The noticeable axis changes found on the ECG of a patient with pericardial tamponade.
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.
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.
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.
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.
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.
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.
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.
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 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.
Symptoms. These are largely dependent on the cause; however, we will ignore trauma as a cause until chapter 7. 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.
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.
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 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.
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.
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.
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.
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.
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.
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.
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 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 chapter 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.
Treatment for VF and pulseless VT was covered earlier in this chapter, 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).