Heart: congestive heart failure
Introduction
- Cause: underlying heart disease:
- Primary:
- Poor diastolic function (compliance failure).
- Poor systolic function (myocardial or pump failure), rare.
- Congenital heart disease.
- Secondary:
- Hyperthyroidism.
- Systemic hypertension.
- Taurine deficiency.
- Arrhythmias.
- Primary:
- Signs: respiratory difficulty, poor appetite, activity intolerance.
- Treatment: control fluid retention, counter adverse neuroendocrine activation, correction of arrhythmia, improving systolic or diastolic function.
- Prognosis: guarded.
Presenting signs
- Dyspnea.
- Increased respiratory rate (tachypnea).
- Progressive abdominal distension (less frequent).
- Anorexia.
- Lethargy.
- Syncope Syncope.
- Rarely cough.
Acute presentation
- Extreme dyspnea.
- Circulatory collapse.
- Signs of acute aortic thromboembolism Thromboembolism: aorta (ie hind limb paralysis) can co-exist with signs of congestive heart failure.
Special risks
Stress
- Treat heart failure symptomatically, eg oxygen, intravenous diuretics, cage rest, before undertaking diagnostic procedures. Drainage of significant pleural or abdominal effusions provides immediate relief.
- Consider thoracic point of care ultrasound (POCUS) Triage for initial assessment if unstable.
Radiographical positioning
- Use dorsoventral (as opposed to ventrodorsal) view to avoid impairing respiration by moving fluid in thorax.
- Often a single lateral view suffices, however this view is relatively insensitive for detection of cardiac enlargement.
- Dorsoventral view usually more useful for detection of atrial enlargement and pulmonary vein congestion.
Sedation
- If dyspneic: sedate safely Sedation or sedative protocol to limit anxiety.
General anesthesia
- See guidance under anesthesia Anesthesia: in cardiovascular insufficiency.
- Avoid if CHF is uncontrolled unless absolutely unavoidable. Warn owner of risks associated with anesthesia.
Intravenous fluid therapy
- Fluids cannot be given if CHF is present.
- See details under fluid therapy Fluid therapy: overview Fluid therapy: for acute circulatory collapse.
Pathogenesis
Etiology
- Systolic failure:
- Dilated cardiomyopathy Heart: dilated cardiomyopathy (DCM). Rare.
- Arrhythmogenic right ventricular cardiomyopathy (affecting right-sided chambers). Rare.
- Diastolic failure:
- Hypertrophic cardiomyopathy Heart: hypertrophic cardiomyopathy. Common.
- Restrictive cardiomyopathy Heart: restrictive cardiomyopathy. Common.
- Pericardial disease Pericardial disease. Rare.
- Secondary to hyperthyroidism Hyperthyroidism.
- Volume overload:
- Severe mitral regurgitation Atrioventricular valve dysplasia.
- Tricuspid regurgitation Atrioventricular valve dysplasia.
- Patent ductus arteriosus Patent ductus arteriosus.
- Ventricular septal defect Ventricular septal defect; large left-to-right shunting.
- Pressure overload:
- Aortic stenosis Heart: aortic stenosis.
- Severe systemic hypertension (rare cause of CHF) Hypertension.
- Pulmonic stenosis.
- Pulmonary hypertension Pulmonary arterial hypertension (PHT).
- Dysrhythmias:
- Ventricular tachycardia Heart: dysrhythmia.
- Supraventricular tachycardia.
- Atrial fibrillation Atrial fibrillation.
- High grade second degree or third degree atrioventricular block Heart: dysrhythmia.
Pathophysiology
- Cardiac injury → activation of sympathetic nervous system, renin-angiotensin-aldosterone and arginine-vasopressin systems to maintain blood pressure → detrimental in chronic cases → decreased cardiac function → progressive vicious cycle.
- Decreased cardiac output → decreased blood pressure activates baroreceptors → reflex increased sympathetic activity/decreased vagal activity → increased heart rate, increased contractility and vasoconstriction → maintain blood pressure.
- Sympathetic activation and poor renal perfusion → activates renin-angiotensin-aldosterone system (RAAS) → further vasoconstriction, sodium and water retention → increased sympathetic outflow and release of vasopressin (antidiuretic hormone) → further vasoconstriction and water retention → increased venous pressures and eventually capillary pressures → extravasation of fluid into lungs and pleura (left-sided heart failure) or liver and abdomen (right-sided heart failure). Pleural effusions are very common in cats with both left and right sided cardiac failure.
- See Pathophysiology of CHF for more detail Heart: pathophysiology of CHF.
Timecourse
- Weeks to months depending on underlying heart disease.
Diagnosis
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Treatment
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Prevention
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Outcomes
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Further Reading
Publications
Refereed papers
- Recent references from PubMed and VetMedResource.
- James R, Guillot E, Garelli-Paar C et al (2018) The SEISICAT study: a pilot study assessing efficacy and safety of spironolactone in cats with congestive heart failure secondary to cardiomyopathy. J Vet Cardiol 20 (1), 1-12 PubMed.
- Ward J L, Lisciandro G R, Ware W A et al (2018) Evaluation of point-of-care ultrasound and NT-proBNP for the diagnosis of congestive heart failure in cats with respiratory distress. JVIM 32 (5), 1530-1540 PubMed.
- Hogan D F, Fox, P R, Jacob K et al (2015) Secondary prevention of cardiogenic arterial thromboembolism in the cat: The double-blind, randomized, positive-controlled feline arterial thromboembolism; clopidogrel vs. aspirin trial (FAT CAT). J Vet Cardiol Supplement 1, S306-317 PubMed.
- MacGregor J M, Rush J E, Laste N J et al (2011) Use of pimobendan in 170 cats (2006-2012). J Vet Cardiol 13 (4), 251-260 PubMed.
- MacDonald K A, Kittleson M D, Kass P H et al (2008) Effect of spironolactone on diastolic function and left ventricular mass in Maine Coon cats with familial hypertrophic cardiomyopathy. JVIM 22 (2), 335-341 PubMed.
- Wall M, Calvert C A, Sanderson S L et al (2005) Evaluation of extended-released diltiazem once daily for cats with hypertrophic cardiomyopathy. JAAHA 41 (2), 98-103 PubMed.
- Fox P (2003) Prospective, double-blinded, multicentre evaluation of chronic therapies for feline diastolic heart failure: interim analysis. JVIM 17, 938.
- Packer M (1998) Neurohormonal interactions and adaptations in congestive heart failure. Circulation 77 (4), 721-730 PubMed.
- Francis G S & Chu C (1994) Compensatory and maladaptive responses to cardiac dysfunction. Current Opinion in Cardiology 9 (3), 280-288 PubMed.
- Roudebush P, Allen T A, Kuehn N F et al (1994) The effect of combined therapy with captopril, furosemide and a sodium-restricted diet on serum electrolyte concentrations and renal function in normal dogs and dogs with congestive heart failure. J Vet Intern Med 8 (5), 337-342 PubMed.
- Dahlström U & Karlsson E (1993) Captopril and spironolactone therapy for refractory congestive heart failure. Am J Cardiol 71 (3), 29A-33A PubMed.
- Bright J M, Golden A L, Gompf R E, Walker M A, Toal R L ( 1991) Evaluation of the calcium channel blocking agents diltiazem and verapamil for treatment of feline hypertrophic cardiomyopathy. JVIM 5 (5), 272-282 PubMed.
Other Sources Of Information
- Boswood A (2017) Heart failure: Clinical Management. In: Textbook of Veterinary Internal Medicine. 8th edn. Eds S J Ettinger, S J & E C Feldman. Philadelphia: W B Saunders. Chapter 247. pp 1163-1176 (well referenced).
- Chetboul V (2017) Feline myocardial disease. In: Textbook of Veterinary Internal Medicine. 8th ed. Eds S J Ettinger & E C Feldman. Philadelphia: W B Saunders. Chapter 253. pp 1278-1304
- Sisson D & Scollan K F (2017) Pathophysiology of heart failure. In: Textbook of Veterinary Internal Medicine. 8th ed. Eds S J Ettinger & E C Feldman. Philadelphia: W B Saunders. Chapter 246. pp 1153-1162.
- Côté E, MacDonald K A, Meurs K M, Sleeper M M (2011) Which drug for which disease? In: Feline Cardiology. Ed Wiley-Blackwell. pp 433-438.