Anesthetizing patients with cardiovascular disease (Proceedings)


I'll review the pathophysiological changes associated with the common congenital and acquired cardiac defects in small animal medicine and discuss the characteristics of anesthetic drugs that may make them desirable of undesirable for each problem.


     • Review the pathophysiological changes associated with the common congenital and acquired cardiac defects in small animal medicine.

     • Discuss the characteristics of anesthetic drugs that may make them desirable of undesirable for each problem.

Canine Valvular Heart Disease (Endocardiosis, myxomatous valve degeneration):

     • CVHD/Mitral insufficiency is a relatively common finding. 10% of all dogs that present to veterinarians have heart disease. Of these, 75% have CVHD.

     • Older, small breed dogs are especially prone to this acquired condition.

     • Males are more commonly affected than females.

     • Usually more rapidly progressive in large dogs.

     • Mitral insufficiency is associated with chronic left ventricular volume overload. The left ventricle at end diastole contains blood that has passed though the atria into the ventricle (normal antegrade filling) AND blood that flowed in a retrograde fashion across the mitral valve during ventricular contraction.

     • The ventricle responds by increasing volume and wall thickness (eccentric hypertrophy). This change is compensatory and helps to maintain function. Atrial dilation occurs as a result of increased volume.

     • Over time, ventricular systolic function decreases.

     • The relationship between atrial pressure and aortic pressure determines the direction and quantity of blood flow.

     • Increased aortic diastolic pressure tends to increase regurgitation of blood into the atria.

     • Patients with mitral regurgitation are in a state of chronic volume overload and sympathetic stimulation. The degree of alteration is related to the severity of disease.

     • Animals with mitral regurgitation are sensitive to volume overload, decreased heart rate, and increased afterload.

     • Thoracic radiographs provide an indication of cardiac enlargement and may indicate the onset of congestive heart failure.

     • Ultrasonic evaluation will confirm the diagnosis of mitral insufficiency, and can provide an indication of myocardial function.

     • Central venous pressure can be useful in determining volume status or onset of congestive heart failure.

     • Exercise tolerance, and other historical and physical findings can provide a good indication of cardiac function and anesthetic risk.

     • The practitioner should be familiar with the ACVIM's guidelines for diagnosis and treatment of canine valvular heart disease:

Summary: ACVIM Consensus Statement, Guidelines for the Diagnosis and Treatment of Canine Valvular Heart Disease (CVHD) 2009

Source: Journal of Veterinary Internal Medicine, November/December 2009, Vol 23, No 6, pp 1142-1150

          o Classification of Disease

               » Modified New York Heart Association

     • Class I: Asymptomatic

     • Class II: Signs only during exercise

     • Class III: Signs during routine, daily activities or mild exercise

     • Class IV: Signs at rest

               » 2001 American College of Cardiology/American Heart Association

     • Stage A: Patients at risk

     • Stage B: Structural heart disease (presence of murmur)

     • B1: Asymptomatic, no radiographic or echocardiographic evidence of remodeling

     • B2: Asymptomatic, cardiac enlargement

     • Stage C: Past or current signs of heart failure

     • Stage D: End stage disease, nonresponsive to standard therapy

          o Diagnosis and Treatment Guidelines

     • Stage A

          o Diagnosis: Yearly auscultation by veterinarian/yearly screening events

     • Treatment: No drug therapy, no breeding if a murmur is discovered

     • Stage B

          o Diagnosis: Thoracic radiograph, blood pressure, +/- echocardiography (recommended in large breeds), basic labwork

          o Treatment:

               » B1: no drug therapy, yearly re-evaluation (radiography, echo; more frequent in large breeds?)

               » B2:

     • Small breeds: no consensus

          o ACEI

          o Beta blocker

          o Mild dietary sodium restriction

          o Some: pimobendan, digoxin, amlodipine, spironolactone

     • Large breed dogs: strengthened recommendations for ACEI, beta blockers, dietary changes

     • Stage C

          o Diagnosis:

               » Differentiate tracheobronchial disease from heart disease

               » Chest radiographs, echocardiography

               » N-terminal pro-B-type naturetic peptide (BNP)-no consensus

               » Obtain signalment, PE, minimum data base (CBC, serum biochemistry, UA)

               » Cachexia (>7.5% loss in weight over course of disease) is a negative prognostic indicator

          o Acute therapy:

               » Oxygen, if needed

               » Furosemide

               » Pimobendan

               » Abdominocentesis or thacocentesis

               » Nursing care

               » Sedation (opioids, acepromazine)

               » Sodium nitroprusside, if nonresponsive pulmonary edema

               » No consensus could be reached on

     • ACEI

     • Nitroglycerin

           o Home-based therapy:

               » Furosemide

     • Allow access to water once dieresis is initiated

               » ACEI

               » Pimobendan

               » No consensus on

     • Spironolactone

     • Digoxin (unless AF)

     • Beta blocker (unless AF...AND only if HF resolved)

     • Diltiazem (some preferred in AF for rate control)

     • Cough suppressants

     • Bronchodilators

               » Adequate caloric intake to prevent cachexia

     • Monitor weight, adequate protein, modest sodium restriction, monitor potassium

     • No consensus on Mg supplementation, n-3 fatty acids

     • Stage D: Note: volume and quality of evidence available is less than for other stages:

          o Diagnosis: As recommended for C and increased as needed to determine response to treatment

          o Acute (Hospital-based) therapy

               » Furosemide

     • Allow access to water once dieresis has been initiated

               » Oxygen therapy

               » Mechanical ventilation, if needed

               » Mechanical fluid removal

               » More vigorous afterload reduction

     • Sodium nitroprusside

     • Hydralazine

     • Amplodipine

     • ACEI

     • Pimobendan

     • Others (no consensus reached)

          o Increased (off-label) doses of pimobendan

          o Nitroprusside

          o Dobutamine

          o Sildenafil

          o Bronchodilators

          o Chronic (Home-based) therapy

               » Furosemide

               » Spironolactone

               » Pimobendan (see below)

               » ACEI

               » No beta blockade unless failure is controlled

               » No consensus on

     • Hydrochlorothiazide

     • Increased dose of pimobendan

     • Digoxin

     • Sildenafil

     • Cough suppressants

     • Bronchodilators

               » Dietary recommendations the same as in C above, but with more aggressive restriction of sodium intake.

     • Anesthetic management of patients with CVHD:

          o Maintain normal or slightly increased heart rate to minimize regurgitant fraction.

          o Manage vascular volume. Interpretation of vascular volume is somewhat difficult as CVP may reflect inadequate forward blood flow OR volume overload. Monitor body weight and perform thoracic radiographs if volume status is questionable. Use a decreased anesthetic fluid rate.

          o Avoid drugs that increase afterload (i.e., medetomidine, xylazine, phenylephrine).

          o Use positive inotropes (i.e., dobutamine) to treat hypotension.

          o Do not discontinue cardiac medications prior to anesthesia. Many patients with mitral regurgitation may be receiving diuretics (may alter serum potassium concentration) and angiotensin converting enzyme inhibitors.

          o Acepromazine, opioids, thiopental, propofol, and isoflurane or sevoflurane are drugs that are frequently used in anesthetic protocols for patients with mitral regurgitation.

Aortic Stenosis (Pulmonic Stenosis):

     • Aortic stenosis is a narrowing (obstruction) of the left ventricular outflow tract that causes a pressure gradient between the left ventricle and the aorta. The degree of stenosis is associated with the magnitude of the pressure gradient.

     • Concentric ventricular hypertrophy is the response to pressure overload of the left ventricle. When severe, aortic stenosis will lead to fibrosis of he left ventricle and decreased compliance (diastolic dysfunction) and contractility (systolic dysfunction).

     • Because of the increase in left ventricular wall mass, increased ejection time, and contraction against a fixed obstruction, the hypertrophic myocardium is prone to ischemia.

     • Animals with aortic stenosis are prone to cardiac dysrrhythmias.

     • Anesthetic management:

          o Maintain preload

               » Appropriate vascular volume

               » Avoid significant vasodilation, if possible

     • Decreases preload

     • Decreases aortic diastolic pressure-leads to decreased coronary artery filling

          o Maintain normal heart rate and rhythm

               » Tachycardia causes increased myocardial work and may be associated with decreased coronary flow.

          o Atrial contraction contributes more to ventricular volume than in normal hearts-so maintenance of normal sinus rhythm is important.

          o Treat hypotension

               » Phenylephrine

               » Positive inotropes will increase contractility and oxygen consumption. They may be used, but cardiac rhythm and rate should be monitored closely

               » Dobutamine vs Dopamine

          o Opioids and benzodiazepines are frequently used in the management of patients with aortic stenosis. Constant rate fentanyl infusion may be used to diminish the amount of inhalant necessary to maintain anesthesia.

Dilated Cardiomyopathy:

     • Dilated cardiomyopathy is seen most commonly in large breeds dogs (i.e., Doberman Pinschers, Great Danes).

     • Systolic function is greatly diminished in dilated cardiomyopathy.

     • Cardiac ultrasonography is useful in quantifying dysfunction.

     • Atrial fibrillation and valvular insufficiency may accompany dilated cardiomyopathy.

          o If atrial fibrillation is present prior to anesthesia, treatment should be initiated to decrease rate of ventricular response.

               » Digoxin

               » Beta antagonists

               » Calcium channel blockers

     • Anesthetic risk is greatly increased in patients with dilated cardiomyopathy.

     • Anesthetic Management:

          o Complete cardiac workup should be performed to evaluate progression of disease.

          o Aggressive patient monitoring is warranted (i.e., direct measurement of arterial blood pressure and central venous pressure).

          o In general, opioids are used extensively to provide analgesia and to minimize the need for inhalant anesthesia.

Hypertrophic Cardiomyopathy:

     • Primarily a disease of cats

     • Diastolic and systolic dysfunction are present.

     • Dynamic outflow obstruction may be present.

     • Animals may be treated with beta antagonists or with calcium channel blocking drugs.

     • Anesthetic Management:

          o Maintenance of normal heart rate is important to preserve cardiac output.

          o Hypotension should be treated with intravenous fluids and with phenylephrine, if necessary. Positive inotropes should be avoided, if possible.

          o Avoid drugs that increase heart rate when possible (anticholinergics).

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