# Seminar 02: Cardiac Emergencies ## Year 3: Emergency Medicine Clerkship --- ## Learning Objectives By the end of this seminar, students will be able to: 1. Recognize ST-elevation myocardial infarction on ECG 2. Initiate time-sensitive ACS management 3. Identify and treat unstable arrhythmias 4. Manage acute decompensated heart failure 5. Diagnose and treat cardiac tamponade 6. Perform synchronized cardioversion --- ## Seminar Outline ### I. Acute Coronary Syndrome Acute coronary syndrome encompasses a spectrum of myocardial ischemia ranging from unstable angina through non-ST-elevation myocardial infarction to ST-elevation myocardial infarction, all resulting from acute disruption of coronary blood flow typically due to atherosclerotic plaque rupture with superimposed thrombosis. The classification depends on electrocardiographic findings and cardiac biomarker elevation, with STEMI defined by characteristic ST-segment elevation of at least one millimeter in two or more contiguous leads, NSTEMI characterized by troponin elevation without ST elevation, and unstable angina representing ischemia without biomarker release. STEMI equivalents including new left bundle branch block, posterior MI pattern with ST depression in anterior leads, and de Winter T waves indicating proximal LAD occlusion demand recognition as indications for emergent reperfusion therapy. This classification determines treatment urgency and strategy, with STEMI requiring immediate reperfusion while NSTEMI and unstable angina follow risk-stratified approaches. STEMI recognition requires systematic ECG interpretation identifying characteristic patterns that localize the infarct territory and predict the culprit coronary artery. Anterior STEMI presents with ST elevation in leads V1 through V4, indicating left anterior descending artery occlusion, the most common STEMI pattern carrying significant morbidity due to large territory at risk. Inferior STEMI manifests as ST elevation in leads II, III, and aVF, typically from right coronary artery occlusion, and should prompt evaluation for right ventricular involvement using right-sided leads. Lateral STEMI shows changes in leads I, aVL, V5, and V6, usually reflecting left circumflex involvement, while posterior STEMI presents subtly with ST depression in V1-V3 that becomes diagnostic elevation when viewed in posterior leads or conceptualized as a mirror image. Time targets in STEMI management reflect the critical relationship between reperfusion delay and myocardial salvage, with every minute of ongoing ischemia causing progressive and irreversible cardiomyocyte death. Door-to-ECG time should not exceed ten minutes, as rapid diagnosis enables appropriate resource mobilization and treatment initiation. Door-to-balloon time for primary percutaneous coronary intervention should remain under ninety minutes when performed at the presenting hospital, representing the primary performance metric for STEMI care quality. When transfer for PCI is required, total first medical contact to device time should not exceed one hundred twenty minutes, though fibrinolysis becomes preferable when transfer times exceed this threshold. Initial ACS management follows established protocols regardless of specific classification, with modifications based on subsequent risk stratification and planned reperfusion strategy. Aspirin three hundred twenty-five milligrams chewed provides rapid antiplatelet effect through oral mucosal absorption and should be administered immediately upon ACS suspicion. P2Y12 inhibitor therapy with clopidogrel, ticagrelor, or prasugrel provides additional platelet inhibition, though timing and agent selection may be deferred pending catheterization laboratory activation. Anticoagulation with heparin prevents thrombus propagation while nitroglycerin provides symptomatic relief and reduces preload, though it must be avoided in right ventricular infarction and hypotension. Morphine use has become more controversial due to potential delayed antiplatelet drug absorption, though it remains appropriate for refractory pain. Panel A: ACS classification algorithm distinguishing STEMI, NSTEMI, and unstable angina based on ECG findings and troponin results. Panel B: STEMI ECG patterns demonstrating territorial localization with corresponding coronary artery anatomy. Panel C: Time target benchmarks showing door-to-ECG, door-to-balloon, and transfer time goals displayed on a timeline. Panel D: Initial ACS management protocol flowchart with medication dosing and contraindication considerations. --- ### II. STEMI Management Reperfusion strategy selection in STEMI balances the superior outcomes of primary PCI against time delays inherent in catheterization laboratory activation or interfacility transfer. Primary PCI represents the preferred reperfusion approach when performed by experienced operators within appropriate time windows, as it achieves higher rates of culprit vessel patency with lower bleeding risk compared to fibrinolysis. Hospitals lacking PCI capability must have established transfer protocols enabling rapid transport to interventional centers, with door-in-door-out times under thirty minutes ensuring transferred patients still achieve timely reperfusion. When anticipated transfer times exceed one hundred twenty minutes from first medical contact, fibrinolytic therapy becomes the appropriate choice despite its limitations, as delayed PCI loses its advantage over timely pharmacologic reperfusion. Fibrinolytic therapy achieves coronary reperfusion through pharmacologic dissolution of the occlusive thrombus, offering the advantage of immediate availability without requiring specialized facilities or personnel. Tenecteplase provides weight-based single bolus dosing that simplifies administration compared to alteplase infusion protocols, while reteplase uses two boluses administered thirty minutes apart. Absolute contraindications including prior intracranial hemorrhage, known cerebral vascular malformation, recent major surgery, and suspected aortic dissection preclude fibrinolytic use. Success is assessed by greater than fifty percent ST-segment resolution within sixty to ninety minutes, with failure to achieve this benchmark indicating need for rescue PCI. Adjunctive therapies in STEMI optimize outcomes beyond acute reperfusion by preventing rethrombosis, limiting infarct size, and addressing secondary complications. Dual antiplatelet therapy with aspirin plus a P2Y12 inhibitor continues beyond the acute phase to prevent stent thrombosis and recurrent events. Anticoagulation with unfractionated heparin, enoxaparin, or bivalirudin maintains during and after PCI according to institutional protocols. Beta-blocker therapy reduces myocardial oxygen demand and prevents arrhythmias when administered to stable patients without contraindications such as hypotension, bradycardia, or acute heart failure. ACE inhibitor therapy initiated within twenty-four hours of stable STEMI provides long-term ventricular remodeling benefits, while high-intensity statin therapy addresses the underlying atherosclerotic disease process. STEMI complications require vigilant monitoring and prompt intervention to prevent progression to cardiogenic shock or death. Cardiogenic shock complicates approximately seven percent of STEMI cases and carries mortality exceeding forty percent, requiring vasopressor support, mechanical circulatory assistance, and early revascularization. Arrhythmias including ventricular tachycardia and fibrillation require immediate defibrillation and may indicate ongoing ischemia demanding accelerated reperfusion. Mechanical complications including ventricular septal defect, papillary muscle rupture with acute mitral regurgitation, and free wall rupture represent surgical emergencies requiring emergent operative intervention. Right ventricular infarction complicating inferior STEMI causes hypotension responsive to volume loading but worsened by nitrates and other preload-reducing agents. Panel A: Reperfusion strategy decision algorithm based on PCI availability and anticipated transfer times. Panel B: Fibrinolytic agent comparison showing dosing regimens, contraindications, and success assessment criteria. Panel C: Adjunctive therapy timeline showing aspirin, P2Y12 inhibitor, anticoagulation, beta-blocker, ACE inhibitor, and statin initiation windows. Panel D: STEMI complication recognition and management including cardiogenic shock, arrhythmias, and mechanical complications. --- ### III. Arrhythmias - Tachycardia The initial approach to any tachyarrhythmia begins with assessment of hemodynamic stability, as unstable patients require immediate electrical cardioversion regardless of the specific rhythm diagnosis. Instability indicators include hypotension with signs of poor perfusion, altered mental status, acute heart failure with pulmonary edema, and ongoing ischemic chest pain, any of which mandate emergent intervention. Synchronized cardioversion interrupts the arrhythmia circuit by depolarizing the entire myocardium simultaneously, allowing the sinoatrial node to resume normal pacemaker function. Stable patients afford time for rhythm diagnosis and rhythm-specific treatment strategies, though continuous monitoring and reassessment remain essential as stability can deteriorate rapidly. Narrow complex tachycardia with QRS duration under one hundred twenty milliseconds indicates supraventricular origin, with specific rhythm identification guiding treatment selection. Sinus tachycardia represents an appropriate physiologic response to underlying stressors such as hypovolemia, pain, fever, or anxiety, requiring treatment of the underlying cause rather than the heart rate itself. Supraventricular tachycardia due to atrioventricular nodal reentrant tachycardia or accessory pathway-mediated tachycardia responds to vagal maneuvers including carotid massage and Valsalva, followed by adenosine if vagal maneuvers fail. Atrial fibrillation and atrial flutter require rate control with atrioventricular nodal blocking agents such as diltiazem or metoprolol, with cardioversion consideration based on duration and anticoagulation status. Wide complex tachycardia with QRS duration exceeding one hundred twenty milliseconds should be presumed ventricular in origin unless prior ECGs demonstrate baseline bundle branch block, as misdiagnosis and inappropriate treatment of ventricular tachycardia as supraventricular tachycardia with aberrancy causes harm. Regular monomorphic wide complex tachycardia in stable patients can be treated with amiodarone or procainamide, agents effective against ventricular tachycardia that also treat supraventricular rhythms with aberrancy. Polymorphic ventricular tachycardia with normal baseline QT interval should be treated as ventricular fibrillation with immediate defibrillation, while polymorphic VT with prolonged QT interval represents torsades de pointes requiring intravenous magnesium sulfate two grams as first-line therapy. Unstable wide complex tachycardia of any morphology requires immediate synchronized cardioversion. Synchronized cardioversion technique ensures shock delivery during the QRS complex to avoid the vulnerable period when shock might induce ventricular fibrillation. Anterior-lateral or anterior-posterior pad placement maximizes current delivery through the myocardium. Initial energy selection of one hundred to two hundred joules biphasic provides effective cardioversion for most tachyarrhythmias, with energy escalation for refractory rhythms. Procedural sedation with agents such as propofol, etomidate, or midazolam with fentanyl provides amnesia and analgesia for conscious patients, though resuscitation equipment must be immediately available for sedation-related complications. Synchronization must be reactivated between shocks, as most defibrillators default to asynchronous mode after each discharge. Panel A: Stability assessment algorithm with indicators for immediate cardioversion versus rhythm-specific management. Panel B: Narrow complex tachycardia differentiation flowchart distinguishing sinus tachycardia, SVT, atrial fibrillation, and atrial flutter with treatment strategies. Panel C: Wide complex tachycardia approach showing VT presumption, medication options, and treatment for monomorphic versus polymorphic patterns. Panel D: Cardioversion procedure steps including synchronization, pad placement, energy selection, and sedation considerations. --- ### IV. Arrhythmias - Bradycardia Symptomatic bradycardia requiring treatment is defined by heart rate inadequate to maintain perfusion with associated symptoms or signs of hemodynamic compromise. Symptoms attributable to bradycardia include lightheadedness, presyncope, syncope, fatigue, dyspnea on exertion, and chest pain, while signs include hypotension, altered mental status, and evidence of heart failure or shock. Asymptomatic bradycardia, even with rates below sixty beats per minute, typically requires only monitoring and treatment of underlying causes without specific antiarrhythmic intervention. Determination of symptom attribution to bradycardia rather than coincidental occurrence guides the aggressiveness of treatment approach. The treatment algorithm for symptomatic bradycardia begins with atropine, which increases heart rate through vagolytic effects on the sinoatrial and atrioventricular nodes. Initial dosing of one milligram intravenously may be repeated every three to five minutes to a maximum dose of three milligrams. Atropine effectiveness varies by the level of block, with good response in sinus bradycardia and first-degree or type I second-degree block but poor response in type II second-degree and third-degree block where the block occurs below the level of vagal innervation. When atropine fails to achieve adequate rate and perfusion, second-line options include transcutaneous pacing, dopamine infusion at two to twenty micrograms per kilogram per minute, or epinephrine infusion at two to ten micrograms per minute. Heart block classification predicts prognosis and guides management intensity based on the anatomic level and completeness of conduction system disease. First-degree block with PR interval prolongation exceeding two hundred milliseconds typically requires no acute treatment beyond observation and identification of reversible causes. Second-degree type I block with progressive PR prolongation culminating in a dropped beat usually localizes to the AV node and responds to atropine if symptomatic. Second-degree type II block with constant PR interval and sudden dropped beats indicates infranodal disease with high risk of progression to complete block, warranting pacing even if currently asymptomatic. Third-degree or complete heart block with atrioventricular dissociation requires pacing regardless of symptoms due to unreliable escape rhythm and risk of asystole. Transcutaneous pacing provides temporary rate support while preparing for transvenous pacing or while reversible causes are addressed. Anterior-posterior pad placement optimizes current pathway through the ventricles. Rate is typically set between sixty and eighty beats per minute, with output increased from minimum until electrical capture is achieved, evidenced by wide QRS complex following each pacing spike. Mechanical capture must be confirmed by pulse palpation, as electrical activity without mechanical response provides no hemodynamic benefit. Transcutaneous pacing causes significant discomfort in conscious patients, requiring sedation and analgesia when clinical status permits. Transvenous pacing provides more reliable capture with less discomfort and represents the bridge to permanent pacemaker placement when indicated. Panel A: Symptomatic bradycardia criteria showing symptoms and signs attributable to inadequate heart rate. Panel B: Bradycardia treatment algorithm progressing from atropine through transcutaneous pacing and vasopressor infusions. Panel C: Heart block classification with ECG examples of first-degree, type I and type II second-degree, and third-degree block with management implications. Panel D: Transcutaneous pacing setup and technique including pad placement, rate and output settings, and capture confirmation. --- ### V. Cardiac Arrest Basic life support forms the foundation of cardiac arrest resuscitation, with high-quality chest compressions providing the circulation necessary to maintain coronary and cerebral perfusion until definitive treatment can restore spontaneous circulation. Recognition of cardiac arrest requires identifying unresponsiveness combined with absent or abnormal breathing, as agonal gasps commonly occur in the initial minutes and should not preclude CPR initiation. Compression quality parameters include rate of one hundred to one hundred twenty per minute, depth of at least two inches in adults, complete chest recoil between compressions, and minimal interruptions. The compression-to-ventilation ratio of thirty to two applies until advanced airway placement, after which continuous compressions with asynchronous ventilation every six seconds becomes appropriate. Shockable rhythms including ventricular fibrillation and pulseless ventricular tachycardia have fundamentally better prognosis than non-shockable rhythms because they respond to defibrillation. Early defibrillation represents the definitive treatment, with survival probability decreasing approximately ten percent for each minute of persistent fibrillation. Defibrillation energy of two hundred joules biphasic or device-specific recommendations should be delivered immediately upon rhythm recognition, followed by immediate CPR resumption without rhythm or pulse check. Epinephrine one milligram is administered after the second shock and repeated every three to five minutes, while amiodarone three hundred milligrams is given after the third shock with additional one hundred fifty milligram dose if needed. Non-shockable rhythms including asystole and pulseless electrical activity carry substantially worse prognosis but still warrant aggressive resuscitation with focus on identifying and treating reversible causes. Asystole must be confirmed in multiple leads to exclude fine ventricular fibrillation that might respond to defibrillation. PEA requires immediate consideration of reversible causes, as organized electrical activity without mechanical output implies a specific pathophysiologic mechanism amenable to targeted treatment. CPR should continue with epinephrine every three to five minutes while the team systematically evaluates and addresses potential causes. The H's and T's mnemonic systematically identifies reversible causes of cardiac arrest that require specific interventions beyond standard ACLS algorithms. Hypovolemia from hemorrhage or severe dehydration responds to volume resuscitation. Hypoxia demands airway management and oxygenation. Hydrogen ion excess indicating severe acidosis may require sodium bicarbonate and treatment of underlying cause. Hypokalemia and hyperkalemia cause arrhythmias addressable with electrolyte repletion or calcium, insulin, and glucose respectively. Hypothermia requires rewarming with modified resuscitation protocols. Tension pneumothorax demands needle decompression. Cardiac tamponade requires pericardiocentesis. Toxins need specific antidotes. Thrombosis causing pulmonary embolism or coronary occlusion may warrant thrombolysis during arrest. Panel A: High-quality CPR parameters including rate, depth, recoil, and interruption minimization displayed with visual guides. Panel B: Shockable rhythm algorithm showing defibrillation timing, epinephrine and amiodarone administration, and CPR integration. Panel C: Non-shockable rhythm management emphasizing reversible cause identification during continuous CPR with epinephrine. Panel D: H's and T's systematic checklist with specific interventions for each reversible cause of cardiac arrest. --- ### VI. Post-Cardiac Arrest Care Immediate priorities following return of spontaneous circulation focus on hemodynamic optimization and prevention of secondary brain injury through careful physiologic management. Mean arterial pressure target of sixty-five millimeters of mercury or higher ensures adequate perfusion, often requiring vasopressor support with norepinephrine or epinephrine in the post-arrest period. Oxygenation should target SpO2 of ninety-four to ninety-eight percent, avoiding both hypoxia and hyperoxia, with the latter associated with increased oxidative injury and worse neurological outcomes. Ventilation targets normocapnia, as both hypocapnia causing cerebral vasoconstriction and hypercapnia indicating inadequate ventilation prove detrimental. Glucose management avoids hypoglycemia while treating significant hyperglycemia to reduce metabolic stress. Targeted temperature management has become standard care for comatose survivors of cardiac arrest based on evidence demonstrating improved neurological outcomes. Current guidelines recommend selecting a target temperature between thirty-two and thirty-six degrees Celsius maintained for at least twenty-four hours. Cooling methods include surface cooling devices, intravenous cold saline, and intravascular cooling catheters, with selection based on institutional resources and expertise. Active prevention of fever for at least seventy-two hours following the cooling period addresses the rebound hyperthermia associated with worse outcomes. Shivering, which undermines temperature control and increases metabolic demand, requires pharmacologic suppression with sedatives, analgesics, and potentially neuromuscular blockade. Neurologic assessment and prognostication require careful timing and multimodal evaluation to avoid premature withdrawal of care in patients who might achieve meaningful recovery. Prognostication should not occur until at least seventy-two hours after return to normothermia, allowing time for sedative clearance and neurological examination accuracy. No single finding reliably predicts poor outcome, mandating multimodal assessment combining clinical examination, electroencephalography, somatosensory evoked potentials, neuroimaging, and biomarkers. Bilateral absence of pupillary and corneal reflexes at seventy-two hours, status myoclonus in the first seventy-two hours, and bilateral absence of N20 cortical responses on somatosensory evoked potentials represent the most specific poor prognostic indicators. Cardiac catheterization decisions in post-arrest patients balance the potential benefit of coronary intervention against procedural risks in hemodynamically unstable patients. STEMI identified on post-ROSC ECG warrants emergent catheterization regardless of neurological status, as cardiac cause likely precipitated the arrest and revascularization offers potential benefit. Absence of obvious STEMI does not exclude coronary etiology, and early catheterization should be considered in patients without clear non-cardiac cause of arrest. Hemodynamic instability from cardiogenic shock may actually increase benefit from catheterization and mechanical circulatory support. Poor neurological prognosis should not delay catheterization, as accurate prognostication cannot occur in the immediate post-arrest period. Panel A: Post-ROSC immediate management priorities showing hemodynamic targets, oxygenation goals, ventilation parameters, and glucose management. Panel B: Targeted temperature management protocol depicting cooling methods, target selection, duration, and fever prevention phases. Panel C: Neuroprognostication timeline showing seventy-two-hour waiting period and multimodal assessment components. Panel D: Post-arrest catheterization decision algorithm based on ECG findings, hemodynamic status, and suspected arrest etiology. --- ### VII. Acute Heart Failure Acute decompensated heart failure presents with symptoms and signs reflecting pulmonary and systemic congestion, with or without evidence of inadequate cardiac output and peripheral hypoperfusion. Patients typically report progressive dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and exercise intolerance developing over hours to days. Physical examination reveals elevated jugular venous pressure, pulmonary crackles, peripheral edema, and frequently a third heart sound. Chest radiograph demonstrates pulmonary vascular congestion with cephalization of pulmonary vessels, interstitial and alveolar edema, pleural effusions, and cardiomegaly. B-type natriuretic peptide or N-terminal pro-BNP elevation supports the diagnosis and aids differentiation from primary pulmonary causes of dyspnea. Hemodynamic profile classification guides treatment selection by categorizing patients based on perfusion adequacy and congestion presence. The warm and wet profile describing adequate perfusion with volume overload represents the most common acute presentation, responding to diuretics and vasodilators. Cold and wet patients demonstrating poor perfusion with congestion require inotropic support in addition to cautious diuresis. Cold and dry patients with poor perfusion but without significant congestion need volume expansion and inotropes rather than diuretics. Warm and dry patients are essentially compensated and benefit from optimization of oral therapy rather than acute intervention. This framework simplifies complex hemodynamics into actionable treatment categories. Treatment of the typical warm and wet presentation targets symptom relief through reduction of pulmonary congestion and afterload. Non-invasive positive pressure ventilation with bilevel support reduces work of breathing and improves oxygenation while decreasing preload and afterload, often dramatically improving patient comfort. Intravenous loop diuretics such as furosemide produce rapid diuresis to relieve congestion, with dosing typically starting at one to two times the patient's home oral dose given intravenously. Vasodilators including nitroglycerin reduce preload and afterload, providing additional relief when systolic blood pressure exceeds one hundred ten millimeters of mercury. Morphine, historically standard therapy, has fallen from favor due to association with increased mortality and should be used sparingly if at all. Cardiogenic shock represents the extreme end of the heart failure spectrum, with cardiac output inadequate to maintain organ perfusion despite adequate or elevated filling pressures. Clinical features include hypotension, cool extremities, altered mental status, oliguria, and elevated lactate reflecting tissue hypoperfusion. Vasopressor support with norepinephrine maintains blood pressure while inotropes such as dobutamine or milrinone augment cardiac output. Mechanical circulatory support devices including intra-aortic balloon pump, Impella, and extracorporeal membrane oxygenation provide escalating levels of hemodynamic support when pharmacologic therapy proves insufficient. Identification and treatment of the underlying cause, particularly acute coronary syndrome, remains essential, as revascularization offers the best chance of meaningful recovery. Panel A: Acute heart failure presentation showing symptom progression, physical examination findings, and diagnostic study results. Panel B: Hemodynamic profile quadrant diagram classifying patients as warm/cold and wet/dry with treatment implications for each category. Panel C: Warm and wet treatment protocol showing NIPPV, diuretic dosing, vasodilator use, and morphine caution. Panel D: Cardiogenic shock management escalation from vasopressors through inotropes to mechanical circulatory support devices. --- ### VIII. Hypertensive Emergencies Hypertensive emergency is defined by severely elevated blood pressure causing acute end-organ damage, distinguishing it from hypertensive urgency where equivalent pressure elevation occurs without evidence of organ injury. The specific blood pressure threshold matters less than the presence of end-organ damage, as patients with chronic hypertension may tolerate higher pressures without acute injury while those with previously normal blood pressure may develop emergencies at lower absolute values. Target organs susceptible to hypertensive injury include the brain, heart, kidneys, eyes, and large vessels. Common presentations include hypertensive encephalopathy, acute coronary syndrome, acute heart failure with pulmonary edema, acute aortic dissection, and acute kidney injury with rapid creatinine rise. End-organ damage manifestations determine both the diagnosis of hypertensive emergency and specific treatment considerations. Neurological involvement may present as encephalopathy with headache, confusion, and visual disturbances, or as ischemic or hemorrhagic stroke. Cardiac manifestations include acute coronary syndrome and acute heart failure with pulmonary edema. Renal involvement causes acute kidney injury with rising creatinine and potentially microangiopathic hemolytic anemia. Retinal findings include papilledema, hemorrhages, and exudates indicating malignant hypertension. Aortic dissection presents with tearing chest or back pain and blood pressure differentials between extremities. Each presentation requires specific blood pressure targets and treatment approach modifications. Treatment principles for hypertensive emergencies balance the need for blood pressure reduction against risks of hypoperfusion from excessive or rapid lowering. The general goal reduces mean arterial pressure by ten to twenty percent within the first hour, with further gradual reduction over the subsequent twenty-four to forty-eight hours. Precipitous blood pressure drops risk watershed infarction in brain and other organs that have adapted to chronic hypertension through autoregulatory shifts. Intravenous medications provide titratable control that oral agents cannot match. Specific targets vary by condition: aortic dissection requires rapid reduction to systolic below one hundred twenty with heart rate below sixty, while ischemic stroke often warrants permissive hypertension unless thrombolysis is planned. Specific antihypertensive agents are selected based on clinical scenario, onset and duration of action, and side effect profile. Nicardipine, a dihydropyridine calcium channel blocker, provides smooth titratable reduction appropriate for most hypertensive emergencies. Labetalol combines alpha and beta blockade, making it particularly useful for aortic dissection where heart rate reduction is essential. Esmolol provides pure beta blockade with ultra-short duration allowing rapid titration. Nitroprusside offers potent vasodilation but requires arterial line monitoring and carries risk of cyanide toxicity with prolonged use. Clevidipine is an ultra-short-acting calcium channel blocker metabolized by esterases. Hydralazine, though commonly available, provides less predictable response and is primarily used in pregnancy-related hypertensive emergencies. Panel A: Hypertensive emergency versus urgency differentiation emphasizing end-organ damage presence rather than specific blood pressure threshold. Panel B: End-organ damage manifestations by system showing neurological, cardiac, renal, retinal, and vascular presentations. Panel C: Blood pressure reduction goals and timeline demonstrating initial ten to twenty percent reduction with subsequent gradual normalization. Panel D: Antihypertensive agent selection guide with specific scenarios favoring nicardipine, labetalol, esmolol, nitroprusside, and hydralazine. --- ### IX. Aortic Emergencies Aortic dissection results from intimal tear allowing blood to enter the media and propagate proximally or distally, creating a false lumen that may compromise branch vessel perfusion or rupture catastrophically. Type A dissection involving the ascending aorta represents a surgical emergency with mortality exceeding one percent per hour when untreated, while Type B dissection limited to the descending aorta can often be managed medically unless complicated by malperfusion or rupture. Classic presentation includes sudden severe tearing or ripping chest pain radiating to the back, though the symptom spectrum varies widely based on dissection location and extent. Physical examination may reveal blood pressure differential exceeding twenty millimeters of mercury between arms, pulse deficits, aortic regurgitation murmur, or focal neurological findings from carotid involvement. Dissection management priorities include blood pressure and heart rate control to reduce aortic wall stress and prevent propagation while arranging definitive imaging and surgical consultation. Beta-blockade constitutes first-line therapy, with esmolol or labetalol providing rapid heart rate reduction targeting below sixty beats per minute to minimize the rate of pressure rise with each cardiac cycle. Blood pressure reduction to systolic below one hundred twenty millimeters of mercury follows heart rate control, using additional agents as needed once beta-blockade is established. CT angiography provides definitive diagnosis with excellent sensitivity and specificity while characterizing dissection extent and branch vessel involvement. Type A dissection requires emergent surgical repair, while uncomplicated Type B dissection typically receives medical management with surgical intervention reserved for complications. Ruptured abdominal aortic aneurysm classically presents with the triad of hypotension, pulsatile abdominal mass, and abdominal or flank pain radiating to the back, though this complete triad appears in only a minority of cases. Many patients present with syncope, isolated back pain, or unexplained hypotension, making clinical suspicion essential in the appropriate demographic. Risk factors include age over sixty-five, male sex, smoking history, hypertension, and family history of AAA. Hemodynamically unstable patients with suspected rupture should proceed directly to the operating room without imaging confirmation, as delays for diagnostic studies allow continued hemorrhage. Permissive hypotension targeting systolic pressure between seventy and ninety millimeters of mercury may reduce ongoing bleeding while preserving coronary and cerebral perfusion until surgical control is achieved. Acute aortic occlusion from embolism or thrombosis presents with sudden onset of bilateral lower extremity pain, pallor, pulselessness, paresthesias, and paralysis representing the classic findings of acute limb ischemia. The abrupt occlusion of the aorta at the bifurcation produces simultaneous bilateral symptoms distinguishing it from more common unilateral peripheral arterial occlusion. Patients may present in profound shock from the acute loss of lower body perfusion. CT angiography confirms the diagnosis and characterizes the occlusion. Treatment requires emergent revascularization through surgical embolectomy, thrombectomy, or bypass depending on the underlying cause and patient condition. Panel A: Aortic dissection Stanford classification showing Type A involving ascending aorta and Type B limited to descending aorta with management implications. Panel B: Dissection management protocol emphasizing beta-blockade first, then blood pressure control to specific targets. Panel C: Ruptured AAA presentation spectrum from classic triad through atypical presentations with management priorities. Panel D: Acute aortic occlusion differentiation from peripheral arterial occlusion showing bilateral simultaneous symptoms and emergent management. --- ### X. Cardiac Tamponade Cardiac tamponade results from pericardial fluid accumulation causing compression of cardiac chambers with impaired diastolic filling and progressive hemodynamic compromise. The pericardial space normally contains fifteen to fifty milliliters of fluid, but the rigid pericardium limits acute expansion, meaning rapid fluid accumulation causes tamponade physiology with relatively small volumes while slow accumulation allows pericardial stretch and tolerance of large effusions. Etiologies include trauma, malignancy, uremia, infection, post-myocardial infarction pericarditis, and iatrogenic causes from procedures such as central line placement or cardiac catheterization. The rate of fluid accumulation rather than absolute volume determines clinical presentation and urgency. Beck's triad describes the classic tamponade presentation with hypotension, jugular venous distension, and muffled heart sounds, though this complete triad appears in only a minority of cases. Hypotension reflects decreased cardiac output from impaired filling, while jugular venous distension results from elevated right atrial pressure as the right ventricle cannot accept venous return. Muffled heart sounds occur when the effusion acoustically insulates the heart from the chest wall. Pulsus paradoxus, defined as greater than ten millimeter of mercury decrease in systolic blood pressure during inspiration, reflects exaggerated ventricular interdependence as the inspiratory increase in right ventricular volume further compromises the already-impaired left ventricle. Diagnosis relies on clinical suspicion confirmed by bedside echocardiography, which has become the standard of care for rapid tamponade evaluation. Echocardiographic findings include pericardial effusion surrounding the heart, right atrial collapse during late diastole, and right ventricular diastolic collapse indicating elevated intrapericardial pressure exceeding chamber pressures. Electrocardiogram may show low voltage and electrical alternans, where the QRS amplitude varies beat-to-beat as the heart swings within the fluid-filled pericardium. Chest radiograph demonstrates enlarged cardiac silhouette with a "water bottle" appearance when the effusion is large, though normal cardiac size does not exclude tamponade from rapid small-volume accumulation. Management of hemodynamically significant tamponade requires emergent pericardiocentesis to relieve the elevated intrapericardial pressure and restore cardiac filling. Temporizing measures while preparing for drainage include intravenous fluid administration to increase filling pressures and maintain cardiac output, though this provides only brief hemodynamic support. Pericardiocentesis is performed using a subxiphoid approach, advancing the needle at a forty-five-degree angle toward the left shoulder under ultrasound or ECG guidance. Even small volume removal often produces dramatic hemodynamic improvement due to the steep pressure-volume relationship of the acutely distended pericardium. Positive pressure ventilation worsens tamponade physiology by increasing intrathoracic pressure and should be avoided or minimized when possible. Definitive management may require pericardial window for recurrent effusions or treatment of underlying cause. Panel A: Tamponade pathophysiology showing pericardial fluid accumulation, chamber compression, and impaired diastolic filling. Panel B: Beck's triad components with pulsus paradoxus measurement technique and significance. Panel C: Echocardiographic findings demonstrating pericardial effusion, right atrial collapse, and right ventricular diastolic collapse. Panel D: Pericardiocentesis procedure showing subxiphoid approach, needle angle, and ultrasound guidance with expected hemodynamic response. --- ## Summary - STEMI requires door-to-ECG under ten minutes and door-to-balloon under ninety minutes, with territory localized by ECG leads to anterior, inferior, lateral, or posterior distribution - Unstable tachycardia of any type requires immediate synchronized cardioversion, while stable narrow complex tachycardia responds to vagal maneuvers followed by adenosine - Wide complex tachycardia should be presumed ventricular tachycardia and treated with amiodarone, while torsades de pointes requires magnesium sulfate - Symptomatic bradycardia management progresses from atropine through transcutaneous pacing to dopamine or epinephrine infusion - Cardiac arrest resuscitation emphasizes high-quality CPR, early defibrillation for shockable rhythms, epinephrine administration, and systematic evaluation of H's and T's - Post-arrest care includes targeted temperature management at thirty-two to thirty-six degrees Celsius with neuroprognostication delayed until seventy-two hours after normothermia - Acute heart failure with warm and wet profile responds to diuretics, vasodilators, and NIPPV, while cardiogenic shock requires vasopressors, inotropes, and possibly mechanical support - Aortic dissection management prioritizes beta-blockade first to reduce heart rate, then blood pressure control, with Type A requiring emergent surgery - Cardiac tamponade presents with Beck's triad and pulsus paradoxus, diagnosed by bedside echo showing chamber collapse, and treated with emergent pericardiocentesis --- ## Key Terms | Term | Definition | |------|------------| | STEMI | ST-elevation myocardial infarction requiring emergent reperfusion therapy | | Door-to-balloon | Time from hospital arrival to coronary artery intervention, target under ninety minutes | | Cardioversion | Synchronized electrical shock delivered during QRS complex for tachyarrhythmia termination | | Defibrillation | Unsynchronized shock for ventricular fibrillation or pulseless ventricular tachycardia | | TTM | Targeted temperature management for post-arrest neuroprotection | | ROSC | Return of spontaneous circulation following cardiac arrest | | Beck's triad | Hypotension, jugular venous distension, and muffled heart sounds indicating tamponade | | Pulsus paradoxus | Greater than ten millimeter mercury systolic blood pressure decrease with inspiration | --- *This content is subject to the [MIT License](https://opensource.org/licenses/MIT). © 2024–2026 Hibbert School of Medicine.*