This patient has classic signs of digitalis toxicity. Digoxin is commonly prescribed to patients with congestive heart failure and atrial fibrillation (A-Fib) or atrial flutter (A-Flutter). Its positive inotropic effects increase cardiac contractility and maintain cardiac output, while its negative chronotropic effects control the ventricular rate of the A-Fib or A-Flutter. Digitalis preparations (ie, Lanoxin, Digoxin) have a narrow therapeutic index—that is, there is a fine line between a therapeutic and toxic dose. You should suspect digitalis toxicity in any patient who takes Digoxin or Lanoxin and presents with complaints such as nausea, vomiting, abdominal pain, anorexia, or blurred/yellow vision. Additionally, virtually any cardiac dysrhythmia can be caused by the toxic effects of digitalis. Treatment involves the administration of Digibind, which is given at the hospital.
According to current emergency cardiac care (ECC) guidelines, absolute contraindications for fibrinolytic therapy include ANY prior intracranial hemorrhage (ie, subdural, epidural, intracerebral hematoma); known structural cerebrovascular lesion (ie, arteriovenous malformation); known malignant intracranial tumor (primary or metastatic); ischemic stroke within the past 3 months, EXCEPT for acute ischemic stroke within the past 3 hours; suspected aortic dissection; active bleeding or bleeding disorders (except menses); and significant closed head trauma or facial trauma within the past 3 months. Relative contraindications (eg, the physician may deem fibrinolytic therapy appropriate under certain circumstances) include, a history of chronic, severe, poorly-controlled hypertension; severe uncontrolled hypertension on presentation (SBP > 180 mm Hg or DBP > 110 mm Hg); ischemic stroke greater than 3 months ago; dementia; traumatic or prolonged (> 10 minutes) CPR or major surgery within the past 3 weeks; recent (within 2 to 4 weeks) internal bleeding; noncompressible vascular punctures; pregnancy; prior exposure (> 5 days ago) or prior allergic reaction to streptokinase or anistreplase; active peptic ulcer; and current use of anticoagulants (ie, Coumadin).
Since oxygen has already been administered to this patient and your partner is attaching the ECG leads, you should administer aspirin (160 to 325 mg, non-enteric-coated). Early administration of aspirin has clearly been shown to reduce mortality and morbidity in patients experiencing an acute coronary syndrome (ACS). After establishing vascular access, you should assess his vital signs and then administer 0.4 mg of nitroglycerin (up to 3 doses, 5 minutes apart), provided that his systolic BP is greater than 90 mm Hg. If 3 doses of nitroglycerin fail to completely relieve his chest discomfort, consider administering 2 to 4 mg of morphine IV, provided that his systolic BP remains above 90 mm Hg.
According to the Einthoven triangle, lead I is assessed by placing the negative (white) lead on the right arm and the positive (red) lead on the left arm. Lead II is assessed by placing the negative lead on the right arm and the positive lead on the left leg. Lead III is assessed by placing the negative lead on the left arm and the positive lead on the left leg.
The patient is experiencing an acute coronary syndrome (ACS). His 12-lead ECG indicates anteroseptal injury with lateral extension (ST elevation in leads V1 through V5). Appropriate treatment includes oxygen (maintain an SpO2 of greater than 94%), vascular access, up to three 0.4 mg doses of nitroglycerin (NTG), and 2 to 4 mg of morphine if NTG fails to relieve his pain and his systolic BP is above 90 mm Hg. Some EMS systems may use fentanyl (Sublimaze) for analgesia. Aspirin, a salicylate, is also given to patients with ACS; however, this patient is allergic to salicylates. Obtain a right-sided 12-lead ECG in patients with signs of inferior wall injury (ST elevation in leads II, III, aVF). Inferior wall infarctions may involve the right ventricle; a right-sided 12-lead ECG will help confirm this. Apply the multi-pads to the patient, not because he is at risk for bradycardia (more common with inferior infarctions), but because he is at risk for cardiac arrest due to V-Fib or pulseless V-Tach.
Although any of the listed conditions could be causing this patient’s condition, the fact that he missed his last three dialysis treatments should make you most suspicious for hyperkalemia. Dialysis filters metabolic waste products from the blood in patients with renal insufficiency or failure. If the patient is not dialyzed, these waste products, including potassium and other electrolytes, accumulate to toxic levels in the blood. In addition to performing high-quality CPR, managing the airway, and administering epinephrine, your protocols may call for the administration of calcium chloride and sodium bicarbonate if hyperkalemia is suspected. Albuterol also has been shown to be effective in treating patients with hyperkalemia becauses it causes potassium to shift back into the cells; it can be nebulized down the ET tube or administered intravenously. Follow your local protocols regarding the treatment for suspected hyperkalemia.
Once vascular access has been obtained (IV or IO), the first drug and dose given to all patients in cardiac arrest—regardless of the rhythm on the cardiac monitor—is epinephrine 1 mg (10 mL) of a 1:10,000 solution, repeated every 3 to 5 minutes. You may consider a one-time dose of vasopressin (40 units) to replace the first or second dose of epinephrine, but not both. Higher doses of epinephrine may be necessary if special circumstances exist (ie, severe beta-blocker toxicity). Consult with medical control as needed.
When assessing the cardiac rhythm of any patient, you must interpret it in the context of his or her clinical status. Before you reach for atropine or a pacemaker, determine if the bradycardia is causing hemodynamic compromise (ie, hypotension, altered mental status, chest pressure or discomfort, pulmonary edema). If the patient is hemodynamically unstable, treat according to established ACLS guidelines (ie, atropine, pacing, etc.). However, if the patient is hemodynamically stable, simply monitor his or her clinical status and transport to the hospital.
Of the cardiac rhythms listed, atrial fibrillation (A-Fib) is the only one that is irregularly irregular. In fact, A-Fib is never seen as a regular rhythm. At a rate of less than 100 beats/min, A-Fib is said to be controlled. Uncontrolled A-Fib, or A-Fib with a rapid ventricular rate (RVR), occurs when the ventricular rate exceeds 100 beats/min. Second-degree AV block type I has a pattern that is regularly irregular; the P-R interval progressively lengthens until a P wave is blocked. Ventricular tachycardia (V-Tach) and supraventricular tachycardia (SVT) are typically regular rhythms.
The correct initial dose and rate of administration of amiodarone for a patient with refractory ventricular fibrillation or pulseless ventricular tachycardia is 300 mg rapid IV or IO push. You may repeat amiodarone one time in 5 minutes at a dose of 150 mg rapid IV or IO push. For patients with hemodynamically stable narrow or wide-complex tachycardias, the correct dose and rate of administration for amiodarone is 150 mg given over 10 minutes.
In general patient assessment, the main purpose of listening to heart sounds is to identify the “lub-dub” that indicates the cardiac valves are functioning properly. S1 (lub) occurs near the beginning of ventricular contraction, when the tricuspid and mitral valves close. S2 (dub) occurs near the end of the ventricular contraction, when the pulmonary and aortic valves close. Although cardiac rate and regularity can be assessed by listening to heart sounds (apical pulse), the quality of the heartbeat can only be assessed by palpating the pulse. The point of maximal impulse (PMI)—also called the apical thrust—is not heard, but rather seen. The PMI, which is normally located on the left anterior part of the chest in the midclavicular line at the fifth intercostal space, occurs when the heart’s apex rotates forward with systole and gently beats against the chest wall, producing a visible pulsation.
According to the 2010 guidelines for CPR and emergency cardiac care (ECC), the correct dosing regimen of adenosine for a hemodynamically stable patient with a narrow-complex tachycardia is 6 mg via rapid (over 1 to 3 seconds) IV push. If needed, adenosine can be repeated in 1 to 2 minutes in a dose of 12 mg rapid IV push.
Because of the typical “sawtooth” flutter (F) waves, this rhythm is interpreted as atrial flutter (A-Flutter). The block is fixed in that the ratio of F waves to QRS complexes is consistent (2:1). A-Flutter with a variable block occurs when the ratio of F waves to QRS complexes is different. Atrial fibrillation (A-Fib) is characterized by an irregularly irregular rhythm with no identifiable P waves. A type II second-degree AV block is characterized by a rhythm in which some P waves are blocked (eg, they are not followed by QRS complexes).
Cardioversion involves delivering a shock that is synchronized to occur during the R wave, which is when the heart is absolutely refractory. This prevents the shock from occurring during the relative refractory period (the downslope of the T wave). Depolarization that occurs during the relative refractory period may induce a non-perfusing ventricular dysrhythmia, such as pulseless V-Tach or V-Fib. Synchronized cardioversion is indicated for patients with supraventricular or ventricular tachycardia who have a pulse, but are hemodynamically unstable.
The process of depolarization begins as sodium ions rush into the cell. At the same time, calcium ions enter the cell—albeit more slowly and through specialized channels—to help maintain the depolarized state of the cell membrane and to supply calcium ions for contraction of cardiac muscle tissue. During repolarization, the sodium and calcium channels close, thus stopping the rapid influx of these ions. Then, special potassium channels open, allowing potassium ions to rapidly exit the cell. This helps restore the inside of the cell to its negative charge; the proper electrolyte distribution is then reestablished by pumping sodium ions out of the cell and potassium ions back in. After the potassium channels close, the sodium-potassium pump helps move sodium and potassium ions back to their respective locations. For every three sodium ions the pump moves out of the cell, it moves two potassium ions into the cell, thereby maintaining the polarity of the cell membrane
Third-degree AV block is caused by a complete block at the AV node. The SA node initiates impulses as usual; however, when they reach the AV node, they are blocked. Resultantly, the ventricles receive no electrical stimulus from the atria, so they initiate their own impulses, although at a much slower rate. On the ECG, this manifests as a bradycardic rhythm with more P waves than QRS complexes. The P-P intervals are regular (some P waves may not be visible because they are buried in a QRS complex), as are the R-R intervals; however, no relationship exists between a given P wave and QRS complex. Second-degree AV block type I (Wenkebach) is caused by a progressive delay at the AV node until an impulse is blocked from entering the ventricles. On the ECG, this manifests as a progressively lengthening P-R interval until a P wave is blocked (not followed by a QRS complex). At this point, the R-R interval becomes irregular, and the presence of this lone P wave increases the ratio of P waves to QRS complexes. Second-degree AV block type I may or may not be associated with bradycardia. Second-degree AV block type II is caused by an intermittent block at the AV node; it occurs when atrial impulses are not conducted to the ventricles. Unlike a second-degree AV block type I, however, a type II block is characterized by consistent P-R intervals of the P waves that are conducted. First-degree AV block is an abnormal delay at the AV node; on the ECG, this manifests with PR intervals greater than 0.20 seconds (120 ms) in duration. In first-degree AV block, all of the atrial impulses are conducted through the AV node and into the ventricles.
The patient in this scenario is likely in ventricular tachycardia (V-Tach). Approximately 90% of wide-complex tachycardias are ventricular in origin. Furthermore, he is hypotensive and has a decreased level of consciousness—signs of hemodynamic compromise. To prevent his condition from deteriorating further, immediate synchronized cardioversion, starting with 100 joules, is indicated. Monophasic (or biphasic equivalent) defibrillation is indicated for patients with pulseless V-Tach and ventricular fibrillation (V-Fib). Amiodarone (150 mg over 10 minutes) is indicated for patients with V-Tach who have a pulse, but are hemodynamically stable; it may also be used as an adjunct for patients with unstable V-Tach when cardioversion alone is not effective. Magnesium sulfate (1 to 2 g) is indicated for patients with torsade de pointes—a variant of polymorphic V-Tach.
Wolff-Parkinson-White (WPW) syndrome is a condition in which accessory pathways—called the bundle of Kent—bypass the atrioventricular (AV) node, causing the ventricles to depolarize earlier than normal (preexcitation). Because the normal delay at the AV node does not occur, the PR intervals in patients with WPW are usually less than 0.12 seconds (120 ms). When conduction occurs down the AV node and simultaneously along the bundle of Kent in an anterograde fashion, the two waves of depolarization meet (fusion). This manifests on the ECG as a delta wave—slurring or notching at the beginning of the QRS complex—which may cause QRS widening. The bundle of Kent is a potential site for a reentry circuit because it allows continued transmission of an electrical impulse from the atria to the ventricles. Therefore, patients with WPW are prone to reentry tachycardias—most notably, AV reentry supraventricular tachycardia (SVT).
Most cases of sudden cardiac arrest (SCA) in the adult population are secondary to a cardiac dysrhythmia, usually ventricular fibrillation (V-Fib). This fact underscores the criticality of early defibrillation. Respiratory failure is the most common cause of cardiac arrest in the pediatric population.
If a patient develops ventricular fibrillation (V-Fib) or pulseless ventricular tachycardia (V-Tach) following synchronized cardioversion, immediately begin CPR (even if it’s just for a short period of time), ensure that the monitor/defibrillator is not in synchronize mode, and defibrillate as soon as possible. CPR should be ongoing as the defibrillator is charging in order to avoid unnecessary delays in performing chest compressions. The synchronize mode must be turned off prior to defibrillation or the device will not deliver a shock; this is because there are no R waves to synchronize with in V-Fib. Vascular access (IV or IO), advanced airway management, and pharmacologic therapy should be performed during the 2-minute cycles of CPR; they are not an immediate priority during early cardiac arrest.
This patient’s clinical presentation and his history of hypertension and transient ischemic attacks (TIAs) suggest acute ischemic stroke. However, his blood glucose level (BGL) is significantly low and must be treated. Untreated hypoglycemia may cause irreversible brain damage or death. Appropriate treatment for this patient involves administering 50% dextrose (consider giving 12.5 g) and then reassessing his BGL to determine the need for additional glucose. Because the patient is confused, and because some patients with acute ischemic stroke lose protective airway reflexes, oral glucose should be avoided. He may not be able to swallow it, which may result in aspiration. Further treatment includes protecting his impaired extremities from injury, monitoring his cardiac rhythm, and transporting him to the hospital. Notify the receiving facility early. Aspirin should be avoided in the prehospital setting for patients with signs and symptoms of a stroke. A CT scan of the head must be performed first to rule out intracranial hemorrhage.
Acute ischemic strokes represent approximately 75% of all strokes. Each cerebral hemisphere controls functions on the contralateral (opposite) side of the body; therefore, sensory and motor deficits (ie, hemiparesis, hemiparalysis) are observed on the side of the body opposite the stroke. However, because the facial nerves do not decussate (cross as they leave the cerebral cortex, move through the brainstem, and arrive at the spinal cord), facial droop is typically observed on the ipsilateral (same) side as the stroke. Pupillary changes, if present, will also occur on the same side as the stroke because of optic nerve crossover in the brain. Other common signs of acute ischemic stroke include dysarthria (slurred speech), dysphasia (difficulty speaking or understanding), aphasia (inability to speak or understand), and mental status changes. In contrast to acute ischemic stroke, acute hemorrhagic stroke (caused by a ruptured cerebral artery) typically presents with more ominous signs, which include a sudden, severe headache that is followed by a rapid decline in level of consciousness. Because bleeding is occurring within the brain, intracranial pressure increases, resulting in signs such as decorticate (flexor) or decerebrate (extensor) posturing, asymmetric or bilaterally dilated pupils, and Cushing’s triad (hypertension, bradycardia, abnormal respiratory pattern).
Although the patient is in supraventricular tachycardia (SVT), she remains stable following your initial efforts to slow her heart rate with vagal maneuvers and adenosine. Her failure to respond to initial treatment does not automatically make her unstable. Simply transport her, closely monitor her en route, and be prepared to cardiovert her if she does become unstable (ie, hypotension, altered mental status, chest pain). Unless specified in your local protocols, pharmacologic therapy beyond adenosine (ie, calcium channel blockers, amiodarone) is typically not indicated in the field for stable patients with SVT, although these medications may be given in the emergency department. However, if your protocols or medical control call for the administration of diltiazem (Cardizem), the initial dose is 0.25 mg/kg.
The rhythm is regular, with a ventricular rate of approximately 40 to 50 beats/min. It has wide (greater than 120 ms [0.12 sec]) QRS complexes and more P waves than QRS complexes. Because there is no relationship between any one P wave to a given QRS complex, this is a third-degree AV block, also called complete heart block. First-degree AV block is characterized by P-R intervals that exceed 200 ms (0.20 seconds [5 small boxes]), although there is a consistent 1:1 P-to-QRS ratio; unless ectopic compexes are present, it is usually a regular rhythm. Second-degree AV block type I is characterized by P-R intervals that progressively lengthen until a P wave is blocked (not followed by a QRS complex); it is an irregular rhythm. Second-degree AV block type II, which may be regular or irregular, is characterized by more P waves than QRS complexes; however, the P-R intervals of the conducted complexes are the same.
In the absence of any significant medical history, this patient’s weakness probably signaled the onset of his atrial fibrillation (A-Fib). New-onset A-Fib of greater than 48 hours’ duration should not be treated with synchronized cardioversion until the patient is adequately anticoagulated first (ie, Coumadin). Blood can stagnate in the fibrillating atria, which increases the risk of clot formation; cardioversion may dislodge these clots, resulting in a stroke, pulmonary embolism, or myocardial infarction. Furthermore, this patient is hemodynamically stable and is not in need of electrical therapy. Appropriate treatment for a patient with A-Fib or atrial flutter (A-Flutter) with a rapid ventricular rate (RVR) involves controlling the ventricular rate with a calcium-channel blocker. Diltiazem (Cardizem) is the most common drug used for this purpose. The initial dose is 0.25 mg/kg, which may be repeated in 15 minutes in a dose of 0.35 mg/kg. Amiodarone may be used to terminate new-onset A-Fib or A-Flutter, but is uncommonly given for this purpose in the prehospital setting. Vagal maneuvers and adenosine are indicated for narrow-complex tachycardias in an attempt to slow the ventricular rate so you can identify the underlying rhythm. You have already identified this patient’s rhythm.
ST segment elevation that is equal to or greater than 1-mm in two or more contiguous leads indicates myocardial injury (eg, an acute MI in progress). ST segment depression and/or dynamic T wave inversion indicates myocardial ischemia. Leads V1 and V2 view the interventricular septum; leads V3 and V4 view the anterior wall of the left ventricle; leads V5, V6, I, and aVL view the lateral wall of the left ventricle; and leads II, III, and aVF view the inferior wall of the left ventricle. Therefore, if a patient is experiencing acute injury involving the interventricular septum and anterior wall of the left ventricle (anteroseptal injury), you would expect the 12-lead ECG tracing to reveal ST segment elevation is leads V1 through V4. It is important to note, however, that an absence of ST elevation does not definitively rule out acute myocardial infarction.
Leads V1 and V2 view the interventricular septum. Leads V3 and V4 view the anterior wall of the left ventricle. Leads V5 and V6 view the low lateral wall of the left ventricle. Leads I and aVL view the high lateral wall of the left ventricle. Leads II, III, and aVF view the inferior wall of the left ventricle. Lead V4R views the right ventricle.
Although the patient’s heart rate is slow, he is hemodyamically stable; therefore, pharmacological or electrical intervention aimed at increasing his heart rate is not indicated at this point. Provide supportive care (ie, oxygen as needed, IV set to a KVO/TKO rate) and transport him to the hospital. Consider administering an antiemetic drug, such as ondansetron (Zofran) or promethazine (Phenergan). If his clinical status deteriorates (ie, chest pain, dyspnea, altered mental status, hypotension), atropine sulfate (0.5 mg) or transcutaneous cardiac pacing (TCP) will be necessary. IV fluid boluses are not indicated at this point because there is no evidence of hypovolemia.
Aspirin (acetylsalicylic acid [ASA]) blocks the formation of thromboxane A2, thus minimizing local coronary vasoconstriction and preventing platelet aggregation. Therefore, aspirin helps prevent an existing clot from getting any larger. Aspirin has clearly been shown to reduce mortality and morbidity from acute coronary syndrome (ACS), and should be given as soon as possible. Examples of blood thinners (anticoagulants) include warfarin sodium (Coumadin) and heparin. Aspirin is not an anticoagulant, nor does it dilate the coronary arteries; nitroglycerin (NTG) does this.
In patients with cardiogenic pulmonary edema (ie, congestive heart failure [CHF]), morphine sulfate causes systemic pooling of blood, which increases venous capacitance and decreases preload (the volume of blood returned to the heart). The net effect is to minimize the volume of fluid that accumulates in the lungs. Note that morphine is not a diuretic and will not remove fluid from the body. This is accomplished by administering furosemide (Lasix), which may be considered for patients with CHF and pulmonary edema.
The sinoatrial (SA) node is the dominant cardiac pacemaker; it sets the inherent rate at which the heart beats. The SA node receives blood from the right coronary artery (RCA); therefore, if the RCA is occluded (ie, acute myocardial infarction), the SA node will become ischemic and may cease functioning. If this occurs, the atrioventricular (AV) node would likely assume the role of the primary pacemaker, although at an inherently slower rate. If the SA node fails, the flow of electricity throughout the atria would likely suffer as well; this would result in a decrease in atrial kick—the volume of blood (about 20%) that is ejected from the atria to the ventricles (the other 80% fills the ventricles by gravity). Sudden cardiac arrest is more likely to occur following occlusion of the left main coronary artery. Ectopic ventricular complexes (eg, PVCs), although benign in many cases, may indicate irritability in the ventricles.
Your first action after establishing return of spontaneous circulation (ROSC) in a patient—regardless of his or her arrest rhythm and duration—is to assess the patient’s ventilatory status. If the patient is not breathing or is breathing inadequately, provide ventilatory support. After assessing and managing airway and breathing, assess the patient’s blood pressure and stabilize it if it is low. Airway and circulatory support are critical following ROSC; inadequate ventilation and/or hypotension following cardiac arrest may lead to a recurrence of cardiac arrest. Depending on your local protocols, IV amiodarone may be given following ROSC. After assessing and maintaining respiratory and circulatory functions, obtain a 12-lead ECG if time allows. If the patient remains comatose following ROSC, consider inducing therapeutic hypothermia.
Your patient has a narrow-complex tachycardia, probably supraventricular tachycardia (SVT). Furthermore, he is hemodynamically unstable as evidenced by his hypotension, respiratory distress, and chest discomfort. Heart rates greater than 150 beats/min often cause hemodynamic compromise because they impair ventricular filling and subsequent cardiac output. Patients with unstable tachycardias require synchronized cardioversion. For the patient with a regular narrow-complex tachycardia (ie, SVT), start with 50 to 100 joules. Consider sedating the patient prior to cardioversion only if doing so does not delay the procedure. If the initial cardioversion attempt is unsuccessful, repeat the cardioversion, increasing the energy setting in a stepwise fashion, and search for potentially reversible underlying causes. Defibrillation is indicated for patients with V-Fib and pulseless V-Tach. Transcutaneous cardiac pacing (TCP) is indicated for patients with hemodynamically unstable bradycardia. Amiodarone, in a dose of 150 mg over 10 minutes, is indicated for patients with stable narrow or wide-complex tachycardias.
Early CPR and defibrillation are the two interventions that will have the greatest impact on patient survival from sudden cardiac arrest (SCA). Early, effective CPR maintains perfusion to the body’s vital organs until defibrillation can be provided. The most common initial cardiac rhythm observed during SCA is ventricular fibrillation (V-Fib). Early defibrillation, in conjunction with early CPR, greatly enhances the chance of establishing return of spontaneous circulation (ROSC). The probability of successful defibrillation decreases over time, especially if CPR is delayed. For each minute that V-Fib persists, the patient’s chance of survival decreases by approximately 7% to 10%.
Atropine sulfate is a parasympathetic blocker (parasympatholytic, vagolytic). It is used to increase the heart rate by opposing the vagus nerve when excessive parasympathetic (vagal) tone causes symptomatic bradycardia. Alpha adrenergic agonists, such as norepinephrine (Levophed), primarily stimulate alpha-1 receptors and cause vasoconstriction. Drugs such as propranolol (Inderal) and prazosin (Minipress) block sympathetic nervous system activity by binding to beta and alpha receptors, respectively. Beta receptor blockade causes a decrease in heart rate (negative chronotropy), a decrease in contractility (negative inotropy), and a decrease in electrical conduction velocity (negative dromotropy). Alpha receptor blockade causes vasodilation, and a subsequent decrease in blood pressure. Drugs that increase cardiac contractility, such as dopamine (Intropin), do so through their positive inotropic effects.
Your patient’s history and clinical presentation is consistent with cardiogenic shock. She has had chest pressure and shortness of breath for 2 days and is now significantly hypotensive with weak pulses. Because of its positive inotropic effect of increasing myocardial contractility, dopamine is the drug of choice for non-hypovolemic shock (eg, cardiogenic shock) and may improve perfusion. Typically, dopamine for cardiogenic shock is started at 2 µg/kg/min and titrated upwards as needed to improve blood pressure and perfusion. At doses of greater than 10 µg/kg/min, dopamine acts predominantly as a vasopressor, which results in systemic vasoconstriction. Clearly, nitroglycerin is contraindicated in any patient with shock; its potent vasodilatory effects would further lower the patient’s blood pressure and worsen her condition. Amiodarone is not the drug of choice for this patient; it is given in a dose of 150 mg over 10 minutes for hemodynamically stable patients with wide or narrow-complex tachycardias that exceed 150 beats/min. Caution must be used if you consider giving a normal saline bolus; the coarse crackles in her lungs indicate pulmonary edema, which could easily be exacerbated by large fluid boluses. Her problem is heart failure, not hypovolemia.
Appropriate treatment for a patient in asystole includes high-quality CPR with minimal interruptions, vascular access, 1 mg of epinephrine 1:10,000 every 3 to 5 minutes, advanced airway management (eg, ET tube, multilumen airway, supraglottic airway), and assessing for and ruling out potentially reversible causes (Hs and Ts). Vasopressin may be given in a one-time dose of 40 units to replace the first or second dose of epinephrine, but not both. Transcutaneous cardiac pacing (TCP) has not shown to be beneficial for patients in asystole and is not recommended. Antidysrhythmic drugs, such as amiodarone and lidocaine, are indicated for patients with ventricular fibrillation or pulseless ventricular tachycardia; they are not given to patients with asystole.
After determining that an adult patient is unresponsive and apneic, you should assess for a carotid pulse for at least 5 seconds but no more than 10 seconds. If the patient has a pulse, open the airway and provide rescue breathing. If the patient does not have a pulse, begin CPR (starting with chest compressions), then open the airway and give 2 rescue breaths. Assess the patient’s cardiac rhythm as soon as a monitor/defibrillator is available.
If a patient has a heart rate that is greater than 150 per minute, and he or she is clinically unstable because of the cardiac rhythm, synchronized cardioversion should be performed. The following initial energy settings are recommended by current emergency cardiac care (ECC) guidelines: narrow and regular, 50 to 100 joules (biphasic or monophasic); narrow and irregular, 120 to 200 joules biphasic (200 joules monophasic); wide and regular, 100 joules (biphasic or monophasic); wide and irregular, defibrillation dose (NOT synchronized). If the initial energy dose is unsuccessful, increase in a stepwise fashion.
Leads V1 and V2 view the interventricular septum. Leads V3 and V4 view the anterior wall of the left ventricle. Leads I, aVL, V5 and V6 view the lateral wall of the left ventricle. Leads II, III, and aVF view the inferior wall of the left ventricle. Myocardial ischemia manifests on the 12-lead ECG with ST segment depression and/or T-wave inversion, whereas myocardial injury manifests with ST segment elevation that is equal to or greater than 1-mm in two or more contiguous leads. Therefore, 3-mm ST segment elevation in leads V3 through V6 indicates injury to the anterior and lateral wall of the left ventricle (anterolateral injury).
Pulseless electrical activity (PEA) exists when an unresponsive, apneic, pulseless patient presents with a regular cardiac rhythm. Treatment for PEA includes immediate high-quality CPR with minimal interruptions, obtaining vascular access (IV or IO), 1 mg of epinephrine every 3 to 5 minutes, advanced airway management (ie, ET tube, multilumen or supraglottic airway), and assessing for and treating reversible causes (Hs and Ts). Vasopressin, in a one-time dose of 40 units, can be given to replace the first or second dose of epinephrine, but not both. There are insufficient data to recommend transcutaneous pacing (TCP) for patients with bradycardic PEA or asystole, and the routine use of calcium chloride during cardiac arrest is not recommended.
Waking up in the middle of the night with severe difficulty breathing (paroxysmal nocturnal dyspnea [PND]) and coughing up blood or blood-tinged sputum (hemoptysis) are consistent with left-sided heart failure and pulmonary edema. Right-sided heart failure typically does not present with respiratory distress; it commonly manifests with jugular venous distention and peripheral edema. Shortness of breath and hemoptysis are not consistent with a gastrointestinal (GI) bleed; signs of a GI bleed include abdominal pain, vomiting up blood (hematemesis), which may be bright red or have a coffee-ground appearance; dark, tarry stools (melena); or bright red blood in the stool (hematochezia). Because left-sided heart failure can be caused by other factors, such as a long history of poorly-controlled hypertension, angina may or may not be present.
First, convert the patient’s weight from pounds to kilograms: 145 ÷ 2.2 = 66 kg. Next, determine the desired dose: 15 µg/kg/min × 66 kg = 990 µg/min. The next step is to determine the concentration of dopamine on hand: 800 mg ÷ 500 mL = 1.6 mg/mL (1,600 µg/mL [1.6 × 1,000 = 1,600]). Now, you must determine the number of mL to be delivered per minute: 990 µg/min [desired dose] ÷ 1,600 µg/mL [concentration on hand] = 0.6 mL/min. The final step is to determine the number of drops per minute that you must set your IV flow rate at: 0.6 mL/min × 60 gtts/mL (drop factor of the microdrip) ÷ 1 (total infusion time in minutes) = 36 gtts/min.
Syncope (fainting) of cardiac origin is caused by a sudden decrease in cerebral perfusion secondary to a decrease in cardiac output. This is usually the result of an acute bradydysrhythmia or tachydysrhythmia. In this particular patient, the presence of frequent premature atrial complexes (PACs), which indicates atrial irritability, suggests paroxysmal supraventricular tachycardia (PSVT) as the underlying dysrhythmia that caused her syncopal episode. In PSVT, the heart is beating so fast that ventricular filling and cardiac output decrease, which results in a transient decrease in cerebral perfusion. Not all patients with PSVT experience syncope. Many experience an acute onset of palpitations and/or lightheadedness that spontaneously resolves.
Immediately following return of spontaneous circulation (ROSC), as evidenced by the presence of a pulse, the paramedic should reassess the patient’s ventilatory status and continue to treat accordingly. Remember, if an advanced airway is placed during cardiac arrest, ventilations are given at a rate of one breath every 6 to 8 seconds (8 to 10 breaths/min) with continuous chest compressions. However, if ROSC occurs and the patient remains apneic, you should deliver one breath every 5 to 6 seconds (10 to 12 breaths/min) for the adult, or one breath every 3 to 5 seconds (12 to 20 breaths/min) for infants and children. Next, assess the patient’s BP and use crystalloid fluid boluses or an inotropic drug (eg, dopamine) to treat hypotension and maintain adequate perfusion. If the patient remains comatose following ROSC, therapeutic hypothermia should be considered. Follow your local protocols.
Cardiac rhythm checks should be performed after every 2 minutes of CPR. If you note a change in the patient’s cardiac rhythm after 2 minutes, especially if it is an organized rhythm, you should check for a carotid pulse for 5 to 10 seconds. In this case, the patient has converted from V-Fib to a wide-complex tachycardia, which is probably V-Tach. If the patient has a pulse, perform synchronized cardioversion with the same energy setting that you used for defibrillation. If the patient is pulseless, however, you should defibrillate and immediately resume CPR, starting with chest compressions. During the 2-minute period of CPR, you can adminster epinephrine, if 3 to 5 minutes have passed, or 300 mg of amiodarone via rapid IV or IO push.
A regular, narrow complex tachycardia at a rate greater than 150 beats/min is consistent with supraventricular tachycardia (SVT). Although the patient is conscious and alert, she is complaining of chest discomfort and is hypotensive. Since she could be experiencing an acute coronary syndrome (ACS), you should instruct her to chew and swallow up to 325 mg of aspirin. Aspirin should be given to any patient suspected of experiencing an ACS, provided there are no contraindications (eg, allergy); it will not affect her blood pressure. Nitroglycerin, however, may exacerbate her hypotension and should be avoided. You can consider administering adenosine; however, the initial dose is 6 mg rapid IV push. Amiodarone, in a dose of 150 mg over 10 minutes, is appropriate for patients with hemodynamically stable wide-complex tachycardias (ie, V-Tach). Closely monitor this patient and be prepared to perform synchronized cardioversion.
A right ventricular infarction (RVI) should be suspected when a patient presents with ECG changes indicative of an inferior wall injury pattern (equal to or greater than 1-mm ST elevation in leads II, III, and aVF; reciprocol ST depression and T wave inversion in leads I and aVL) AND has equal to or greater than 1-mm ST elevation in lead V4R when a right-sided 12-lead ECG is obtained. Patients experiencing an RVI are preload dependent and often present with hypotension; therefore, vasodilators (eg, nitroglycerin, morphine) should be avoided. Instead, IV fluid boluses should be given to maintain adequate perfusion. Other signs of an RVI include jugular venous distention and peripheral edema. Pulmonary edema and coughing up blood (hemoptysis) are indicative of left ventricular failure.
Unless associated with a fast rate (> 100 beats/min) and hemodynamic compromise (eg, hypotension, altered mental status, pulmonary edema), treatment for atrial flutter is usually not necessary in the prehospital setting. Administer supplemental oxygen if indicated, transport, and monitor the patient’s hemodynamic status en route. For this patient, you should treat his nausea with an antiemetic, such as ondansetron (Zofran), 4 mg; or promethazine (Phenergan), 12.5 to 25 mg.
Patient assessment involves simple questioning techniques. You should ask open-ended questions, whenever possible; this is especially true when determining the onset and quality of a patient’s pain. Asking a leading question, such as “Do you have sharp chest pain?” will often lead the patient to say “yes,” even though that is not the true quality of his or her pain. Allow the patient to use his or her own words when describing symptoms.
Toprol (metaprolol) is a commonly prescribed beta-blocker used to treat various cardiovascular conditions, including hypertension and tachydysrhythmias. Proscar (finasteride) is used to treat benign prostatic hyperplasia (BPH). Fluoxetine (Prozac) is a selective serotonin reuptake inhibitor (SSRI) antidepressant. It is used to treat conditions such as depression, generalized anxiety disorder, and obsessive-compulsive disorder (OCD). Lansoprazole (Prevacid)—a proton pump inhibitor—is used to treat conditions such as heartburn, acid reflux disease, and ulcers. Clonazepam (Klonopin) is a benzodiazepine sedative-hypnotic; it is used to treat anxiety.
Nitroglycerin (NTG) is a vasodilator. It relaxes the smooth muscle of the vascular walls, which promotes systemic venous pooling of blood. As a result, venous return to the right atrium (preload) is decreased; this decreases the cardiac workload. The amount of resistance that the left ventricle must contract against (afterload) is also decreased secondary to vasodilation. By dilating the coronary arteries, NTG increases blood supply to ischemic myocardium and may relieve the chest pain, pressure, or discomfort associated with acute coronary syndrome (ACS). Nitroglycerin is not an analgesic; if it relieves the patient’s pain, it is because myocardial oxygen supply and demand have been rebalanced.
A transmural myocardial infarction involves the entire thickness of the left ventricular wall from endocardium to epicardium; it is associated with ST-segment elevation and, eventually, the development of pathologic Q waves. A subendocardial infarction involves multiple areas of myocardial necrosis confined to the inner one third to one half of the left ventricular wall; subendocardial infarctions are also referred to as non-Q-wave infarctions. Myocardial ischemia caused by focal areas of spontaneous coronary vasospasm, which may lead to infarction, is called Prinzmetal’s (variant) angina; the exact cause of this spontaneous coronary vasospasm is largely unknown.
The cardiac rhythm described is a third-degree (complete) AV block, and the patient is clinically unstable (ie, hypotension, altered mental status, shortness of breath). Third-degree AV block is characterized by a slow ventricular rate and no P-to-QRS relationship (AV dissociation). Patients with high-grade AV blocks (eg, second-degree type II, third-degree) are often clinically unstable and require immediate transcutaneous cardiac pacing (TCP). Atropine is an appropriate drug for clinically unstable patients with sinus bradycardia and bradycardia associated with low-grade AV blocks (eg, first-degree, second-degree type I); it is not recommended for high-grade AV blocks. If TCP is unsuccessful for this patient, consider an epinephrine infusion (2 to 10 µg/min) or a dopamine infusion (5 to 10 µg/kg/min), either of which may increase her heart rate and blood pressure. The patient’s hypotension is secondary to severe bradycardia, not hypovolemia; therefore, a rapid IV fluid bolus is not indicated. If you have reason to suspect that the patient is experiencing an acute coronary syndrome (ACS), aspirin should be given.
Diltiazem hydrochloride (Cardizem) is a calcium channel blocking drug that is used to treat rapid ventricular rates associated with atrial fibrillation or atrial flutter. It can also be used after adenosine to treat refractory reentry supraventricular tachycardia in hemodynamically stable patients. The initial dose of diltiazem is 0.25 mg/kg IV over 2 minutes; the average initial dose is 15 to 20 mg. It may be repeated in 15 minutes in a dose of 0.35 mg/kg IV over 2 minutes; the average second dose is 20 to 25 mg. A 165-pound patient weighs 75 kg. Therefore, the initial dose of diltiazem for a patient of this weight would be 18.75 mg (approximately 19 mg), and the second dose would be 26.25 mg (approximately 26 mg).
Since this rhythm has narrow (less than 0.12 seconds) QRS complexes and a rate greater than 150 beats/min, it should be interpreted as supraventricular tachycardia (SVT), which means that its site of origin is above (supra) the level of the ventricles. SVT can be either atrial or junctional in origin. Atrial fibrillation is characterized by an irregularly irregular rhythm and no discernable P waves. Atrial flutter is characterized by flutter (F) waves that resemble a saw tooth. Ventricular tachycardia (V-Tach), in contrast to SVT, is characterized by wide (greater than 0.12 seconds) QRS complexes and no visible P waves.
The first drug given to any patient in cardiac arrest is epinephrine in a dose of 1 mg (10 mL of a 1:10,000 solution) via the IV or IO route. This dose should be repeated every 3 to 5 minutes. Alternatively, a one-time dose of vasopressin (40 units) can be given to replace the first or second dose of epinephrine, but not both. Do NOT hyperventilate the patient as doing so increases intrathoracic pressure and can impair venous return (preload) and cardiac output, which would decrease the effectiveness of chest compressions. After an advanced airway has been placed during cardiac arrest, deliver one breath every 6 to 8 seconds (8 to 10 breaths/min) and ensure that chest compressions are uninterrupted. There is presently no evidence to support the efficacy of transcutaneous cardiac pacing (TCP) in patients with bradycardic PEA or asystole.
Angina pectoris occurs when the heart’s demand for oxygen exceeds it’s available supply (ischemia) and is a sign of coronary artery disease (CAD). Angina is classified as being stable or unstable. Stable angina typically follows a predictable pattern (ie, chest pain, pressure, or discomfort induced by exertion), lasts less than 15 minutes, and is usually relieved with rest and/or nitroglycerin. While unstable angina (preinfarction angina) can also occur during exertion, it more commonly occurs when the patient otherwise would not expect it to, such as when he or she is asleep or is otherwise resting. Furthermore, unstable angina is often not relieved by rest and/or nitroglycerin and typically lasts longer than 15 minutes. Chest pressure, tightness, or discomfort occurs in patients with both stable and unstable angina. If a patient is experiencing angina, you would expect to see ST segment depression and/or T wave inversion on the 12-lead ECG as these are indicators of myocardial ischemia. ST segment elevation indicates myocardial injury (eg, acute MI in progress).
In multifocal atrial tachycardia (MAT), the pacemaker of the heart moves within various areas of the atria. MAT is characterized by a ventricular rate that is greater than 100 beats/min. MAT is irregularly irregular, with variation between R-R intervals based on the site of the pacemaker for that particular complex. P waves are present, upright, and precede each QRS complex; however, the shapes of the P waves vary as an indication of their different sites of origin. The P-R interval generally measures between 0.12 and 0.20 seconds, but also varies slightly based on the origin of the particular complex. Atrial fibrillation (A-Fib) is also an irregularly irregular rhythm; however, there are no discernable P waves. A wandering atrial pacemaker essentially contains all the components of MAT; unlike MAT, however, the ventricular rate is typically less than 100 beats/min. Atrial flutter (A-Flutter) has characteristic flutter waves (F waves) that resemble a saw tooth. If accompanied by aberrancy, A-flutter has QRS complexes that are greater than 0.12 seconds in duration, which indicates abnormal (aberrant) ventricular conduction.
The mnemonic “MONA” is used to help remember the medications given to patients who are experiencing an acute coronary syndrome (ACS). Although it does not represent the correct sequence in which the medications should be given, it is a useful mnemonic to remember. The appropriate sequence of medications is oxygen (as needed to maintain an SpO2 of greater than 94%), aspirin (160 to 325 mg), nitrogylcerin (0.4 mg up to 3 times), and morphine (2 to 4 mg) if the nitroglycerin does not relieve the chest pain. Pain relief is very important in patients experiencing ACS (eg, unstable angina or AMI) because it reduces anxiety and subsequent oxygen consumption and demand.
Normally, there is a physiologic delay of an impulse at the AV node that allows the atria to empty into the ventricles. On the ECG, this manifests as a P-R interval—the period of time that includes atrial depolarization and the delay at the AV node—that is between 0.12 and 0.20 seconds (120 to 200 ms). A pathologic delay at the AV node, such as what occurs with a first-degree AV block, would manifest with a P-R interval that is greater than 0.12 seconds (120 ms) in duration. By contrast, A P-R interval that is less than 0.12 seconds indicates that an impulse is traversing the AV node too fast or is bypassing it altogether, such as what occurs with Wolff-Parkinson-White (WPW) syndrome, a preexcitation syndrome in which the electrical impulse follows accessory pathways around the AV node (bundle of Kent) and prematurely depolarizes the ventricles. A wide (> 0.12 seconds [120 ms]) QRS complex indicates an intraventricular conduction delay, such as a bundle branch block. P waves that vary in morphology (appearance) indicate more than one atrial pacemaker site; an example of this is an ectopic atrial rhythm.
Angina pectoris is a sign of coronary artery disease (CAD), and is the result of an imbalance in myocardial oxygen supply and demand. Stable angina occurs when the patient experiences chest pain or discomfort after a certain, predictable amount of exertion. Furthermore, the patient with stable angina typically knows what actions to take to relieve the pain (ie, rest, nitroglycerin). By contrast, unstable angina is characterized by noticeable changes in the frequency, severity, and degree of chest pain or discomfort. The patient experiences symptoms, which are often not relieved with rest and/or nitroglycerin, when myocardial oxygen demand is otherwise low (ie, sleep, rest). Unstable angina indicates advanced CAD; it is commonly referred to as preinfarction angina.
The Los Angeles Prehospital Stroke Screen (LAPSS) is a useful tool for indentifying patients who are possibly experiencing a stroke. It requires the paramedic to rule out other causes of abnormal neurologic signs (eg, seizures, hypoglycemia). There are six components to the LAPSS. If any one of these items is checked “yes” or “unknown,” you should notify the receiving facility as soon as possible and inform them that the patient is potentially experiencing a stroke. Bear in mind, however, that some patients who are experiencing a stroke may have unremarkable findings on the LAPSS (eg, all components of the LAPSS are checked “no”). Following are the six components of the LAPSS: (1) Age > 45 years; (2) History of seizures is absent; (3) Patient is not normally bedridden or confined to a wheelchair; (4) Blood glucose level is between 60 and 400 mg/dL; (5) Symptom duration is < 24 hours; (6) Unilateral asymmetry in any of the following categories: Facial smile/grimace, Grip strength, or Arm strength (eg, arm drift).
The most common cause of right ventricular failure (RVF) is left ventricular failure (LVF). When the left ventricle fails, blood backs up into the lungs and eventually into the pulmonary circulation, resulting in pulmonary hypertension. Because the right ventricle must work harder to overcome the increased resistance in the pulmonary circulation, it eventually fails as an effective forward pump. As a result, blood backs up into the systemic circulation, resulting in jugular venous distention, hepatomegaly (enlarged liver), and peripheral edema—especially to dependent areas of the body (eg, extremities, the sacrum in bedridden patients). In patients with severe RVF, total body edema (anasarca) may be present. Hypotension may be observed in patients with RVF, and commonly occurs as the result of right ventricular infarction (RVI). Treat the hypotensive patient with crystalloid fluid boluses (250 to 500 mL), which will increase preload and may improve contractility via the Starling effect. Vasodilators (ie, morphine, nitroglycerin) should not be administered to patients with RVF; they may induce or exacerbate hypotension.
The patient in this scenario has likely experienced an acute myocardial infarction and is now in cardiogenic shock (pump failure). Cardiogenic shock is characterized by general signs of shock (eg, tachycardia, diaphoresis), hypotension, altered mental status, and pulmonary congestion—a sign of significant left ventricular damage and decreased stroke volume. After ensuring airway patency and adequate oxygenation and ventilation, your priority is to improve perfusion. Crystalloid fluid boluses, at least not large fluid boluses (ie, 20 mL/kg), are not appropriate for this patient; they may exacerbate his pulmonary edema and further impair pulmonary respiration. Dopamine is a more appropriate intervention. In a dosing range of 5 to 10 µg/kg/min, dopamine possesses positive inotropic effects, which increases myocardial contractility and may improve cardiac output. Rapid transport for this patient is essential; because of your extended transport time, start the dopamine infusion en route. Unfortunately, true cardiogenic shock has a high mortality rate.
A major emphasis is placed on minimizing interruptions in CPR. Evidence has shown that even a brief pause in chest compressions can result in a significant decrease in coronary and cerebral perfusion. Therefore, CPR should be continuing—even as the defibrillator is charging. When the defibrillator is charged, ensure (visually and verbally) that nobody is touching the patient, and then deliver the shock. When defibrillating a patient with V-Fib, you must ensure that the synchronizer is off; the synchronizer will not be able to identify an R wave in V-Fib due to the chaotic nature of the dysrhythmia. Cardiac arrest patients (adults, children, and infants) should be ventilated at a rate of 8 to 10 breaths/min after an advanced airway device has been placed (eg, ET tube, multilumen airway, supraglottic airway). Excessive ventilation rates should be avoided; they cause increased intrathoracic pressure, which may impair venous return and cardiac output.
Aortic dissection occurs when the layers of the aorta undergo destructive changes, resulting in an aneurysm (weakening and ballooning of the arterial wall). In dissection of the ascending aorta, the patient typically experiences an acute onset of ripping, tearing, or stabbing pain in the anterior chest or in between the scapulae. In some patients, it may be difficult to differentiate the pain of acute aortic dissection from that of acute myocardial infarction (AMI); however, a number of distinctive features may help. The pain of an AMI is often preceded by prodromal symptoms (eg, nausea, weakness, sweating). Although pain from an AMI is acute, it gradually intensifies over time and is typically described as a squeezing or pressure sensation. By contrast, the pain of aortic dissection is acute, is of maximal intensity from the onset, and is usually described as a ripping, tearing, or stabbing feeling. Other signs and symptoms depend on the extent and location of the dissection. In dissections of the ascending aorta, one or more of the vessels of the aortic arch may be compromised. Disruption of blood flow through the innominate artery, for example, is likely to produce a difference in blood pressure between the arms. The onset and pain characteristics of abdominal aortic dissection are similar to those of ascending aortic dissection; however, the pain typically begins in the abdomen or lower back. Pulse deficits in the femoral arteries may be present, and if the aneurysm is leaking blood into the retroperitoneal space, the patient may complain of an urge to defecate and exhibit signs of shock.
The patient most likely experienced an acute myocardial infarction (AMI); however, since he did not receive timely treatment, extensive myocardial damage has resulted in pump failure. His low BP; weak, rapid pulses; and altered mental status indicate that he is systemically hypoperfused. Hypoperfusion (shock) secondary to a cardiac etiology (ie, pump failure, fast or slow heart rate) is called cardiogenic shock. True cardiogenic shock, which occurs when the myocardium is extensively and permanently damaged and can no longer meet the metabolic needs of the body, has a high mortality rate.
Thromboxane A2 is produced by activated platelets. It is a potent vasoconstrictor, it stimulates activation of new platelets, and it increases platelet aggregation. Aspirin (acetylsalicylic acid [ASA]) blocks the production of thromboxane A2, which inhibits vasoconstriction, inhibits activation of new platelets, and inhibits platelet aggregation (ie, it makes the platelets less “sticky”). Aspirin does not destroy a clot in a coronary artery—it prevents it from getting larger. Furthermore, by inhibiting local coronary vasoconstriction, it may enhance blood flow around the clot. Fibrinolytic agents (ie, alteplase [Activase], streptokinase [Streptase], tenecteplase [TNKase]) convert the body’s own clot-dissolving enzyme from its inactive form, plasminogen, to its active form, plasmin. Plasmin then destroys the fibrin matrix of the clot—hence the term “fibrinolysis.”
If return of spontaneous circulation (ROSC) occurs, you must focus on preventing recurrent cardiac arrest and providing optimal conditions that enhance neurologic recovery. Immediately following ROSC, reassess the patient’s airway and breathing and treat accordingly. For this patient, you should insert an airway adjunct and assist her ventilations with a bag-mask device and high-flow oxygen. If her breathing does not improve, and she remains unresponsive, an advanced airway device should be considered. Her heart rate (70 beats/min) does not require treatment, although you must closely monitor it. Her blood pressure, however, is low and should be treated. Marked hypotension must be corrected in order to minimize cerebral ischemia; this is usually accomplished initially with crystalloid fluid boluses. If fluid boluses are unsuccessful, an inotropic drug (eg, dopamine) should be considered. Because the patient is still unresponsive, you should consider inducing therapeutic hypothermia, depending on your local protocols. The induction of hypothermia following ROSC has been shown to improve neurologic recovery. The postresuscitation cardiac rhythm should be stabilized to the extent possible. If the arrest rhythm was V-Fib or pulseless V-Tach, consider an antidysrhythmic bolus (eg, lidocaine, amiodarone), followed by an infusion of that same drug.
Pulseless electrical activity (PEA) refers to the presence of an organized cardiac rhythm (except V-Tach), despite the absence of a pulse; it can result from a variety of conditions, such as hypovolemia, overdose, hypothermia, and trauma, among others. Treatment for PEA includes high-quality CPR with minimal interruptions, 1 mg of epinephrine 1:10,000 every 3 to 5 minutes, advanced airway management, and treating potentially reversible causes. A one-time 40-unit dose of vasopressin can be given to replace the first or second dose of epinephrine, but not both. After an advanced airway device is in place, perform asynchronous CPR; the compressor delivers at least 100 compressions/min and the ventilator provides 8 to 10 breaths/min (one breath every 6 to 8 seconds). Do not hyperventilate the patient; doing so may impair venous return to the heart and decrease cardiac output. A ventilation rate of 12 to 20 breaths/min is appropriate for infants and children who are apneic, but have a pulse. An apneic adult with a pulse should be ventilated at a rate of 10 to 12 breaths/min. Dopamine is not indicated for patients in cardiac arrest, and current evidence does not support the use of transcutaneous cardiac pacing (TCP) in patients with PEA or asystole.
Dyspnea that occurs in the context of an acute coronary syndrome (ACS)—that is, unstable angina or acute myocardial infarction—should be assumed to be the result of left side congestive heart failure with resultant pulmonary congestion/edema. The majority of myocardial infarctions involve the left ventricle. The damage may be so extensive that myocardial contractility is impaired and blood backs up into the lungs. Cor pulmonale—acute right heart failure secondary to pulmonary hypertension—typically presents with systemic venous congestion (ie, JVD, peripheral edema), not pulmonary congestion. Anxiety is very common with ACS, and can potentially exacerbate the patient’s condition due to increases in myocardial oxygen consumption and demand. In the interest of the patient, however, assume that any complaint of dyspnea in conjunction with ACS is the result of the worst case scenario—pulmonary edema and impaired oxygenation.
Transcutaneous cardiac pacing (TCP) involves passing small, repetitive electrical currents through the patient’s skin (transcutaneous) across the heart between one externally placed pacing pad and another. The pacemaker is set at a specific rate, usually 60 to 80/min. The energy is then increased—usually by 10 to 20 milliamps (mA) every few seconds—until the heart begins to respond to the electrical stimulus. Electrical capture has been achieved when the stimulus depolarizes the ventricles; this appears as a wide QRS complex immediately following each pacemaker spike. If the QRS complex is not present, the pacemaker current is not depolarizing the ventricles and electrical capture has not been achieved. Mechanical capture is achieved when the patient’s palpated pulse rate corresponds with the paced rate on the ECG.
Sinus tachycardia in the adult—that is, a heart rate less than 150 beats/min—is usually a manifestation of an underlying problem, such as hypovolemia or hypoxia. Therefore, the treatment for sinus tachycardia should focus on treating the underlying cause (ie, fluid boluses, oxygen). Rate-related hemodynamic compromise is uncommon in patients with a heart rate less than 150 beats/min. Tachycardia in the patient with myocardial ischemia is NOT good; it increases myocardial oxygen demand and consumption, which can exacerbate ischemia. Calcium channel blockers (eg, diltiazem [Cardizem]) are commonly used for ventricular rate control in patients with atrial fibrillation or atrial flutter. Synchronized cardioversion is indicated for patients with hemodynamic compromise secondary to supraventricular tachycardia (narrow complex; heart rate > 150 beats/min) and ventricular tachycardia (wide complex; rate > 100 beats/min [often > 200 beats/min]).
Cardiomyopathy is a progressive weakening of the myocardium. This condition is commonly the result of chronic hypertension or a history of multiple myocardial infarctions. An enlarged myocardium is called cardiomegaly.
The S3 or third heart sound is a soft, low-pitched sound that is caused by vibrations of the ventricular walls, resulting from the rapid filling period of the ventricle during the beginning of diastole. An S3 sound should occur 120 to 170 milliseconds after S2, if it is heard at all. An S3 sound may be a normal clinical finding in children and young adults, although a cardiac evaluation should be performed to determine this. When it is heard in older adults, however, it signifies moderate to severe heart failure. S1 is heard near the beginning of ventricular contraction (systole), when the tricuspid and mitral valves close. S2 is heard near the beginning of ventricular relaxation (diastole), when the pulmonic and aortic valves close.
When you arrive at a scene and find bystanders performing CPR, you should briefly pause and confirm that the patient is pulseless and apneic. In some cases, you will find CPR being performed on patients who do not require it. Once cardiac arrest is confirmed, resume high-quality CPR and assess the patient’s cardiac rhythm as soon as possible. According to the 2010 guidelines for CPR and emergency cardiac care (ECC), the precordial thump should not be used for unwitnessed out-of-hospital cardiac arrest. However, it may be considered for patients with witnessed, monitored unstable ventricular tachycardia, including pulseless ventricular tachycardia, if a defibrillator is not immediately ready for use.
Hypovolemia is the most easily correctable cause of PEA, provided that immediate treatment is given in the prehospital setting. In addition to CPR, airway management, and epinephrine, fluid boluses are repeatedly given, followed by a reassessment of the patient’s condition. Remember, myocardial contraction is dependent on electricity and pressure. This pressure is caused as blood fills the heart. If there is no blood, the heart will not pump, even though electrical activity continues. Drug overdose is the underlying cause of asystole that would most likely respond to immediate prehospital treatment, especially in younger patients. Hypokalemia is treated with potassium chloride, which is not administered in the prehospital setting. Lactic acidosis is treated with effective ventilation first, and then sodium bicarbonate if local protocol permits. While sodium bicarbonate can be given in the prehospital setting, paramedics do not have the ability to quantify the pH or bicarbonate level of the patient’s blood; this requires arterial blood gas analysis.
The precordial (chest) leads view the following aspects of the heart: V1 and V2, interventricular septum; V3 and V4, anterior wall; V5 and V6, lateral wall. ST segment depression and/or T wave inversion in two or more contiguous leads indicates ischemia. ST segment that is equal to or greater than 1-mm in two or more contiguous leads indicates injury. A developing Q wave may be seen in conjunction with ST segment elevation associated with myocardial injury. Therefore, 4-mm ST segment elevation in leads V1 through V4 indicates an anteroseptal injury pattern (acute MI in progress). Infarcted (dead [necrotic]) myocardium is characterized by poor R wave progression in the precordial leads and/or the presence of a pathologic Q wave in two or more contiguous leads. By definition, a pathologic Q wave is wider than 0.04 seconds (40 ms) or deeper than one third the height of the R wave that follows it.
CPR alone rarely, if ever, converts asystole—or any other cardiac arrest rhythm—to a perfusing rhythm. Furthermore, if one of the leads detaches from the patient’s chest, you will more likely see something that resembles massive artifact, not ventricular fibrillation (V-Fib). If you see V-Fib on the cardiac monitor, defibrillate one time with 360 monophasic joules (or equivalent biphasic) and then immediately resume CPR, starting with chest compressions. Assessing for a carotid pulse in a patient who is clearly in V-Fib wastes time; it delays defibrillation and CPR. After 2 minutes of CPR, reassess the patient’s cardiac rhythm; if V-fib is still present, defibrillate one time and immediately resume CPR. If you see an organized cardiac rhythm, assess for a pulse for at least 5 seconds but no more than 10 seconds, and then resume CPR if indicated.
Patients with an acute coronary syndrome (ACS)—that is, unstable angina or acute myocardial infarction—often clench their fist when describing the quality of their chest pain or discomfort. This is called Levine’s sign, and it conveys a feeling of pressure in the chest. The pain associated with ACS may also be described as a dull or aching sensation or as a feeling of heaviness. An ACS patient who complains of fluttering in the chest should make you suspicious for a cardiac dysrhythmia (ie, SVT, V-Tach). Cullen’s sign is characterized by periumbilical bruising and indicates blood in the peritoneal space. Grey-Turner’s sign—bruising to the flank area—also indicates blood in the peritoneal space. Beck’s triad is a trio of clinical findings that indicates a cardiac tamponade; it includes jugular venous distention, muffled or distant heart sounds, and a narrowing pulse pressure.
Because third-degree AV block (complete heart block)—an inherently slow cardiac dysrhythmia—represents total atrioventricular dissociation, it is associated with hemodynamic compromise in most cases and should be treated with immediate transcutaneous cardiac pacing (TCP). Signs of hemodynamic compromise include ongoing chest pain, pulmonary edema, decreased level of consciousness, shortness of breath, and hypotension. First-degree AV block is typically a benign rhythm and is not commonly associated with hemodynamic compromise. Evidence has shown TCP to be of little or no benefit to patients with PEA or asystole, and it is clearly of no benefit to patients with prolonged asystole.
When a patient reports taking nitroglycerin (NTG) for chest pain, you should determine how many tablets or sprays he or she took, and whether or not the NTG relieved his or her pain. Failure of NTG to relieve cardiac-related chest pain can occur for one of two reasons—the pain is of extraordinary severity, such as that associated with acute myocardial infarction, or the NTG has been open too long and has lost its potency. Fresh, potent NTG has certain distinct side effects, including a throbbing headache, a burning sensation under the tongue, and a bitter taste. If the patent did not experience any of these side effects, chances are the drug was outdated or had lost its potency. However, if the patient experienced any of these side effects, but is still experiencing chest pain, you should suspect that he or she is experiencing continued myocardial ischemia and is in the process of having an acute myocardial infarction. A 12-lead ECG and other diagnostic tests (ie, echocardiography) are required to determine if permanent myocardial damage has occurred.
Acute ischemic stroke, which is caused by an occluded cerebral artery, is characterized by an acute onset of confusion, slurred speech, facial droop, and unilateral weakness (hemiparesis), among other signs. This patient has two major risk factors for a stroke: hypertension and atrial fibrillation (A-Fib). Although hypertension could be a contributing factor, it is more likely that his A-Fib resulted in the stroke. In A-Fib, a small blood clot can dislodge from the wall of the fibrillating atria, enter the systemic circulation, and occlude a cerebral artery. An epidural hemorrhage is unlikely; it is generally the result of blunt head trauma—most often to the temporal lobe. Furthermore, patients with an epidural hemorrhage tend to deteriorate rapidly and exhibit signs of increased intracranial pressure. Epidural hemorrhage is most often the result of injury to the middle meningeal artery, which bleeds rapidly. Hypoglycemia can also present with acute confusion and slurred speech; however, hemiparesis is a less common finding. Clearly, you should assess the blood glucose level of any patient with an altered mental status. Patients with a space-occupying intracranial lesion (eg, brain tumor) typically have a slow onset and insidious progression of symptoms—often over a period of months. In some patients with a brain tumor, a seizure may be the only presenting clinical manifestation.
The patient is in monomorphic ventricular tachycardia with a pulse. He is clinically unstable, as evidenced by his decreased level of consciousness, profuse diaphoresis, and weak radial pulses. Assessing his BP will yield little additional information; therefore, you should perform synchronized cardioversion with 100 joules. Consider sedating the patient, but do not delay cardioversion. Amiodarone, 150 mg IV over 10 minutes, would be an appropriate intervention if the patient was clinically stable. Adenosine is used for clinically stable patients with narrow-complex tachycardias and can be considered for clinically stable patients with wide-complex monomorphic tachycardias.
Patients with atrial fibrillation (A-Fib) are commonly prescribed digoxin (a digitalis preparation) and warfarin sodium (Coumadin), which is a blood thinner. As the atria fibrillate, blood has a tendency to stagnate and form microemboli that can be ejected from the heart and occlude a pulmonary, cerebral, or coronary artery.
Your patient has signs and symptoms of an acute coronary syndrome (ACS)—a spectrum of cardiac diseases that includes unstable angina pectoris and acute myocardial infarction. In ACS, tachycardia increases myocardial oxygen consumption and demand, and may exacerbate myocardial ischemia or injury. Therefore, her heart rate of 120 beats/min is the most significant clinical finding. Stimulation of the sympathetic nervous system increases the production of sweat, resulting in diaphoresis. Although this is a clinically significant finding, it is not detrimental to the patient. The patient’s mental status—conscious, alert, and oriented—indicates that her brain is adequately perfused; obviously, this is a positive sign. Her respiratory rate of 20 breaths/min is consistent with the upper limit of normal for an adult.
Ejection fraction (EF) is the percentage of blood that is pumped from the ventricle per contraction. The total volume of blood pumped out of the ventricle per contraction is called the stroke volume (SV). If the ventricle contains 100 mL of blood before a contraction, but only ejects 55 mL when it contracts (SV), the ejection fraction is 55% (100 mL × 0.55 = 55 mL). Ejection fraction should be at least 65% in the adult. Cardiac output (CO) is the volume of blood ejected from the left ventricle each minute, and is calculated by multiplying the stroke volume by the heart rate; in the adult, this is typically 5 to 6 L/min.
A junctional rhythm is characterized by inverted P waves in lead II. If seen, the inverted P waves precede or follow the QRS complex. At a rate of 90 beats/min, the rhythm is further defined as an accelerated junctional rhythm. QRS complexes greater than 0.12 seconds (120 ms) indicate aberrant (abnormal) ventricular conduction (ie, bundle branch block). A wandering atrial pacemaker is characterized by P waves that precede each QRS complex, but vary in morphology. An ectopic atrial rhythm is also characterized by P waves of varying morphologies as well as varying PR intervals. A second- or third-degree AV block should be suspected when there are more P waves than QRS complexes.
Enalapril maleate (Vasotec) is an ACE (angiotensin converting enzyme) inhibitor that is used to treat hypertension. Angiotensin II, a potent chemical produced by the kidneys that causes vasoconstriction, is formed from angiotensin I in the blood by the angiotensin converting enzyme. ACE inhibitors inhibit the activity of this enzyme, which decreases the production of angiotensin II. As a result, the blood vessels dilate and blood pressure is reduced. Beta blockers, which are also used to treat hypertension, include drugs such as metoprolol (Lopressor), propranolol (Inderal), and atenolol (Tenormin), among others. Calcium channel blockers are also used to treat hypertension, and include drugs such as diltiazem (Cardizem), verapamil (Calan; Isoptin), and amlodipine (Norvasc), among others. Atropine sulfate is a parasympathetic blocker (vagolytic) that is used to treat patients with hemodynamically unstable bradycardia.
The rhythm shown is sinus tachycardia at a rate of approximately 100 to 110 beats/min. First-degree AV block is characterized by a PR interval that is greater than 0.20 seconds, the normal being 0.12 to 0.20 seconds (120 to 200 milliseconds). The fact that the patient does not have a pulse indicates pulseless electrical activity (PEA). PEA is not a specific rhythm; it is a condition in which a pulseless, apneic patient presents with an organized cardiac rhythm (except for pulseless V-Tach).
On visualization of the chest, you may be able to see the apical thrust, or point of maximal impulse (PMI). The PMI is normally located on the left anterior part of the chest, in the midclavicular line, at the fifth intercostal space. This thrust occurs when the apex of the heart rotates forward during systole, gently beating against the chest wall and producing a visible pulsation.
Energy settings for manual biphasic defibrillators are device-specific—typically 120 joules (rectilinear) or 150 joules (truncated). However, if the appropriate initial energy setting is unknown, you should defibrillate with 200 joules. For subsequent shocks, use the same or higher energy setting. Whether you are using a monophasic or biphasic defibrillator, you should only perform 1 shock, followed immediately by CPR (starting with chest compressions).
Lidocaine is not given prophylactically to patients suspected of experiencing an acute coronary syndrome (ACS). In addition to assessing the responsive patient’s ABCs and vital signs, you should obtain a 12-lead ECG as early as possible and promptly notify the receiving facility of your findings. Obtaining a SAMPLE history may provide you with additional information that may affect your treatment. Treatment includes supplemental oxygen (maintain an SpO2 of greater than or equal to 94%), 160 to 325 mg of baby aspirin, IV access, up to three doses of nitroglycerin (if the systolic BP is greater than 90 mm Hg), and 2 to 5 mg of morphine sulfate if nitroglycerin fails to completely relieve the patient’s chest pain or discomfort and his or her systolic BP remains above 90 mm Hg. Transport the patient as soon as possible, obtain additional 12-lead tracings en route to the hospital, and monitor his or her vital signs and level of pain.
The 2010 guidelines for CPR and emergency cardiac care (ECC) have added a fifth link to the chain of survival, integrated post-arrest care. In addition to supporting the patient’s airway and ventilatory status and supporting his or her blood pressure with IV fluid boluses or an inotropic agent (ie, dopamine), you should assess for and correct any glucose abnormalities. If the patient is unable to follow verbal commands or remains comatose following return of spontaneous circulation (ROSC), therapeutic hypothermia (89.6°F to 93.2°F [32°C to 34°C]) has been shown to improve neurologic recovery and should be considered (follow your local protocols regarding therapeutic hypothermia). Once ROSC has been established, you should continue to ventilate the adult patient at a rate of 10 to 12 breaths/min (one breath every 5 to 6 seconds) if he or she remains apneic. DO NOT hyperventilate the patient as this may impair venous return to the heart and compromise cardiac output. If the patient is able to follow verbal commands following ROSC, obtain a 12-lead ECG tracing and assess for signs of acute MI (ie, ST elevation). Depending on your transport time, you may consider starting a maintenance infusion of the antidysrhythmic drug that was administered during the arrest, which in this case, would be amiodarone (1 mg/min).
After determining that a patient is in pulseless electrical activity (PEA), you should resume CPR, establish vascular access (IV or IO), and administer 1 mg of epinephrine 1:10,000. Consider inserting an advanced airway (ie, ET tube, multilumen airway, supraglottic airway), but DO NOT interrupt CPR to do this. Focus on ruling out potentially reversible causes (Hs and Ts). Routine administration of sodium bicarbonate during cardiac arrest is not recommended; its administration should be guided by arterial blood gas (ABG) values. Synchronized cardioversion is indicated for hemodynamically unstable patients with wide and narrow complex tachycardias, not PEA.
A patient who presents with or develops symptomatic bradycardia needs to be treated in a manner that will increase the heart rate, thus improving cardiac output, blood pressure, and mental status. Altered mental status, hypotension, chest pain or pressure, and shortness of breath are indications for treatment of the bradycardic patient. After ensuring adequate oxygenation and ventilation, establish vascular access and give 0.5 mg of atropine; this may be repeated every 3 to 5 minutes to a maximum dose of 3 mg. If the patient is severely compromised or does not respond to atropine, begin transcutaneous cardiac pacing (TCP) without delay. If the patient is in a second-degree type II or third-degree AV block, TCP is the first-line treatment. Atropine and TCP-refractory bradycardia may require a sympathomimetic infusion, such as epinephrine or dopamine. The body’s normal physiologic response to hypovolemia is tachycardia, not bradycardia. Therefore, fluid boluses are not the initial treatment for the hypotensive, bradycardic patient. In fact, they may cause further harm to the patient. With a slow heart rate and decreased cardiac output, a sudden increase in preload may result in acute pulmonary edema. After stabilizing the patient’s heart rate and improving perfusion, obtain a 12-lead ECG to assess for signs of acute myocardial ischemia or injury.
The patient in this scenario is hemodynamically stable. Premature ventricular complexes (PVCs) are generally not a cause for concern unless they are frequent (> 6 per minute) or occur in the context of acute coronary syndrome (ACS) or hemodynamic compromise. Nonetheless, any change in the patient’s condition warrants reassessment. Continue monitoring the ECG and his vital signs. If the PVCs become more frequent, or if his condition deteriorates, an antidysrhythmic (eg, lidocaine, amiodarone) may be indicated. The patient’s current vital signs are not suggestive of hypovolemia; therefore, a fluid bolus is not indicated at this point. Call your radio report to the receiving facility as usual and report your findings at that time; there is no need to contact them “immediately.”
As the right side of the heart fails, blood is not effectively ejected into the pulmonary circulation; therefore, it backs up beyond the right atrium and into the systemic venous system. This is most noticeable by the presence of engorged or distended jugular veins. Orthopnea, nocturnal dyspnea, and coughing up blood-tinged sputum are indicators of left-sided heart failure as they all indicate fluid in the lungs.
As ventricular contraction begins, the atrioventricular valves (tricuspid and mitral) close and the semilunar valves (pulmonic and aortic) are forced open. As a result, blood moves from the right ventricle through the pulmonary arteries and from the left ventricle through the aorta and into the systemic circulation. The majority of ventricular filling occurs by gravity. Atrial kick is the volume of blood that the atria contribute to ventricular filling; this occurs before ventricular contraction. Increased pressure within the myocardium (ie, increased blood volume) causes stretching of the myocardial walls, thus increasing the force of its contraction (Starling effect); this process precedes ventricular contraction.
The first and most crucial intervention for any patient in cardiac arrest is immediate high-quality CPR. With CPR ongoing, you or your partner can apply the defibrillation pads and assess the patient’s cardiac rhythm. If a shock is indicated, deliver it and immediately resume CPR, starting with chest compressions. During the 2-minute cycles of CPR, vascular access can be obtained, cardiac drugs can be administered, and the patient’s airway can be secured with an advanced device if necessary. It is absolutely critical to minimize interruptions in chest compressions; if you must interrupt compressions, do so for no longer than 10 seconds. The precordial thump is not indicated for unwitnessed cardiac arrest; it may be considered for patients with witnessed V-Tach, however, but has a low success rate.
Paroxysmal nocturnal dyspnea (PND), the sudden awakening from sleep with the feeling of being suffocated, along with the dried blood around the patient’s lips (likely due to coughing up blood-tinged sputum), are classic indicators of left-sided congestive heart failure (CHF). In left-sided CHF, stroke volume (the amount of blood ejected from the ventricle per contraction) is decreased secondary to a weakened or damaged myocardium. Decreased stroke volume causes blood to regurgitate into the upper chamber of the heart and ultimately backs up into the lungs and causes pulmonary edema.
The Q-T interval represents the time from the beginning of ventricular depolarization to the end of ventricular repolarization, and is measured from the start of the QRS complex to the end of the T wave. In a patient with a heart rate between 60 and 100 beats/min, the Q-T interval in lead II is considered to be prolonged if it is greater than one half the distance between any two R waves (R-R interval). If the Q-T interval is prolonged, the patient is at increased risk for developing a lethal dysrhythmia; an electrical impulse may fire during the relative refractory period (downslope of the T-wave), resulting in monomorphic or polymorphic ventricular tachycardia (with or without a pulse) or ventricular fibrillation. If lead II suggests Q-T prolongation, a 12-lead ECG should be obtained to quantify this finding. In a normocardic patient (heart rate of 60 to 100 beats/min), the corrected Q-T interval (QTc) should range between 0.36 and 0.44 seconds (360 to 440 milliseconds) on the 12-lead ECG. The Q-T interval is corrected based on the patient’s heart rate. The faster the heart rate, the narrower the Q-T interval; the slower the heart rate, the wider the Q-T interval.
According to the 2010 guidelines for CPR and emergency cardiac care (ECC), vasopressin, in a one-time dose of 40 units, can be given to replace the first OR second dose of epinephrine for adult patients in cardiac arrest. There are no definitive data to support superiority of vasopressin over epinephrine. There are insufficient data to make a recommendation for or against the use of vasopressin in pediatric cardiac arrest.
The patient in this scenario is in supraventricular tachycardia (SVT); her heart rate is 170 beats/min and her QRS complexes are narrow (< 0.12 seconds). Despite appropriate treatment for her rhythm (ie, vagal maneuvers, adenosine), her rhythm remains unchanged, although she remains hemodynamically stable. Lightheadedness is common in patients with SVT, but it is not a clinical indicator of hemodynamic instability. A cardiac rhythm of ventricular origin (eg, ventricular tachycardia) is characterized by QRS complexes that are greater than 0.12 seconds in duration; this patient's QRS complexes are 0.08 seconds in duration. If vagal maneuvers and adenosine are unsuccessful in converting her rhythm, transport immediately without further treatment (other than oxygen); her present condition indicates that she is tolerating the cardiac rhythm. However, if signs of hemodynamic instability are noted (ie, hypotension, decreased level of consciousness, chest pain, shortness of breath), perform synchronized cardioversion at 50 to 100 joules without delay.
The patient is likely experiencing an acute ischemic stroke. Determining the time of onset of his symptoms is critical; fibrinolytic therapy must be administered within the first 3 hours following a stroke in order to be of maximum benefit. Treatment includes supplemental oxygen (a nasal cannula is appropriate, given his room air oxygen saturation), blood glucose assessment (hypoglycemia can mimic certain signs of a stroke), vascular access, cardiac monitoring, and prompt transport with early notification of the receiving facility. Do not give aspirin to suspected stroke patients in the field; it can cause further harm to the patient with a hemorrhagic stroke. Aspirin may be given at the hospital after a hemorrhagic stroke is ruled out with a computed tomography (CT) scan of the brain. Antihypertensive therapy should also be avoided in the field; it should be performed in the controlled setting of a hospital, where the patient has invasive hemodynamic monitoring. Lowering a patient’s BP in the field is dangerous and can have disastrous effects; inadvertently inducing hypotension in the stroke patient may exacerbate cerebral ischemia.
Side effects of atropine sulfate may include thirst, dry mouth, pupillary dilation (mydriasis), tachycardia, hypertension, and urinary retention. Acute urinary retention is especially common in older men with benign prostatic hyperplasia (BPH), also known as an enlarged prostate gland.
You witnessed your patient’s deterioration to cardiac arrest, and he is now in ventricular fibrillation (V-Fib). You should immediately start CPR and defibrillate as soon as possible. Deliver a single shock with 360 monophasic joules or the equivalent biphasic setting, and immediately resume CPR (starting with chest compressions). Perform 5 cycles (about 2 minutes) of CPR and then reassess his cardiac rhythm. If V-Fib persists, defibrillate again and immediately resume CPR, starting with chest compressions. During CPR, establish vascular access (if not already done), and give 1 mg of epinephrine 1:10,000. After 2 minutes of CPR, reassess the patient’s cardiac rhythm. If V-Fib persists, defibrillate again and immediately resume CPR, starting with chest compressions. It would then be appropriate to administer 300 mg of amiodarone. Synchronized cardioversion is indicated for patients with narrow or wide-complex tachycardias who are hemodynamically unstable but have a pulse.
This patient is in ventricular tachycardia (V-Tach). Furthermore, he is hemodynamically unstable as evidenced by his confusion, hypotension, and labored breathing. Therefore, he requires prompt synchronized cardioversion, starting with 100 joules. Consider sedation with midazolam (Versed) or diazepam (Valium), but do not allow this to delay cardioversion. Amiodarone would be an appropriate intervention if the patient was hemodynamically stable. Vagal maneuvers and adenosine are appropriate for stable patients with narrow complex tachycardias (eg, SVT). Fluid boluses will likely not improve the patient’s blood pressure; his hypotension is the result of inadequate ventricular filling and decreased cardiac output due to his cardiac rhythm—not hypovolemia.
More than 500,000 deaths occur each year as the result of acute myocardial infarction (AMI). Sixty to seventy percent of these deaths occur outside the hospital, usually during the first few hours after the onset of symptoms. Of all deaths from AMI, 90% are due to dysrhythmias—usually ventricular fibrillation—which typically occur during the early hours of the infarct; this should be your primary concern. Many patients experiencing an anterior wall MI are hyperdynamic—that is, they are hypertensive and tachycardic; hypotension is not as common. Depression of the CNS (respiratory depression, bradycardia, and hypotension) should be a concern any time you administer a narcotic analgesic (ie, morphine); however, most patients do not experience significant CNS depression with 5 mg of morphine. Pain relief is an important aspect in the management of the patient with AMI; minimizing pain minimizes anxiety, which can limit the size of the infarct.
A single shock (360 monophasic joules or the biphasic equivalent) should be administered to the patient with V-Fib or pulseless V-Tach cardiac arrest. Immediately following this single shock, begin or resume CPR, starting with chest compressions. Assessing the patient’s cardiac rhythm and pulse immediately following defibrillation causes an unnecessary delay in CPR, and delays in CPR have been directly linked to poor patient outcomes. Most patients who are defibrillated—especially if their arrest interval is prolonged—remain in V-Fib/pulseless V-Tach or convert to another non-perfusing rhythm (ie, asystole, PEA). Either way, the patient is still in cardiac arrest and needs immediate CPR. After 2 minutes of CPR, reassess the patient’s rhythm, and if necessary, a pulse (if an organized cardiac rhythm appears), and repeat defibrillation (single shock) if indicated, followed immediately by CPR.
Epinephrine stimulates alpha and beta receptors. However, it is used during cardiac arrest because of its vasopressor effects that result from stimulation of alpha-1 receptors. In conjunction with high-quality CPR, epinephrine’s vasoconstrictive effects improve coronary and cerebral perfusion, thus keeping these organs viable until the underlying cardiac dysrhythmia can be terminated.
The rhythm shown is sinus tachycardia. Any increase in cardiac workload, such as an increase in heart rate, contractility, or blood pressure, will increase the amount of oxygen that the myocardium demands and consumes. In patients experiencing an acute coronary syndrome (ie, unstable angina [UA], acute myocardial infarction [AMI]), this could extend the area of ischemia or infarction.
The patient in this scenario is in a third-degree (complete) AV block, which is causing his signs and symptoms. Complete heart block should be treated with immediate transcutaneous cardiac pacing (TCP). Given the patient’s clinical presentation, it is clear that he is hemodynamically unstable; obtaining a complete set of vital signs will yield very little, if any, additional information. A 12-lead ECG should be obtained, but not before addressing the most immediate problem of hemodynamic compromise. Atropine should be avoided in patients with high-grade AV heart blocks (eg, second-degree AV block type II and third-degree AV block). Atropine may worsen the patient’s condition—especially in cases of third-degree AV block—by increasing sinus node discharge without any effect on the ventricles. Remember, if the rhythm is perfusing, but is slow and wide, begin TCP without delay.
Correct lead placement is critical in obtaining an accurate 12-lead ECG tracing. Lead V1—the first precordial (chest) lead—is placed in the fourth intercostal space, just to the right of the sternum. Lead V2 is placed in the fourth intercostal space, just to the left of the sternum.
A QRS duration of greater than 120 ms (0.12 seconds [3 small boxes]) signifies an intraventricular conduction delay (IVCD), such as a bundle branch block. A left bundle branch block (LBBB) is characterized by a QRS duration of greater than 120 ms and a terminal S wave in lead V1 (the second half of the QRS complex terminates in an S wave); terminal R waves are seen in leads I, aVL, and V6. A right bundle branch block (RBBB) is characterized by a QRS duration of greater than 120 ms and a terminal R wave in lead V1 (the second half of the QRS complex terminates in an R wave); terminal S waves are seen in leads I, aVL, and V6.
A second-degree AV block Mobitz Type II (classic second-degree AV block) is characterized by more P waves than QRS complexes. However, the P-R intervals of the conducted complexes (P waves that are followed by a QRS complex)—whether shortened, normal, or prolonged—are consistent. By contrast, a second-degree AV block Mobitz Type I (Wenkebach) is characterized by a progressive lengthening of the P-R interval until a P wave is blocked (not followed by a QRS complex). The ventricular rate of a second-degree AV block may be normal or slow. Dissociation of the P waves and QRS complexes is characteristic of a third-degree (complete) AV block.
Sympathomimetic medications, such as epinephrine and norepinephrine, cause increases in myocardial oxygen demand and consumption. If given to patients with hypoxemia or acute coronary syndrome (eg, unstable angina, acute myocardial infarction), this effect can result in cardiac arrhythmias. Therefore, you should monitor the cardiac rhythm of any patient who receives a sympathomimetic drug. Sympathomimetic drugs cause an increase in heart rate, not a decrease. Hypotension and respiratory failure are not common following the administration of a sympathomimetic drug.
The initial dose of amiodarone for a patient with refractory ventricular fibrillation or pulseless ventricular tachycardia is 300 mg via rapid IV or IO push. A second dose of 150 mg via rapid IV or IO push may be repeated one time in 5 minutes. For supraventricular tachycardia or ventricular tachycardia with a pulse, amiodarone should be given in a dose of 150 mg over 10 minutes; this same dose may be repeated as needed.
The progressive lengthening of the PR interval until a P wave is blocked (not followed by a QRS complex) makes this cardiac rhythm a type I second-degree AV block, also referred to as “Wenckebach.” This type of AV heart block represents a progressive delay at the AV node/junction until an electrical impulse is completely blocked from entering the ventricles. A type II second-degree AV block is characterized by more P waves than QRS complexes; however, the P-R intervals of the conducted complexes are consistent. In complete AV dissociation (ie, third-degree AV block), there are more P waves than QRS complexes, and no relationship exists between a given P wave and QRS complex. A wandering atrial pacemaker is characterized by varying morphologies of P waves.
Chest pain of cardiac origin is most often described as crushing, dull, pressure, or as a feeling of heaviness or discomfort. The pain is typically constant, not intermittent, and is usually not palliated or exacerbated by movement. Bear in mind that these are typical pain descriptions. The paramedic should not rule out a cardiac problem if the patient describes the pain differently. Sharp (pleuritic) pain is often associated with conditions such as pleurisy, pulmonary embolism, or spontaneous pneumothorax. A tearing sensation should alert you to the possibility of acute aortic dissection.