Cardiovascular emergencies are life-threatening disorders that must be diagnosed quickly to avoid delay in treatment and to minimize morbidity and mortality. Patients may present with severe hypertension, chest pain, dysrhythmia, or cardiopulmonary arrest. In this chapter, we will review the clinician's approach to these disorders and their treatments and provide links to other informative resources. Acute coronary syndromes are covered elsewhere in this text.

Cardiopulmonary arrest

Causes

Cardiopulmonary arrest occurs as a result of a multitude of cardiovascular, metabolic, infectious, neurologic, inflammatory, and traumatic diseases. However, the clinician must be aware of several specific causes, including drug toxicity or overdose, myocardial ischemia or infarction, hyperkalemia, torsades de pointes, cardiac tamponade, and tension pneumothorax. The marked differences in therapeutic intervention among these various causes underscore the need for accurate recognition. The end point of these disorders is commonly pulseless ventricular tachycardia or ventricular fibrillation, pulseless electrical activity, symptomatic bradycardia, or asystole.

Prevalence

An estimated 250,000 people per year in the United States experience sudden cardiac death. However, national statistics on the actual prevalence of cardiopulmonary arrest are unreliable because no single agency collects data relating to the number of patients who receive cardiopulmonary resuscitation (CPR) annually. Ischemic cardiovascular disease underlies many cardiopulmonary arrests in adults.

The value of early CPR and immediate defibrillation has been proven in many community-based studies. ^1–4 Additionally, among adults, in whom ventricular tachycardia, ventricular fibrillation, or both is more common, the increased use of automated external defibrillators (AEDs) by emergency medical services (EMS), businesses, and airports has improved survival. ^5–8 Without defibrillation, mortality from ventricular tachycardia, ventricular fibrillation, or both increases by approximately 10% per minute. ^9–12

Diagnosis and Therapy

The American Heart Association, in collaboration with the International Liaison Committee on Resuscitation, has established guidelines for resuscitation of cardiac arrest patients. ^13,14 In each resuscitation scenario, four concepts should always apply:

1. Activate EMS or the designated code team.
2. Perform basic life support (CPR).
3. Evaluate heart rhythm and perform early defibrillation as indicated.
4. Deliver advanced life support (e.g., intubation, intravenous [IV] access, transfer to a medical center or intensive care unit).

Ventricular Tachycardia or Ventricular Fibrillation

1. Conduct a primary ABCD survey (airway, breathing, circulation, differential diagnosis). Place airway device as soon as possible. Confirm placement, secure device, and confirm oxygenation and ventilation. Establish IV access, identify rhythm, and administer drugs appropriate for rhythm and condition. Search for and treat identified reversible causes, with focus on basic CPR and early defibrillation.
2. On arrival to an unwitnessed cardiac arrest or downtime longer than 4 minutes, five cycles (approximately 2 minutes) of CPR are to be initiated before evaluation of rhythm. If the cardiac arrest is witnessed or downtime is shorter than 4 minutes, one shock may be administered immediately if the patient is in ventricular fibrillation or pulseless ventricular tachycardia (see below).
3. If the patient is in ventricular fibrillation or pulseless ventricular tachycardia, shock the patient once using 200 J on biphasic (or equivalent monophasic, 360 J).
4. Resume CPR immediately after attempted defibrillation, beginning with chest compressions. Rescuers should not interrupt chest compression to check circulation (e.g., evaluate rhythm or pulse) until five cycles or 2 minutes of CPR have been completed.
5. If there is persistent or recurrent ventricular tachycardia or ventricular fibrillation despite several shocks and cycles of CPR, perform a secondary ABCD survey with a focus on more advanced assessments and pharmacologic therapy. Pharmacologic therapy should include epinephrine (1-mg IV push, repeated every 3 to 5 minutes) or vasopressin (a single dose of 40 U IV, one time only).
6. Consider using antiarrhythmics for persistent or recurrent pulseless ventricular tachycardia or ventricular fibrillation. These include amiodarone, lidocaine, magnesium (if there is a known hypomagnesemic state), and procainamide (class indeterminate for persistent and Class IIb for recurrent).
7. Resume CPR and attempts to defibrillate.

Pulseless Electrical Activity

1. Assess the patient and conduct a primary ABCD survey.
2. Review for the most frequent causes of pulseless electrical activity, the five Hs and five Ts: hypovolemia, hypoxia, hydrogen ion (acidosis), hyperkalemia (or hypokalemia), and hypothermia and tablets (drug overdose, accidents), tamponade (cardiac), tension pneumothorax, thrombosis (coronary), and thrombosis (pulmonary embolism).
3. Administer epinephrine (1-mg IV push repeated every 3 to 5 minutes) or atropine (1 mg IV if the heart rate is slow, repeated every 3 to 5 minutes as needed, to a total dose of 0.04 mg/kg).
4. Conduct a secondary ABCD survey.

Bradycardia

1. Determine whether the bradycardia is slow (heart rate less than 60 beats/min) or relatively slow (heart rate less than expected relative to underlying condition or cause).
2. Conduct a primary ABCD survey.
3. Check for serious signs or symptoms caused by the bradycardia.
4. If no serious signs or symptoms are present, evaluate for a type II second-degree atrioventricular block or third-degree atrioventricular block.
5. If neither of these types of heart block is present, observe.
6. If one of these types of heart block is present, prepare for transvenous pacing. If symptoms develop, use a transcutaneous pacemaker until the transvenous pacer is placed.
7. If serious signs or symptoms are present, begin the following intervention sequence:
   1. Atropine, 0.5 up to a total of 3 mg IV
   2. Transcutaneous pacing, if available
   3. Dopamine, 5 to 20 mcg/kg/min
   4. Epinephrine, 2 to 10 mcg/min
   5. Isoproterenol, 2 to 10 mcg/min
8. Conduct a secondary ABCD survey.

Asystole

1. Conduct a primary ABCD survey.
2. Perform transcutaneous pacing immediately if needed. Consider transvenous pacing if transcutaneous pacing fails to capture.
3. Administer epinephrine (1-mg IV push, repeated every 3 to 5 minutes) or atropine (1 mg IV repeated every 3 to 5 minutes, up to a total of 3 mg).
4. Conduct a secondary ABCD survey.
5. If asystole persists, consider withholding or ceasing resuscitative efforts.

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Hypertensive emergency

Definition

A hypertensive emergency is an acute, severe elevation in blood pressure accompanied by end-organ compromise. In newly hypertensive patients, a hypertensive emergency is usually associated with a diastolic blood pressure higher than 120 mm Hg. Nephrosclerosis that causes acute renal failure frequently complicates hypertensive emergencies, with resultant hematuria and proteinuria. Nephrosclerosis also may perpetuate the elevation of systemic pressure through ischemic activation of the renin-angiotensin system. Ocular involvement with retinal exudates, hemorrhages, or papilledema connotes a worse prognosis. ^15,16

Complications of particular concern include hypertensive encephalopathy, aortic dissection, and eclampsia. Hypertensive encephalopathy signals the presence of cerebral edema and loss of vascular integrity. If left untreated, hypertensive encephalopathy may progress to seizure and coma. ^17,18 Aortic dissection is associated with severe elevations in systemic blood pressure and wall stress, requiring immediate lowering of the blood pressure and emergent surgery to reduce morbidity and mortality. Eclampsia, the second most common cause of maternal death, occurs from the second trimester to the peripartum period. It is characterized by the presence of seizures, coma, or both, in the setting of preeclampsia. Delivery remains its only cure. ¹⁹

Causes

Hypertensive emergencies result from an exacerbation of essential hypertension or have a secondary cause, including renal, vascular, pregnancy-related, pharmacologic, endocrine, neurologic, and autoimmune causes (Box 1).

Prevalence

The prevalence of hypertension rises substantially with increasing age in the United States and is greater among blacks than among whites in every age group. ^20,21 Based on the National Health and Nutrition Examination Survey (NHANES III), the prevalence of hypertension in those older than 70 years was found to be approximately 55% to 60% of the U.S. population. ^22,23 A British study has revealed that fewer than 1% of patients with primary hypertension progress to hypertensive crisis. ²⁴ This study also showed that, despite increasingly widespread therapy, the number of patients presenting with hypertensive crises did not decline between 1970 and 1993.

Pathophysiology

Any syndrome that produces an acute rise in blood pressure may lead to a hypertensive crisis. Cerebral vasomotor autoregulation is a key facet of a patient's symptomatic presentation. Patients without chronic hypertension will develop hypertensive crisis at a lower blood pressure than those with chronic hypertension. Although not completely understood, an initial rise in vascular resistance mediated by vasoconstrictors such as angiotensin II, acetylcholine, or norepinephrine is responsible for the acute increase in blood pressure. This cascade exceeds the vasodilatory response of the endothelium, mediated primarily by nitric oxide. Mechanical destruction of the endothelium by shear stress leads to further vascular obstruction, platelet aggregation, inflammation, and subsequent blood pressure elevation. The rate at which this occurs determines the rate of increase in systemic vascular resistance as well as the acuity of a patient's presentation.

Clinical Evaluation

The symptoms and signs of a hypertensive emergency vary widely. Symptoms of end-organ involvement include headache, blurry vision, confusion, chest pain, shortness of breath, back pain (e.g., aortic dissection) and, if severe, seizures and altered consciousness. ^15,16 Physical examination should assess end-organ involvement, including detailed fundoscopic, neurologic, and cardiovascular examinations, with emphasis on the presence of congestive heart failure and bilateral upper extremity blood pressure measurements. Laboratory evaluation should include measurement of the complete blood count with differential and smear evaluations, measurements of electrolyte, blood urea nitrogen, and creatinine levels, and electrocardiography, chest radiography, and urinalysis.

Treatment

No large randomized clinical trials have assessed therapy in hypertensive emergency; therapeutic intervention is largely a result of expert opinion. All patients with end-organ involvement should be admitted for intensive monitoring and have an arterial blood pressure line placed. ¹⁶

Pharmacologic Therapy

IV vasodilator therapy to achieve a decrease in mean arterial pressure (MAP) of 20% to 25% or a decrease in diastolic blood pressure (DBP) to 100 to 110 mm Hg in the first 2 hours is recommended. Decreasing the MAP and DBP further should be done more slowly because of the risk of decreasing perfusion of end-organs. ¹⁶ Several drugs have proven beneficial in achieving this goal ( Table 1 ).

At our institution, we focus on reducing shear forces and combine a beta blocker with sodium nitroprusside (SNP). In cases of marked catecholamine level elevation, large doses of IV beta blockers may be required to achieve blood pressure reduction. One exception to the use of large doses of beta blockers is cocaine overdose, for which vasodilators and benzodiazepines are the mainstays of therapy.

Additional Considerations

1. In addition to reducing MAP and DBP with medications as described above, early surgical intervention for type A dissection has proved to reduce morbidity and mortality. Reduction in shear stress is best achieved with IV beta blockade and SNP. ^25,26
2. In addition to delivery, IV magnesium, hydralazine (pregnancy class B drug), and labetalol (pregnancy class B drug) have value in the treatment of preeclampsia and prevention of eclampsia. ¹⁹ Angiotensin-converting enzyme inhibitors are strictly contraindicated because of adverse effects to the fetus, although this occurs in the first trimester.
3. Antihypertensive therapy remains controversial in the presence of stroke because a high cerebral perfusion pressure may be neurologically beneficial. Prompt neurologic consultation should be obtained.

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Aortic dissection

Definition

Aortic dissection is a tear of the aortic intima that allows the shear forces of blood flow to dissect the intima from the media and, in some cases, penetrate the diseased media with resultant rupture and hemorrhage (Fig. 1). ²⁷ Sixty-five percent of dissections originate in the ascending aorta, 20% in the descending aorta, 10% in the aortic arch, and the remainder in the abdominal aorta. ^28,29

By the Stanford system, a dissection that involves the ascending aorta is classified as type A, and one that does not is classified as type B (Fig. 2). Dissections are further classified by chronicity as acute (shorter than 2 weeks) or chronic (longer than 2 weeks); mortality peaks at 2 weeks at approximately 80% and then levels off. ²⁸

Causes

Any disease that weakens the aortic media predisposes patients to dissection. These include aging, hypertension, Marfan syndrome, Ehlers-Danlos syndrome, bicuspid aortic valve (associated with medial degeneration), coarctation, and Turner's syndrome. Pregnancy poses a unique risk to women with any of these diseases because of increased blood volume, cardiac output, and shear forces on the aorta. Of dissections in women younger than 40 years, 50% occur in the peripartum period. ³⁰ Trauma from catheters or intra-aortic balloon pumps may also dissect the aortic intima. ³¹ Aortic dissection is infrequently associated with blunt trauma.

Clinical Presentation

Most patients present with acute chest pain that is often tearing or ripping in nature, which peaks in intensity at its onset. Uncommonly, patients may present with congestive heart failure (from accompanying acute aortic insufficiency, tamponade, or both), cerebrovascular accident (involvement of the carotid artery or vertebrobasilar system), syncope (tamponade), or cardiac arrest. ^32,33 On physical examination, hypertension is usually present, either as the primary cause of dissection or secondary to renal artery involvement. Acute aortic insufficiency with a resultant diastolic murmur may complicate ascending dissections. Loss of pulse, decrease in blood pressure, or both, often asymmetrically, are also found in the many patients. ³² Dissection of the spinal arteries, although rare, may produce secondary paraplegia.

Chest radiographs may reveal an abnormality in approximately 70% to 80% of patients, such as a widened mediastinum or loss of the demarcation of the aortic knob, pleural effusion, or pulmonary edema. ³² Importantly, a normal chest radiograph is not incompatible with an aortic dissection. The electrocardiogram (ECG) may reveal left ventricular hypertrophy, ST depression, T wave inversion, or ST elevation. Electrocardiographic changes indicating inferior territory injury may herald right coronary ostial involvement in 1% to 2% of aortic dissection cases.

Diagnosis

Recognition of several signs is essential in the imaging of aortic dissection because they affect treatment and outcome:

1. Involvement of the ascending aorta
2. Location of dissection flap, intimal tear
3. Presence of pericardial fluid, cardiac tamponade
4. Involvement of coronary ostia

Magnetic resonance imaging (MRI) has a sensitivity and specificity of approximately 98% for detection of dissection. Transesophageal echocardiography has a sensitivity of approximately 98%; however, its lower specificity, 77% to 97%, reflects differences in operator experience. ^29,35 Computed tomography sensitivity for detection of dissection is approximately 83% to 94%, whereas its specificity ranges from 87% to 100%, depending on the study. ^34,35 Choice of testing should be based on the medical center's expertise, hemodynamic stability of the patient, and access to the imaging modality. ^34–36 Although MRI remains the gold standard, its lack of portability, limited access, and long duration of imaging make this a less favorable option in the care of acute aortic dissection in some centers. ³⁶

Treatment

Surgery

Surgical therapy is the best option for an acute aortic dissection involving the ascending aorta. Studies have shown that delaying surgical intervention, even to carry out left heart catheterization, aortography, or both, results in worse outcomes. ^37–39 Surgical repair in patients with type B dissection is generally reserved for those with end-organ compromise or those who do not respond to medical therapy.

Medical Therapy

Medical therapy should be initiated in all patients with acute dissection. Reductions of shear force and blood pressure should be the primary goals. Beta blockers should be given parenterally and titrated to effect (generally, pulse 50 to 60 beats/min). In our institution, we then add SNP because of its rapid onset and ease of titration, aiming for a MAP of 65 to 75 mm Hg.

In the hypotensive patient, pericardial tamponade, aortic rupture, myocardial infarction, or a combination of these should be suspected. Volume replacement and early surgical intervention should be pursued. Pericardiocentesis should be avoided if tamponade is present, because immediate surgical intervention is the therapy of choice. If hypotension persists, norepinephrine and phenylephrine are the vasopressors of choice because of their limited effects on shear force. Endovascular stenting, a rapidly growing field, remains investigational in this setting.

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Acute pulmonary edema

Definition

Acute pulmonary edema is an emergency that necessitates admission to the hospital. It has two major forms, cardiogenic and noncardiogenic. We will focus on cardiogenic pulmonary edema, which generally is more reversible than the noncardiogenic form.

Cardiogenic pulmonary edema results from an absolute in-crease in left atrial pressure, with resultant increases in pulmonary venous and capillary pressures. In the setting of normal capillary permeability, this increased pressure causes extravasation of fluid into the alveoli and overwhelms the ability of the pulmonary lymphatics to drain the fluid, thus impairing gas exchange in the lung. ^40,41

Causes and Pathophysiology

Left ventricular systolic dysfunction, left ventricular diastolic dysfunction, and obstruction of the left atrial outflow tract are the primary causes of increased left atrial pressure. Left ventricular systolic dysfunction is the most common cause of cardiogenic pulmonary edema. ⁴⁰ This dysfunction can be the result of coronary artery disease, hypertension, valvular heart disease, cardiomyopathy, toxins, endocrinologic or metabolic causes, or infections.

Diastolic dysfunction results in impaired left ventricular filling and elevation in left ventricular end-diastolic pressure. In addition to myocardial ischemia, left ventricular hypertrophy, hypertrophic obstructive cardiomyopathy, and infiltrative or restrictive cardiomyopathy are all causes of diastolic dysfunction.

Left atrial outflow obstruction is often a result of valvulopathy, such as mitral stenosis or mitral regurgitation, but also can be caused by tumors (atrial myxoma), dysfunctional prosthetic valves, thrombus, and cor triatriatum. It is imperative to distinguish between mitral regurgitation and mitral stenosis, given their very different treatments.

Diagnosis

Pulmonary edema is diagnosed by the presence of various signs and symptoms, including tachypnea, tachycardia, crackles (reflecting alveolar edema), hypoxia (secondary to alveolar edema), and S3 or S4 heart sounds, or both. Additionally, if hypertension is present, it may represent diastolic dysfunction, decreased left ventricular compliance, decreased cardiac output, and increased systemic vascular resistance. The presence of increased jugular venous pressure indicates increased right ventricular filling pressure secondary to right ventricular or left ventricular dysfunction. Finally, the presence of peripheral edema indicates a certain chronicity to the patient's condition.

Laboratory data associated with pulmonary edema include hypoxemia on arterial sampling and a chest radiograph showing bilateral perihilar edema and cephalization of pulmonary vascular marking. Cardiomegaly, pleural effusion, or both may be present. Two-dimensional echocardiography may be helpful in the acute setting to assess left ventricular and right ventricular size and function and to look for valvular stenosis or regurgitation and pericardial pathology. The electrocardiogram (ECG) may reflect ongoing ischemia, injury, tachycardia, and atrial or ventricular hypertrophy.

Treatment

Mainstays of immediate therapy include improving oxygen delivery to end organs, decreasing myocardial oxygen consumption, increasing venous capacitance, decreasing preload and afterload, with careful attention to MAP, and avoiding hemodynamic embarrassment. All patients should receive supplemental oxygen to maximize oxygen saturation of hemoglobin. Administration of continuous positive airway pressure provides positive airway pressure, increases gas exchange, and perhaps decreases preload via decreased intrathoracic pressure. ^42,43

Endotracheal intubation and mechanical ventilation should be used immediately if noninvasive supplemental oxygenation proves inadequate. In our experience, repeated attempts to improve oxygenation with noninvasive positive pressure ventilation often prove futile, and restoration of oxygenation is best achieved via endotracheal intubation.

Pharmacologic Therapy

The pharmacologic agents most commonly used in the treatment of acute pulmonary edema are nitroglycerin, SNP, nesiritide, and diuretics. ⁴⁴

Nitroglycerin acts immediately to decrease preload and afterload. ⁴⁵ It should be used for the management of patients with pulmonary edema who are not in cardiogenic shock. Sublingual administration allows rapid delivery of a large dose, which is often required to decrease preload. Parenteral administration also should be used in the nonhypotensive patient and, based on symptoms, titrated to a MAP of approximately 70 to 75 mm Hg.

SNP is an effective vasodilator that is often required for the treatment of the hypertensive patient with pulmonary edema. ⁴⁶ Its use requires arterial blood pressure monitoring. SNP should be used with caution in the setting of liver dysfunction, although thiocyanate toxicity is uncommon and usually occurs after prolonged infusion at high doses. Concomitant use of nitroglycerin should be strongly considered in the ischemic patient.

A recent addition to the pharmacologic armamentarium, nesiritide is a vasodilator that acts by increasing the level of cyclic guanosine monophosphate, which, in turn, causes smooth muscle cell relaxation. In one trial, it proved superior to low-dose IV nitroglycerin. ^47,48 Its serum half-life and blood pressure–lowering effect are much longer than SNP; therefore, it should be used with caution in a patient with a low or low-normal MAP. However, the use of the drug does not require invasive hemodynamic monitoring.

Intravenous diuretics are most helpful for the treatment of volume overload in chronic congestive heart failure. Their vasodilatory and diuretic properties also are useful in the management of pulmonary edema. Diuretics should be used with caution in the euvolemic patient to avoid compromising cardiac output and oxygen delivery.

Summary

• Cardiopulmonary arrest has several causes, all of which require prompt resuscitative efforts.
• Hypertensive emergency warrants admission for intensive monitoring and arterial blood pressure line placement.
• Aortic dissection categorized as type A requires emergent surgery, whereas type B is managed medically.
• Acute pulmonary edema should be treated by improving oxygen delivery to end organs, decreasing myocardial oxygen consumption, increasing venous capacitance, and decreasing preload and afterload.

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Suggested Readings

• ACOG practice bulletin. Diagnosis and management of preeclampsia and eclampsia. Number 33, January 2002. Obstet Gynecol. 99: 2002; 159-167.
• Diagnostic imaging in the evaluation of suspected aortic dissection. Old standards and new directions. N Engl J Med. 328: 1993; 35-43.
• Acute heart failure: A novel approach to its pathogenesis and treatment. Eur J Heart Fail. 4: 2002; 227-234.
• 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 112: 2005; IV1-IV203.
• American Heart Association Emergency Cardiovascular Committee; Council on Cardiopulmonary, Perioperative, and Critical Care; Council on Clinical Cardiology: Lay rescuer automated external defibrillator (“public access defibrillation”) programs: Lessons learned from an international multicenter trial: Advisory statement from the American Heart Association Emergency Cardiovascular Committee; the Council on Cardiopulmonary, Perioperative, and Critical Care; and the Council on Clinical Cardiology. Circulation. 21: 2005; 3336-3340.
• Experience with the use of automated external defibrillators in out-of-hospital cardiac arrest. Resuscitation. 37: 1998; 3-7.
• 2005 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Circulation. 112: 2005; III1-III136.
• Predicting survival from out-of-hospital cardiac arrest: A graphic model. Ann Emerg Med. 22: 1993; 1652-1658.
• The failure of malignant hypertension to decline: A survey of 24 years' experience in a multiracial population in England. J Hypertens. 12: 1994; 1297-1305.
• NHANES III health data relevant for aging nation. JAMA. 277: 1997; 100-102.
• Does coronary angiography before emergency aortic surgery affect in-hospital mortality?. J Am Coll Cardiol. 15: 2000; 889-894.
• Aortic dissection. Lancet. 349: 1997; 1461-1464.
• Magnetic resonance imaging of thoracic aortic aneurysm and dissection. Semin Roentgenol. 36: 2001; 295-308.
• Acute ascending aortic dissection during pregnancy. Am J Crit Care. 10: 2001; 430-433.
• Diagnostic accuracy of transesophageal echocardiography, helical computed tomography, and magnetic resonance imaging for suspected thoracic aortic dissection: Systematic review and meta-analysis. Arch Intern Med. 166: 2006; 1350-1356.
• Hypertensive emergencies. Lancet. 356: 2000; 411-417.