National Registry Paramedic Exam: Cardiology, Cardiac Emergencies, and Resuscitation

Objectives
- Describe cardiovascular anatomy and physiology.
- Identify normal and abnormal electrical cardiac rhythms.
- Interpret 12-lead ECGs (electrocardiograms).
- Differentiate, assess, and treat cardiac emergencies. 

In most systems, cardiac-related emergencies make up a significant portion of a paramedic’s call volume, especially when you consider all the ailments that can result from a failing cardiovascular system. Each year, new treatments are added and some are taken away from the repertoire of assessment and treatment possibilities for the patient with a cardiac condition. This guide will focus on all things cardiac, from anatomy to electrophysiology.

1. Cardiovascular Anatomy and Physiology
The human heart is a muscular structure about the size of a fist and consists of 4 separate chambers. It is uniquely designed to pump blood throughout our bodies. The entire heart is encapsulated by the pericardium, a tough fibrous sac that protects the heart from other structures of the chest and contains lubricating fluid to reduce friction generated by the moving heart. There are 3 layers to the muscular walls of the heart.

- The epicardium is the outermost layer of the heart and protects the muscle from friction generated when it beats.
- The myocardium is the actual contractile muscle of the heart. All the myocytes (muscle cells) are able to not only contract and conduct electrical impulses efficiently through them to neighboring myocytes but also generate their own electrical impulse in the absence of a coordinated, propagated impulse that normally occurs and initiates the contraction of the heart.
- The final layer of the heart is the endocardium, which is the layer that lines the inside of the heart and protects muscle tissue from the friction of the blood traveling through it.

The cardiac muscle tissue needs all these levels of protection to function properly because any outside irritation could generate an electrical and mechanical impulse and start a new beat when the heart is not ready to beat.
Despite being surrounded by and, in fact, bathed in blood, the heart derives none of its O2 supply from the blood within its chambers; it has its own vasculature and is entirely supplied by the coronary arteries. Two coronary artery sinuses originate in the root of the aorta and flow along the surface of the heart.

- The right coronary artery (RCA) follows the AV sulcus between the right atrium and the right ventricle, and the branches from the RCA service the right atrium and ventricle and part of the left ventricle and septum. The RCA services the AV node in approximately 85% of the population.
- The left main coronary artery (LMCA) comes off the aorta and travels about 10–25 mm and branches into the left anterior descending (LAD) and the left circumflex (LCx) arteries. These heavily branched arteries deliver blood to the left atrium; the left ventricle’s lateral, posterior, and anterior walls; and most of the septum. The LCx provides most of the blood for the lateral wall and the posterior wall. A branch of the LCx services the AV node in those people whose AV node does not get its blood supply from the RCA.

This extensive network of branches, called collateral circulation, creates multiple routes of flow for oxygenated blood to reach the cells. It develops across time to ensure continuous blood flow to the heart.


Figure: Arterial Supply to the Heart

As with any capillary system, the capillaries empty into venules and eventually veins that go around the heart in a groove called the coronary sulcus. They empty into the coronary sinus before making their way back into the right atrium directly.


Figure: Venous Drainage of the Heart

Blood Flow through Heart and Cardiac Structure
To make a complete circuit from systemic circulation back to systemic circulation, a blood cell must go through the heart twice. The heart is actually 2 pumps within the same organ, with each having 2 distinct purposes. The right side of the heart is responsible for the pulmonary circuit and getting O2 from the lungs, whereas the left side is responsible for the systemic circuit and getting blood to every cell of the body. Each blood cell begins its travel through the heart at the vena cava.


Figure: Bloodflow through the Heart

- The vena cavae are the collecting veins

where all the blood drains as it completes its circuit through the body. They are named according to their relative position to the heart: the superior vena cava drains the head and upper limbs, and the inferior vena cava drains the lower extremities, abdomen, and pelvis. They both empty into the right atrium.
- The right atrium is the initial holding spot for blood and is the site of the sinoatrial (SA) node. (The SA node will be discussed in more detail later when the electrical system is discussed.) The atria contract together under normal circumstances. The right atrium sends our red blood cell through a valve called the tricuspid valve and into the right ventricle.
- The tricuspid valve is composed of 3 leaflets that are designed to prevent the backflow of blood during ventricular contraction into the atrium and make up the physical barrier between the right atrium and right ventricle. During atrial systole, or contraction, the leaflets are pushed open. As the atria relax, the valve leaflets swing shut again. The leaflets of the valve are prevented from inverting, or prolapsing, because they are attached to chordae tendineae. These “heart strings” are attached at the other end to the wall of the right ventricle to specialized muscles called papillary muscles.
- After the right ventricle squeezes out its blood, relaxes, and refills, the motion of relaxing draws in blood from the right atrium down the pressure gradient. When the atria beat, they kick a little extra blood into the ventricles than would otherwise be able to fit. This is called the atrial kick, which has the effect of stretching the ventricles just a fraction more, helping maintain cardiac output. The blood cell being followed is now in a 2nd larger chamber called the right ventricle. This chamber is more muscular than the previous one because it is responsible for moving blood through all the lung capillaries.

Blood Vessels
Blood vessels have basically the same structure, whether in an artery or a vein. Three distinct layers of tissue in the walls of the blood vessel surround the lumen: the tunica adventitia, the tunica media, and the tunica intima. The tunica intima is the innermost layer and provides a smooth surface for blood to slide against. The tunica media is the middle layer, which is thickest in arteries and is composed of smooth muscle. The tunica media is responsible for the dilation and constriction of arteries and veins. The tunica adventitia is the outermost layer and is composed of a fibrous connective tissue that holds the vessels together against the high pulsing pressures.

Tip: To remember the layers, the tunica intima is intimate with blood and the tunica media is the medium layer. Therefore, the tunica adventitia is the outside layer.

The arteries are the most sensitive to nervous system signals because they have the most smooth muscle. Therefore, they are instrumental in regulating blood pressure. Blood pressure is based on the total systemic vascular resistance and the cardiac output. The veins are thinner because much of the pressure produced by the pulse is dissipated in the capillary bed. Some of the fluid that was present on the arteriole side of the capillary got squeezed out and will return to the heart as lymph.


Figure: Structure of Blood Vessels

2. Electrical Conduction System
The heart is special in that it is the only organ to completely generate its own electrical impulse, conduct it completely through the entire muscle, and operate completely free on innervation. Four properties contribute to this unique ability of the heart.

- The myocytes possess automaticity, which is the ability for any cell in the heart to initiate an electrical impulse.
- Excitability refers to a cell’s responsiveness to that electrical impulse simply by being in contact with the cell next to it; this does not happen in skeletal or smooth muscle.
- Conductivity is the ability of each cell to pass along the electrical impulse.

The SA node is the pacemaker of the heart and is an area in the right atrium that normally sets the rate of the heart. However, any area that sets the heart rate is called the pacemaker site. For now, the focus will be on the normal electrical pathways of the heart and what passage of the electrical impulse through these pathways means for both the mechanical action of the heart and the appearance on the electrocardiogram (ECG). To fully understand all of this, a discussion on cellular polarity, depolarization, and repolarization is needed.
When muscle cells are relaxed, an electrical potential is established across the muscle cell membrane. Muscles actively pump out positively charged sodium ions into the intercellular space, which leaves the inside of the cell negatively charged relative to the outside. This establishes an electric gradient across the cell membrane of approximately –90 millivolts (mV), indicating that the inside of the cell is negatively charged. Once this is established, the cell is said to be polarized.

Tip: “Potential” here means difference in electrical charge, which also is known as voltage. It does not mean “possible.” Although, thinking about it, without this potential, muscle contractions would not be possible.

When the cell receives the signal from the nervous system, or in this case the electrical conduction system of the heart, this polarized muscle cell depolarizes. When this happens, the permeability of the muscle cell membrane changes, and Na+ ions rush into the cell along with some calcium ions, effectively reducing the electrical gradient to 0 mV. In muscle cells, a depolarized cell is contracted. Therefore, when it is said that, for example, “the ventricles are depolarized” or “a part of the ECG refers to the depolarization of the ventricles,” this means that the ventricles are contracted or contracting at that time.
Once a cell has depolarized, it cannot do anything more until it has repolarized. Repolarization can begin only when the stimulus to the cell to contract or depolarize is removed. To begin repolarization chemically, the sodium and calcium channels that allowed those ions into the cell during depolarization close, shutting off the flow of these ions into the cell. Meanwhile, the potassium channels simultaneously open, allowing potassium to flow out of the cell, which allows for a rapid reestablishment of the electrical gradient needed for depolarization to occur. However, potassium is not the correct ion that is needed on the outside of the cell. Next, the potassium channels close, and specialized pumps aptly named the sodium-potassium pump in the cellular membrane work to move 3 Na+ ions out of the cell and 2 K+ ions back into the cell. At the end of this process, Na+ ions are back outside the cell, and K+ ions are now back inside the cell where they belong, and the polarity of the cell has been reestablished at –90 mV. The cell is now ready to depolarize once again.
As mentioned earlier but worth repeating, while the cell is depolarized, it cannot respond to any electrical stimulus any more than it already has. This is referred to as the refractory period. In the heart, there is an absolute refractory period and a relative refractory period. During the absolute refractory period, no amount of external stimulus will cause another contraction. During the relative refractory period, cells that have fully repolarized can and will depolarize if the stimulus is strong enough, whereas the others that have not yet completed repolarization will remain unaffected. Stimulus during the relative refractory period can cause electrical rhythm disturbances that could prove to be lethal, such as ventricular fibrillation.
After understanding depolarization and repolarization chemically and what it means for the heart mechanically, it will now be applied to the creation of a normal ECG. When the SA node discharges, the electrical impulse travels down the internodal pathways and pauses briefly at the atrioventricular (AV) node near the AV junction. As the impulse travels through the internodal pathways, the atria are caused to depolarize and contract. On the ECG, this event is represented as the 1st upward deflection or the P wave.


Figure: Cardiac Conduction System

The AV node then “collects” the charge transmitted through the internodal pathways and delays transmitting it for approximately 0.12 seconds, which gives the atria time to empty into the ventricles. This pause is represented on the ECG as the PR interval (PRI). When the AV node discharges, the electrical charge travels through the bundle of His. The bundle subsequently divides into the right and left bundle branches, which travel down the septum and divide further into the Purkinje fibers. The Purkinje fibers divide countless times, and each branch will ultimately innervate only a single cardiac muscle cell. This system is efficient enough to deliver the charge to every cell in the ventricles in about 0.08 seconds, allowing the large ventricles to depolarize and contract simultaneously and uniformly. This event is represented on the ECG as an upright spike called the QRS complex. The final notable part of the ECG is a hump immediately after the QRS complex, which is the repolarization of the ventricles and is referred to as the T wave.


Figure: Normal Pattern of ECG

P wave: atrial depolarization
QRS complex: ventricular depolarization (40–100 msec)

R wave: 1st upward deflection after the P wave
S wave: 1st downward deflection after an R wave
T wave: ventricular repolarization
PR interval: start of the P wave to start of the QRS complex (120–200 msec); mostly due to conduction delay in the AV node
QT interval: start of the QRS complex to the end of the T wave; represents duration of the action potential (see Figure 4-6)
ST segment: ventricles are depolarized during this segment; roughly corresponds to the plateau phase of the action potential
J point: end of the S wave; represents isoelectric point

Note: Height of waves is directly related to (a) mass of tissue, (b) rate of change in potential, and (c) orientation of the lead to the direction of current flow.

Nervous System Control of Heart
The heart is under complete control of the autonomic nervous system, meaning that its activities are completely regulated outside of conscious direction. The autonomic nervous system has 2 branches that are always working in opposition to each other: the sympathetic and parasympathetic nervous systems. The parasympathetic nervous system exerts its control on the heart through the vagus nerve. The parasympathetic nervous system has a slowing effect on the heart and has as its neurotransmitter acetylcholine, which acts directly on the SA node. Parasympathetic stimulation unopposed by sympathetic nervous input may result in profound bradycardia. The sympathetic nervous system is responsible for speeding up the heart and increasing its contractility, conduction, and thus the cardiac output.

Cardiac Monitoring
One of the most common procedures a paramedic will perform is placing a patient on the cardiac monitor. This is done alike for patients with and without a cardiac condition. Although it is rather simple to accomplish, accuracy is important to be able to get the best views of the heart that cardiac monitoring can afford, especially in cases of heart attack. Cardiac monitoring will allow you to observe the electrical activity of the heart from a variety of different views and allow you to determine the rhythm that the patient’s heart is displaying. It also can allow you to figure out not only if but also where a patient is having a heart attack or other ischemic problem. This section explains everything about cardiac monitoring, including how to apply it to your patient and what the paper can tell you about your patient’s rhythm. The section concludes by delving even deeper into the normal ECG, expounding on what has been learned already.
Every patient who requires advanced care beyond the scope of the EMT–Basic will need to be placed on a cardiac monitor for continuous monitoring. This is accomplished through any 1 of the 3 standard limb leads—lead I, lead II, and lead III—but most commonly lead II. Capturing the limb leads requires the placement of 4 electrodes on the patient, 1 on each limb, hence the name. The leads are color coded regardless of the manufacturer and can be placed on the patient in any order; however, they need to be placed in the following specific locations:

- The white lead is placed on the right arm or shoulder.- The red lead is placed on the left hip or anywhere on the lateral surface of the left leg.
- The green lead is placed on the right hip or anywhere on the lateral surface of the right leg.

The leads are placed in these locations to establish Einthoven’s triangle. Similar to a battery that has positive and negative ends, or poles, each of the standard limb leads has 1 of the electrodes designated either positive or negative, which means that leads I, II, and III are the bipolar leads. The green lead is always the ground lead, which means that it helps minimize artifact generated from skeletal muscle activity or patient motion of any kind.


Figure: Leads I, II, III (left) and augmented voltage leads (right).

Using just these 3 electrodes, the cardiac monitor is able to generate 3 alternate views of the heart, called the augmented voltage leads. These leads are unipolar leads in that only 1 of the electrodes on the patient has a true polarity. The 2nd

pole is an average of the 2 remaining electrodes. The augmented voltage leads are designated by the letters aV followed by the 1st letter of the electrode that is the positive pole. For example, the lead that has as its positive pole the red lead, near the left foot, is designated as lead aVF; the lead that has as its positive pole the white lead, near the right arm, is designated as lead aVR; finally, the lead that has as its positive pole the black electrode, near the left arm, is designated lead aVL.

Polarity of Electrodes
 

The precordial leads are 6 electrodes that are placed on the anterior and lateral left chest, basically circling around the heart. These 6 leads, combined with the 6 limb leads, comprise the 12-lead ECG, which is the gold standard in cardiology for determining cardiac events. These leads also are referred to as the V leads because they are all designated with a capital V followed by a subscript number, V1 to V6. The precordial leads are all unipolar leads that are positive at the point of electrode placement, and the negative terminal is at a calculated point of reference, which is called Wilson’s central terminal. The location and order of placement of these electrodes is specific:

- V1: 4th intercostal space, immediately to the right of the sternum
- V2: 4th intercostal space, immediately to the left of the sternum
- V4: 5th intercostal space, midclavicular line- V5: 5th intercostal space, anterior axillary line (directly between V

Figure: Precordial Lead Placement

All of the electrodes pick up small electrical currents traveling through the body, and the monitor converts these signals to the image on the screen and the rhythm strip on the paper. The flat part of the ECG tracing is known as the isoelectric line, and every electrical activity of the heart, whether depolarization or repolarization, can be seen as a deflection from the isoelectric baseline. If the overall direction of the electrical impulse is toward the positive electrode, it will be seen as a positive deflection above the isoelectric line. If the overall direction of the electrical impulse is away from the positive electrode, it will be seen as a negative deflection below the isoelectric line. When the overall electrical impulse is traveling perpendicular to the lead, there may be no discernible deflection at all in that lead, whereas it can be found in others. Finally, there could be a portion of time where the impulse is traveling toward the positive electrode followed immediately by a period of time where it is traveling away or vice versa. In this instance, the deflection is described as biphasic where part of it is above the baseline and another part is below the baseline.

ECG Paper and Appropriate Interval Lengths
ECG paper is designed to help you determine the rate and regularity of the heart’s rhythm. The paper moves at 25 mm per second under normal use, which means that horizontally, the paper represents time. The deflections generated by the heart’s electrical activity are vertical, which represent voltage, specifically millivolts. Each small box is 1 mm square. Two large boxes represent 1 mV; although this value is adjustable, it defaults to the 1 mV value. The small and large boxes are each necessary in discerning the time component to the ECG. Each large box has 5 small boxes. Each large box represents 0.20 second; therefore each small box is 0.04 second. It takes 5 large boxes to make up 1 second, and 15 large boxes to make up 3 seconds. At the top of the paper, hash marks represent 3-second intervals, which can help you count the heart rate. Each component to the ECG discussed previously will print out against this paper and, therefore, have normal interval ranges of which the paramedic needs to be aware in determining the rhythm.


Figure: ECG Paper and Normal ECG

ECG Waves and Intervals

Calculating Heart Rate Using Rhythm Strip

- 6-Second Strip. For this method, simply count the number of QRS complexes that appear between the 1st and 3rd of 3 sequential hash marks on the top of the strip (remember, from 1 hash mark to the next is 3 seconds) and then multiply by 10. (This is the only method of the 3 methods given that should be used for irregular rhythms.)
- Sequence Method. This method is a quick way of estimating the rate of a regular rhythm. It is not particularly helpful for irregular rhythms. Find a QRS complex that is on a heavy line—one of the lines that outlines the large boxes. Then recite the following numbers on each successive heavy line until the next QRS complex is reached: 300, 150, 100, 75, 60, 50. Chunking the numbers together in the following way is helpful to remember this because it becomes almost rhythmic, so say to yourself, “300, 150, 100,. . . 75, 60, 50.” If the QRS complex falls between 2 heavy lines, estimate the value, but remember that the lighter lines represent logarithmic values. For example, the light lines between 100 and 75 are not 95, 90, 85, and 80 but really 94, 88, 83 and 79. It is not necessary, nor is it realistically possible, to memorize every light line.
- 1500 Method. This method is highly accurate; however, it should be used only for regular rhythms, particularly those with rates in excess of 150 beats per minute. Start by counting the number of small boxes between 2 sequential QRS complexes; this is known as the R-R interval. Then divide that number into 1500. For example, a certain regular rhythm has 8 small boxes between QRS complexes. Doing the math, 1500/8 gives a heart rate of about 187 beats per minute.

3. Dysrhythmias
This section addresses the likely rhythms that a patient may generate. Each rhythm is described in the same manner, which will coincide with the process described later of how to differentiate between each rhythm. A picture of each rhythm strip is included to illustrate its typical appearance. The treatment plan for a patient exhibiting the rhythm, whose chief complaint can be attributed to being in that rhythm, then follows.

Sinus and Atrial Rhythms
Sinus and atrial rhythms are generated either within the SA node or from the automaticity of the atrial muscle tissue.

Sinus Bradycardia

Origination Point: SA Node	Differential Causes
P Wave	- Athletes (not clinically significant) - Increased vagal tone - Myocardial infarction (MI) - Increased ICP - Hypothermia - Beta-blocker and calcium channel blocker overdose - Hypoxemia - Sick sinus syndrome - Electrolyte imbalances - Hypothyroidism - Idiopathic
Shape	Upright
P rate	<60
P wave for every QRS?	Yes
QRS complex for every P wave?	Yes
PRI
Duration	<0.20 second
QRS Complex
Shape	Normal
Duration	0.08–0.12 second
R-R Interval
Regularity	Regular
Rate	<60
Treatment Options. The treatment for sinus bradycardia is largely dependent on the hemodynamic stability of the patient and the root cause for the bradycardia. If the patient is stable and has not displayed any change in mentation while in this rhythm, aggressive treatment likely is not indicated. - For situations thought to be related to increased vagal tone or parasympathetic stimulation, 0.5–1 mg atropine is the first-line treatment of choice. If this fails and the patient remains symptomatic, transcutaneous pacing (TCP) should be considered and initiated. The TCP procedure is discussed later in this guide. - In cases of acute myocardial infarction (AMI), increasing the rate may have a negative effect on the condition of the patient because of the concurrent increase in myocardial O2 demand. In this case, increasing blood pressure without appreciably increasing the workload of the heart is desirable. This can be accomplished with fluid. - For presumed hypoxemia, administer O2. This is particularly important for pediatric patients. - An overdose of any of a variety of drugs can cause symptomatic bradycardia. An effort should be made to determine the drug and administer its antidote; in cases of opiate or calcium channel blocker overdose, administer naloxone or calcium, respectively. If unable to determine the specific drug, treat the patient symptomatically and support the ABCs.

Sinus Tachycardia

Sinus Arrhythmia

Sinus Arrest and Sick Sinus Syndrome

Wandering Atrial Pacemaker

Multifocal Atrial Tachycardia

Atrial Flutter

Atrial Fibrillation

Supraventricular Tachycardia

Junctional Rhythms and AV Blocks
When the SA node and subsequently the atria fail to maintain the pacemaking duties for the heart, the junction, or the AV node, will take over. These are referred to as junctional rhythms. These 3 rhythms are closely related, varying only in rate. In distinguishing these rhythms apart from each other, pay particular attention to the rate.
AV blocks vary by how well the atria successfully communicate with the AV node and therefore the ventricles. For example, in 1st-degree block, there is still a 1:1 ratio of P:QRS, but the PRI is lengthened. In a 2nd-degree Mobitz type I block, the PRI lengthens until 1 entire QRS complex is omitted; then the process begins anew. In a Mobitz type II block, there is a regular ratio of P:QRS, but it is not 1:1. It can be 2:1, 3:1, or even 3:2; it is similar to banging on a door multiple times until it opens. Finally, in 3rd-degree heart block, there is no communication whatsoever between the SA node and the ventricles, and, therefore, no relationship of P waves to QRS complexes; they each just do their own thing at their own rate.

Junctional

Accelerated Junctional

Junctional Tachycardia

First-Degree AV Block

Second-Degree AV Block, Mobitz Type I, Wenckebach

Second-Degree AV Block, Mobitz Type II

Third-Degree AV Block

4. Ventricular Rhythms 
Ventricular rhythms are those that originate in the ventricles.

Idioventricular Rhythm

Accelerated Idioventricular

Ventricular Tachycardia

Ventricular Fibrillation

Polymorphic Ventricular Tachycardia (Torsades de Pointes)

Asystole

Artificial Pacing
In situations when medications can no longer increase the heart rate or maintain adequate blood pressure, a patient will receive an implanted artificial pacemaker, which is designed to send small electrical impulses to the heart to generate a beat. The pacemaker consists of a small case that houses the battery and generator of the electrical pulse and 1 or 2 wires that connect directly into the myocardium. The pulse generator is about the size of half a deck of cards and is generally housed in the soft tissue of the anterior left shoulder. Two common types are used: the ventricular pacemaker and the AV sequential pacemaker.
The ventricular pacemaker has 1 wire leading from it to the heart and is attached somewhere in the ventricle, usually near the apex of the internal right ventricle. Ventricular pacing produces a rhythm similar to what is shown; however, the exact tracing will vary based on where in the ventricle it is attached. The vertical spike seen just before the wide and bizarre QRS complex is the small electrical current the pacemaker delivers to the myocardium. It is not always visible, and it is not visible in every lead. The spike will likely be upright, but it may be inverted or biphasic.


Figure: Ventricular Artificial Pacemaker Trace

The 2nd type of pacemaker is the AV sequential pacemaker. This pacer has a 2nd lead coming from it, in addition to the lead attached to the internal right ventricle. This lead follows the same pathway but attaches to the right atrium. The 2 leads fire sequentially, first the atrial lead followed a short time later by the ventricular lead. This can possibly result in 2 pacer spikes visible on the ECG; the first just prior to what looks like a P wave, and a 2nd following the P wave ahead of the wide QRS complex.


Figure: AV Sequential Artificial Pacemaker Trace

Ectopic Rhythm Disturbances
Occasionally, within an otherwise normal heart rhythm similar to those discussed previously, a beat occurs earlier than it would have been predicted to happen. This premature beat comes from a place other than the baseline pacemaker and therefore looks different from the other complexes in the strip. If this beat originates somewhere in the atria, it is called a premature atrial contraction (PAC). If it comes from the junction, it is called a premature junctional contraction (PJC). Finally, if it comes from somewhere within the ventricles, it is called a premature ventricular contraction (PVC). PACs and PJCs can be caused by various different drugs, including caffeine, nicotine, and cocaine, or they could be caused by ischemia or an underlying heart problem that has not shown itself in any other way. They are mostly of little cause for concern beyond documenting their presence and seldom require treatment in the field. PVCs are somewhat more complicated.


Figure: Premature Atrial Contraction


Figure: Premature Junctional Contraction

PVCs can be caused by the same issues as PACs and PJCs; however, more often, they are caused by ischemia within the ventricular tissue. This ischemia causes the tissue to become irritable and spontaneously depolarize, generating a beat within the entire heart that appears on an ECG as a wide and bizarre complex among the baseline rhythm. PVCs may be unifocal, be multifocal, or occur in couplets or runs. Unifocal PVCs originate from 1 location or focus in the ventricles and have the same morphology or shape on the ECG. Multifocal PVCs appear on an ECG as premature complexes that originate in the ventricles but have different shapes. The different shapes indicate that the complexes are coming from 2 or more locations within the ventricles. When 2 premature ventricular complexes occur back to back without an intrinsic, or baseline, beat between them, they are called couplets. Three or more premature ventricular complexes in a row constitute a run of VT and are the most ominous sign of all.


Figure: Unifocal Premature Ventricular Contractions

PVCs also may become frequent enough that their presence creates recognizable patterns with the normal (intrinsic) beats. When PVCs alternate with normal beats in a 1:1 ratio, the pattern is called bigeminy. If the PVC-to-normal beat ratio drops to 1:2, the rhythm is referred to as trigeminy.


Figure: Multifocal PVCs in a Bigeminy Pattern


Figure: Multifocal PVCs in a Trigeminy Pattern

12-Lead ECG Interpretation
The 12-lead ECG is the defining method for rhythm interpretation and a determination of what is happening within the heart. It provides a snapshot of the patient’s heart rhythm at the time it was taken and combines 12 different views on 1 page. The leads are always arranged in the same way. Each lead represents a particular area of the heart. Leads I, aVL, V5, and V6 look at the left lateral wall of the heart. Leads II, III, and aVF look at the inferior wall. Leads V1 and V2 represent the junction and the ventricular septum. Finally, leads V3 and V4 look at the anterior wall of the heart.


Figure: Colors indicate which leads represent the same general area of the heart.

Approaching the ECG in a systematic way is necessary to not miss anything on it. This is true whether attempting to preliminarily determine the rhythm from a running strip or a 12-lead ECG. The following are the steps to help you determine the rhythm and the questions you should ask yourself systematically until a rhythm name is reached to a reasonable degree of confidence.

- P Waves. Are they upright and smooth? Are they the same shape? Is there a P wave for every QRS?
- PR Interval. Is it <0.20 second (1 large box)? Is it the same duration in each sequential cycle?
- QRS Complex. Is it <0.12 second in width? Is there a QRS for every P wave?
The following is specific to 12-lead interpretation, not to running strips.

Axis Determination
Every muscle cell, or myocyte, emits a small amount of electrical current as it depolarizes. This electrical current has a defined direction or travel associated with it. Any value that has both magnitude and direction associated with it is called a vector. If you were able to add together all these tiny vectors, which means taking into consideration both the magnitude and direction of each, the result would be called the resultant vector. In the heart, this vector has a special name called the axis, and in the normal heart, this axis is down and to the patient’s left. If there is damage to the heart, or if 1 side of the heart were much larger than normal, this axis can shift from the normal predicted area. Paramedics can determine if there has been what is called an axis deviation by looking at lead I and lead aVF and evaluating the orientation of the QRS complex in each of those 2 leads.


Table: Determining Axis from QRS Direction

Conduction Disturbances
After the electrical impulse leaves the bundle of His, it divides into the right and left bundle branches. Because of damage to the area of the septum that contains the bundles, whether ischemia or infarction, the electrical impulse may travel noticeably slower through 1 bundle versus the other. This is referred to as a bundle branch block and can be seen by evaluating the QRS complex in lead V1.

Right Bundle Branch Block
Characterized by an RSRʹ appearance, often referred to as rabbit ears, and a widening of the QRS beyond 0.12 second found in lead V1. In this appearance, there is first a positive deflection, which represents the first R followed by a downward deflection, which constitutes the S. In normal ECGs, this is where it ends; however, in a right bundle branch block (RBBB), there is a 2nd, larger positive deflection that is labeled as Rʹ (said “R-Prime”). The S wave does not have to make it back down to or below the baseline to be considered an S wave, nor does 1 of the R waves need to be larger than the other to be identified as an RSRʹ pattern; the QRS could simply appear notched and it qualifies. This can be confirmed by observing terminal S waves in the lateral wall leads, leads I, aVF and V6.

Left Bundle Branch Block
Left bundle branch block (LBBB) can be seen when there is a widening of the QRS beyond 0.12 second and a terminal S wave in lead V1. Although there is normally a terminal S wave in lead V1, the key here is a widened complex overall. A LBBB can be further confirmed by observing terminal R waves in the lateral wall leads: leads I, aVL, V5, and V6. 
The 12-lead also can identify enlarged chambers of the heart. The following describes the hallmark signs to look for on an ECG tracing to identify enlargement of 1 or more of the heart’s chambers.
Also called right atrial dilation, which results from chronic pulmonary disorders, it can be seen as a P wave >2.5 mm in height in lead II and/or >1.5 mm in lead V1.
Though it can be a normal finding in an athletic heart, it is more commonly caused by systemic hypertension or mitral or aortic valve stenosis. Stenosis is a fancy word that means abnormal narrowing of an opening or passageway of the body.
Left atrial enlargement is illustrated on an ECG with the following:

- Notched P wave
- Notches in P wave >0.04 second (1 small box) apart
- P wave in lead V1 inverted (negative deflection)
- P wave duration >0.12 second in duration
- Right ventricular hypertrophy (RVH)

Hypertrophy refers to the enlargement of any organ or tissue as a result of the enlargement of its own cells. RVH is characterized on the ECG when finding a large R wave in V1 and/or an R wave in lead aVR taller than 5 mm or 0.5 mV.
Most commonly caused by systemic hypertension and high afterload, left ventricular hypertrophy (LVH) is an enlargement of the left ventricle. It is not possible to completely diagnose LVH exclusively with the ECG. The ECG can confirm only that the patient’s heart meets the voltage criteria for LVH. Another test, an echocardiogram, is needed to confirm the diagnosis. Here is what is seen on an ECG when the patient meets the voltage criteria for LVH.

- Deepest S wave between leads V1 and V2 measured in millimeters from baseline to peak, plus
- Tallest R wave between leads V5 and V6 measured in millimeters from baseline to peak is >35 mm, and/or
- R wave in lead aVL >1.1 mV (11 mm when 1 mV is represented by 2 large boxes)

ST and T Wave Changes
The goal of the 12-lead ECG is to identify and localize the location of ischemia and injury or infarct. This can be accomplished through systematic evaluation of the ST segment and T wave in each and every lead on the ECG. Although it is true that identifying the location or severity of the ischemia and active infarction will not change the treatment the paramedic provides overall, it could shorten the time the patient has to wait to receive definitive treatment. Any amount of time saved when a patient is actively infarcting will serve to minimize the long-term damage done to the heart.
So, the paramedic plays a key role in not only treating the out-of-hospital patient with acute coronary syndrome (ACS) but also impacts the length of stay of the patient in the hospital and has a direct impact on his or her quality of life after discharge. With that in mind, it is crucial that the paramedic minimize time spent on scene working to obtain a 12-lead ECG, or initiating treatment in the field, and perform as much treatment as possible, including the 12-lead ECG, en route to the hospital. Accomplishing all this time-sensitive work as efficiently as possible will come with time, rest assured, but it is all in concert with the American Heart Association goals of reducing “door to balloon” time, or the amount of time the patient spends between arrival time at the hospital until the balloon of the angioplasty is inflated to open up blocked arteries.
Ischemia and infarct can be seen on the ECG in most patients. If it is to be seen on the ECG, it will show up as changes in the Q wave, J point and ST segment, and T wave. Let’s look at each change as the patient progresses from normal to ischemia to evolving injury (or active infarction) to completed infarction or cellular death.

Q Waves
The first negative deflection after the P wave is the Q wave and is considered pathologic (abnormal) if it is wider than 1 small box or 0.40 second. Q waves also must be deeper than 1/3 the height of the succeeding R wave in lead II. The presence of a Q wave indicates an old MI that has completed evolving, typically after several hours or days.

ST Segment and J Point
The ST segment and the J point are the areas to pay the most attention to in a patient with suspected ACS. Because the J point represents the start of the ST segment, referring to the ST segment is inclusive of the J point. Therefore, we will refer to this area exclusively as the ST segment. Under normal circumstances, the ST segment is isoelectric; however, during a cardiac event, the ST segment can fall below or elevate above the isoelectric line. As an area of the heart begins to get ischemic, or lack nutrients and O2, the ST segment will start to dip below the baseline, referred to as ST depression. As this ischemia progresses to injury, and the cells that were ischemic now begin to die, that is to say an infarct begins to evolve, the ST segment quickly reverses course and rises above the isoelectric baseline.
When the ST segment rises >1 mm above the isoelectric line, it is considered pathologic for an MI. As the infarct worsens in the area, the ST segment will continue to elevate, sometimes nearing the point of the R wave, some 7–10 mm above the baseline. QRS complexes with their associated ST segments elevated this high are said to look like the silhouette of a fire helmet viewed from the side or the outline of a tombstone. During the time that the ST segment is elevated, indicating the ongoing evolution of an MI, the patient is said to be having an ST elevation MI (STEMI). It is important to know that only approximately 50% of patients with active injury and infarction will have a STEMI. The other 50% of people will have what is referred to as a non-STEMI because their ECGs are normal or have nondiagnostic changes on the ECG. More on diagnostic versus nondiagnostic a little later in the text.
Once the injury to the tissue has reached its maximum, through either reperfusion of the area or full thickness MI, the ST segment will return to baseline, leaving a Q wave as a marker for what happened prior.

T Wave
The T wave also is an area of dynamic change in the ECG during ischemia, injury, and infarction. Normally, the T wave is upright and smooth, however, as ischemia begins in an area of the heart, the T wave may present inverted in corresponding leads.

Although T wave inversion is a classic sign of ischemia, hyperacute and broad-based upright T waves also could indicate ischemia. Hyperacute T waves are T waves that are larger than normal, exceeding half the height of the QRS in that lead. These T waves often also are seen as broad based because there is initially less of a discernible ST segment. Here, the T wave almost seems to begin at the J point.
As with the ST segment, situations with the T wave may mimic ischemic conditions. Although hyperacute T waves could indicate ischemia, tall, pointed, or sharply peaked T waves in all leads could indicate hyperkalemia. If hyperkalemia is suspected, P waves will flatten, and in patients who are severely hyperkalemic, the QRS will widen. The opposite of hyperkalemia, hypokalemia results in flattened T waves and often a 2nd wave called a U wave after the T wave.
ST segment and T wave changes may be diagnostic or nondiagnostic, as mentioned earlier. These changes, (for example, ST elevation), are considered diagnostic of an AMI when it appears in 2 or more contiguous leads. By extension, this also means that finding ST elevation isolated in 1 lead on the ECG is said to be a nondiagnostic finding. In leads that represent areas of the heart that are serviced by the same artery, it is possible to have ST changes in >1 area. For example, there may be an occlusion in the LAD that causes ST changes in both the septal and anterior leads. The following lists them according to the area of the heart to which they correspond:

- Inferior wall: leads II, III, and aVF
- Septum: leads V1 and V2
- Anterior wall: leads V3 and V4
- Lateral wall: leads V5, V6, I, and aVL

Reciprocal Leads
Finding ST elevation on a 12-lead ECG in the contiguous leads often is enough to isolate and diagnose an evolving AMI. However, 2 special cases of AMI result in reciprocal changes in leads opposite the area of the heart in which the AMI is occurring. When ST elevation is in the lateral leads—V5, V6, I, and aVL—ST depression often can be seen in the inferior leads II, III, and aVF. The opposite also is true; if ST elevation is in the inferior leads, ST depression often can be seen in 2 or more of the lateral leads. Reciprocal changes are not required for a diagnosis of AMI to be made when ST elevation is seen in inferior or lateral leads. However, when this does happen, it is something that should be documented.
Unfortunately, it is not possible for paramedics to evaluate old ECGs to compare with the current ECG to look for new onset changes. Essentially, until proven otherwise, observation of any deviations from what is considered normal on an ECG should be believed to be acute and treated as such.

5. Cardiac Emergencies: Pathophysiology, Assessment, and Treatment
So far, we have been talking at length about 1 tool in our assessment arsenal for patients who are suspected of having a cardiac event: the ECG. We have not in any meaningful way covered the patient interrogation and physical examination of the cardiac patient. Every assessment as mentioned previously needs to address ensuring scene safety first and foremost, followed by evaluation and rapid treatment of the ABCs. During the evaluation of the history of present illness, use the OPQRST and SAMPLE mnemonics to guide questioning. In the following sections, we will cover questions that should be asked that are specific to the cause of the problem that are not obviously addressed elsewhere in SAMPLE or OPQRST. We will then go into cardiovascular emergencies you will likely encounter in the field, including additional questions for those patient populations. Each cardiovascular emergency section also will cover the treatments recommended for that ailment.

Acute Coronary Syndrome

Pathophysiology
ACS refers to any of a variety of symptoms associated with coronary artery disease (CAD) that results in symptoms of cardiac ischemia, including Prinzmetal angina, stable and unstable angina pectoris, and AMI. Symptoms of ACS can include any of the following: chest pain, pressure, tightness, or general discomfort; shortness of breath; nausea with or without vomiting; dizziness; weakness; or syncope. Patients also may become diaphoretic and pale while experiencing the pain. Each of these has a different pathophysiology; however, the prehospital management for each is highly similar. Paramedics are not required to differentiate between the ultimate cause for the symptoms or diagnose the patient as having 1 cause of ACS versus another.
Coronary artery spasm is the principal cause of Prinzmetal angina. It causes a sudden onset of chest pain or pressure and often occurs while at rest, usually during sleep. It occurs in a younger population than would be expected to be in the advanced stages of CAD from atherosclerotic plaque buildup. This also is closely associated with cocaine use or smoking. The spasming coronary artery interrupts blood flow to the myocardium, resulting in severe pain.
Stable and unstable anginas differ in their predictability. Stable angina is highly predictable and typically occurs after exertion of some kind. It is caused by advanced CAD and occurs during exercise because of the increased workload placed on the heart at that time. The narrowing of the coronary arteries limits the amount of blood and, therefore, O2 that can get to areas of the heart, resulting in ischemia. The level of exercise that will cause a bout of chest pain from stable angina does not have to be much; it can simply be walking up a flight of stairs. The amount of exercise varies from patient to patient but is predictable, nonetheless.
Unstable angina is far more serious because it can occur at any time and without warning. Unstable angina indicates a higher degree of obstruction to at least 1 of the coronary arteries. It also is unpredictable in duration, degree of pain felt, and frequency of occurrences. With unstable angina, exercise and stress are not required to precipitate an event.
The ACS of greatest concern to the paramedic however is the AMI or heart attack. This occurs when there is a blockage to coronary blood flow for a long enough period of time that death to the myocardium occurs. This blockage can have several causes.

- Thrombus. A clot can form in the already narrowed artery, preventing blood flow to areas beyond.
- Embolus. A clot formed elsewhere in the body can travel to the coronary artery.
- Spasm. Similar to Prinzmetal angina but for a much longer duration than that typically associated with Prinzmetal angina, a spasm could be severe enough and of long enough duration to cause permanent damage to the heart muscle.

The location, size, and severity of an MI depend on the location of the blockage, as we have seen in the 12-lead discussion. If the full thickness of the cardiac muscle is involved in the infarction, it is called a transmural MI; if the infarction is affecting only the inner layers of muscle, it is called a subendocardial MI. The area surrounding the infarcting area will be ischemic yet still viable. This area can become irritable and therefore the potential source of dysrhythmias. All this information should be thought of as “nice to have” rather than “need to have” because knowing any of it will not change the prehospital management for the most part and should not be evaluated if it means delaying treatment or transport to the nearest appropriate facility.

Assessment of ACS
No patient with ACS will have exactly the same complaints as others with ACS nor will every patient have a single complaint in common. That said, there is a basket of symptoms and examination findings that tend to go hand in hand for patients experiencing ACS. To make sure we approach each of these cases systematically, we will fill in the blanks for SAMPLE and OPQRST with questions and answers, followed with pertinent head-to-toe physical examination findings.
Symptoms. Chest pain or discomfort and shortness of breath are common complaints associated with ACS. In fact, for every patient who complains of chest pain or discomfort, ask him or her about shortness of breath, and vice versa. Nausea, with or without vomiting also may occur, so be prepared to manage this potential complication. Some patients will complain of dizziness or syncope if cardiac output is impaired as a result of the syndrome.
It is worth noting that up to 25% of people actively experiencing an MI or other ACS do not experience chest pain. This is particularly common among women, the elderly, patients with a heart transplant, and patients with diabetes, so be alert to other subtle, seemingly unrelated complaints and be aware of general or nonspecific complaints. Seemingly unrelated complaints could be upper abdominal (epigastric) pain, back pain, or shoulder pain without identifiable trauma. General or nonspecific complaints could include general malaise, the global feeling of being run down or ill. When an elderly female patient with a history of diabetes complains of “just not feeling well,” this may be the subtle, atypical presentation of a heart attack.
Allergies. These are patient specific. Because aspirin and morphine sulfate are an important part of prehospital ACS treatment, make sure to ask specifically about these.
Medications. These are important to evaluate, and the patient’s list of medications should be gathered and taken to the hospital with the patient. Common medications for the patient with CAD will include antihypertensives, statins for cholesterol, and calcium channel blockers for heart rhythm. Here, also evaluate if the patient is compliant with his or her medication regimen. Because the administration of NTG is the hallmark treatment for ACS, be sure to inquire about medications commonly prescribed for erectile dysfunction and primary pulmonary hypertension, including sildenafil, tadalafil, and vardenafil.
Past Medical History. Patients may have a history of a previous heart attack or cardiac-related chest pain, so they may be able to state whether their current situation resembles in any way that of previous episodes. Note all of their history. Also, note if they have any history that could compromise their feeling of chest pain, such as open heart surgeries, especially valve replacements or heart transplants.
Last Oral Intake. Although mostly important to know what may be coming back up if the patient vomits, knowing this could help determine what caused this new problem. For example, heart attacks often occur after a large meal, particularly a meal high in sodium, because the heart will have to work harder to get blood to the gut for digestion. In addition, the systemic parasympathetic stimulation could have a vasoconstrictive effect on the coronary arteries, enhancing the chances of a blockage to occur.
Events Prior. This leads the assessment nicely into OPQRST. Evaluation of what the patient was doing at the onset of the complaint can help differentiate between stable and unstable angina but not necessarily between angina and an AMI.
Onset. What were you doing when this started? This is of particular concern if the pain started while at rest or while sleeping.
Provocation/Palliation. Does anything make this feeling better or worse? Have you done anything to make it better, such as take a medication or rest? Did the pain start suddenly or come on gradually over time? Patients experiencing Prinzmetal, stable, or unstable angina may be able to obtain full relief from NTG administration, either on their own or from the paramedics. For those suffering an AMI, NTG may not provide any relief. Because the AMI is not, in most cases, caused by spasms or constriction of the vessels and is more likely the result of a clot, NTG is not able to remove or break up the clot. If they are previous angina sufferers, they may be able to explain that the feeling would normally be able to be made better with NTG, but this time it is not.
Quality. How would you describe the pain? Although open-ended questions should be used whenever possible, a patient may need some guidance with this question. Offering multiple options can help the patient select the best description or help the patient find his or her own description. If you were trying to make me feel the same pain, what would you do to me to give me that same feeling? ACS pain often is described as a pressure, tightness, or a squeezing sensation and less commonly as a stabbing or tearing pain. Patients also may describe it as someone or something is sitting on their chest.
Radiation. Can you show me where the pain is? Does the pain you are having go anywhere? Does it go to the shoulder? Back? Abdomen? Neck or jaw? ACS pain frequently radiates to nearby structures, such as the left shoulder, neck, jaw, back, and abdomen. A patient who indicates radiation of pain should be treated as if he or she has a cardiac problem until proven otherwise.
Severity. On a scale of 1–10, with 10 being the worst pain you have ever had and 1 being very minor or no pain, what number would you give this feeling? The first time the patient answers this question establishes a baseline for tracking changes in pain as treatments are administered because what is a 10 to a person may be only a 4 for another. A move from an initial answer of 8 to a reassessed answer after some treatment has been given of 6 denotes a potential improvement in patient condition. Serial evaluations of this question help the paramedic decide what is working and perhaps what is not.
Time. When did this begin? Is it constant or intermittent? ACS pain, specifically pain related to an AMI, often will be constant and increasing as the ischemic or infarcting area broadens. If the pain is intermittent and the patient gets relief from NTG, it is likely it is unstable angina or something not cardiac related.
Physical Examination. The patient may present a variety of physical examination findings, but the following are the most common and concerning. The patient may be pale and diaphoretic. Either of these by themselves is cause for concern; both together likely indicates a serious emergency.
Vital Signs. Monitoring the patient’s vital signs is paramount as they may change without warning if the condition worsens. The pulse rate could be fast, slow, or normal, and the blood pressure could be high, low, or normal depending on what part of the heart is affected.

Treatment of ACS
The patient with ACS is 1 of the most critical and time-sensitive patients a paramedic will encounter. A lot of things can and should be done for the patient before arrival at the emergency department; however, none of it should cause a delay in the arrival to the hospital. The following are the treatments that should be attempted and considered for all patients with ACS.
Ensure that the patient is in a place of emotional and physical rest. The best thing a paramedic can do for a patient experiencing ACS would be to keep him or her calm and mitigate as much anxiety as possible. This will reduce myocardial O2 demand to a reasonable extent and essentially help the patient help himself or herself.
Monitoring ECG and Obtaining 12-Lead. These are essential to determine the rhythm of the patient and identify the existence of ischemia or infarct. Whenever possible, the 12-lead should be obtained prior to the administration of any medications because they may change the overall baseline rhythm. The prehospital 12-lead has effectively lowered door-to-balloon times for patients experiencing a heart attack. Some systems have even implemented a process where the 12-lead can be continuously transmitted to the hospital receiving the patient so that the emergency physicians and cardiac catheterization team can remain up-to-date on the incoming patient and offer real-time treatment suggestions, should they become applicable.
Oxygen. This formerly was given in high quantities to every patient with a complaint of chest pain; however, in recent years, research has shown that unless a patient is hypoxic with a reliable pulse oximetry reading <94%, supplemental O2 can actually worsen a patient’s prognosis. Because of the prevalence of reperfusion therapies, where the obstruction to the coronary artery is removed and fresh oxygenated blood is able to get to the previously ischemic area of the heart, high levels of O2 cause reperfusion arrhythmias, occasionally leading to sudden cardiac arrest. Only administer O2 enough to maintain a pulse oximetry reading at or >95%.
Aspirin. A patient with chest pain of a cardiac origin or symptoms thought to indicate a cardiac problem should be given 162–324 mg chewable baby aspirin as soon as possible. This will help the patient by preventing further platelet aggregation in any clots. Ensure that the patient does not have any history of gastrointestinal bleeding or aspirin allergy before administration. If the patient has taken aspirin within an hour of calling the ambulance it is acceptable to avoid repeating the dosage.
Initiation of Intravenous Access. This is largely preventive in the event that if the patient’s condition deteriorates, access has already been established. In addition, if the patient’s blood pressure drops after the administration of NTG, the paramedic is ready to quickly administer fluids. Although not necessarily required to happen before NTG is given, it is strongly recommended in case of an adverse event.
Nitroglycerine. In the case of ACS, 0.4 mg NTG is given sublingually as a spray or a tablet. NTG is a potent smooth muscle relaxant that dilates the coronary arteries with the hope of getting more O2 to the ischemic areas of the heart. It also reduces myocardial preload because it dilates the venous side of the vasculature. NTG can be repeated every 3–5 minutes up to a total of 3 doses as long as the patient still has pain and the SBP remains >100. The patient should be advised not to chew or swallow the medication and that it may cause side effects of a burning sensation under the tongue and a headache. NTG should not be administered if the patient has taken any erectile dysfunction medications in the past 24–36 hours. NTG should be withheld in patients who are having an MI that affects the right ventricle. Decreases in preload resulting from NTG administration can be catastrophic if given to a patient with ischemia or infarct extending to the right ventricle. Right-sided involvement is a concern only in patients whose 12-lead ECG shows an inferior MI (ST elevation in leads II, III, and aVF). To assess this crucial piece of information, whenever the 12-lead ECG shows that a patient is having an inferior MI, take the lead V4 and move it over to the mirror image position on the right side of the patient’s chest and rerun the 12-lead. This will give you a lead called V4R. If in V4R, the ST segment is altered—either elevated or depressed—it indicates right-sided involvement of the MI, and NTG should be withheld until medical control is contacted.
Morphine Sulfate. For pain that continues despite NTG administration, 2–4 mg morphine as an intravenous bolus can be administered. Morphine, in addition to providing pain relief, also can help the patient relax because as it takes the pain away, the patient slowly stops thinking about his or her condition. Morphine should be withheld for patients with a SBP <100 and used with caution in patients who are at risk for respiratory compromise. Morphine, like NTG, can have the effect of reducing preload. Therefore, for the same reasons, morphine should be withheld in patients having an MI involving the right side of the heart. Fentanyl citrate can be an alternative to morphine because it has a faster onset and fewer side effects than morphine. If fentanyl is the analgesic of choice, administer 1 mcg/kg slowly over 1–2 minutes intravenously.

Congestive Heart Failure

Pathophysiology
CHF occurs whenever the heart is unable to pump effectively. As a result, blood backs up into the systemic circuit, the pulmonary circuit, or both. Most commonly, the left side of the heart fails before the right side for 1 or more of several reasons. First, the left side is more likely to sustain damage from a heart attack than the right side. This damage can then limit the overall function of the heart and reduce its ability to empty the chambers. The heart now has a reduced ability to push blood around the body, which leads to pooling. Second, the left side must consistently push against afterload, which, especially in cases of long-term hypertension, can cause LVH. The thickened walls of the left ventricle have a more difficult time squeezing together, further worsening the heart's ability to eject the blood.
These 2 cases are further impacted by a normally functioning right side of the heart. As the right side continues to function, it efficiently moves blood through the lungs to the poorly functioning left side of the heart. This causes a backup of blood behind the left ventricle into the left atrium and, eventually, the lungs. Slow transit of blood through the lungs combined with increased pressures in the pulmonary capillaries causes those capillaries to become leaky, which allows some of the plasma to enter the alveoli and bronchioles. This is where it gets the term congestive because the lungs are now congested with excess fluid, similar to how they can get congested with mucus during an infection.
As the fluid enters the alveoli, it inhibits gas exchange between the alveoli and blood. As more and more alveoli are affected, poor oxygenation will result in hypoxemia. This hypoxemia is then recognized by the body’s chemoreceptors, triggering the body to attempt to rectify the problem. This actually makes matters worse for the patient because the body’s reaction is to activate the sympathetic nervous system. Most sympathetic responses will actually make matters worse for the patient with CHF. First, the heart rate will increase in an effort to try and move more blood through the lungs and body. This only worsens the backup of blood into the lungs and the rest of the body. Second, the peripheral arteries constrict in an effort to shunt blood to the vital structures in the chest and abdomen. This serves to further increase the afterload on the left ventricle, further limiting its ability to eject blood. Third, the bronchioles dilate in an effort to allow more air to reach the alveoli. Unfortunately, this serves to actually further increase the pressure in the lungs, increasing the amount of fluid that escapes the pulmonary capillaries and worsening the hypoxemia. If not addressed quickly, further deterioration can result in cardiac arrest.
Eventually, as the left side continues to fail and pressures build up in the lungs, right-sided heart failure can begin. Left-sided heart failure is the most common reason for right-sided heart failure. As the right side of the heart fails, blood backs up behind the right ventricle that is no longer able to push blood through the lungs and back into systemic circulation. The venous side of the vasculature can hold fluid when it is in excess—but only to a point. Once that point is exceeded, the fluid begins to leak out of the venules of the capillary beds. This is particularly true of those capillary beds in the dependent areas of the body—the legs and feet of patients capable of sitting upright and standing and the sacral and lower back area of those who are bedridden. In something of a surprising twist, right-sided heart failure can actually help left-sided heart failure because as the right side fails, it can no longer push blood into the already failed left side. This reduces left-sided preload and, therefore, the workload of the left side of the heart.

Assessment of CHF
CHF generally results in a syndrome, or several signs and symptoms that generally occur together and relate to the same problem. When we talked about ACS, we said patients may exhibit any of a basket of symptoms. However, in CHF, patients typically present with similar signs and symptoms. As with ACS, we will approach assessment of the patient with CHF systematically and will fill in the blanks for SAMPLE and OPQRST with questions and answers, followed with pertinent head-to-toe physical examination findings.
Symptoms. Shortness of breath is the most common chief complaint for patients in the throes of CHF. Chest pain or discomfort may or may not be present and often is related more to the workload of the heart exceeding its O2 supply because of the poor oxygenation status in the lungs rather than from blockage. That said, keep in mind that it is possible to have a heart attack and CHF concurrently, so chest pain here is worth assessing in the same fashion as previously. Some patients will complain of dizziness or syncope, most likely caused by the overall drop in O2 in the blood. Nausea, with or without vomiting, is always a possibility with increased sympathetic tone, so be prepared to manage this potential complication.
Allergies. These are patient specific. Morphine sulfate is again a treatment option for patients with CHF because of its mild diuretic properties in addition to analgesia, so ask specifically about morphine allergies.
Medications. These are important to evaluate, and the patient’s list of medications should be gathered and taken to the hospital with the patient. Common medications for the patient with CHF will include many of the same as for CAD in addition to diuretics, such as furosemide or bumetanide, and positive inotropes, such as digoxin, to help the heart beat more forcefully. Also evaluate if the patient is compliant with his or her medication regimen. Because administration of NTG in large quantities is the treatment of choice in patients with CHF, once again ask about medications commonly prescribed for erectile dysfunction and primary pulmonary hypertension, including sildenafil, tadalafil, and vardenafil.
Past Medical History. Patients may have a history of a previous heart attack, which is now causing them to go into CHF. They also may have had episodes of CHF before, so they may be able to state whether their current situation resembles in any way that of previous episodes. They also may be able to tell you what worked best for them in the past.
Last Oral Intake. Although mostly important to know what may be coming back up if the patient vomits, knowing this could help determine what caused this new problem. For example, a recent meal that was high in sodium, which transiently increases blood pressure, may have been enough to “tip the scales” and send the patient into CHF.
Events Prior. This leads the assessment nicely into OPQRST. Evaluation of what the patient was doing and how the patient was feeling over the hours or days leading up to the call is important.
Onset. What were you doing when this started? This may not yield a specific answer because CHF takes time to develop and worsen to the point that the patient will call for an ambulance. A common answer might be something like “Nothing specific, but I have been getting more and more short of breath over the past few days.” At this point, it is worth looking into the progression of the issue. This may include when the patient first noticed a change in breathing and, what, if anything, changed or started at that time that he or she can think of.
Provocation/Palliation. Does anything make this feeling better or worse? Have you done anything to make it better, such as take a medication or rest? With these questions, patients may indicate symptoms of orthopnea, or difficulty breathing based on position. This might manifest as the inability to sleep lying flat or needing to sleep propped up on multiple pillows. The patient also may state that he or she sleeps in a recliner rather than a bed.
Quality. How would you describe the pain? This one does not make the most sense to ask in a patient with CHF unless he or she is having associated chest pain or pressure.
Radiation. Can you show me where the pain is? Does the pain you are having go anywhere? Does it go to the shoulder? Back? Abdomen? Neck or jaw? Again, reserve these questions for patients with chest pain associated with the respiratory distress.
Severity. On a scale of 1–10, with 10 being the worst pain you have ever had and 1 being very minor or no pain, what number would you give this feeling? At first look, this may seem to be a question to avoid asking; however, if we reword it slightly to “On a scale of 1–10, with 10 being the shortest of breath you have ever been and 1 being not short of breath at all, how would you rank today’s shortness of breath?” Now we can establish a numerical baseline and follow how the treatments are improving the patient’s status.
Time. When did this begin? Is it constant or intermittent? This is related to the onset questions noted previously but focuses more on timing.
Physical Examination. The patient will very likely be pale and diaphoretic and cool to the touch because of the shunting of blood away from the skin and the increased sympathetic tone. The patient will likely have JVD when evaluated, with the patient sitting upright or in the semifowlers position with the head raised higher than 45°. Evaluation of lung sounds will reveal rales in the dependent areas, usually the bases, from fluid seeping into the alveoli. Lung sounds also may include wheezing from the interstitial pressure narrowing the bronchioles. Patients with CHF also will have pitting edema in the dependent areas of the body. The edema is said to be pitting when you push your thumb into the edematous tissue and the indent remains for an extended period of time.
Vital Signs. The patient’s vital signs in CHF also can be predictable. The heart rate will be elevated, often in the 120–130 range. The patient will be hypertensive, with blood pressure values often exceeding 200/100 on both the SBP and DBP numbers. The patient also will be breathing faster than usual, sometimes in excess of 30 breaths per minute. He or she also will present with a decreased pulse oximetry, sometimes so low that the pulse oximeter cannot even pick up a signal.

Treatment of CHF
The primary goal in treating the patient with CHF is to increase oxygenation. This will reduce the patient’s work of breathing and, therefore, the anxiety associated with not being able to get enough O2. Secondarily, the goal should be reducing the blood pressure so that the workload being placed on the heart can be reduced. Both angles of CHF management will be discussed here. Before initiating any of the following, ensure that the patient is at least in a full fowlers position (seated upright with the legs outstretched). Ideally, although difficult to achieve in an ambulance, the patient should be seated with the legs dangling to aid in venous pooling, limiting the amount that can return to the heart.
Oxygen. In ACS, administration of O2 was restricted to those with a pulse oximetry <95%. Here, begin treatment with high-flow O2 via a non-rebreathing mask at 15 LPM. In some patients, this will not improve their pulse oximetry into the desired range of >95%, so CPAP will be needed. Moving to CPAP quickly in the patient with CHF can avert the need for intubation and ventilation, treatment from which the patient may not ever recover.
Monitoring ECG and Obtaining 12-Lead. Continuous cardiac monitoring is essential to determine the rhythm of the patient. It also helps monitor patient improvement. If possible, obtain a 12-lead ECG to rule out ischemia and infarct; however, obtaining a 12-lead ECG should not delay initiation of the CPAP or other treatments that follow here.
Initiation of Intravenous Access. This is largely preventive in the event that the patient’s condition deteriorates, access has already been established. In addition, if the patient’s blood pressure drops after the administration of NTG, the paramedic is ready to quickly administer fluids. Although not necessarily required to happen before NTG is given, it is strongly recommended in case of an adverse event.
Nitroglycerine. In CHF, NTG is given sublingually as a spray or a tablet and depends on the blood pressure. If the SBP is between 100 and 140, 0.4 mg NTG is given. If the SBP is between 140 and 180, 0.8 mg NTG is given. Finally, if the SBP is >180, 1.2 mg NTG is given. The NTG is given primarily to reduce myocardial preload and create more venous pooling. The patient should be advised not to chew or swallow the medication and that it may cause side effects of a burning sensation under the tongue and a headache. NTG should not be administered if the patient has taken any erectile dysfunction medications in the past 24–36 hours. If the patient is on CPAP, whenever possible, the seal of the mask of the CPAP should not be broken to administer the NTG. In this situation, if local protocols allow, apply 1 inch of NTG paste to the patient’s chest.
Morphine Sulfate. Morphine can be given to patients to assist the NTG with reducing preload and increasing venous pooling. A typical CHF dose of morphine is between 2 and 6 mg. Because morphine is not usually used in CHF for its pain-relieving properties, fentanyl citrate is not an ideal alternative because its smooth muscle relaxant properties are not as potent as morphine.
Beta-adrenergics. Inhaled beta-adrenergic medications should be used with caution in the patient who is wheezing. Frequently, when the patient presents with wheezing and other symptoms consistent with CHF, such as pitting edema, hypertension, and orthopnea, administering albuterol can cause the patient to have what is called flash pulmonary edema, or flash CHF. It gets this name because rales appear, and the patient’s work of breathing dramatically increases in a very short period of time. It is recommended that these medications be given only after initiation of the above treatments and on orders from medical control.

Cardiac Tamponade

Pathophysiology
Cardiac tamponade occurs when fluid accumulates between the tough fibrous membrane surrounding the heart, called the pericardial sac, and the heart itself. The fluid can be blood if a coronary aneurysm ruptures or a myocardial rupture occurs after a heart attack; it also can be serous fluid resulting from an infection. Blunt chest trauma also can result in myocardial rupture. Regardless of the fluid type and cause, it can build up, putting pressure on the heart. If unrecognized, the fluid can build to the point that the heart collapses and is no longer able to expand, preventing the chambers from filling. This can go on until there are no more palpable pulses, at which point in time the patient is essentially in cardiac arrest.

Assessment of Cardiac Tamponade
Symptoms. These are largely dependent on the cause. Slow onset of progressively worsening chest pain is a common symptom. Dizziness or syncope become more likely as the stroke volume, and by extension the blood pressure, drops. Finally, if the cause is an infection, the patient can present with fever.
There are 3 signs and symptoms that when found together strongly signal pericardial tamponade. They are JVD, muffled or distant heart sounds, and low and narrowing pulse pressure. Collectively, these are known as Beck's Triad. 


Figure: The noticeable axis changes found on the ECG of a patient with pericardial tamponade.

Electrical alternans may also be observed. Electrical alternans is a condition that manifests on the ECG running rhythm later in the tamponade. As the fluid builds up, each contraction of the heart causes it to swing around in the fluid that now surrounds it. This causes variations in the size of the QRS complexes throughout each lead.
Allergies and Medications: These are related to the patient’s health history and often do not offer any clues that would lead toward a notion of tamponade.
Past Medical History. If the patient has a history of a heart attack, cardiac rupture is a possible cause. The heart attack causes myocardial tissue to die, which over time weakens the structure of the heart. A patient with this and a history of uncontrolled or poorly controlled high blood pressure is at high risk for cardiac rupture.
Last Oral Intake. Important only for documentation purposes. This information likely will not impact any treatment plans.
Events Prior. Evaluate what led up to the patient calling for an ambulance.
Onset. What were you doing when this started? This may not yield a specific answer if the tamponade develops over time. Again, clarify when the patient first noticed the symptoms of which he or she is complaining.
Provocation/Palliation. Does anything make this feeling better or worse? Have you done anything to make it better, such as take a medication or rest? With these questions, patients may indicate that chest pain and dizziness get better when they lie down. This can happen because the fluid around the heart spreads out and allows the ventricles to fill more efficiently; also, a lower overall blood pressure is needed when lying down to get blood to the brain.
Quality. How would you describe the pain?
Radiation. Can you show me where the pain is? Does the pain you are having go anywhere? Does it go to the shoulder? Back? Abdomen? Neck or jaw?
Severity. On a scale of 1–10, with 10 being the worst pain you have ever had and 1 being very minor or no pain, what number would you give this feeling? Now we can establish a numerical baseline and follow how the treatments are improving the patient’s status. Because chest pain is a very common complaint with this issue, it is not unreasonable to assess or treat this patient as if he or she is having ACS. Remember, chest pain is ACS until proven otherwise.
Time. When did this begin? Is it constant or intermittent? This pain is likely to be constant and progressively worsening over time. Dizziness, if present, also would be worsening over time, especially when changing positions (going from lying down to sitting or sitting to standing).
Physical Examination. The skin color and texture of a patient with cardiac tamponade can vary from normal, to cool, to pale and diaphoretic depending on the degree of tamponade that has already occurred. JVD will be present in later stages as venous return to the heart becomes impaired. Heart sounds will be muffled and sound distant compared with normal heart sounds.
Vital Signs. Tachycardia is frequently present as the body raises the heart rate to try and maintain blood pressure. The respiratory rate tends to not be significantly altered. Blood pressure may be normal or hypotensive. As the tamponade progresses, the pulse pressure—the difference between the SBP and DBP—narrows or becomes progressively smaller with each sequential blood pressure measurement. 

Treatment of Cardiac Tamponade
Prehospital treatment of tamponade is very limited and focused on supportive measures, including maintaining an airway, providing O2, and managing pain if present. A fluid bolus of 500 mL NSS may be given to help support blood pressure; however, this should be given with an abundance of caution because too much fluid could precipitate pulmonary edema because of the poor functioning of the heart. Ultimately, the patient needs to receive a procedure called pericardiocentesis. This procedure involves inserting a long needle into the pericardial sac and drawing off the fluid. This is not a procedure typically performed by paramedics because it is extremely dangerous and carries with it many possible side effects. With this in mind, rapid transport to the nearest facility often is the best treatment.

Cardiogenic Shock

Pathophysiology
Cardiogenic shock occurs when >40% of the left ventricular muscle is damaged as a result of a heart attack or a series of heart attacks. This level of damage ultimately prevents the heart from ejecting enough blood to move it around the body and prevents the heart from maintaining a viable blood pressure. It often is lethal to the patient and, therefore, is always a true emergency.

Assessment of Cardiogenic Shock
Symptoms. Shortness of breath and extreme fatigue or general malaise are the most common chief complaints for cardiogenic shock. Chest pain or discomfort also may be a complaint if the developing cardiogenic shock is caused by an ongoing AMI. Some patients will complain of dizziness or syncope related to the hypotension. Nausea, with or without vomiting, is always a possibility with increased sympathetic tone, so be prepared to manage this potential complication.
Allergies. These are patient specific.
Medications. These are patient specific and widely varied depending on the patient’s history. Because cardiogenic shock usually follows an MI, the patient will likely be on medications consistent with CAD.
Past Medical History. Patients often have a history of a recent heart attack.
Last Oral Intake. This information will seldom be important to the overall assessment. It may be helpful only if the patient ate recently to help prepare for the potential to vomit.
Events Prior. Evaluation of what the patient was doing and how the patient was feeling over the hours or days leading up to the call is important.
Onset. What were you doing when this started? Patients who suffer from cardiogenic shock typically are not very active, resulting from their diminished cardiac ejection fraction and poorly functioning heart. This answer, therefore, will vary from patient to patient.
Provocation/Palliation. Does anything make this feeling better or worse? Have you done anything to make it better, such as take a medication or rest? With these questions, patients may indicate symptoms of orthopnea. This might manifest as the inability to sleep lying flat or needing to sleep propped up on multiple pillows. This condition can mimic CHF in a variety of ways, including what makes the feeling better or worse.
Quality. How would you describe the pain? Chest pain concurrent with cardiogenic shock is unlikely because the AMI often has already passed.
Radiation. Can you show me where the pain is? Does the pain you are having go anywhere? Does it go to the shoulder? Back? Abdomen? Neck or jaw? Reserve these questions for patients with chest pain associated with the respiratory distress.
Severity. On a scale of 1–10, with 10 being the worst pain you have ever had and 1 being very minor or no pain, what number would you give this feeling? Because pain may not be present, this should be ascertained only if the patient has pain, or it can be adjusted to evaluate respiratory status and severity.
Time. When did this begin? Is it constant or intermittent? The patient may be able to share when this happened. Most likely, the shortness of breath or general malaise felt with cardiogenic shock will be constant and possibly progressively worsening.
Physical Examination. The patient may present with an altered mental status resulting from poor cerebral perfusion from the hypotension. The patient will very likely be pale and diaphoretic and cool to the touch because of peripheral vasoconstriction and increased sympathetic tone as the body tries to correct the blood pressure. The patient may have JVD when evaluated with the patient sitting upright or in the semifowlers position with the head raised higher than 45° because the heart is not able to move blood around the body, leading to venous pooling. Evaluation of lung sounds will reveal rales in the dependent areas, usually the bases, from fluid seeping into the alveoli. Lung sounds also may include wheezing from interstitial pressure narrowing the bronchioles. Depending how long the patient’s heart has been failing overall, the patient may have dependent pitting edema. If all of this is a relatively sudden onset, he or she may not have peripheral edema.
Vital Signs. Patients with cardiogenic shock will be tachycardic with low blood pressure—the clinical picture of shock. Their respiratory rate could be slow, normal, or fast depending on how well they are compensating. Pulse oximetry will be low, owing to poor blood flow through the lungs and the resulting pulmonary edema.

Treatment of Cardiogenic Shock
Increasing oxygenation and increasing cardiac output are the primary goals for treating the patient with cardiogenic shock. Position the patient according to his or her mental status in the position. If the patient is able to maintain consciousness in a semifowlers or high fowlers position, do this because it will help with the pulmonary edema. If the patient is unable to maintain consciousness in this position or needs to have an airway adjunct placed, he or she should be transported in the supine position.
Oxygen. Begin treatment with high-flow O2 via a non-rebreathing mask at 15 LPM. CPAP does not improve the patient outcome in cardiogenic shock as it does in CHF, so it is not a treatment option here, despite similar presentations. If the patient’s pulse oximetry does not improve with high-flow O2, consider placing an advanced airway as soon as possible, especially in cases of severe altered mental status or unresponsiveness.
Monitoring ECG and Obtaining 12-Lead ECG. Continuous cardiac monitoring is essential to determine the rhythm of the patient. It also helps monitor patient improvement. If possible, obtain a 12-lead ECG to rule out ischemia and infarct; however, obtaining a 12-lead ECG should not delay other treatments that follow here. Treat any rhythm disturbances appropriately.
Initiation of Intravenous Access. The patient will need intravenous access for medication administration. If the patient does not have JVD when the head of the bed is elevated >45°, it is possible that the patient is hypovolemic in addition to cardiogenic shock. This patient may benefit from a fluid bolus of 200 mL. If, however, the patient does have JVD when the head of the bed is elevated, the patient is likely fluid overloaded and would not benefit from a fluid challenge.
Vasopressors. Depending on the transport time to the hospital, paramedics may need to start a vasopressor that is a positive inotrope and has minimal impact on renal blood flow and myocardial oxygen demand. Dopamine is the preferred choice because it maintains renal blood flow at low doses while increasing myocardial contractility. The dose is typically started at 5 mcg/kg/min and titrated upward to obtain the desired effect of a systolic blood pressure between 90 and 100 mmHg. A dopamine drip is commonly prepared by injecting 400 mg into a 250 mL intravenous bag of normal saline. This yields a 1,600 mcg/mL concentration of dopamine.

Aortic Aneurysm

Pathophysiology
An aneurysm is a widening of any blood vessel. The vessel can be anywhere in the body, in this case, specifically the aorta. An aneurysm can form in 3 areas in the aorta: the ascending aorta leading from the aortic valve, the aortic arch, and the descending or abdominal aorta. Because the aorta endures higher pressures during systole than any other vessel in the body, it stands a greater chance of sustaining damage, especially those with untreated or poorly managed hypertension. Degenerative weakening in the middle layer, the tunica media, allows for a ballooning out of the aortic wall. Consequently, the tunica intima is left to bear the brunt of the systolic pressure, which will inevitably cause it to tear under the pressure. This tear will allow blood to get in between the intima and the media, effectively tearing the 2 layers apart. This is referred to as a dissecting aortic aneurysm.
Aortic aneurysms are differentiated by their location. When damage to the aorta is localized to the ascending aorta or the aortic arch, it can be called a thoracic aortic aneurysm. This aneurysm is concerning because the damage may not be limited to the aorta. The vessels branching off the aorta in this area also could sustain damage. In addition, the dissection could move toward the heart and involve the aortic valve. Because this is the area where the coronary arteries begin, they too could become compromised, therefore altering coronary artery blood flow. In an abdominal aortic aneurysm (AAA), the descending portion of the aorta is involved. Although there are many smaller arteries that branch off the descending aorta and service the abdominal viscera and the spinal column, damage to these is less concerning.
Symptoms. Chest or abdominal pain are the most common symptoms with an aortic aneurysm. Back pain is sometimes the chief complaint.
Allergies. These are patient specific.
Medications. These are patient specific and widely varied depending on the patient’s history. Because aortic aneurisms are more common in people with uncontrolled or poorly controlled hypertension, patients often are on several antihypertensive medications.
Past Medical History. Patients may have a documented history of hypertension; however, if they have not been seeing their primary care physician regularly, they may not have had any diagnoses.
Last Oral Intake. This information will seldom be important to the overall assessment. It may be helpful only if the patient ate recently to help prepare for the potential to vomit.
Events Prior. Evaluation of what the patient was doing and how the patient was feeling over the hours or days leading up to the call is important. This line of questioning is important to help decide between possible causes of the symptoms you are finding.
Onset. What were you doing when this started? Frequently, the pain from the aneurysm starts suddenly and at any time so this can vary widely from person to person.
Provocation/Palliation. Does anything make this feeling better or worse? Have you done anything to make it better, such as take a medication or rest? The AAA causes pain that is excruciating and constant, as long as the dissection is progressing. Many patients will not be able to find a position of comfort that suits them for the duration of the patient contact.
Quality: How would you describe the pain? This pain is frequently described as tearing, shredding, ripping or stabbing pain. It also is most often the worst pain of the patient’s life.
Radiation: Can you show me where the pain is? Does the pain you are having go anywhere? Does it go to the shoulder? Back? Abdomen? Neck or jaw? Pain from an AAA that starts in the abdomen frequently radiates around the flank to the back. In a thoracic aortic aneurysm, the pain often is described as straight through to the back. Occasionally, if the dissection travels down into 1 of the branches of the aorta in the pelvis, pain can be felt in the pelvis or down into the legs. Radiation will be heavily dependent on the location of the original dissection.
Severity: On a scale of 1–10, with 10 being the worst pain you have ever had and 1 being very minor or no pain, what number would you give this feeling? Almost always, it will be the worst pain the patient has ever experienced.
Time. When did this begin? Is it constant or intermittent? The patient may be able to pinpoint the exact starting time of the pain because this tends to start so suddenly.
Physical Examination. In helping differentiate between an AAA and other abdominal ailments, a complete and thorough physical examination is crucial so that important signs are not missed or overlooked. Skin color and temperature often are pale and diaphoretic owing to the increased sympathetic tone and the body’s response to severe visceral pain.
In a thoracic aortic aneurysm, blood flow may be disrupted into any of the 3 major branches coming off the aortic arch. If the aortic dissection affects either the brachiocephalic or left subclavian artery, the blood pressure in each arm may be different. This also is true if the aneurysm exists between the 2 arteries, so whenever an aortic aneurysm is suspected, take the blood pressure in both arms. Disruption of blood flow into either the brachiocephalic or the left common carotid artery may cause stroke symptoms, including 1-sided weakness, visual and speech disturbances, or facial droop.


Figure: Thoracic Aorta and Branches of the Aortic Arch

In an AAA, there may be a palpable pulsating mass near the midline during the abdominal examination. If this is found, gently release the pressure placed over the abdomen and do not palpate that area again. Palpating it only adds to the already high pressure in the area and could accelerate a complete tear of the aortic wall, leading to intra-abdominal bleeding. This bleeding can be so intense that the patient completely exsanguinates (bleeding sufficient to cause death) in minutes. One leg may be cooler than the other. The same leg that is cooler also will likely have a notably weaker or possibly absent pulse; it also may appear mottled or pale compared with the other leg.
Vital Signs. More than likely the patient will be hypertensive. A patient who is hypotensive with any of the above signs, symptoms, or complaints may very well be bleeding out and rapidly approaching death. The patient’s heart rate will most likely be normal to tachycardic. The ECG will be unremarkable except in the case of a thoracic aortic aneurysm that is affecting blood flow into the coronary arteries. If this is the case, the ECG may show ischemia or infarct and greatly complicates treatment. The respiratory rate will probably be elevated because of the pain, but breathing will not necessarily be labored. Pulse oximetry will be at the patient’s usual baseline.

Treatment of Aortic Aneurysm
The primary goal of prehospital care of an aortic aneurysm is to calm and reassure the patient. Anything that can be done to reduce the patient’s anxiety will go a long way in helping the patient reduce his or her blood pressure. Next is to help manage the patient’s pain because this also will help reduce the patient’s blood pressure. Paramedics do not frequently carry antihypertensive medications other than NTG, so directly addressing the blood pressure is not likely to happen in a meaningful way in the field. Therefore, rapid, stress-free transport is always indicated for the patient with an aortic aneurysm. Keep lights and siren use to a minimum so as not to alarm or agitate the patient because this will serve to only increase the blood pressure.

Hypertensive Emergencies

Pathophysiology
The full pathophysiology of hypertension, and why some people are chronically hypertensive whereas others are not, is poorly understood. The most widely accepted explanation is associated with progressing atherosclerosis, which has the ultimate effect of narrowing the arteries and reducing their elasticity. As this worsens over time, the afterload of the heart increases, which causes the heart to work harder, resulting in systemic hypertension. People walk around on a daily basis with hypertensive blood pressures and generally do not experience any symptoms that would require a hospital visit. It is when their hypertension is uncontrolled during an extended period of time that the symptoms develop and systemic problems arise. Left-sided heart failure and aortic aneurysm, discussed previously, are 2 conditions closely tied to hypertension. Paramedics may encounter a hypertensive blood pressure in a patient that can be associated with stress and anxiety of the situation; however, this is not likely to be life threatening. A sudden onset of hypertension, in very rare instances, can cause a condition known as posterior reversible encephalopathy syndrome (PRES), which can be devastating. The discussion about hypertension will center on this issue.
PRES is at greatest risk of occurring when the blood pressure exceeds 200/130, or, more specifically, whenever the MAP exceeds 150 mmHg. Recall that MAP is calculated by taking 1/3 the difference of the SBP and adding to that value the DBP:

As the MAP exceeds 150 mmHg, the vessels in the brain begin to become leaky, resulting in cerebral edema, particularly in the occipital and parietal regions. This causes a breakdown of the all-important blood brain barrier and increases ICP. The areas of the brain most affected will determine the type and severity of the symptoms the patient will exhibit.
Patients may present with widely varied symptoms, but headache, dizziness, ringing in the ears (tinnitus), and visual disturbances are most common. These also can be accompanied by nausea and vomiting. Occasionally, global muscle twitching can be seen as a result of neuromuscular irritability, possible progressing to seizures. Sudden onset of confusion also is seen as the encephalopathy worsens.

Treatment of Hypertensive Emergencies
Lowering catastrophically high blood pressure must be done in a highly controlled and gradual fashion. Therefore, prehospital treatment of this issue is largely related to supportive treatment, including maintaining an airway and adequate oxygenation, establishing intravenous access, and monitoring the patient’s ECG for the duration of the transport. Paramedics working in areas with transport times >30 minutes or so may need to initiate more definitive treatment related to lowering the blood pressure.
Labetalol is the drug of choice for PRES because it has alpha- and beta-blocking effects. As an alpha blocker, it helps relieve peripheral vasoconstriction, and its beta blocking effects prevent the possibility of rebound tachycardia that may accompany a drop in blood pressure. The beta blockade also will have negative inotropic effects. To administer, mix 250 mg in 250 mL NSS and begin to infuse as an intravenous piggyback at a rate of 2 mg/min, being careful to avoid accidentally giving the patient a large bolus of labetalol. Assess the blood pressure every 2–3 minutes and turn off the infusion when the desired blood pressure is reached.
If labetalol is not available, 0.4 mg NTG sublingually can be used in its place. In this case, multiple doses may need to be given to achieve the desired blood pressure. Ensure that adequate time passes between each administration of NTG so that there is not a large, sudden drop in blood pressure.

Cardiac Arrest
Cardiac arrest can have many etiologies, including massive AMI, severe respiratory distress, drug overdose, and electrolyte imbalance to name a few. Ultimately, in cardiac arrest, the heart is simply not producing a palpable pulse. We saw earlier in the guide that the resulting rhythm can be the primary cause for pulselessness in the cases of VF and VT. However, occasionally, the electrical cardiac rhythm looks as if it should be generating a pulse, possibly even completely normal. This is referred to as PEA. When presented with a patient with PEA, assess the patient for the following reversible causes, often referred to as the H’s and T’s. In the following list, the H or T that will serve as the memory aid is listed first, then the problem if it is not completely obvious, followed by a description of how the problem can present as cardiac arrest. Finally, each section will address the requisite treatment for the particular cause.

H’s

- Hypoxia. If the patient does not get enough O2 for a long enough period of time, the heart will lose the ability to contract forcefully enough to generate a pulse. To treat this, ensure high-flow O2 at all times and continually monitor pulse oximetry.
- Hypovolemia. It is possible for a person to have lost such a large amount of his or her circulating volume that the heart is beating normally, with an organized electrical rhythm, but will not produce a palpable pulse, even when the patient is supine. This can be caused by profound fluid loss from burns, sepsis, dehydration, or severe bleeding. Treatment for this situation involves aggressive fluid replacement therapy. Fluid boluses of 500–1,000 mL are common during any cardiac arrest situation; however, it is essential if hypovolemia is a suspected contributing cause.
- Hypoglycemia. As the blood sugar level drops in a patient, he or she will first lose consciousness as the body works to reduce its glucose consumption. If it drops far enough, the heart will stop moving but will continue to display a normal electrical rhythm. If the patient is a diabetic, or perhaps intentionally overdosed on insulin, hypoglycemia should be suspected. Check the patient’s blood sugar level using a glucometer. If it is found to be <60 mg/dL, administer 25 g of a 50% solution of dextrose (D50). Administering D50 should not be a routine treatment in all cardiac arrest cases; however, it is a first-line treatment in hypoglycemia.
- H+ Acidosis. As we talked about in this guide, the body needs to maintain the blood acidity within a fairly narrow pH range: 7.35–7.45. If it deviates outside this range, the cellular enzymes necessary for the metabolism of nutrients and other cellular activities begin to fail as the proteins that make them begin to change shape. Most commonly, the blood becomes more acidic (pH decreases) because of the production of metabolic acids and ketones and/or the inability for the body to reduce CO2. Treating this involves 1 of 2 options—or both. In the cardiac arrest situation, CO2 can build up in the blood because the patient is no longer breathing adequately. Here, treatment will focus first on restoring a patent airway and adequate ventilation and oxygenation. This should remedy most of the acidosis in cardiac arrest. If the patient is on dialysis or is a diabetic who has not taken insulin, metabolic acidosis may be playing more of a role than simply inadequate ventilation. In this case, while reestablishing an airway and ventilation remain the priority, 1 mEq/kg sodium bicarbonate may be beneficial in attaining a viable pH.
- Hyperkalemia/Hypokalemia. Cardiac arrest can be caused when the potassium levels are either elevated or deficient. Hyperkalemia is possible in patients who are on dialysis, especially if they do not follow their diet or have missed treatments, or in cases of profound cellular damage such as rhabdomyolysis. Rhabdomyolysis should be suspected in patients with a crush injury that has not been relieved for >1 hour, fall victims who have not been able to move for a couple days, or weight lifters who have overdone the workout. Any of these situations will cause potassium to enter the blood in lethal quantities where it does not belong; as long as potassium remains within the cells, it tends to be relatively harmless. Hypokalemia is much less common and can occur in patients who have consumed excess volumes of water (relative hypokalemia) or more likely overdosed on potassium-wasting diuretics, such as furosemide, or in profound diabetic ketoacidosis. Prehospital providers can moderately treat hyperkalemia only with the administration of 1 g of calcium chloride or calcium gluconate as an intravenous bolus.
- Hypothermia. Long-term exposure to cold temperatures can result in slowing of the metabolism and eventually death. Treatment for this is slow, controlled rewarming, including warm intravenous fluids. 

T’s

- Thrombosis (Cardiac Thrombus). This is better known as a massive AMI. If the blockage is in the left main coronary artery, this could be sufficient enough to put the patient into sudden cardiac arrest because that would effectively eliminate blood flow to the entire left ventricle and therefore its ability to contract. Because the electrical signal would come from an area unaffected by the blockage, it would continue uninterrupted and unchanged. Treatment is minimal in the prehospital and hospital environments once the patient has gone into cardiac arrest. Unless pulses can be restored, this is likely a lethal event for the patient.
- Thrombosis (Pulmonary Thrombus). Also known as a PE, which was discussed at length here. If the blockage occurs in a larger pulmonary vessel, profound and irreversible hypoxemia will quickly ensue. This is usually enough to cause catastrophic systemic cellular failure, resulting in patient death. This is irreversible in the field and in many cases in the hospital as well. The best treatment for this situation is aggressive ventilation and oxygenation with intubation and BVM ventilations.
- Tamponade (Cardiac Tamponade). Cause and treatment were discussed earlier in here.
- Tension Pneumothorax. Cause and treatment were discussed here.
- Trauma. This refers to multisystem trauma, which involves more than just the heart. It could involve complicated and irreversible head injury, spinal cord transection, or disseminated intravascular coagulation. All these issues could be lethal to the patient without the traumatic event directly affecting the heart. Treatment for a traumatic event is largely supportive.
- Toxins (Drug Overdose). Nearly every drug—street, prescription, or over the counter—in the right concentration can result in an overdose. Even docile water can be a toxin in the right quantity. Paramedics carry an antidote only for 1 family of medications and can mitigate only the effects of others. Opiate overdoses can quickly and effectively be treated in the field with 0.4–2 mg naloxone. Calcium channel blocker overdoses can be overcome with administration of 1 g calcium chloride or calcium gluconate. Other overdoses, such as aspirin, acetaminophen, benzodiazepines, and beta blockers, need to be treated in the hospital and can be treated only symptomatically in the prehospital environment. Maintenance of the ABCs is of primary concern in overdoses that cannot be definitively treated. This includes CPR, ventilation, establishing an intravenous line, and evaluation of the blood sugar level.

Treatment for VF and pulseless VT was covered earlier in this guide, but it is worth a review of the global treatment options for a patient in cardiac arrest. First and foremost, high quality CPR must be performed at a rate of at least 100 per minute. The chest should be compressed 1/3 
to 1/2 the diameter of the chest or about 5 cm. Ensure that the chest fully recoils so that the heart has an opportunity to refill. Compressions should be alternating with ventilations at a ratio of 30 compressions to 2 ventilations until the patient has a definitive airway in place, at which point compressions should not be stopped to allow for a breath. Furthermore, compressions should not be stopped for >30 seconds at any given time (e.g., patient movement). Each ventilation should be delivered slowly over 1 second so that the risk of gastric insufflation is minimized. Adequate time for exhalation of the previous breath should be allowed. After 2 minutes or 5 cycles of CPR, the electrical rhythm may be rechecked and the patient evaluated for a pulse.
Electrical defibrillation is needed for the patient who presents with VF or pulseless VT. If either of these are the presenting initial rhythm, give 1 defibrillation at 360 J or the manufacturer’s recommended dose (often 200 J) as soon as possible if EMS witnessed the arrest or after 2 minutes of CPR if EMS did not witness the arrest. Defibrillations then should happen after 2 minutes or 5 cycles of CPR at about the same time as the pulse/rhythm check described above. Follow each shock immediately with high-quality CPR and ventilations for 2 minutes. Defibrillation is not a treatment option for patients in PEA or asystole.
An intravenous or intraosseous line should be established early in the resuscitation attempt for fluid and medication administration. In most cases, running the intravenous line wide open is recommended. The first medication of choice is 1 mg of 1:10,000 epinephrine. Epinephrine should be given every 3 to 5 minutes for the duration of the resuscitation attempt. Medications should always be followed with CPR so that the medication can be moved around the body and reach the central circulation and exert its effects. The first dose of epinephrine should be followed by an appropriate antidysrhythmic medication when the patient is in VF or VT. Choose between 300 mg amiodarone and 1.5 mg/kg lidocaine as the first-line antidysrhythmic. Whichever medication is chosen should be continued for the duration of the resuscitation. Do not alternate medications or use both at any time on a patient.
Although epinephrine can be continued throughout as mentioned earlier, amiodarone and lidocaine cannot be given during a cardiac arrest more than a couple times. Amiodarone can be given only a 2nd time, approximately 10 minutes after the first dose at 150 mg. After the initial dose of lidocaine, each subsequent dose should be 1/2 the previous until a maximum of 3 mg/kg has been given. For example, if the 1st dose is 1.5 mg/kg, the 2nd dose given about 5 minutes later is 0.75 mg/kg, and the 3rd and generally accepted final dose 5 minutes after that would be approximately 0.5 mg/Kg.
Waveform capnography is the best way to confirm effective CPR. After intubation, or the placement of another alternative airway such as a Combitube, monitor the patient’s exhaled CO2. If the patient is still metabolizing glucose at a cellular level, CO2 will still be produced. As long as that CO2 can make it to the lungs, it will be picked up by the EtCO2 sensor. If a sudden spike is noticed in the EtCO2, it is very likely that the patient has had or will have a return of spontaneous circulation (ROSC).

6. Electrical Therapies
Paramedics can perform several different therapies involving direct delivery of electricity to the heart, including transcutaneous pacing, synchronized cardioversion, and defibrillation. In this section, each will be described in the following manner: indications, contraindications, recommended settings or dose, precautions, considerations, and therapeutic process.

Transcutaneous Pacing
TCP is the temporary application of an electrical pacemaker to the chest of a patient. TCP delivers a small electrical current to the heart, stimulating it to beat faster than it already is. It will help the patient reach the hospital in a better overall cardiovascular condition than he or she otherwise would without this procedure.
Indications. Bradycardic rhythm with hemodynamic compromise, refractory to atropine and fluid administration. If the patient is in a rhythm with associated signs of hemodynamic compromise that does not respond to the initial dose of atropine—typical bradydysrhythmias that do not respond to atropine include high 2nd- and 3rd-degree AV blocks and idioventricular rhythms—then move rapidly to initiate TCP.
Contraindications. Bradydysrhythmias without hemodynamic compromise or pulseless bradycardic rhythms. Aggressive treatment of bradydysrhythmias that are not hemodynamically unstable is not warranted because the patient is maintaining blood pressure and mentation successfully, despite the bradycardic rhythm. Although it may seem that a pulseless bradycardic rhythm is the ultimate description of hemodynamically unstable, pacing a person in this condition often is fruitless. For pulseless bradycardic rhythms, instead of TCP, look to treat underlying problems such as hypoxia or hypovolemia along with providing high-quality CPR.
Recommended Settings or Dose. Eighty pulses per minute, 80 mA to start, titrate milliamps to the minimum needed for electrical and mechanical capture.
Precautions. Wet patients and excessively hairy patients. Patients whose chest area is wet, either from perspiration or being in water (shower, bath, pool, ocean, etc.) need to be dried off prior to the initiation of therapy. This step helps prevent arcing of the electricity across the chest and helps the pads adhere more effectively throughout the course of treatment. The hair on a patient’s chest could prevent the pads and electrode gel from making a strong contact with the chest, possibly leading to electrical burns to the patient’s chest or, worse, setting the hair on fire. If a patient with excessive hair is encountered, a recommended practice is to firmly apply 1 set of pads and rip them off, hopefully taking a swath of the patient’s hair with them. Next, place a new set of pads in the newly waxed area and proceed as normal. Shaving also works; however, it takes longer and there is a greater chance of injury to the patient.
Considerations. Pain management and/or sedation in patients who are conscious at the start of the procedure or whose consciousness improves with TCP. There is no hiding it; having electricity course through one’s chest wall cannot possibly be a pleasant experience under any circumstance. In these cases, consider pain management or sedation but not until after obtaining electrical and mechanical capture. Once capture is obtained, the patient’s hemodynamic status should improve by observing better blood pressure and mentation. At that point, the paramedic can address the pain and discomfort caused by the electrical current. This can be accomplished with fentanyl 1 mcg/kg for pain or with 2–5 mg of midazolam. Midazolam is preferred because it not only sedates but also induces amnesia.

Therapeutic Process

- Take standard precautions if not already done. The patient should meet criteria described above, including hemodynamic instability and atropine unsuccessful at raising the heart rate. Obtain and document an initial set of vital signs, including an initial cardiac rhythm strip and whenever possible a 12-lead ECG.
- Place pacing pads on the patient. One pad should be placed inferior to the right clavicle, and the other should be placed on the left anterior axillary line at about the level of the 5th intercostal space. It is important that you explain to the patient and any family members who are present what is about to happen.
- Attach wires from the pads to the pacing/defibrillation cable of the cardiac monitor.
- On the monitor, activate the pacer. Different monitor manufacturers accomplish this differently. Be familiar with the one you will use.
- Set the pacing rate to 80 pulses per minute.
- Set the pacing current to 80 mA and adjust until there is electrical and mechanical capture. Electrical capture is represented on the running ECG lead when there is a wide and bizarre QRS complex following most if not all pacer spikes. Mechanical capture is verified when a palpable pulse matches the pacer output rate. That is, 80 beats can be counted at any pulse point on the patient.
- Now that capture has been achieved, this should be the lowest energy that achieves consistent capture. To check this, drop the current slightly until capture is lost.
- Once it is lost, return it back to the level that capture is consistent. This step helps minimize discomfort for the patient. Obtain a rhythm strip for documentation purposes and transport the patient to the closest facility capable of TCP, transvenous pacing, or pacemaker placement.
- Consider sedation and pain management.

Synchronized Cardioversion
Synchronized cardioversion is used to interrupt the cardiac cycle of tachydysrhythmias with the delivery of an impulse of electricity. To reset the heart rate at a lower rate while simultaneously minimizing the chances of setting off a lethal dysrhythmia such as VF, this electrical impulse must be delivered at precisely the right moment in the cardiac cycle. If the electricity is delivered on the first half of the T wave, nothing will happen, and the electricity could serve only to hurt the patient. Similarly, if the electricity is delivered on the 2nd half of the T wave, the heart could be sent into VF or VT, either option potentially leading to death. Therefore, the impulse delivery is synchronized with the QRS complex the heart is already generating. The monitor predicts when the next QRS will fall and discharges the electricity only then. This creates a momentary disruption in the entire cardiac cycle, allowing the heart’s pacemaker to take over at a presumably slower rate, immediately improving cardiac output.
Indications. Unstable SVT, unstable VT with pulses, and unstable atrial fibrillation (AF) with rapid ventricular response. These rhythms are hemodynamically unstable because they are too fast to support viable cardiac output for an extended period of time. Although more stable versions of the same rhythms can and should be treated with medications, unstable rhythms need to be treated more aggressively with electricity to promptly restore effective cardiac output. An unstable rhythm is characterized by any of the following symptoms: dizziness, syncope, altered mental status, hypotension, or orthostatic hypotension.
Contraindications. Stable SVT, stable VT with pulses, stable AF with rapid ventricular response, and pulseless VT. The stable rhythms are treated with a variety of medications. Pulseless VT is treated with defibrillation and medications.
Recommended Settings or Dose. For atrial rhythms (SVT, AF, atrial flutter), start at 50–100 J, with sequential doses increasing to 150 J, 200 J, 300 J, and 360 J. For VT, start at 100–150 J, with sequential doses increasing to 200 J, 300 J, and 360 J.
Precautions. Electrical shock, postcardioversion cardiac arrest, and wet and/or hairy patients. The electrical impulse delivered during cardioversion is much larger than that given during TCP, so the possibility of bystanders or rescuers getting a shock is very real. It is important to “clear” the patient before delivering the shock. This means to announce that the shock is about to be delivered and perform a visual inspection around the patient so that no one is in contact with either the patient or anything the patient is in contact with, including the stretcher, the ETT, or the intravenous line. After the shock is delivered, reevaluate your patient not just for the resulting rhythm and ensure that your patient is not now in cardiac arrest, a possible untoward effect of the treatment. Patients who are wet and hairy should be handled as described in the TCP section.
Considerations. Pain management and/or sedation in patients who are conscious at the start of the procedure and SYNC button deactivation. In these cases, consider pain management or sedation early in the process but do not delay electrical therapy to provide sedation. One option is to have another paramedic prepare and give the medication as the other prepares the patient for the procedure. This can be accomplished with fentanyl 1 mcg/kg for pain or with 2–5 mg midazolam. Midazolam is preferred because it not only sedates but also induces amnesia. Some machines automatically turn off the SYNC button after the synchronized shock has been delivered, whereas others leave it activated. Therefore, if another synchronized cardioversion is needed, make sure the SYNC button is reactivated. Similarly, if a defibrillation is now needed, ensure that the SYNC button is deactivated.

Therapeutic Process

- Take standard precautions if not already done. The patient should meet criteria described above. Obtain and document an initial set of vital signs, including an initial cardiac rhythm strip and whenever possible a 12-lead ECG.
- Place pacing pads on the patient. One pad should be placed inferior to the right clavicle, and the other should be placed on the left anterior axillary line at about the level of the 5th intercostal space. It is important that you explain to the patient and any family members who are present what is about to happen.
- Attach wires from the pads to the pacing/defibrillation cable of the cardiac monitor.
- If time permits, have another paramedic sedate the patient.
- Turn on the SYNC button. Failure to perform this step will result in defibrillation, not cardioversion, and increase the odds of a negative outcome for the patient.
- Select your initial setting according to above.
- Charge the system. During the time that the system is charging, clear all personnel and bystanders from the patient.
- Announce loudly, “Everyone clear!”
- Press and hold the SHOCK button until the shock is delivered. Remember the shock must be delivered at a specific time in the cardiac cycle, so the button must be held until that point is predicted by the machine and the shock is delivered.
- Reassess the patient immediately, focusing on electrical rhythm, the presence of a pulse, and blood pressure if the pulse is present.
- Still in the same rhythm? Increase the joule level and repeat the process. New rhythm and improved blood pressure? Treat to prevent reentry into that rhythm. Cardiac arrest? Initiate CPR and treat according to appropriate protocol for the resulting rhythm.

Defibrillation
Defibrillation delivers a surge of electricity to a heart that is currently generating disorganized electrical activity in the hopes of reorganizing that activity. The amount of electricity delivered through defibrillation is significantly higher than that used in TCP and cardioversion. This is because in defibrillation, the amount of electricity delivered needs to overcome that which is already present and redirect it, whereas in TCP, just enough electricity needs to be delivered to stimulate a single myocyte to contract, creating a cascade where the rest of the heart contracts.
Indications. VF and pulseless VT. Defibrillation can be used only when the heart is fibrillating and displaying a rhythm of VF. Pulseless VT is treated identically to VF.
Contraindications. Any rhythm with pulses. including AF and SVT; asystole and PEA. A patient with pulses in any rhythm, including VT, should not be defibrillated. AF should not be defibrillated, even though part of the heart is, in fact, fibrillating. SVT can sometimes look like VT if it is conducted aberrantly (through an alternate electrical pathway), but similarly, it should not be defibrillated. In addition, SVT, aberrantly conducted or not, will have pulses. Pulseless VT and VF are shockable cardiac arrest rhythms; asystole and PEA are not. Defibrillation needs the heart to have its own electrical activity to reorganize it into a meaningful rhythm that produces a pulse. Asystole does not have any electrical activity to reorganize. In PEA, the electrical activity is already organized; it is just not producing a palpable pulse for any of a variety of reasons.
Recommended Settings or Dose. Biphasic machines: 200 J to start or the manufacturer’s recommended setting for first and successive doses. Monophasic machines: 360 J, all shocks.
Precautions. Electrical shock, SYNC button activated, patients who are wet and/or hairy. The electrical impulse delivered during defibrillation is much larger than that given during TCP, so the possibility of bystanders or rescuers getting a shock is very real. It is important to “clear” the patient before delivering the shock. This means to announce that the shock is about to be delivered and perform a visual inspection around the patient so that no one is in contact with either the patient or anything the patient is in contact with, including the stretcher, the ETT, or the intravenous line. If the defibrillation shock will not deliver despite the machine being charged and pads making good contact with the patient’s skin, ensure that the SYNC button is not activated. If it is, the machine is waiting to figure out when to deliver the shock. This will never happen because there is no QRS to find in VF. Patients who are wet and hairy should be handled as described in the TCP section.
Considerations. Continuity of CPR. Minimize interruptions in CPR during pulse and rhythm checks or intubation attempts. The continuity of high-quality compressions at a rate of at least 100 per minute and approximately 2 inches deep is crucial to the patient having any chance of survival. After the shock is delivered, immediately resume CPR for 2 minutes unless the patient immediately regains and maintains consciousness.

Therapeutic Process
- Take standard precautions if not already done. The patient should meet criteria described above.
- Place pads on the patient. One pad should be placed inferior to the right clavicle, and the other should be placed on the left anterior axillary line at about the level of the 5th intercostal space. It is important that you explain to any family members who are present what is about to happen.
- Attach wires from the pads to the pacing/defibrillation cable of the cardiac monitor.
- Ensure the SYNC button is not activated.
- Select your initial setting according to above.
- Charge the system. During the time that the system is charging, clear all personnel and bystanders from the patient.
- Announce loudly, “Everyone clear!”
- Press the SHOCK button. The machine will discharge the shock immediately.
- Resume CPR immediately, unless the patient regains consciousness. This is regardless of whether there was a rhythm change.
- Repeat until the patient regains spontaneous circulation, enters a nonshockable rhythm such as PEA and asystole, or a physician gives orders to terminate the resuscitation effort.

Postresuscitation Care
When a patient achieves ROSC, the paramedic’s new priority is to take steps to prevent a reentry back into cardiac arrest. This is a multistep process that involves stabilizing the heart rate and rhythm, maintaining a viable blood pressure, and maintaining an airway and ventilation if not previously secured.

1. Stabilize the Rhythm
For patients coming out of a cardiac arrest that at any time during the resuscitation presented with either VF or VT, preventing recurrence of these rhythms is the first important priority. If not done during the resuscitation, administer a loading bolus dose of either amiodarone or lidocaine. Once the bolus has been administered, initiate an infusion of that same medication. For lidocaine, inject 100 mg into 100 mL NSS to create a 1 mg/mL solution and run the infusion at 1–4 mg/min according to medical control’s direction. For amiodarone, the infusion should be run at 1 mg/min for the first 6 hours after ROSC.

2. Stabilize the Heart Rate
Frequently, a patient’s heart will start off slowly and accelerate to a more normal heart rate after conversion from a nonperfusing rhythm. If the patient’s rhythm is bradycardic, consider a bolus of 0.5–1 mg atropine intravenously, especially if the blood pressure is low. If the atropine does not work, initiate TCP for bradycardia with low blood pressure (symptomatic bradycardia).

3. Stabilize the Blood Pressure
In stabilizing the blood pressure, first provide a fluid bolus of at least 500 mL prior to beginning more aggressive treatment. This will directly increase preload, which should translate into a higher blood pressure. More than that amount in a short amount of time on an already sick heart could precipitate pulmonary edema and other signs of fluid overload. This is not a case where if some is good, more is better. If a fluid bolus has not sufficiently increased blood pressure to the target systolic pressure of 100 mmHg, the physician may order a vasopressor to be given. The options available to the paramedic are epinephrine and dopamine. Prepare the epinephrine infusion by injecting 1 mg into a 100 mL bag of NSS to create a 10 mcg/mL concentration. Run this at 0.1–0.5 mcg/kg/min and titrate to effect. For dopamine, inject 400 mg into a 250 mL bag of NSS to create a 1,600 mcg/mL concentration. Run this at 2–5 mcg/kg/min to start and titrate to effect up to 20 mcg/kg/min. The effect to which the titration is being performed is an SBP of 100 mmHg. Once that value is achieved, turn down the infusion rates and maintain that blood pressure. Finally, if the blood pressure allows, raise the head of the bed to about 30° to help with cerebral drainage and keep the patient warm as part of the shock treatment plan.

Withholding Resuscitative Efforts
Withholding CPR means either deciding not to provide it in the first place or ceasing efforts once they have begun. A paramedic may encounter 3 situations that will signal that the patient has already been in cardiac arrest for too long to merit any attempts to even begin. First and most obvious is putrefaction and signs inconsistent with life. If the patient has been deceased for so long that they actually have begun to putrefy or rot, nothing can be done. Furthermore, other signs inconsistent with life may be present, such as decapitation. 
Second is rigor mortis. Rigor begins to set in approximately 8 hours after death and lasts for about 12–16 hours. During this time, the body is stiff from all the muscles becoming rigid. 
The 3rd and final situation is if dependent lividity is observed. Lividity is the pooling of blood in the lowest areas of the body in response to gravity. Lividity begins to be noticeable approximately 30 minutes after death and continues indefinitely because the the heart is no longer pushing the blood around.
These situations are pretty straightforward and easily observable. But, when it comes to deciding when to stop resuscitative efforts after they have been begun—whether by the paramedics, other first responders, or bystanders—it can be much more difficult. There are very few hard and fast rules as to when to stop CPR versus bringing the patient to the hospital. For example, the patient’s family may expect you to bring the patient to the hospital; bystanders similarly may view the paramedics and other responders negatively if they appear to just “give up.” Next to consider is what to do with the body? It is becoming increasingly common to terminate resuscitations in the field rather than waste prehospital and in-hospital resources on a futile effort. The recommendation at this point is that if the paramedic believes that continuing resuscitative efforts will only prolong the inevitable, contact medical control and solicit their input and acceptance. This is particularly true in the following situations:

- ROSC did not occur after all first-line treatments have been completed.
- The patient has been in asystole for an extended period with no rhythm changes; no shocks administered.
- No bystander CPR provided at any time.
- Unwitnessed arrests.