Congestive Heart Failure

Causes

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• ​Congestive heart failure (CHF) is a condition in which fluid builds up (congests) due to the heart’s reduced ability to pump blood efficiently throughout the body.

• The Primary functions of the cardiovascular system are to maintain

  • normal blood pressure and

  • normal cardiac output, both at a

  • normal venous/capillary pressure

• It is most commonly due to a chronic disease that results in a severe decrease in myocardial contractility, severe regurgitation or shunting, or severe diastolic dysfunction.

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• Causes of CHF- 

  • Dilated cardiomyopathy

  • Valvular disease

  • Defects in the walls of the heart

  • Congenital cardiac defects

  • Arrhythmias

  • Narrowing of major blood vessels

  • Heartworms

  • Accumulation of fluid in the pericardium (sack around the heart)

  • Infection (endocarditis)

  • Tumors or cancer

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Pathophysiology

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• Heart failure occurs only with severe, overwhelming heart diseases like valvular leaks (eg, mitral regurgitation) and shunts (eg, patent ductus arteriosus, ventricular septal defect).

• To compensate for these diseases, the kidneys retain sodium and water, thereby increasing blood volume and thus venous return to the heart.

• The increase in venous return initially increases the diastolic pressure or stress on the myocardium, causing it to stretch. This stretch turns on the myocardium's genetic machinery to produce new sarcomeres (contractile elements) in the myocytes, causing longer cells to grow. The net result is that the ventricle grows a larger chamber. This phenomenon, called volume overload or eccentric hypertrophy. The compensation for a decrease in contractility (eg, dilated cardiomyopathy) is similar.

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•  Conversely, a disease that results in an increase in systolic pressure in a ventricle (eg, stenotic lesions such as subaortic and pulmonic stenosis, or systemic hypertension) causes pressure overload, or concentric hypertrophy. 

• ​With concentric hypertrophy, the heart grows a thicker wall to compensate for the increased systolic pressure, the thicker heart wall allows a ventricle to contract normally in the face of an increased force that is impeding contraction.

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• Volume overload (eccentric hypertrophy) results from the addition of sarcomeres in series (end to end) in myocytes whereas, pressure overload (concentric hypertrophy) results from the addition of new sarcomeres in parallel (side by side) in myocytes.

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Stages of Congestive Heart Failure

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• Stage A

  • The dog is at a high risk of developing heart disease based on age and breed. However, they aren’t showing any overt clinical signs, such as weakness or a persistent cough. This stage can last for years.

• Stage B

  • The dog has a heart murmur that can be heard with a stethoscope. They may not be exhibiting clinical signs of heart failure.

• Stage B2

  • The dog has a detectable heart murmur but isn’t showing clinical signs. There are structural changes to the dog’s heart that can be seen with an X-ray or electrocardiogram.

• Stage C

  • The dog is showing signs of heart disease and is responsive to cardiac medications.

• Stage D

  • This stage is referred to as “end-stage,” because the dog is exhibiting severe symptoms and is no longer responding to cardiac medications or treatments.

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Symptoms and Types

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• CHF can be described as right-sided or left-sided:

  • Left-sided CHF: The more common type to occur in dogs occurs when blood backs up in the lungs, causing swelling in the lungs (pulmonary edema). Dogs with left-sided CHF will usually have a cough and difficulty breathing. 

     

  • Right-sided CHF: When the right side of the heart malfunctions, the main circulatory system becomes backed up with blood throughout the body, and fluid gathers in the abdomen (ascites) or limbs (peripheral edema).

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• Symptoms of CHF in dogs can be one or more of the following clinical signs:

  • Coughing, sometimes even coughing up foam

  • Difficulty breathing

  • Increased rate of breathing, even when resting

  • Inability to exercise

  • Fatigue, lethargy and weakness

  • Cyanotic (blue) gums 

  • Distended abdomen

  • Collapse or sudden death

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Diagnosis

• Blood and urine test

• Chest X-rays

• EKG 

• Ultrasound 

• Heartworm antigen test

• Holter monitor 

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• While a cage-side echocardiogram (eg, assessment of left atrial size) can provide support for a diagnosis of CHF if needed, the stress of a full echocardiogram could further decompensate the patient without providing additional information.​

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• Thoracic radiographs often confirm the diagnosis of left-sided CHF but should be postponed if the patient is unstable (FIGURE 1). Radiographic cardiomegaly can be documented, and the presence of an interstitial/alveolar pattern centered on the perihilar region, consistent with pulmonary edema, confirms the diagnosis of CHF. While dilated pulmonary veins can be suggestive of left heart failure, in acute cases, it is not uncommon for these to be normal in size.

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• The clinical signs and history can also help in increasing the clinical suspicion of CHF. Sympathetic stimulation associated with heart failure should cause tachycardia, while cough and crackles are nonspecific signs.

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Treatment

• First-Line Therapy

  • Any dyspneic patient should initially be provided oxygen supplementation to increase tissue oxygenation. This can be achieved several ways. The most effective is an oxygen cage with the ability to vary the oxygen content and control temperature. Oxygen cages have the additional benefit of reducing activity, hence reducing oxygen use by the muscles. However, some larger dogs can become hyperthermic in small oxygen cages. If an oxygen cage is not an option, flow-by oxygen, masks, and nasal prongs may be used.

  • In dogs with a diagnosis of acute congestive heart failure, oxygen should be used in conjunction with a potent loop diuretic, such as furosemide. Ideally, an intravenous catheter is placed and furosemide is given IV. If the patient is too unstable, furosemide can be administered IM and the patient returned to the oxygen cage, pending improvement.

  • Exact doses depend on the severity of the presenting signs; furosemide 2 to 4 mg/kg IV or IM is used initially. Response to treatment should be closely monitored over the next 1 to 2 hours.1 Ideally, after 1 hour, the respiratory rate and effort should start to decline; however, some severely affected dogs require several doses before improvement is noted. However, if the patient has not responded after oxygen and furosemide have been administered, referral consultation with a specialist should be considered.

  • Close monitoring of respiratory rate is a noninvasive way to tailor diuretic therapy. The production of large amount of dilute urine is an encouraging sign that furosemide is having an effect. If there is no improvement, the dose can be repeated as a bolus, or the patient can be placed on a constant-rate infusion (CRI). CRI doses of furosemide 0.6 to 1 mg/kg/hr IV have been suggested; this high dose should be carefully monitored and decreased by 50% as the patient improves, or major electrolyte disturbances will be seen.1

  • Pimobendan should also be administered as soon as CHF is diagnosed. This inodilator causes vasodilation via phosphodiesterase 3 inhibition and augments contractility of the heart, supporting the failing heart by promoting calcium binding to troponin C within the cardiomyocyte. Left atrial pressure declines with pimobendan in experimental models and likely in the clinical setting.2

  • If the patient appears stressed as a result of dyspnea, opioids can be beneficial to reduce anxiety and provide mild sedation. This must be balanced against the potential to depress the respiratory centers. Butorphanol at 0.1 to 0.2 mg/kg IV or IM is often used.

• Second-Line Options

  • Following these treatments, the next parameter to evaluate is blood pressure. Due to the sympathetic drive, these patients may be normo- or hypertensive, and this afterload is an extra burden on the failing myocardium. If the patient is hypertensive, arterio dilators can be used to decrease the afterload for dogs with severe mitral regurgitation to achieve a systolic blood pressure of about 100 mm Hg.

  • Historically, sodium nitroprusside was the treatment of choice. This drug was given as a CRI, and the dose was increased to reduce the blood pressure to the required level. It required close monitoring of the blood pressure and could only be used for 24 to 48 hours at the risk of developing cyanide toxicity. Unfortunately, it has now become prohibitively expensive.

  • Topical nitroglycerine ointment has been used, but studies and clinical experience have questioned its effectiveness. Amlodipine can be given orally but is slower in onset of action. Injectable nitrate compounds have been used anecdotally.

  • Hydralazine is a potent arterio dilator and has been used at 0.5 to 3 mg/kg IV bolus q12h or as a CRI at 1.5 to 5 mcg/kg/min IV. Reflex tachycardia and hypotension are the most serious side effects seen.

  • For patients that are hypotensive (eg, dogs with dilated cardiomyopathy (DCM) and some dogs with DMVD), pressor agents may be required to increase blood pressure.3 Dopamine or, more commonly, dobutamine (which is less arrhythmogenic) have been used as CRIs, and, in my clinical experience, the beneficial effects seem to last for 4 to 6 weeks.

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