Definition

• A severe manifestation of forward heart failure. Profound impairment of cardiac function results in poor cardiac output, inadequate forward blood flow, and poor tissue perfusion in the presence of adequate intravascular volume.
• Cardiac impairment may result from systolic dysfunction (dilated cardiomyopathy, sepsis, myocarditis, and ischemia), diastolic dysfunction (hypertrophic cardiomyopathy, restrictive cardiomyopathy, tension pneumothorax or mediastinum, restrictive pericarditis, and pericardial tamponade), conduction defects and arrhythmias, valvular diseases, obstructive diseases, pulmonary thromboembolism, and structural defects. Understanding the underlying defect and its hemodynamic consequences is imperative to institute appropriate therapy.
• In congestive heart failure (CHF), sometimes referred to as backward heart failure, the ventricle cannot pump out all of the blood that comes into it resulting in systemic and/or pulmonary edema. This is in contrast to forward heart failure, when the heart is not pumping enough blood out to meet the needs of the body. Most, but not all, veterinary patients that present in cardiogenic shock will have concurrent CHF.

Pathophysiology

• Decreased cardiac output leads to hypotension and systemic hypoperfusion.
• Hypotension decreases coronary perfusion pressure resulting in coronary ischemia that provokes further myocardial dysfunction.
• Peripheral vasoconstriction increases myocardial work and exacerbates tissue ischemia and energy depletion resulting in organ dysfunction.

Systems Affected

• Cardiovascular-cardiac dysfunction is causative. Myocardial ischemia exacerbates cardiac dysfunction.
• Endocrine-hyperglycemia and insulin resistance.
• Gastrointestinal-mucosal necrosis and sloughing, hemorrhage, and bacterial translocation.
• Hemic-homeostatic imbalances lead to microvascular thrombosis.
• Hepatobiliary-hepatocellular enzyme leakage, cholestasis, reduced clearance of bacteria and bacterial by-products, and abnormal synthetic function. Hepatic congestion may result from right-sided CHF.
• Musculoskeletal-weakness.
• Nervous-altered mental status.
• Renal-ischemic tubular damage, oliguria and development of acute kidney injury.
• Respiratory-as cardiac dysfunction progresses and ventricular end diastolic pressure increases, pulmonary edema and pleural effusion develop. Ultimately pulmonary gas exchange is affected and hypoxemia results.

Genetics

Many breeds are predisposed to specific cardiac diseases.

Incidence/Prevalence

Unknown

Geographic Distribution

Unknown

Signalment

• Dogs and cats
• Any breed, age, or sex

Signs

Causes

Risk Factors

• Underlying cardiac disease
• Concurrent illness causing hypoxemia, acidosis, and electrolyte imbalances, or as in sepsis, the release of myocardial depressant factors.

Differential Diagnosis

CBC/Biochemistry/Urinalysis

Other Laboratory Tests

• Blood gas analysis may reveal metabolic acidosis, hypoxemia (if concurrent CHF), and evidence of increased oxygen extraction by tissues (a widened arteriovenous oxygen difference and or a decreased venous oxygen concentration in a patient that is not hypoxemic or anemic).
• Hyperlactatemia (tissue hypoperfusion).
• Increased cardiac troponin I levels (sensitive and specific marker of myocardial injury).
• NT-proBNP may be useful in ruling out significant intrinsic cardiac dysfunction.

Imaging

Diagnostic Procedures

Thoracocentesis, abdominocentesis, and pericardiocentesis when indicated may provide insight to underlying etiology.

Pathologic Findings

Cardiac abnormalities consistent with various underlying etiologies. Other abnormalities consistent with tissue hypoxia.

Appropriate Health Care

Emergency inpatient intensive care management

Nursing Care

• Minimize stress as these patients are extremely fragile and at risk of cardiac arrest.
• Oxygen supplementation is critical.
• Significant pleural effusion (CHF) should be relieved with thoracocentesis.
• Patients exhibiting respiratory failure may need to be mechanically ventilated.
• Most patients in cardiogenic shock should NOT receive ANY fluid therapy until the etiology of the underlying cardiac dysfunction is understood and cardiac function improved. The exceptions to this rule include patients in cardiogenic shock secondary to pericardial tamponade, tension pneumothorax/mediastinum, and pulmonary thromboembolism.
• Pericardial tamponade should be relieved with emergency pericardiocentesis.

Activity

Minimize patient exertion

Diet

Free choice access to water; withhold food until shock is resolved.

Client Education

Warn of the danger of imminent cardiac arrest and discuss a “code status” in advance whenever possible.

Surgical Considerations

• Bradyarrhythmia may require implantation of a pacemaker device.
• Tension pneumothorax may require thoracostomy tube placement or exploratory thoracotomy.
• Caval syndrome secondary to Dirofilaria immitis infection will require worm extraction.

Drug(s) Of Choice

• Fast-acting positive inotropes to improve cardiac function and preserve end-organ perfusion in patients with reduced myocardial contractility (dobutamine 5–20 µg/kg/min CRI in dogs; 2.5–15 µg/kg/min CRI in cats; pimobendan 0.25 mg/kg PO q12h in dogs only).
• Arrhythmia and conduction abnormalities should be corrected promptly with antiarrhythmic therapy, cardioversion, or pacemaker implantation.
• Ventricular tachycardia:
  • Dogs may respond to lidocaine (2 mg/kg IV loading dose then 50 µg/kg/min CRI) or procainamide (10–15 mg/kg IV loading dose then 25–50 µg/kg/min CRI).
  • Boxers with arrhythmogenic right ventricular cardiomyopathy may respond favorably to sotalol (2 mg/kg PO q12h) alone, or combined with mexiletine (5–8 mg/kg PO q8h).
• Supraventricular tachyarrhythmia:
  • Treatments to slow the heart rate in dogs with supraventricular tachyarrhythmia include vagal maneuvers, calcium channel blockers (diltiazem 0.125–0.35 mg/kg IV over 2–3 minutes or 0.125–0.35 mg/kg/h CRI), beta-blockers (esmolol 0.5 mg/kg IV over 1 minute), and procainamide (6–8 mg/kg IV over 5–10 minutes then 20–40 µg/kg/min CRI).
  • Patients that do not respond to vagal maneuvers or emergency drug therapy may require DC cardioversion or overdrive pacing.
• Bradyarrhythmia:
  • Treatment of choice for severe bradyarrhythmia is cardiac pacing. However, some patients may benefit from atropine (0.02–0.04 mg/kg IV) or isoproterenol (0.4 mg in 250 mL D5W slowly to effect).
• Concurrent CHF:
  • Furosemide to treat pulmonary edema and enhance oxygenation in dogs and cats with CHF (2–8 mg/kg IV or IM; or 0.5–1.0 mg/kg/h CRI). The IV route is preferable, but IM is appropriate when IV access would require manual restraint.
  • Relief of pain or anxiety with morphine sulfate (0.1–0.5 mg/kg/h IV CRI, or 0.2–2 mg/kg IM) can reduce excessive sympathetic activity and decrease oxygen demand, preload, and afterload.

Contraindications

• Avoid diuretic therapy in patients with pericardial effusion, tension pneumothorax/mediastinum, and pulmonary thromboembolism.
• Avoid beta-blockers and calcium channel blockers in patients with reduced myocardial contractility.

Precautions

• Catecholamine infusions must be carefully titrated to maximize coronary perfusion pressure with the least possible increase in myocardial oxygen demand.
• Afterload reducers and vasodilators (angiotensin-converting enzyme inhibitors, nitroglycerin and nitroprusside) should be used with caution because of the risk for worsening hypotension and decreasing coronary blood flow.

Alternative Drug(s)

Dopamine may be used to improve systolic function as an alternative to dobutamine at a dose of 5–10 µg/kg/min (dogs and cats).

Patient Monitoring

• Serial subjective and objective assessment of perfusion (mentation, mucous membrane color, capillary refill time, pulse quality, muscle strength, temperature, serum lactate, urine output, heart rate, blood pressure, and oxygenation indices), respiratory rate and effort, and pulmonary auscultation is required to optimize therapy.
• Blood gas analysis and pulse oximetry to follow tissue oxygenation, ventilation, and acid-base balance.
• Packed cell volume, serum total protein, serum electrolytes, hepatocellular enzymes, blood urea nitrogen, and serum creatinine to monitor effects of systemic tissue hypoxia.
• Daily monitoring of cardiac troponin I (cTn-I) to assess level of myocardial injury.
• Blood pressure measurement may document hypotension.
• Electrocardiography may aid in the detection and characterization of arrhythmias.
• Pulse oximetry may document low oxygen saturation in patients with concurrent CHF.
• Central venous pressure monitoring may aid in assessment of cardiac preload and central venous oxygen saturation.
• Hemodynamic monitoring to assess mixed venous oxygen saturation, cardiac output and systemic vascular resistance.

Prevention/Avoidance

Prevention strategies aimed at the various underlying etiologies

Possible Complications

• CHF
• Cardiac arrhythmias
• Syncope
• Acid-base and electrolyte disturbances
• Renal dysfunction
• Cardiac arrest

Expected Course and Prognosis

Dependent on underlying etiology. Patients with primary cardiac disease have generally worse prognosis (poor to grave) as compared to those with secondary cardiac dysfunction.

See Also

• Atrioventricular Block
• Cardiomyopathy
• Congestive Heart Failure, Left-Sided
• Congestive Heart Failure, Right-Sided
• Endomyocardial Diseases-Cats
• Myocarditis
• Pericardial Effusion
• Pericarditis
• Pneumothorax
• Pulmonary Thromboembolism
• Sepsis and Bacteremia
• Shock, Hypovolemic
• Shock, Septic
• Sick Sinus Syndrome
• Supraventricular Tachycardia
• Ventricular Tachycardia

Abbreviations

• CHF = congestive heart failure
• GFR = glomerular filtration rate