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Author: Dr. Robin Pinto, MBBS, MD, DM (Cardiology)


Cardiovascular emergencies are a life-threatening disorders   that  must  be  recognized  immediately  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 review the  clinician’s  approach  to  these  disorders   and their treatments and provide links to other informative resources.

Cardiopulmonary  arrest  Etiology

Cardiopulmonary  arrest  is  a  sudden  and  unexpected loss of perfusing pulsatile blood flow attributable to cessation of cardiac mechanical activity. It occurs as a result of a multitude of cardiovascular, metabolic, infectious, neurologic, inflammatory, and traumatic diseases.

These diseases can be generally classified into 5

H’s and 5 T’s (Hypovolemia, Hypoxemia, Hydrogen ion (acidosis), Hypo- or Hyperkalemia, Hypothermia, Tension pneumothorax, Tamponade, Toxins, and Thrombosis – both pulmonary and cardiac). The endpoint of these disorders is commonly pulseless ventricular tachycardia (VT) or ventricular fibrillation (VF), pulseless electrical activity, or asystole.

Diagnosis and therapy

The American Heart Association and European Society of Cardiology have published revised resuscitation   guidelines.   The   new   guidelines   still include the major steps below:

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

The new changes are as follows:

  1. Changing   the  Airway  (A) –  Breathing  (B) – Circulation (C) sequence to C-A-B.  This change was made to emphasize the importance of rapid initiation of chest compressions because in the old guidelines, significant time is potentially wasted performing airway evaluation. Airway evaluation and  initiation  of  mouth-to-mouth  breathing  may be a complex, time-consuming process for the layperson,   and  may  delay  chest  compressions. The phrase “Look, listen and feel” has also been removed from the algorithm to prevent time delays.
  2. More emphasis on the quality of CPR performed, including the rate and depth of compressions, allowing complete chest recoil, and minimizing interruptions in compressions. Less emphasis on pulse checks.
  3. Highlighting  the   importance   of   professional healthcare rescue teams performing multiple tasks during CPR such as establishing an airway or delivering advanced cardiac life support drugs.

Pulseless VT or VF

  1. Start chest compressions as early as cardio- pulmonary arrest is identified. Place airway device as soon as possible 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 (5 H’s and 5 T’s), with focus on basic CPR and early defibrillation.
  2. On arrival to an unwitnessed cardiac arrest or downtime longer than 4 minutes, five cycles (~2 min) of CPR (each cycle is 30 compressions at a rate of ~100 compressions per minute) 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 VF or pulseless VT followed by five cycles of CPR.
  3. If the patient is in VF or pulseless VT, shock the patient once using 200 J on biphasic (on equivalent monophasic, 360 J).
  4. Resume  CPR  immediately  after  attempted defib- rillation, 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 VT or VF despite several shocks and cycles of CPR, perform a secondary ABC survey with a focus on more advanced assessments and pharmacologic therapy. Pharmacologic therapy should include epinephrine (1 mg IV push, repeated every 3-5 min) or vasopressin (a single dose of 40 U IV, one time only).
  6. Consider using antiarrhythmics for persistent or recurrent pulseless VT or VF. These include amiodarone, lidocaine, magnesium, and procain – amide
  7. Resume CPR and attempts to defibrillate

If spontaneous circulation returns, start immediate post-cardiac arrest care. This includes optimization of oxygenation and ventilation with emphasis on avoiding hyperventilation, treating hypotension by starting vasopressor infusion or inserting intra-aortic balloon pump, assessing neurologic status and starting induced hypothermia if indicated and assessing need for coronary reperfusion if high suspicion for acute coronary syndrome.

Pulseless electrical activity or asystole

  1. Assess the patient and begin chest compressions immediately.
  2. Administer epinephrine (1 mg IV push repeated every 3-5 min). Consider transcutaneous pacing if asystole.
  3. Conduct a secondary ABC survey and consider reversible causes (5 H’s and 5 T’s).
  4. Resume immediate post-cardiac arrest care if there is a return of spontaneous circulation as above.


  1. Heart rate typically <50 beats per minute.
  2. Identify and treat underlying cause if patient is stable (5 H’s and 5 T’s).
  3. Check for serious signs of low cardiac output due to bradycardia such as hypotension, altered mental status, or acute heart failure.
  4. If serious signs or symptoms are present, begin the following intervention sequence:
    1. Atropine, 0.5 mg, up to a total of 3 mg IV
    2. Transcutaneous pacing, if available
    3. Dopamine, 5 to 20 µg/kg/min
    4. Epinephrine, 2 to 10 µ/min
    5. e. Isoproterenol, 2 to 10 µ/min
    6. Consider glucagon for beta-blocker toxicity, calcium infusion for calcium channel blocker toxicity.
  5. If no serious signs or symptoms are present, evaluate for a type II second-degree atrioventricular block or third-degree atrioventricular block.
  6. If neither of these types of heart block is present, observe.
  7. If one of these types of heart block is present, prepare for transvenous pacing.
  8. Resume immediate post-cardiac arrest care if there is a return of spontaneous circulation as above.

Hypertensive emergency

A  hypertensive  emergency  is  an  acute,  severe elevation in blood pressure accompanied by end-organ compromise. It is usually associated with a systolic blood pressure  (SBP) equal to or  higher  than 180 mm  Hg  and/or  a  diastolic  blood  pressure  (DBP) equal to or higher than 120 mm Hg.

End-organ compromise includes acute renal failure due to nephrosclerosis, ocular involvement with retinal exudates, hemorrhages, or papilledema, hypertensive encephalopathy, acute stroke or intracranial  hemorrhage,  acute  myocardial infarction, aortic dissection, and eclampsia.

Hypertensive encephalopathy signals the pres- ence of cerebral edema and loss of vascular integ- rity. If left untreated, hypertensive encephalopathy may progress to seizure and coma.

Aortic dissection is associated with severe elevations  in  systemic  blood  pressure   and  wall stress, requiring immediate lowering of the blood pressure and emergent surgery for type A dissection 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.

Acute pulmonary edema

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

Cardiogenic pulmonary edema results from an absolute increase in left atrial pressure, with resultant increases in pulmonary capillary and venous 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.


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 the S3 or S4 heart   sounds,   individually   or   in   combination. 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 degree of chronicity to the patient’s condition.

Laboratory data associated with pulmonary edema include hypoxemia on arterial blood 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 transthoracic echocardiography is usually helpful in the acute setting to assess biventricular size and function, to identify valvular stenosis or regurgitation, and to determine the presence or absence of pericardial pathology.

The ECG may reflect ongoing ischemia, injury, tachycardia, and atrial or ventricular hypertrophy. In many cases, differentiating cardiogenic and noncardiogenic pulmonary edema can be challenging and requires the insertion of a pulmonary artery catheter to measure the pulmonary capillary wedge pressure.


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 compromise. All patients should receive supplemental oxygen to maximize hemoglobin oxygen saturation. Administration of continuous positive airway pressure can increase gas exchange,   and  may  perhaps  decrease  preload  via increased intrathoracic pressure.In our experience, however, repeated attempts to improve oxygenation with noninvasive positive pressure ventilation often prove inadequate. In such cases,  restoration of oxygenation is best achieved via prompt endotracheal intubation and initiation of mechanical ventilation.

Pharmacologic  therapy

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

Nitroglycerin acts immediately to decrease preload and afterload.It should be used for the management of patients with pulmonary edema who are not hypotensive. Sublingual administration allows rapid delivery, which is often required to decrease preload. IV administration of nitroglycerin 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. Due  to  the  rapid and potent effects of SNP, its use requires continuous invasive monitoring of arterial blood pressure. The issues of methemoglobinemia, cyanide, and thiocyanate toxicity rarely become significant, but since patients receiving continuous infusions will often develop tachyphylaxis – a progressive resistance to the drug’s effects – frequent blood testing is necessary.

SNP should be used with caution in the setting of hepatic dysfunction, since the liver is responsible for transformation of the cyanide radical into thiocyanate. Patients with renal dysfunction will tend to accumulate thiocyanate more rapidly than those with normal kidney function, since thiocyanate is excreted in the urine. Finally, through its effects on coronary arteriolar resistance vessels, SNP can potentially cause coronary “steal,” drawing blood flow away from ischemic myocardium. We generally co-administer nitroglycerin along with SNP to dilate conductance vessels and lessen this theoretical risk.

IV diuretics are most helpful for the treatment of volume overload in chronic congestive heart failure. Their vasodilative 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.

IV morphine can be used in certain select patients to decrease their “air hunger,” anxiety, and sympathetic tone, which can in turn help reduce their afterload.

Aortic Dissection

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.

Most patients present with acute chest pain that peaks in intensity at onset, and is often self-described as “tearing” or “ripping” in nature. Uncommonly, patients present with congestive heart failure from accompanying acute aortic valve insufficiency, tamponade, or both. Also seen are cerebrovascular accidents due to involvement of the carotid artery or vertebrobasilar system, syncope from tamponade, or cardiac arrest.

It is essential to recognize several key signs in the imaging of aortic dissection, because they dramatically affect treatment and outcome:

Involvement of the ascending aorta.

Location  of  dissection flap,  intimal tear  and  the major vessels involved.

Presence of pericardial effusion or cardiac tamponade.

Involvement of coronary ostia.

The sensitivity of computed tomography angiography (CTA) for detecting aortic dissection is approximately 83%  to 100%,  and its specificity ranges from 87%  to 100%, depending on the study


Surgical therapy is the best option for 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 outcome.Mortality  increases by 1% per hour while waiting for surgery.  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 intravenously and titrated to the desired effect.

In the hypotensive patient, diagnoses of pericardial tamponade, aortic rupture, aortic insufficiency, myocardial infarction, or a combination of these should be suspected and tested for. 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 increasing cardiac contractility. Endovascular stenting, a rapidly growing field, remains investigational in this acute setting and is sometimes used in very high-risk surgical patients with type B aortic dissections or aneurysms.


Cardiovascular emergencies are common in the practice of medicine and quick action is necessary.

Cardiopulmonary arrest has several possible causes, all of which require prompt resuscitative efforts. The American Heart Association guidelines have proposed changes that make chest compressions a priority before assessment of airway and breathing, in order to minimize time delays. All healthcare professionals need to be aware of these changes.

Hypertensive emergency causes end-organ damage and warrants admission for intensive monitoring, including continuous arterial blood pressure measurement, and treatment.

Aortic  dissection categorized as Stanford type A requires emergent surgery, whereas type B is generally managed medically unless end-organ damage can be demonstrated.

Acute pulmonary edema should be treated by improving oxygen delivery to end organs, decreasing myocardial oxygen consumption, and safely decreasing preload and afterload.