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Table of Contents

Reviewed July 14, 2004

Matthew
Hook, MD

Department of
Cardiovascular
Medicine

Deepak L.
Bhatt, MD

Department of
Cardiovascular
Medicine

Print Chapter

     Cardiopulmonary      Arrest and      Resuscitation

     Hypertensive      Emergencies

     Therapy

     Acute
     Pulmonary
     Edema

ETIOLOGY

Cardiopulmonary arrest occurs as a result of a multitude of cardiovascular, metabolic, infectious, neurologic, inflammatory, and traumatic diseases. However, the clinician must be keenly aware of several specific causes, including drug toxicity or overdose, myocardial ischemia or infarction, hyperkalemia, torsade de pointes, cardiac tamponade, and tension pneumothorax. The marked differences in therapeutic intervention among these various etiologies underscore the need for their accurate recognition. The endpoint of these disorders is commonly:

• pulseless ventricular tachycardia/ventricular fibrillation,
• pulseless electrical activity,
• symptomatic bradycardia, or
• asystole.

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 proved in many community-based studies.^1,2 Additionally, among adults, in whom ventricular tachycardia and/or ventricular fibrillation is more common, the increased use of automated electrical defibrillators by emergency medical systems (EMS), businesses, and airports has improved survival.^3,4 Without defibrillation, mortality from ventricular tachycardia and/or ventricular fibrillation increases by approximately 10% per minute.^5,6

The American Heart Association in collaboration with the International Liaison Committee on Resuscitation have established guidelines for resuscitation of cardiac arrest patients.^7,8 In each resuscitation scenario, four concepts should always apply:

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

Ventricular Tachycardia/Ventricular Fibrillation

1. Conduct a primary ABCD survey (A = Airway. Place airway device as soon as possible. B = Breathing. Confirm placement, secure device, and confirm oxygenation and ventilation. C = Circulation. Establish IV access, identify rhythm, and administer drugs appropriate for rhythm and condition. D = Differential Diagnosis. Search for and treat identified reversible causes.) with focus on basic CPR and early defibrillation.Assess for and shock the ventricular fibrillation/pulseless ventricular tachycardia patient up to three times at 200 J, 200 to 300 J, 360 J, or equivalent biphasic (120J, 200J) if necessary. Check the cardiac rhythm after each shock.If, after three shocks, there is persistent or recurrent ventricular tachycardia/ventricular fibrillation, 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).Resume attempts to defibrillate (one time at 360 J or equivalent biphasic within 30 to 60 seconds).Consider using antiarrhythmics for persistent or recurrent pulseless ventricular tachycardia/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).
2. Resume attempts to defibrillate.

Pulseless Electrical Activity

1. Assess the patient and conduct a primary ABCD survey.Review for the most frequent causes of pulseless electrical activity-the 5 Hs and 5 Ts. These stand for hypovolemia, hypoxia, hydrogen ion (acidosis), hyper/hypokalemia, hypothermia, tablets (drug overdose, accidents), tamponade (cardiac), tension pneumothorax, thrombosis (coronary), and thrombosis (pulmonary embolism). 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).
2. Conduct a secondary ABCD survey.

Bradycardias

1. Determine whether the bradycardia is slow (heart rate less than 60 bpm) or relatively slow (heart rate less than expected relative to underlying condition or cause).Conduct a primary ABCD survey.Check for serious signs or symptoms due to the bradycardia.If no serious signs or symptoms are present, then evaluate for type II second-degree atrioventricular block or for third-degree atrioventricular block.If neither of the above types of heart block is present, observe.If one of the above types of heart block is present, prepare for transvenous pacing. If symptoms develop, use a transcutaneous pacemaker until the transvenous pacer is placed.If serious signs or symptoms are present, begin the following intervention sequence:
   1. Atropine 0.5 to 1.0 mg IVTranscutaneous pacing, if availableDopamine 5 to 20 µg/kg per minuteEpinephrine 2 to 10 µg/min
   2. Isoproterenol 2 to 10 µg/min
2. Conduct a secondary ABCD survey.

1. Conduct a primary ABCD survey.Perform transcutaneous pacing immediately if needed. Consider transvenous pacing if transcutaneous pacing fails to capture.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 0.04 mg/kg).Conduct a secondary ABCD survey.
2. If asystole persists, consider withholding or ceasing resuscitative efforts.

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 greater than 120 mm Hg. Nephrosclerosis that causes acute renal failure frequently complicates hypertensive emergencies, with resultant hematuria and proteinuria. Nephrosclerosis also may perpetuate elevation of systemic pressure through ischemic activation of the renin-angiotensin system. Ocular involvement with retinal exudates, hemorrhages, and/or papilledema connotes a worse prognosis.^9,10

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.¹¹ 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 in the setting of preeclampsia. Delivery remains its only cure.¹²

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

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, and norepinephrine is responsible for the acute rise 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 rise in systemic vascular resistance as well as the acuity of a patient's presentation.

The symptoms and signs of a hypertensive crisis vary widely. Symptoms of end-organ involvement include headache, blurry vision, confusion, chest pain, shortness of breath, back pain (eg, aortic dissection), and if severe, seizures and altered consciousness.^9,10 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 evaluation; measurements of electrolyte, blood urea nitrogen, and creatinine levels; and an electrocardiogram (ECG), chest radiograph, and urinalysis.

Drug 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 mm Hg to 110 mm Hg in the first 2 hours is recommended. Decreasing the MAP/DBP further should be done more slowly, as one risks decreasing perfusion of end-organs.¹⁰ Several drugs have proved beneficial in achieving this goal (Table 2).

At our institution, we focus on reducing shear forces and combine a beta-blocker with sodium nitroprusside (SNP). In cases of marked catecholamine 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.

Aortic Dissection
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.^16,17

Preeclampsia/eclampsia
In addition to delivery, IV magnesium and hydralazine and labetalol (both pregnancy Class B) have value in the treatment of preeclampsia and prevention of eclampsia.¹² Angiotensin-converting enzyme inhibitors are strictly contraindicated due to adverse effects on the fetus.

Cerebrovascular Accident
Antihypertensive therapy remains controversial in the presence of stroke because a high cerebral perfusion pressure may be neurologically beneficial. Prompt neurologic consultation should ensue.

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 instances, penetrate the diseased media with resultant rupture and hemorrhage (Figure 1). Sixty-five percent of dissections originate within the ascending aorta, 20% within the descending aorta, 10% within the aortic arch, and the remainder within the abdominal aorta.^18,19

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 (Figure 2). Dissections are further classified by chronicity as acute (less than 2 weeks) or chronic (greater than 2 weeks); mortality peaks at 2 weeks at approximately 80% and then levels off.¹⁸

Any disease that weakens the aortic media predisposes patients to dissection. These include aging, hypertension, Marfan's 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 due to increased blood volume, cardiac output, and shear forces on the aorta. Fifty percent of dissections in women under age 40 occur in the peripartum period.²⁰ Trauma from catheters or intra-aortic balloon pumps may also dissect the aortic intima.²¹ Aortic dissection is infrequently associated with blunt trauma.

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.²² Importantly, a normal chest radiograph is not incompatible with an aortic dissection. ECG may reveal left ventricular hypertrophy, ST depression, T-wave inversion, or ST elevation. An inferior current of injury may herald right coronary ostial involvement in 1% to 2% of aortic dissection cases.

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

• Involvement of the ascending aorta
• Location of dissection flap/intimal tear
• Presence of pericardial fluid/cardiac tamponade
• Involvement of coronary ostia

Magnetic resonance imaging 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.¹⁹ Computed tomographic sensitivity for detection of dissection is approximately 83% to 94%, whereas its specificity ranges from 87% to 100%, depending on the study.²³ Choice of testing should be based on the medical center's expertise, hemodynamic stability of the patient, and access to the imaging modality.^23,24 Although magnetic resonance imaging 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.²⁴

Medical therapy should be initiated in all patients with acute dissection. Reduction of shear force and blood pressure should be the primary goal. Beta-blockers should be given parenterally and titrated to effect (generally pulse 50 bpm to 60 bpm). In our institution, we then add sodium nitroprusside due to its rapid onset and ease of titration, aiming for a MAP of 65 mm Hg to 75 mm Hg.

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

Cardiogenic pulmonary edema results from an absolute increase in left atrial pressure with a resultant increase in pulmonary venous and capillary pressure. 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 within the lung.^26,27

Left ventricular systolic dysfunction is the most common cause of cardiogenic pulmonary edema.²⁶ This dysfunction can be due to myocardial ischemia, coronary artery disease, hypertension, valvular heart disease, cardiomyopathy, toxins, endocrinologic and 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 due to 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 from a variety of 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. If increased jugular venous pressure is present, this reflects increased right ventricular filling pressure secondary to right ventricular or left ventricular dysfunction. Finally, if peripheral edema is present, this reflects 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 and/or pleural effusion may or may not 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. ECG may reflect ongoing ischemia, injury, tachycardia, and atrial and/or ventricular hypertrophy.

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. Continuous positive airway pressure provides positive airway pressure, increases gas exchange, and perhaps decreases preload via decreased intrathoracic pressure.²⁸

Endotracheal intubation and mechanical ventilation should be used immediately when 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.

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

Nitroglycerin
Nitroglycerin acts immediately to decrease preload and afterload. 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 mm Hg to 75 mm Hg.

Sodium Nitroprusside
SNP is an effective vasodilator that is often required in the treatment of the hypertensive patient with pulmonary edema.²⁹ Its use requires arterial blood pressure monitoring. SNP should be used with caution in the setting of liver dysfunction, although thiocyanate toxicity is uncommon. Concomitant use of nitroglycerin should be strongly considered in the ischemic patient.

Nesiritide
A recent addition to the pharmacologic armamentarium, nesiritide is a vasodilator that acts by increasing cyclic guanosine monophosphate, which, in turn, causes smooth muscle cell relaxation. In one trial, it proved superior to low-dose IV nitroglycerin.³⁰ Its' serum half-life and blood pressure-lowering effect is much longer than SNP; therefore, it should be used with caution in a patient with low or low to normal MAP.

Diuretics
Parenteral diuretics are most helpful in 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 great caution in the euvolemic patient to avoid compromising cardiac output and oxygen delivery.

Return to Medicine Index

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