Neo Conduction System & Pericardium Flashcards
A 78-year-old woman with a past history of ischemic stroke is brought to the emergency department because of chest pain and diaphoresis. The patient has no history of congestive heart failure, diabetes, or hypertension. The image shows a portion of an ECG performed on the patient. Blood pressure is stable. She is started on aspirin, nitroglycerin, beta-blockers, and heparin. After treatment is initiated, the patient no longer has chest pain, and troponin and creatine kinase-MB levels are normal. Which of the following drugs is most appropriate for this patient immediately after stabilization?
A. Aspirin
B. Atropine
C. Morphine
D.Propylthiouracil
E.Warfarin
Answer E
ReKap
Atrial fibrillation is characterized by a lack of detectable P waves and fluctuating R-R intervals.
Atrial fibrillation that has been ongoing for more than 48 hours or for an uncertain amount of time (such as in this patient) is associated with thrombus formation in the atria.
After stabilization with rate-controlling medications (such as a beta-blocker) and initial anticoagulation with heparin, an oral agent such as warfarin should be administered to reduce the risks of embolic events from a possible atrial thrombus.
Non-vitamin K oral anticoagulants such as dabigatran are also appropriate therapeutic choices for long-term anticoagulation.
Analysis
The correct answer is E. The patient has atrial fibrillation (AF). There are no discernable P waves on the ECG and the ventricular rhythm is erratic (irregularly irregular). Following initial stabilization, rate control, chronic arrhythmia, and anticoagulation must be addressed. Warfarin is generally used for the long-term treatment of AF.
While this patient appears to have ST elevations on the single ECG tracing shown here, an ST-elevation myocardial infarction (STEMI) cannot be diagnosed with a single-lead ECG. Additionally, aspirin has already been given to this patient and their pain is well-controlled. This means that two of the typical treatments for suspected STEMI, aspirin (choice A) and morphine (choice C), are not urgently required in this patient.
This question examines the issue of anticoagulation in AF. It is important to note that when choosing the most appropriate treatment, it must be considered that the patient also has two primary risk factors: age over 75 years and past history of thromboembolic disease. The altered flow in the fibrillating atrium can cause clot formation, and thus anticoagulation must be initiated in order to prevent another stroke or other embolic disease. Because warfarin takes 3–4 days to reach its full therapeutic effect, heparin therapy (along with warfarin) is generally started immediately after a diagnosis is made. Heparin is then generally discontinued after 4–5 days once the patient has achieved the desired INR. Heparin acts at multiple sites in the coagulation process. However, its primary effect is achieved by binding to antithrombin III, catalyzing the inactivation of thrombin and other clotting factors. Warfarin acts by inhibiting vitamin K-dependent coagulation factor synthesis (II, VII, IX, X, proteins C and S).
Newer, non-vitamin K oral anticoagulants (e.g., dabigatran, rivaroxaban, apixaban) are also appropriate therapeutic choices for long-term anticoagulation. Bridging therapy with heparin may be omitted depending on specific patient characteristics when initiating these agents.
Aspirin (choice A) has been used for its antiplatelet effects in low-risk atrial fibrillation patients under the age of 75 without a past history of thromboembolic disease. In this question, the patient has both advanced age and a past history of a stroke; hence, aspirin would not be indicated. This brings up the widely used CHA2DS2-VASc score for AF stroke risk. Given this patient’s age, sex, and stroke history, she would earn a score of 5, where anything greater than 2 normally warrants anticoagulation rather than only an antiplatelet medication like aspirin.
Atropine (choice B) is a muscarinic cholinergic antagonist and would speed up electrical conduction. This would exacerbate the problem. When it comes to cardiac questions, atropine would rarely be used for anything except bradycardia per the ACLS algorithms. This patient has tachycardia.
Morphine (choice C) is incorrect. Once the patient is stabilized and rate controlled, the patient’s pain should subside. There is thus no need for opiate analgesia.
Propylthiouracil (choice D) is used in the treatment of hyperthyroidism. It inhibits thyroid peroxidase and also diminishes the peripheral deiodination of thyroxine (T4) to triiodothyronine (T3). Hyperthyroidism can lead to atrial fibrillation, but there is nothing to indicate that the patient’s atrial fibrillation is due to hyperthyroidism. In either case, the patient needs anticoagulation first, so warfarin is a better choice.
ReKap
The sinoatrial node is in the wall of the right atrium.
It is close to the point of entry of the superior vena cava behind the right third intercostal space near the sternal border.
Analysis
The correct answer is E. The sinoatrial (SA) node is in the wall of the right atrium near the point of entry of the superior vena cava. A penetrating wound in the right third intercostal space near the sternal border might injure this part of the right atrium. The right atrium projects to the right of the sternum. The function of the SA node is to initiate cardiac depolarization. The specialized cardiac muscle cells in the SA node depolarize spontaneously at a rate faster than any other cardiac muscle cells and thus serves as the pacemaker.
The ascending aorta (choice A) might be injured by a penetrating wound in the right second intercostal space near the sternal border.
The atrioventricular (AV) node (choice B) is in the subendocardium of the interatrial septum. The AV node is retrosternal, and would not likely be injured by a wound in the right third intercostal space. From the AV node, the Purkinje fibers of the atrioventricular bundle enter the interventricular septum to carry impulses to the ventricle. The function of the AV node is to slow down the conduction of the cardiac impulses so that ventricular systole occurs after atrial systole.
The chordae tendineae attached to the mitral valve (choice C) are found in the left ventricle. A penetrating wound near the left border of the heart, which is further to the left than the sternal border, could injure the left ventricle. The left ventricle is behind the left third, fourth, and fifth intercostal spaces, close to the midclavicular line. The function of the chordae tendineae is to control the closure of the mitral valve. See the image below.
The moderator band (choice D) is found in the right ventricle. A penetrating wound in the left fourth or fifth intercostal space, close to the sternal border, would injure the right ventricle in the region of the moderator band. The moderator band passes from the interventricular septum to the anterior papillary muscle of the right ventricle. It carries Purkinje fibers from the right bundle branch to this papillary muscle to cause this muscle to contract at the very beginning of systole.
ReKap
Autoimmune pericarditis, also known as Dressler syndrome, generally occurs 4 to 6 weeks after a myocardial infarction.
Pericarditis would show ECG changes with diffuse ST elevations.
Affected patients usually present with fever, positional substernal chest pain, and a loud friction rub on cardiac auscultation.
Analysis
The correct answer is A. This patient has Dressler syndrome, an autoimmune post-MI phenomenon resulting in fibrinous pericarditis. Fibrinous pericarditis presents with fever and chest pain that is positional, with patients generally preferring to remain upright and leaning forward. On physical examination, a loud, three-component, pericardial friction rub is sometimes heard on auscultation. Associated ECG changes include diffuse ST segment elevations (“diffuse” means that the ST changes are present in many of the limb leads). Patients with autoimmune pericarditis typically present 4–6 weeks (but occasionally months, and rarely, days) after a MI.
Infective endocarditis (choice B) generally presents with high fever and new-onset heart murmur, usually of valvular regurgitation instead of friction rub. Physical exam findings include Roth spots (white spots on the retina), Osler nodes (painful raised lesions on fingers and toe pads from circulating immune complexes), Janeway lesions (erythematous lesions on palms and soles from infected microemboli), and splinter hemorrhages. Infective endocarditis is not a post-MI complication.
Inferior MI secondary to stent thrombosis (choice C) is certainly possible in this patient who had a stent placed for an inferior wall MI. ECG would show ST elevations in the inferior leads (II, III, and aVF, which is what the patient had initially) as opposed to diffuse ST elevations, which characterize pericarditis.
Papillary muscle rupture (choice D) is a complication generally seen 5–10 days after myocardial infarction. Findings include a new apical, holosystolic murmur of mitral regurgitation since the papillary muscle is not functional to prevent bowing of the valve into the left atrium. Other physical examination findings include rales at the lung bases (if severe mitral regurgitation is present) and signs of left-sided heart failure.
Prinzmetal angina (choice E) refers to chest pain secondary to coronary artery vasospasm. ECG will show ST elevations in the associated leads as opposed to diffuse ST elevations.
ReKap
Third-degree atrioventricular (AV) block, otherwise known as complete heart block, is characterized by atrial impulses not being conducted through the AV node. The ventricular rate is subsequently determined by the intrinsic escape rhythm.
Atenolol is a beta-1-selective blocker and at high doses may cause different degrees of heart block, including complete heart block.
Analysis
The correct answer is B. Atenolol is a selective beta-1-adrenergic receptor antagonist. In high doses, it can cause bradycardia and varying degrees of atrioventricular (AV) block. This patient has a third-degree AV block, also called complete heart block. Additional side effects of atenolol include impotence, bradycardia, heart failure, and CNS adverse effects (sedation, seizures, sleep alterations).
In third-degree AV block there is no relationship between P waves and QRS complexes. Impulses are not transmitted through the AV node. A pacemaker develops in the ventricles, with both the atria and ventricles beating at their own rates because action potentials from the atria cannot reach the ventricles. Characteristics include a steady rhythm (usually) and very low ventricular heart rate (usually). There are no consistent PR intervals because impulses are not transmitted through the AV node. The rate for P waves (atrial depolarization) are different from the rate for R waves (first upward deflection after P wave; early ventricular depolarization).
Third-degree AV block is most commonly caused by coronary artery disease or iatrogenic-related inhibition of the cardiac conduction system with medications/procedures known to cause AV block. The initial management of bradycardia (third-degree AV block, in this case) can be with atropine, isoproterenol, and dopamine.
None of the other options are associated with complete heart block:
Albuterol (choice A), a beta-2 agonist, can cause tachyarrhythmias in high doses, not bradyarrhythmias. It is a bronchodilator used in the treatment of asthma and bronchospasm.
Glyburide (choice C) is a sulfonylurea used in the treatment of type 2 diabetes mellitus. It stimulates the pancreas to release insulin from the beta cells, increases insulin sensitivity at peripheral target sites, and decreases glucose output from the liver. In high doses, it can cause hypoglycemia.
Levothyroxine (choice D) is a synthetic form of thyroid hormone. It is used in the treatment of hypothyroidism. High doses of levothyroxine can cause sinus tachycardia and other tachyarrhythmias.
Pentoxifylline (choice E) lowers blood viscosity and improves erythrocyte flexibility. It is indicated for the treatment of intermittent claudication, and is generally well tolerated with few side effects; however, it has been associated with the development of dyspnea and mild hypotension.
ReKap
Fibrinous pericarditis:
May be seen a few days after myocardial infarction (early post-myocardial infarction pericarditis).
Late post-myocardial infarction pericarditis may be seen 2 to 10 weeks after MI and is most likely an autoimmune reaction (Dressler syndrome).
Causes characteristic chest pain that is worse with inspiration and improves when leaning forward.
Analysis
The correct answer is B. This patient had an acute myocardial infarction (MI) two months ago and now presents with a late post-MI fibrinous pericarditis. This condition is most likely an autoimmune reaction and classically occurs 2 to 10 weeks after an acute MI or heart surgery.
An early post-MI fibrinous pericarditis may also occur. This condition manifests during the infarction event when myocardial inflammation and vasodilation are at a peak (3–5 days following MI) and involve the pericardium.
Typical symptoms of pericarditis include a low-grade fever, pleuritic chest pain that worsens with respiration and improves with leaning forward, pericardial friction rub, pulsus paradoxus (drop >10 mm Hg on inspiration), and sometimes pericardial effusion. Other potential causes of fibrinous pericarditis include uremia (secondary to renal failure), acute rheumatic fever, systemic lupus erythematosus, and viral etiologies.
Caseous pericarditis (choice A) is generally due to tuberculosis, although certain fungal infections may also precipitate this condition. This form of pericarditis is important because it is a common cause of chronic constrictive pericarditis, which can result in reduced cardiac output and classically produces a pericardial knock from filling of the heart against a rigid pericardium.
Hemorrhagic pericarditis (choice C) can be seen with tuberculosis, with malignant tumors, in patients with bleeding diatheses, and following chest surgery. Irritation of the pericardium by contents within the blood results in symptoms of pericarditis. This phenomenon is similar to how blood leaking into cerebrospinal fluid during subarachnoid hemorrhage can result in meningeal irritation and produce meningeal signs.
Purulent pericarditis (choice D) is seen when pyogenic infections involve the pericardium. Major contexts for this condition include thoracic surgery, nosocomial bloodstream infections, and immunosuppression.
Repeat myocardial infarction (choice E) should always be on your differential for chest pain following a MI. However, in this context, it is unlikely given the history. The chest pain characterized by the patient is pleuritic in nature and changes with position, not characteristic of MI. Additionally, the two-day history of pain, coupled with fever, is much more consistent with pericarditis rather than MI.
ReKap
In a patient who has been to the woods and develops a bull’s eye rash (erythema migrans), neurologic symptoms, cardiac problems, and/or musculoskeletal problems, think of Lyme disease.
Lyme disease is caused by Borrelia burgdorferi, a spirochete transmitted by the tick Ixodes scapularis.
Analysis
The correct answer is C. This patient is suffering from first degree AV nodal heart block as a consequence of Lyme disease. This infection, caused by the spirochete Borrelia burgdorferi, is transmitted by the deer tick genus Ixodes, which is also the vector for Babesia microti. First-degree heart block is defined as a slowing of the PR interval to >200 msec.
Erythema migrans can be the first sign of the illness, although it is not seen in all patients. Erythema migrans is a red patch that slowly expands as the center blanches, beginning at the point of the tick bite, to produce a classic expanding bull’s-eye lesion. Patients may not even remember the tick bite.
Generally, patients also have constitutional symptoms, such as fever and chills, during this phase. Stiff neck may develop, along with other signs of meningeal irritation, because of an aseptic meningitis. Other neurologic complications of Lyme disease include Bell palsy due to the involvement of branches of the facial nerve. Arthritis is a prominent feature in about half the patients and results from an immune-complex hypersensitivity. It tends to appear several months after the infection, but may persist for several years. The course of chronic arthritis shows exacerbations and remissions; the most commonly affected joints are the knees and hips.
Below is a summary of the three distinct phases of Lyme disease: early localized, early disseminated, and late disease. NOTE: The clinical features of each stage may overlap with one another. Also, some individuals may present in a later stage of Lyme disease without a past history of prior signs or symptoms.
Oral doxycycline, amoxicillin, and cefuroxime axetil can be used for the treatment of early Lyme disease. Doxycycline is generally considered the drug of choice since it is effective in treating Anaplasma phagocytophilum, which is a common coinfection agent. However, all cardiac and serious neurologic manifestations should be treated with intravenous ceftriaxone. Since this patient developed first degree AV nodal heart block, she should be treated with ceftriaxone.
Yellow fever is transmitted by Aedes aegypti (choice A) and is associated with high fever, jaundice, epistaxis, anuria, and hematemesis. It does not occur in the continental United States.
Malaria transmitted by Anopheles gambiae (choice B) does not occur in the continental United States. The disease is characterized by a periodic 2-3 day fever paroxysm followed by drenching sweats, exhaustion, and hemolytic anemia.
The human body louse, Pediculus humanus (choice D), is responsible for the transmission of relapsing fever caused by Borrelia recurrentis. This disease is associated with poverty and crowding and is endemic in Sudan and Ethiopia but would not be expected in the United States. The disease is characterized by a raised red rash, fever, jaundice, and hepatosplenomegaly.
The rat flea, Xenopsylla cheopis (choice E), transmits bubonic plague, which is caused by Yersinia pestis. In the United States, plague is a zoonosis in the desert southwest and presents with the development of hemorrhagic lymph nodes, high fever, conjunctivitis, and septicemia.
ReKap
Severe cell damage caused by burns, crush injuries, and other traumatic events releases potassium into the bloodstream, producing hyperkalemia.
On ECG, hyperkalemia may be associated with abnormally tall T waves, lengthening of the PR interval, and widening of the QRS complex.
Analysis
The correct answer is C. The ECG recording shows tall, tented T waves, which are characteristic of hyperkalemia.
Approximately 98% of total body K+ stores are contained within cells, with a significant proportion of this total being located within skeletal muscle. Tissue damage caused by burns, trauma, or crush injuries allows intracellular K+ stores to enter the circulation in amounts that can overwhelm the kidneys’ ability to maintain plasma levels within a normal range, resulting in hyperkalemia.
Clinical manifestations of hyperkalemia include muscle weakness and paralysis and cardiac conduction abnormalities. These symptoms reflect the effects of the depression of the electrochemical gradient driving transmembrane K+ efflux in excitable tissues (neurons and myocytes; see figure). Slow hyperkalemia-induced membrane depolarization inactivates voltage-dependent Na+ channels and impairs membrane repolarization. Early signs of hyperkalemia may include peaked T waves on the ECG as shown. As the severity of the hyperkalemia increases, the PR interval and QRS duration may widen and progress to ventricular fibrillation. This is why hyperkalemia is such a serious metabolic abnormality.
Treatment typically includes:
Calcium (calcium gluconate or calcium chloride) to stabilize the myocardium and prevent arrhythmias.
Insulin + dextrose to stimulate Na+-K+ ATPase and cause K+ to be internalized by healthy cells, the dextrose being given to prevent hypoglycemia.
Beta-agonists may similarly cause a K+ shift from extracellular fluid to intracellular fluid.
Sodium polystyrene sulfonate may be given to decrease potassium absorption by the gut.
Dialysis to help clear the excess K+ from the body.
Increased serum Ca2+ (hypercalcemia; choice A) will manifest on an ECG as a shortened QT interval with an abridged or absent ST segment (as will also occur with hyperkalemia). With increased serum Ca2+, the T wave will not be as tall as the R wave, as shown above. In addition, blood pressure (systolic and diastolic) would be elevated and the patient would be vomiting.
Increased Cl– (hyperchloremia; choice B) is rare in the absence of metabolic acidosis. The patient above has normal O2 saturation and respirations.
Increased serum Mg2+ (hypermagnesemia; choice D) will result in prolonged PR and QT intervals on an ECG, hypotension, and respiratory depression. Since the patient can move his fingers, there are no signs of impaired acetylcholine release, which is present with hypermagnesemia. One of the first signs of hypermagnesemia is reduced deep tendon reflexes. This is often monitored in pregnant patients with pre-eclampsia receiving magnesium therapy.
Increased serum Na+ (hypernatremia; choice E) results in nausea, vomiting, confusion, delirium, irritability, and muscle twitching.
ReKap
Pericarditis is characterized by sharp, pleuritic chest pain that is often positional and is relieved by leaning forward.
ECG shows diffuse ST-segment elevations with upright T waves.
Analysis
The correct answer is A. The patient’s signs and symptoms are consistent with acute pericarditis.
Key points:
Symptoms: Sharp, substernal chest pain that worsens with inspiration.
Positional pain improves with sitting up and leaning forward.
Physical examination is often normal. Patients may have a pericardial friction rub, which is a three-component, scratchy, pericardial heart sound.
ECG: Diffuse ST-elevations.
Generally preceded by a viral upper respiratory illness.
It is important to understand some of the key points to differentiate the common causes of acute chest pain. The important components in the differential diagnosis include: aortic aneurysm, myocardial infarction, and pericarditis.
Dissecting aortic aneurysm (choice B) can present with sharp, knifelike chest or back pain that radiates to the mid-back. The characteristic radiation of the chest pain is due to the posterior location of the aorta. Differing blood pressures in either arm may be present. Additionally, it may present with acute aortic regurgitation Unless the dissection includes the coronary vessels, it would not be expected to show any abnormalities on ECG. However, a chest x-ray would likely show widening of the mediastinum.
While the history of myocardial infarction (MI) would raise suspicion for having another MI (choice C), this presentation would be atypical. Acute MI generally presents as substernal chest pressure that occasionally radiates to the left arm, jaw, and/or neck. ECG would show ST-segment changes in the leads corresponding to the affected coronary vessel. Chest x-ray would be expected to be normal. Creatinine kinase MB (CK-MB) would likely be elevated secondary to cardiac myocyte injury.
Myocarditis (choice D) can also present with variable substernal chest pain, often in the context of a preceding viral illness. It would be unlikely to see ECG changes or an abnormal chest x-ray in these patients. CK-MB may be mildly elevated.
Pulmonary embolism (choice E) generally presents with the acute onset of pleuritic chest pain. Pulmonary embolism usually occurs in the context of predisposing factors for clot formation such as vascular stasis, hypercoagulability, and/or endothelial injury. Patients will also commonly be tachycardic on examination with decreased oxygen saturation. ECG would not show diffuse ST-elevations. Chest x-ray would likely be normal.
ReKap
The pericardial cavity is a potential space between the two layers of pericardium: the epicardium (visceral pericardium) and the parietal pericardium.
Accumulation of fluid in the potential space between these two layers compresses the heart, resulting in cardiac tamponade.
Analysis
The correct answer is A. With a dropping blood pressure and elevated heart rate, there are two possibilities for the cause in this scenario:
Blood loss into the thorax (thus hypovolemic shock)
Tamponade (thus cardiogenic shock)
The elevated jugular venous pulse (JVP) points toward tamponade (JVP would be low to normal in hypovolemic shock). This is further suggested by the enlarged cardiac silhouette, which is also seen in cardiac tamponade.
The pericardial space is located between the epicardium (also known as the visceral pericardium) and the parietal pericardium. A tear of a blood vessel immediately outside of the heart will cause bleeding into the pericardial space, which reduces the heart sounds. Accumulating blood also exerts external pressure on the cardiac chambers, collapsing the right heart, restricting diastolic filling (cardiac tamponade), and causing jugular venous distension. Reduced preloading results in reduced cardiac output and reduced blood pressure. This is a life-threatening condition. Blood in the pericardial space may be removed by pericardiocentesis, thus relieving the pressure on the heart.
The region between the fibrous pericardium and the parietal pleura (choice B) is outside of the pericardial space. It is part of the mediastinum and is the region in which structures such as the vagus nerve and the phrenic nerve are found. Accumulation of blood here is more likely to cause hypovolemic shock due to loss of fluid in the mediastinum (thus no elevated JVP) rather than cardiogenic shock since there is no compression of the heart. Irritation of the mediastinum may cause chest pain.
The epicardium (also known as the visceral pericardium) is fused to the myocardium and is the outer layer of the heart wall. There is no potential space between the epicardium and the myocardium (choice C).
The parietal pericardium and the fibrous pericardium are fused into a single layer that forms the outer wall of the pericardial space. There is no potential space between the parietal pericardium and the fibrous pericardium (choice D).
The space between the parietal pleura and the visceral pleura (choice E) is the pleural space. Accumulation of blood in the pleural space would cause symptoms of shortness of breath and chest pain rather than the symptoms we see in this patient. Additionally, imaging would show accumulation of blood in the pleural space rather than enlargement of the cardiac silhouette.
ReKap
Because digoxin has a narrow therapeutic window, toxicity can easily develop, resulting in a range of signs and symptoms including nausea, vomiting, malaise, yellow vision (xanthopsia), hyperkalemia, and cardiac dysrhythmias.
The incidence and severity of digoxin toxicity is greatly increased when hypokalemia or renal failure is present.
Treatment with digoxin immune (Fab) antigen-binding fragments is indicated in cases of significant hyperkalemia or the development of life-threatening arrhythmias.
Analysis
The correct answer is B. Digoxin is a cardiac glycoside that directly inhibits the cardiac Na+-K+ ATPase. This indirectly inhibits the Na+-Ca2+ exchanger used to clear Ca2+ from the sarcoplasm following excitation, which leads to increased intracellular Ca2+ and positive inotropy. Digoxin also inhibits the neuronal Na+-K+ ATPase, resulting in increased vagal nerve activity and a decrease in heart rate. Digoxin is used for congestive heart failure (increases inotropy) and supraventricular tachycardias (decreases atrioventricular conduction and depresses the sinoatrial node).
Digoxin has a low therapeutic index. Early toxic doses include anorexia, nausea, and ECG changes. Later signs include disorientation and visual effects (e.g., blurred vision, yellow-green halos; may have contributed to Van Gogh’s “Yellow Period”). Toxic doses can cause a variety of cardiac arrhythmias, a life-threatening complication. If toxicity occurs, the patient can be treated with digoxin immune Fab, which binds to digoxin, making it unavailable to bind to the Na+-K+ ATPase and facilitating its removal from the body. Correction of electrolyte imbalances is also important.
Digoxin toxicity is unlikely to result in the development of acute renal failure (choice A) or hyponatremia (choice D). Tonic-clonic seizures may occur (choice E), but this is extremely rare.
It is important to note that digoxin toxicity does not cause hypokalemia (choice C). However, hypokalemia can lead to digoxin toxicity at any therapeutic concentration. This occurs because digoxin binds to the K+ site on the Na+-K+ ATPase. If potassium concentrations are reduced, digoxin binds more easily.
ReKap
The combination of hypotension with a normal or increased pulse pressure and a heart rate of 30 to 45/min should suggest the diagnosis of a complete heart block.
Dissociation of atrial and ventricular excitation with a ventricular escape rhythm strongly implicates third-degree atrioventricular (AV) block.
Third-degree AV block with ventricular rate below 45/min usually causes hemodynamic instability.
Analysis
The correct answer is C. Dissociation of atrial and ventricular rhythms occurs in complete, or third-degree heart block (atrioventricular [AV] nodal block):
P waves are uncoupled from QRS complexes.
If the block occurs at the level of the AV node, the node takes over as pacemaker:
Nodal cells have an intrinsic rate of 45-60 beats/min.
QRS complexes are narrow (i.e., normal) because contractions are still coordinated by the bundle of His and Purkinje system.
Patients are hemodynamically stable.
If the block occurs below the node, Purkinje cells can generate an escape rhythm.
Purkinje cells have an intrinsic rate of <40 beats/min.
QRS complex is wide.
Patients are hemodynamically unstable.
Stroke volume (SV) tends to increase as heart rate (HR) decreases because diastole lengthens and allows for increased ventricular preloading. When SV increases, a greater amount of blood must be accommodated within the arterial tree with each heartbeat, which causes an increased systolic blood pressure (SBP). The pulse pressure (SBP minus diastolic blood pressure) is 50 mm Hg in this patient (normal pulse pressure is 30-50 mm Hg) despite her hypotension (mean arterial pressure [MAP] is ~57 mm Hg).
None of the other choices result in complete dissociation of the atrial and ventricular rhythm.
Aortic valve obstruction (choice A; e.g., aortic stenosis) promotes left ventricular (LV) hypertrophy and chronically increased LV pressure. The higher pressure is required to force blood through the valve’s reduced surface area. MAP remains normal until the surface area is critically reduced, at which point the patient may experience syncope. HR would tend to be increased.
Fluid accumulating within the pericardial sac (tamponade; choice B) compresses the heart chambers and limits LV preloading. Cardiac output (CO) falls, along with MAP. HR would be increased to compensate. Patients with acute tamponade typically experience chest pain and dyspnea.
The decreased contractility associated with heart failure (choice D) limits CO and, in the later stages, would cause MAP to fall. Patients experience dyspnea upon exertion and syncope. HR would tend to be increased to compensate for impaired output.
Mitral valve obstruction (choice E) limits LV filling. Left atrial pressure rises to compensate, which backs up into the pulmonary vasculature and causes pulmonary hypertension. Patients experience dyspnea and fatigue. MAP would be reduced as a result of decreased CO, but HR would tend to be increased.
ReKap
Atrial fibrillation is characterized by indistinct P waves and fluctuating R-R intervals.
Digoxin decreases conduction through the atrioventricular node.
Digoxin can be used to treat atrial fibrillation with rapid ventricular rate.
Analysis
The correct answer is B. The patient has atrial fibrillation (AF), a supraventricular tachyarrhythmia characterized by uncoordinated atrial activation with the subsequent decline of atrial function. ECG shows replacement of consistent P waves by fibrillatory waves that vary in size, shape, and timing. There may also be an irregular (frequently rapid) ventricular response, which accounts for the classic “irregularly irregular” heart rhythm heard on physical examination. While generally asymptomatic AF can also cause palpitations, dyspnea, or chest pain in the case of rapid ventricular rate, if coronary artery disease is also present.
The primary goals of drug therapy for AF are to maintain sinus rhythm, avoid the risk of complications (i.e., stroke), and minimize symptoms. Warfarin remains a cornerstone of anticoagulant therapy for AF patients at moderate to high risk of thromboembolic events. Previously, warfarin was the only anticoagulant approved for the prevention of stroke in AF; however, newer data has shown that two novel oral anticoagulants have comparable efficacy. These include Xa inhibitors (e.g., rivaroxaban and apixaban) and the direct thrombin inhibitor, dabigatran. Although not commonly used as first-line therapy for the treatment of AF, digoxin is still an acceptable treatment option; it acts by slowing conduction through the atrioventricular (AV) node.
The effects of digoxin on the myocardium are dose-related and involve both a direct and indirect action on the cardiac muscle. The indirect actions involve a vagomimetic response, which decreases the conduction rate through AV node. Beta blockers, such as esmolol and metoprolol, and calcium channel blockers, such as verapamil and diltiazem, are other conventional choices for the treatment of atrial arrhythmia. These agents are generally considered before digoxin in patients without evidence of heart failure; however, of the answer choices listed, digoxin is the most appropriate treatment choice and acts by decreasing AV nodal conduction.
Atropine (choice A) is an anticholinergic agent that has been used in the treatment of atrioventricular heart block to increase the rate of conduction through the AV node, when increased vagal tone is a major factor in the conduction defect. Atropine is used in the ACLS protocol for symptomatic bradycardia but would not be appropriate to use in this tachycardic patient.
Lidocaine (choice C) is an antiarrhythmic agent indicated for the treatment of ventricular arrhythmias. Lidocaine has a variable effect on AV nodal conduction rate. For the most part, rate of conduction through the AV node remains unchanged.
Procainamide (choice D) is a class IA antiarrhythmic agent indicated for the treatment of ventricular arrhythmias. It may cause AV nodal conduction rate to be slightly increased. Procainamide may be used to cardiovert patients in atrial fibrillation to a normal rhythm in the emergency and inpatient setting.
Quinidine (choice E) is indicated for the conversion of atrial fibrillation/flutter. However, quinidine exerts an indirect anticholinergic effect that will decrease vagal tone and facilitate conduction through the AV node.
ReKap
In Mobitz type II AV block, the ECG will show intermittently nonconducted atrial beats with consistent PR intervals.
Metoprolol is a selective beta-1 blocker that can cause different degrees of AV blockade.
Analysis
The correct answer is C. Metoprolol is a selective beta-1 adrenergic receptor blocker that can cause bradycardia and varying degrees of atrioventricular (AV) block. In this case, the patient has a Mobitz type II second-degree AV block. Some action potentials traverse the AV node in Mobitz type II AV block, while others do not. Typically, patients have a regular rhythm with a P:QRS ratio greater than 2:1 and a consistent PR interval.
Second-degree heart block is typically subclassified as follows:
In Mobitz type I (Wenckebach) AV block, the PR interval progressively lengthens, with the RR interval shortening before the blocked beat. There is progressive PR interval prolongation for several beats preceding a dropped QRS complex.
ReKap
In Mobitz type II AV block, the ECG will show intermittently nonconducted atrial beats with consistent PR intervals.
Metoprolol is a selective beta-1 blocker that can cause different degrees of AV blockade.
Analysis
The correct answer is C. Metoprolol is a selective beta-1 adrenergic receptor blocker that can cause bradycardia and varying degrees of atrioventricular (AV) block. In this case, the patient has a Mobitz type II second-degree AV block. Some action potentials traverse the AV node in Mobitz type II AV block, while others do not. Typically, patients have a regular rhythm with a P:QRS ratio greater than 2:1 and a consistent PR interval.
Second-degree heart block is typically subclassified as follows:
In Mobitz type I (Wenckebach) AV block, the PR interval progressively lengthens, with the RR interval shortening before the blocked beat. There is progressive PR interval prolongation for several beats preceding a dropped QRS complex.
Mobitz type I block may occur as a result of medications (e.g., beta-blockers, digoxin, calcium channel blockers) or increased vagal tone. Mobitz type II block may also occur as a result of medications (listed above), but is usually associated with an organic lesion in the conduction pathway; a pacemaker may be required in these cases. Mobitz type I AV block is often transient or temporary. However, Mobitz type II AV block is almost always permanent, and frequently progresses to third-degree (complete) heart block.
The other options are not associated with heart block:
Felodipine (choice A) is a dihydropyridine calcium channel blocker. It inhibits calcium ion flux into vascular smooth muscle and the myocardium. Unlike verapamil and diltiazem, which are non-dihydropyridine calcium channel blockers, it is not associated with bradycardia or AV block.
Hydrochlorothiazide (choice B) is a thiazide diuretic. It inhibits sodium and chloride reabsorption in the distal convoluted tubule.
Terazosin (choice D) is a peripherally acting alpha-1 adrenergic receptor blocker. It is used for the treatment of hypertension and benign prostatic hyperplasia.
Triamterene (choice E) is a potassium-sparing diuretic. It inhibits sodium influx through channels in the luminal membrane of the late distal and cortical collecting tubules. Because potassium secretion is coupled with sodium influx in this area, potassium is spared.
ReKap
Digoxin is a cardiac glycoside that inhibits Na+-K+ ATPase.
Digoxin is used for the treatment of congestive heart failure and supraventricular tachycardia (including paroxysmal supraventricular tachycardia).
Signs of digoxin toxicity include gastrointestinal distress, xanthopsia, and new-onset arrhythmias.
Treatment is supportive and can involve F(ab) antibodies.
Analysis
The correct answer is A. Digoxin is a cardiac glycoside that inhibits the Na+-K+ ATPase and weakens the Na+ gradient used by the Na+-Ca2+ exchanger to clear Ca2+ from the sarcoplasm following cardiac excitation. The resulting increase in intracellular Ca2+ increases myocardial inotropy. Digoxin also inhibits the neuronal Na+-K+ ATPase, which increases vagal activity and decreases heart rate. Digoxin is indicated for heart failure (increases contractility) and atrial fibrillation (increases parasympathetic stimulation to the atrioventricular and sinoatrial nodes).
Symptoms of digoxin toxicity include nausea, vomiting, diarrhea, yellow-green visual distortion, and xanthopsia (yellow halos around lights). Because digoxin blocks the Na+-K+ ATPase, it can cause hyperkalemia. ECG changes include a decreased QT interval, an increased PR interval, T-wave inversion, atrioventricular (AV) block, and almost any kind of arrhythmia (including paroxysmal supraventricular tachycardia ).
Factors predisposing to digoxin toxicity include renal failure (decreased drug excretion), drug interactions (verapamil, quinidine, amiodarone), and hypokalemia (K+ competes with digoxin for binding sites on the Na+-K+-ATPase; hypokalemia results in increased digoxin binding). Initial treatment of digoxin toxicity includes anti-digoxin Fab fragments, correction of any underlying electrolyte abnormalities (e.g., hyperkalemia, hypomagnesemia), and managing the dysrhythmia.
Milrinone is an inotrope indicated for the short-term treatment of patients with acute decompensated heart failure. It inhibits phosphodiesterase (choice B), thus increasing cAMP levels and protein kinase A activation; this increases Ca2+ influx into the cardiac myocyte during excitation. Milrinone can cause a variety of arrhythmias, but it is not associated with nausea nor xanthopsia.
Diltiazem, an example of an L-type calcium channel blocker, inhibits calcium ion influx (choice C) into vascular smooth muscle and the myocardium. This decreases peripheral vascular resistance, dilates coronary arteries, and prolongs the atrioventricular (AV) node refractory period. Diltiazem is used to treat hypertension, chronic stable angina, and supraventricular tachycardias (including rate control in atrial fibrillation). Side effects include hypotension and AV block.
Esmolol and acebutolol are examples of drugs that selectively antagonize beta-1-adrenergic receptors (choice D). They are used for supraventricular tachyarrhythmias. Side effects include bradycardia, AV block, heart failure, and asthma exacerbation.
Procainamide is an example of class IA antiarrhythmic agent that decreases the slope of phase 0 of the action potential (choice E) by blocking Na+ channels. It also increases the action potential duration and effective refractory period. Side effects include hypotension, cardiac arrhythmias, and lupus erythematosus.
Pilocarpine is an example of a cholinomimetic drug that stimulates muscarinic cholinergic receptors (choice F). It decreases the heart rate by decreasing AV conduction velocity. Common side effects include diaphoresis, flushing, rhinitis, and dizziness.
Symptoms of digoxin toxicity include nausea, vomiting, diarrhea, yellow-green visual distortion, and xanthopsia (yellow halos around lights). Because digoxin blocks the Na+-K+ ATPase, it can cause hyperkalemia. ECG changes include a decreased QT interval, an increased PR interval, T-wave inversion, atrioventricular (AV) block, and almost any kind of arrhythmia (including paroxysmal supraventricular tachycardia ).
Factors predisposing to digoxin toxicity include renal failure (decreased drug excretion), drug interactions (verapamil, quinidine, amiodarone), and hypokalemia (K+ competes with digoxin for binding sites on the Na+-K+-ATPase; hypokalemia results in increased digoxin binding). Initial treatment of digoxin toxicity includes anti-digoxin Fab fragments, correction of any underlying electrolyte abnormalities (e.g., hyperkalemia, hypomagnesemia), and managing the dysrhythmia.
Milrinone is an inotrope indicated for the short-term treatment of patients with acute decompensated heart failure. It inhibits phosphodiesterase (choice B), thus increasing cAMP levels and protein kinase A activation; this increases Ca2+ influx into the cardiac myocyte during excitation. Milrinone can cause a variety of arrhythmias, but it is not associated with nausea nor xanthopsia.
Diltiazem, an example of an L-type calcium channel blocker, inhibits calcium ion influx (choice C) into vascular smooth muscle and the myocardium. This decreases peripheral vascular resistance, dilates coronary arteries, and prolongs the atrioventricular (AV) node refractory period. Diltiazem is used to treat hypertension, chronic stable angina, and supraventricular tachycardias (including rate control in atrial fibrillation). Side effects include hypotension and AV block.
Esmolol and acebutolol are examples of drugs that selectively antagonize beta-1-adrenergic receptors (choice D). They are used for supraventricular tachyarrhythmias. Side effects include bradycardia, AV block, heart failure, and asthma exacerbation.
Procainamide is an example of class IA antiarrhythmic agent that decreases the slope of phase 0 of the action potential (choice E) by blocking Na+ channels. It also increases the action potential duration and effective refractory period. Side effects include hypotension, cardiac arrhythmias, and lupus erythematosus.
Pilocarpine is an example of a cholinomimetic drug that stimulates muscarinic cholinergic receptors (choice F). It decreases the heart rate by decreasing AV conduction velocity. Common side effects include diaphoresis, flushing, rhinitis, and dizziness.
ReKap
Torsade de Pointes is a polymorphic ventricular tachycardia associated with prolongation of the QT interval.
Antiarrhythmic drugs that prolong the QT interval include class 1A antiarrhythmics (quinidine, procainamide, disopyramide) and class III antiarrhythmics (sotalol, dofetilide, amiodarone).
Analysis
The correct answer is E. The characteristic twisting of the QRS complexes with changes in amplitude around the isoelectric line demonstrates torsades de pointes (twisting of the points). The patient’s symptoms of palpitations, chest pain, and syncope also support this diagnosis. These arrhythmias are initiated by a ventricular premature beat in the setting of abnormal ventricular repolarization characterized by prolongation of the QT interval. Class IA, IC, and III antiarrhythmics are associated with torsade.
Sotalol is a class III antiarrhythmic (and non-selective beta-blocker) used in the treatment of atrial fibrillation/flutter and ventricular tachycardia. It is associated with QT prolongation and torsades de pointes, heart failure, bradycardia, and bronchospasm.
Atenolol (choice A) is a beta1-adrenergic antagonist that decreases sinoatrial (SA) and atrioventricular (AV) nodal activity and decreases the slope of phase 4 of the nodal action potential. It does not affect the QT interval.
Dabigatran (choice B) is an anticoagulant that directly and reversibly inhibits thrombin. Its primary adverse effect is bleeding. It has no impact on the QT interval.
Digoxin (choice C) is a cardiac glycoside that inhibits Na+-K+ ATPase activity, decreases AV conduction, and increases vagal activity. It also decreases nodal action potential duration and can shorten the QT interval. Shortening the QT interval does not predispose patients to TDP.
Metformin (choice D) is a biguanide that decreases hepatic gluconeogenesis and increases insulin. Serious side effects include lactic acidosis and hepatotoxicity. It does not affect the QT interval.
Verapamil (choice F) is a calcium channel blocker that decreases SA and AV nodal activity and decreases phase 0 and phase 4 of the nodal action potential. It does not affect the QT interval.
ReKap
Oral mexiletine and intravenous lidocaine are both class IB antiarrhythmics that block Na+ channels, shorten the duration of cardiac action potentials, and treat and prevent ventricular arrhythmias after myocardial infarction.
Amiodarone (class III antiarrhythmic) is a first-line agent for stable ventricular tachycardia but contains iodine, which increases the risk of severe reactions in patients with allergy to iodinated contrast dye.
Analysis
The correct answer is D. Sustained monomorphic ventricular tachycardia that is hemodynamically tolerated and asymptomatic can be treated initially with intravenous amiodarone, lidocaine, or procainamide. Symptomatic ventricular tachycardia requires emergent synchronized cardioversion per ACLS guidelines.
Lidocaine is a class IB antiarrhythmic indicated for the treatment of ventricular tachycardia. This agent blocks sodium channels and shortens action potential duration, but has no effect on conduction velocity. Both mexiletine and tocainide are also class IB antiarrhythmic agents that shorten the action potential duration and refractory period. These agents produce a modest suppression of sinoatrial (SA) node automaticity, as well as atrioventricular (AV) node conduction. Both of these agents have oral formulations and can be used to treat ventricular tachycardia.
Amiodarone (choice A) is a class III antiarrhythmic agent commonly used due to its compatibility with structural heart disease. It would be the first-line agent for chronic oral treatment of stable ventricular tachycardia. However, it is contraindicated in this patient due to his severe reaction to iodine.
Diltiazem (choice B) and verapamil are non-dihydropyridine calcium channel blocking agents and class IV antiarrhythmics. They act by decreasing and slowing SA and AV nodal conduction. Diltiazem is not used for managing ventricular tachycardia but can be used for atrial fibrillation with a rapid ventricular response.
Esmolol (choice C) is a class II antiarrhythmic agent that acts as an ultra-short acting beta-1 adrenergic blocking agent with cardioselective properties. Because of its short half-life, it is only administered intravenously. While this patient will require beta-blocker therapy after his myocardial infarction, this is not an appropriate agent for that indication, nor will it adequately suppress his stable ventricular tachycardia. It is typically used in the acute management of atrial fibrillation with a rapid ventricular response.
Procainamide (choice E) and quinidine are class IA antiarrhythmics that block Na+ and K+ channels. They all decrease myocardial excitability, conduction velocity (less than class IC agents), contractility, and automaticity. They also prolong the effective refractory period and action potential duration and block vagal stimulation of the AV node. They are also associated with an increased frequency of premature ventricular contractions, which can be dangerous in post-MI patients. They are typically only used as a last-line treatment due to this significant potential for harm.
ReKap
Acute coronary syndromes, including non-ST elevation myocardial infarction (NSTEMI), can lead to fatal arrhythmias in the post-MI period.
Torsades de pointes is a type of ventricular tachycardia that appears as a shifting sinusoidal waveform on ECG and can progress to ventricular fibrillation.
QT interval prolongation predisposes patients to torsades de pointes.
One common etiology of QT prolongation is the use of medications such as amiodarone, a class III antiarrhythmic.
Analysis
The correct answer is A. Amiodarone is a class III antiarrhythmic drug that blocks K+ channels in cardiac myocytes. It may be used to treat or prevent arrhythmias after acute coronary syndromes, such as non-ST elevation myocardial infarction (NSTEMI), as noted on this patient’s initial ECG. Although it is an antiarrhythmic drug, it may precipitate certain arrhythmias, including torsades de pointes, by prolonging the QT interval (>500 ms).
Torsades de pointes is a type of ventricular tachycardia that appears as a shifting sinusoidal waveform on ECG and is associated with the use of QT interval-prolonging medications. In addition to amiodarone, QT interval prolongation can be caused by many other drugs including:
Antiemetics (ondansetron)
Antibiotics (especially macrolides and quinolones)
Antifungals (azoles)
Opiates (methadone)
Other antiarrhythmic medications: class Ia (quinidine, procainamide, disopyramide) and class III (dofetilide, ibutilide, sotalol)
Typical and atypical antipsychotics
Aspirin (choice B) and clopidogrel (choice C) are not associated with QT interval prolongation on ECG. Both medications are antiplatelet drugs that are used in the treatment of patients with acute coronary syndrome and ischemic heart disease.
Heparin (choice D) is an anticoagulant that is not associated with QT interval prolongation. It is a standard-of-care treatment used for acute coronary syndrome and serves as a bridge to cardiac catheterization if coronary revascularization is indicated.
Metoprolol (choice E) is a cardioselective beta-blocker agent that helps to reduce myocardial oxygen demand by decreasing heart rate and contractility. It may help to relieve angina related to ischemia. It does not cause QT interval prolongation and is generally safe to use in the post-MI recovery period.
Simvastatin (choice F) is an HMG-CoA reductase inhibitor that decreases cholesterol biosynthesis in patients with hyperlipidemia. It improves lipid profiles mainly by reducing low-density lipoprotein levels. It does not cause QT interval prolongation.
