Heart Failure Flashcards
What is the difference between preload and afterload?
PRELOAD = left ventricular end-diastolic volume or pressure (volume of blood in ventricles before contraction)
AFTERLOAD = resistance/pressure the ventricles are pumping against
(left CO = right CO)
How is MAP calculated? CO?
MAP = CO x SVR
CO = SV x HR
What is heart failure? What 4 things does it lead to?
inability of the heart to maintain normal venous/capilary pressures, CO, and/or systemic BP that occurs secondary to severe, overwhelming cardiac disease
- volume overload
- pressure overload
- impaired LV filling (pump/myocardial failure)
- primary myocardial disease
What are 3 of the heart’s priorities?
- maintain normal systemic arterial pressure
- maintain normal tissue blood flow
- maintain normal systemic and pulmonary capillary pressures
Why is heart failure a vicious cycle?
the heart overcompensates and the mechanisms meant to preserve function leads to failure
What are 6 mechanisms used for cardiac compensation (that can ultimately lead to failure)?
- Starling’s Law
- endocrine - RAAS
- sympathetic nervous system
- neurohormones
- renal effects
- remodeling to accommodate for changes in volume and pressure
What are the 3 major causes of CHF?
- decreased CO - infarction, myocarditis, volume/pressure overload, genetics
- renal responses - water and sodium retention, vasoconstriction, cardiac remodeling (RAAS, aldosterone, ADH, sympathetic NS, neurohormones)
- decompensation - pulmonary edema, ascites, pleural effusion
What are 4 results of compensated heart failure?
- no clinical signs
- increased RAAS
- increased adrenergic systems
- cardiac remodeling
What are 3 results of decompensated heart failure (CHF)?
- clinical signs - water retention exceeds vessel capacity, leading to accumulation of fluid in body cavities
- increased RAAS
- increased adrenergic systems
How does the activation of the RAAS progress throughout heart disease?
- mechanical or functional abnormalities of the valves upregulates the RAAS with no clinical signs for years
- onset of clinical signs begins years later, ultimately leading to death within months
How does right-sided and left-sided heart failure compare?
RIGHT - blood cannot pump blood into the heart properly, so it backs up in the BODY, resulting in ascites, poor organ function, and distended veins
LEFT - blood cannot pump into the heart properly, so it backs up in the LUNGS, resulting in pulmonary edema
What is the Frank Starling mechanism? What does this result in?
acute increases in ventricular filling (preload) induces greater contraction force and blood ejection, allowing for beat-to-beat adjustments that balance the output of the 2 ventricles in response to acute increases in hemodynamic load
ventricular output increases as preload increases = heart can change its force of contraction and SV
What role does the Frank Starling mechanism take part in during compensation for heart failure? How is it limited?
buffers the fall in CO to preserve sufficient blood pressure when there is poor emptying and higher preload by stretching to allow for better contraction and preservation of CO
can cause muscle failure —> poor compensation leading to end diastolic volume and left ventricular pressure increase —> pulmonary edema
Cardiac compensation:
increase in catecholamines is not enough to increase contraction enough at a certain point
How does heart failure affect the endocrine system? When does this activate?
increases RAAS and ADH, resulting in water and sodium retention to increase circulating volume
later in heart disease when there is renal artery hypoperfusion, resulting in decreased filtered Na reaching the macula densa which increases SNS activity and renin release
RAAS:
things that cause renin release are targeted by cardiac drugs
What 2 local effects does angiotensin II have on the heart? What else does it do?
- enhances sympathetic affections
- promotes tissue remodeling - hypertrophy, inflammation, fibrosis
- vasoconstrictor
- releases aldosterone from adrenal cortex —> increases thirst and salt appetite
- stimulated ADH release
What 2 local effects does aldosterone have on the heart and kidneys? What else does it do?
- mediates inflammation and fibrosis
- pathologic cardiac changes
- promotes sodium and chloride reabsorption in renal collection tubules
- promotes potassium and hydrogen secretion in collection tubules
How does heart failure affect the nervous system? How does it do this?
decreased CO activates the SNS to compensate by stimulating beta receptors and increase contractility and HR
maintains CO by causing vasoconstriction and increased inotropy/chronotropy to increase venous return
What inhibitory and excitatory inputs affect SNS activation with heart failure?
INHIBITORY - baroreceptors, mechanoreceptors (maintain pressure)
EXCITATORY - non-baroreflex peripheral chemoreceptors, muscle metaboreceptors
What are 4 results of chronic SNS activation with heart failure? What ultimate response is seen?
- increased afterload stress
- increased myocardial O2 demands
- cellular damage
- myocardial fibrosis
persistent sympathetic innervation reduces cardiac sensitivity to catecholamines, resulting in arrhythmias in later disease
What are 3 other neurohormones that play a role in abnormal cardiovascular hypertrophy or fibrosis?
- free radicals from oxidative stress
- cytokines - TNFa
- endothelins - ET-1, 2, and 3 produced in response to hypoxia and vascular mechanical factors, angiotensin II, ADH, NE, and cytokines act as potent vasoconstriction
What role do most neurohormones play in heart failure? What happens as failure worsens?
prolonged vasoconstriction = increases workload by reducing forward CO and exacerbating valvular regurgitation
neurohormone activation increases —> increased endothelins and inflammatory cytokines
What are 5 endogenous mehanisms that oppose the vasoconstrictor responses caused by heart failure? Why does heart failure often still result?
- natriuretic peptides - natriuresis/diuresis, vasodilation, inhibits RAAS and SNS (ANP, CNP, NT-proBNP)
- vasodilatory prosraglandins - PGE2, PGI2
- adrenomedullin
- nitric oxide
- bradykinin
as heart failure progresses, the influence of vasoconstriction predominates despote activation of vasodilatory mechanisms
How do the kidneys respond to heart failure? What happens with chronic heart failure? What effects do diuretics have?
efferent glomerular arteriolar constriction - maintains GFR in the face of reduced cardiac output and renal blood flow, enhances reabsorption of tubular fluid and sodium (promoted by angiotensin II)
clinical edema and effusions
magnify azotemia and electrolyte loss and further reduces CO and activates NH mechanisms
How does the heart remodel in response to heart failure? What 3 things contribute to this change? What does this ultimately result in?
cardiac hypertrophy —> takes place way before hear failure manifests clinically
- abnormalities with cell energy production
- calcium fluxes
- contractile protein function
ventricular function deteriorates as contractility and relaxation becomes deranged
What 4 things are responsible for cardiac hypertrophy with heart failure? What changes take place>
- pressure
- volume
- neurohormones
- cytokines
myocardial cell hypertrophy/apoptosis, interstitial matric formation, fibrosis, collagen destruction (dilation)
What different responses happen with pressure overload and volume overload?
PRESSURE = concentric hypertrophy, thickening
VOLUME = eccentric hypertrophy, dilation (spreading of muscle)
Cardiac remodeling:
What 4 things is LV remodeling influenced by?
- hemodynamics
- neurohormones
- epigenetic
- genetic
What causes eccentric hypertrophy? What 3 things does this result in?
volume overload
- addition of sarcomeres in series (elongated)
- increased LV lumen diameter
- poor contractility
What causes concentric hypertrophy? What 3 things does this result in?
pressure overload
- addition of sarcomeres in parallel (side by side)
- increased cross-sectional area
- decreased LV luminal diameter and compliance, which impairs relaxation (diastolic dysfunction)
What are 3 causes of eccentric hypertrophy?
- valvular insufficiency - MMVD, aortic insufficiency
- systolic dysfunction - DCM, myocarditis, nutritional cardiomyopathy
- congenital volume overload - PDA, ASD, VSD
What are 3 causes of concentric hypertrophy?
- pressure overload - aortic/pulmonic stenosis, systemic hypertension, hyperthyroidism, systolic anterior motion of mitral valve (SAM)
- genetic - hypertrophic cardiomyopathy, myocarditis, nutritional cardiomyopathy
- infiltrative - neoplasia, amyloidosis, lysosomal disorders
Other than hypertrophy, what are some cardiac changes expected with heart failure?
- impaired contraction and relaxation - most prominent during high HR
- necrosis/myocyte death - ischemia, myocardial injury, toxin exposure, infection, inflammation, and neurohormonal activation (AT-II, endothelins, TNF)
- fibrotic scar/fibrosis - alters myocardial function, cell signaling, and electrical transduction
What are the 4 most common presentations of heart failure?
- pulmonary edema - LS-CHF, common in dogs and cats
- pleural effusion - LS/RS-CHF, cat > dog
- ascites - RS-CHF, dog > cat
- SQ edema - RS-CHF, dogs/cats < horses/cows
How does systolic dysfunction lead to heart failure?
- decreased SV
- higher systolic volume
- higher diastolic volume and pressure in LA through open mitral valve, then to pulmonary vein and capillaries
- TRANSUDATION of fluid into pulmonary interstitium where cap hydrostatic pressures are >20 mmHg
- LEFT HEART FAILURE
How does diastolic dysfunction lead to heart failure?
- reduced champer compliance
- high end diastolic filling pressure (incomplete filling) to RS through open tricuspid valve
- TRANSUDATION of fluid into dependent tissue interstitium (lower extremities, liver, GIT)
- RIGHT HEART FAILURE
What are some clinical manifestations of heart failure? What is not seen in cats?
- increased respiratory rates, coughing
- reduced exercise capacity
- normal CO at rest, but cannot increase in response to exertion (exercise intolerance)
- inadequate forward output, poor diastolic filling
- pulmonary edema, pleural effusion
- impaired peripheral vasodilation contributes to inadequate skeletal muscle perfusion and fatigue
- increased vascular wall sodium and interstital fluid pressure stiffen and compress vessels
coughing —> can be caused by HW, but adults live in lungs and cause pneumonitis
What are some important historical questions to ask in patients seemingly in heart failure?
- diet
- PU/PD history
- indoor vs outdoor
- activity level
- coughing, frequency/character
- vomiting/gagging
- history of episodes of fainting/weakness
- changes in gum or tongue color, cyanosis
- history of any medication
- history of travelq
What breeds are predisposed to developing valvular disease, DCM, and HCM?
VALVULAR - CKCS, Dachshunds, Poodles, Papillon, Maltese, Chihuahua
DCM - Doberman, Boxer, American Cocker Spaniel, Newfoundlands, Irish Wolfhounds, Portuguese Water Dogs, Mastiffs, Great Danes
HMC - males > females, Main Coons, Persians, American Shorthair, Ragdolla
How does MMVD compare to other valvular diseases?
small breeds predisposed, but large breeds get it with faster disease progression
What are some common symptoms of heart failure?
- audible heart murmur Grade III/VI or higher
- cough (often productive with edema) in dogs
- respiratory cackles with severe CHF
- pale MM, poor CRT
- arrhythmia, pulse deficits
- tachycardia
- anxious/restless
- open mouth breathing
- orthopnea and abducted elbows
- tachypnea - short and shallow
- hypernea - increased depth
What are the most common findings with left and right heart failure?
LEFT = cough caused by enlarged LA pressing on trachea/mainstem bronchi and chronic pulmonary edema (cats rarely cough)
RIGHT = increased jugular pulses and ascites caused by increased venous pressures
What are important parts of clinical pathology for diagnosing heart failure?
- CBC/CHEM/UA - electrolytes, renal function, glucose
- thyroid function tests
- heartworm test
- complete neuro exam
- blood cultures (if diastolic murmur/fever)
What are 4 parts of the basic cardiac workup? What else can be included?
- thoracic radiographs
- cardiac U/S
- arterial blood pressure
- ECG - rest, post-exercise, vagal maneuver, in-house continuous (Holter, event monitoring, ZIO, implants)
cardiac biomarkers - NT-proBNP, cardiac troponin I
What are the 2 major cardiac biomarkers used to assess cardiac function?
- NT-proBNP - ventricular stretch (bedside good for emergency cases in clinical patients - screening); can rule out cardiac disease with negatives
- cardiac troponin I - myocardial damage, monitored over time
What are the major diagnostic and therapeutic indications for performing cardiac catheterization?
DIAGNOSTIC - complicated congenital abnormalities, evaluating pressures
THERAPEUTIC - pre-surgical, ballooning, pulmonic stenosis in Bulldogs
(+ research for cardiac therapeutics)
What symptoms occur with left-sided CHF?
everything is backed up at the LA
- pulmonary edema - dyspnea, coughing, orthopnea, tachypnea, exercise intolerance, cyanosis
- hypotension - pale MM, increased CRT, elevated HR, weak pulses
- lethargy/depression
- weakness
- syncope
- prerenal azotemia
(pleural effsion seen in cats with right or left heart failure)
What are the most common symptoms associated with right-sided CHF?
- ascites
- distention of jugular veins (venous distention)
- increased hydrostatic pressure - caudal vena cava, hepatic vein, hepatic sinusoids
- hepatosplenomegaly
- pleural effusion
- hypotension
- weak pulses
- syncope
When is syncope most commonly seen with heart failure? What are the most common signs? How does this compare to seizures?
right-sided heart failure and pulmonary hypertension
- exertion or excitement
- rear limb weakness
- sudden collapse (tend to get right back up)
- lateral recumbency
- stiffening of forelimbs and opisthotonos
- micturition
- vocalization
- hypoxia
SEIZURE = tonic/clonic motion, facial fits, defecation, aura, post-ictal dementia, neurologic deficits
What are the 5 major treatment strategies to treating heart failure?
- control edema and effusions
- improve CO
- reduce cardiac workload
- support myocardial function
- manage concurrent arrhythmias
What are the most common ways to control signs of congestion in cases of CHF?
- diuretics
- dietary salt restriction
- vasodilators
- abdominocentesis/pleurocentesis
How can neurohormone response be modulated in cases of heart failure?
- ACEi
- aldosterone
- sympathetic antagonists
What is the most easily monitored sign associated with the development of stage C heart disease?
resting respiratory rate (RHRR) at home
- > 35/30 resting/sleeping bpm is highly suggestive of heart failure
- at home preferred since RR will be increased due to excitement/agitation in-hospital
CHF causes:
What are the 4 major classes of drugs used to treat heart failure?
- DIURETICS - Furosemide, Torsemide
- ACEi - Benazepril
- CONTRACTILITY IMPROVEMENT - Pimobendan
- ALDOSTERONE INHIBITOR - Spironolactone
What is the purpose of using diuretics to treat heart failure? What are 4 options?
decrease venous congestion by increases Na and water loss through the kidneys
- FUROSEMIDE - proximal tubule, Na/K/2Cl
- TORSEMIDE - 10x more potent (SID), Na/K/2Cl
- SPIRONOLACTONE - weak, K sparing
- HYDROCHLOROTHIAZIDEDE - Na/Cl cotransporter i distal tubule
Why must Hydrochlorothiazide be carefully used in cases of heart failure?
potentiates Furosemide, which can lead to dehydration and renal disease
Diuretics:
What are 3 classes of drugs used to control/inhibit RAAS?
- ACEi - Enalapril, Benazepril
- Angiotensin II receptor antagonists - reduce action to prevent blood vessel constriction; Lostartan, Telmisartan
- aldosterone antagonists - Spironolactone (also prevents remodeling)
COMBO: Benazepril + Spironolactone = very effective
How does Pimobendan work? What 3 effects does it have?
positive inotrope and vasodilator –> improves myocardial contractility through calcium sensitivity
- reduces afterload
- decreases LA pressure
- makes MV annulus smaller and decreases MR
(can be given before clinical heart failure to prolong time until heart failure develops)
Other than medication, what 4 treatments are recommended when treating heart failure?
- diet - decrease sodium
- exercise
- monitoring - NT-proBNP, at home RR
- resolving concurrent diseases
