Define congestive heart failure
Failure of the heart to maintain cardiac output and resulting congestion of blood in the venous system
What are the clinical signs of left heart failure?
- Decreased stroke volume resulting in hypotension:
- Pale mm
- Prolonged CRT (>2sec)
- Tachycardia
- Weak pulses
- Lethargy
- Depression
- Weakness
- Exercise intolerance
- Pre-renal azotemia
- Increased pressure in the pulmonary veins–> pulmonary edema
- Coughing
- Dyspnea
- Orthopnea
- Tachypnea
- Cyanosis
What are the clinical signs of right heart failure?
- High end-diastolic pressure resulting in increased pressure in anterior and posterior vena cavae
- Distention of jugular and peripheral veins
- Ascites
- Hepato- and splenomegaly
- Pleural effusion
- Rare peripheral edema
- Forward heart signs
- Hypotension
- Lethargy
- Depression
- Weakness
- Pre-renal azotemia
Differentiate between heart failure and heart disease
Heart disease consists of problems with the heart such as arrhythmias, murmurs, and other abnormalities.
Only when the compensation for heart disease results in insufficient cardiac output does the rocess progress to heart failure.
Describe the normal physiological responses to decreased cardiac output
- Baroreceptors detect a decrease in BP and activate the sympathetic nervous system –> inc. contractility (+ inotropy) and inc. heart rate (+ chronotropy)
- Inc. sympathetic activity –> veno-, arterio-constriction –> redirects blood to vital organs
- Prolonged depressed CO (hemorrhage) can cause decreased renal blood flow –> activation of RAAS –> peripheral vasoconstriction (veins and arteries) via angiotensin II and Na and H2O retention via aldosterone (both activated by kidneys)
- Inc. blood volume (aldosterone) + venoconstriction (angiotensin II) = inc. venous return
- Inc. venous return stretches myocardial fibers in heart –> inc. myoconttractility and CO (Frank Starling relationship)
- Angiotensin II causes arterioconstriction –> inc. peripheral resistance –> maintain BP
T/F: Abnormal hearts cannot respond to the SNS appropriately and increased peripheral resistance leads to decreased blood flow and hypotension
TRUE
What are 2 ways in which positive chronotropic effects (from physiological changes due to heart failure) might exacerbate heart failure?
- Lead to increased myocardial oxygen consumption
- Decreased flow + increased oxygen requirements = not enough oxygen to the heart
- chronotropy = less time in diastole = decreased coronary perfusion
- Sympathetic stimulation may also further damage the myocardium and predispose the heart to arrhythmias (coronary vasospasm)
- chronotropy = less time in diastole = decreased coronary perfusion
T/F: Catecholamines are good for the heart, even at prolonged elevated levels
FALSE–catecholamines are BAD for the heart at prolonged elevated levels
Physiological changes that occur with heart failure and how they might exacerbate the failure:
Frank Starling relationship?
Increased preload–> ?
Chronic vasoconstriction increases/decreases?
- Frank Starling relationship is not as pronounced in the diseased heart as it is in the healthy heart–CO is not as increased as it could be
- Increased preload –> pulmonary edema –> hypoxia –> more heart strain
- Chronic vasoconstriction increases afterload and oxygen requirements of the heart but decreases forward blood flow –> hypotension
Negative effects of angiotensin II during heart failure?
Negative effects of aldosterone?
- Angiotensin II
- Increased sympathetic activity, hypertrophy, and remodeling of ventricles
- Aldosterone
- Vascular and myocardial fibrosis, direct vascular damage, baroreceptor dysfunction–blocks parasympathetic activity, potentiates norepi effets
Eccentric hypertrophy–all the things
Atrial eccentric hypertrophy?
- Caused by increased diastolic pressure–volume overload
- Cells become elongated by adding sarcomeres in series
- Larger ventricle with increased chamber size and normal wall thickness
- Normal contractility, increased end diastolic volume, increased afterload, increased oxygen requirements
- Atrial eccentric hypertrophy = increased compliance to prevent increased atrial pressure–but increased venous pressure and edema
Concentric hypertrophy–all the things
- Caused by increased systolic ventricular pressure
- Pressure overload
- Seen with aortic stenosis or systemic hypertension
- Sarcomeres relicate side by side/parallel causing wider cells and a thicker ventricular wall
- Less ability for the wall to dilate during diastoly (lysotropy)
- Decreased filling –> increased preload –> edema
- Increased wall thickness –> increased oxygen requirements –> anaerobic metabolism if not met
- Resulting hypoxia decreases myocardial contraction efficiency and promotes arrhythmias
Describe the different stages of left sided CHF
- Phase I–heart disease but no clinical signs
- Phase II–cough, fatigue, and dyspnea with normal or strenuous exercise
- Phase III–cough, fatigue, dyspnea and orthopnea at night and with ANY activity
- Phase IV–cough, fatigue, dyspnea, orthopnea and cyanosis at rest with exacerbated signs
List the steps (general) for the treatment of heart failure
- Handle with extreme care (avoid excitation/stress)
- Can use drugs
- Enhance oxygen
- Reduce edema
- ACE inhibitors
- Improve cardiac contractility
- Low sodium fluids
- Treat arrhythmias
- Restrict sodium
How can you reduce excess excitation and stress in an animal with heart failure?
- Handle with extreme care!
- Transport on a stretcher and confine in cage until stabilized
- Morphine–reduces stress, vasodilator
- May cause nausea and vomiting (bad)
- Diazepam can also be used but butorphanol is effective and safe in cats/dogs
How can you enhance oxygenation for heart failure patients?
What is the goal?
Should you give 100% oxygen?
- Remove pleural fluid and any froth blocking the airways if needed
- Goal–maintain PaO2 > 60mmHg
- 100% oxygen for prolonged periods is toxic to the respiratory epithelium; usually give 30-50% O2 humidified with sterile saline to prevent drying of the respiratory mucosa
What are the different devices available for enhancing oxygenation in a heart failure patient?
- Oxygen mask–mut fit snugly (resistance) and requires high flow rate 8-12 L/min
- Oxygen collars–oxygen host led into an E collar sealed with plastic wrap; allow opening for CO2 to escape
- Nasal catheters–pre-measure infant feeding tubes to the carnassial tooth; pass tube through nostril dorsomedially then ventromedially; suture/super glue the tube to the muzzle; connected to sterile catheter connected to a saline IV bottle w/ oxygen bubbled in (humidification)
- 50-100 mL/kg/min
- Oxygen cages–minimal stress caused, but patient is isolated from contact
- Monitor O2, CO2, and humidity w/in cage
- Ventilatory support–for patients who cannot maintain a PaCO2 < 60mmHg on O2
- IPPV will decrease venous return by increasing the positive pressure w/in the lungs–can lead to severe systemic hypotension
What is the main go-to for reducing edema in a heart failure patient?
- Decrease circulating blood volume by using diuretics
- Furosemide
- MOST IMPORTANT DRUG IN THE TREATMENT OF CHF
- Prolongs life/improves quality of life
- Given IV or CRI until dyspnea improves and RR decreases; then given orally
- Activates RAAS and may cause decreased CO, hypotension, dehydration, azotemia, and electrolyte imbalances
- Give lowest dose possible to avoid; can also decrease Na and use ACE inhibitor
Reducing edema:
Acute situation
Chronic situation
- Reduce preload by trapping blood in the peripheral venous system and away from the heart and lungs–using dilators
- Acute
- Topical nitroglycerin cream (venodilator)
- IV sodium nitroprusside (mixed dilator)
- Chronic
- ACE inhibitors (mixed dilator)
- Slow progression, blunten remodeling and fibrosis (due to angiotensin II and aldosterone), reduce furosemide dosage (and reduce electrolyte imbalances), prolong and improve quality of life
- Side effects of ACE inhibitors
- Signs of hypotension and azotemia
- If BUN and Cr are excessively high, reduce furosemide dose (30%)
- Pimobendan–phosphodiesterase inhibitor
- ACE inhibitors (mixed dilator)
Reducing edema:
Cardiac contractility
Sodium fluids
Arrhythmias
Sodium
- Improve cardiac contractility
- CRI of dobutamine if animal is in cardiogenic shock (inc. rate until BP > 100mmHg and animal improves clinically)
- Outpatients: digoxin sometimes given, but pimobendan much safer/more effective (very effective in mngmt of heart failure in dogs due to cardiomyopathy or mintral insufficiency)
- Low sodium fluids up to 25% of the maintenance rate
- Treat arrhythmias (treat first if cause of failure) and underlying cause of heart failure
- Sodium-restricted diet–dec. Na and water retention and lower drug doses
- Check drinking water
- Severe restriction can cause hypotension and renal dysfunction (esp. w/ ACE inhibitors)
How should you monitor a patient being treated for CHF?
- Frequent clinical exams–TPR
- BP monitoring
- Bloodwork–electrolytes, Na, BUN, CREA
- X-rays, ECG, U/S–monitor changes in the heart
- Biomarkers–ANP, BNP elevated during heart dz and failure (cannot differentiate between)
- Cardiac troponin-1–also detects heart dz/failure (cannot differentiate)
- Have owners monitor resting RR at home (less stressed than in hospitals)
-
Neuro examination28
-
Neurology 121
-
Neurology 235
-
Neurology 347
-
Neurology 437
-
Neurology 540
-
Electrocardiography20
-
Arrhythmias41
-
Examination of the heart and circulatory system18
-
Heart failure21
-
Congenital heart diseases47
-
Acquired heart conditions52
-
Canine heartworm34
-
Respiratory introduction41
-
Diseases of the nasal cavity49
-
Tracheobronchial diseases--dogs31
-
Tracheobronchial diseases--cats15
-
Pulmonary disease69
-
Pleural disorders19
-
Antibiotics9
