Heart Failure Flashcards
what is heart failure?
pathologic state and clinical syndrome. heart impaired in ability to eject to eject (systolic) or receive blood (diastolic)
- CO doesn’t meet perfusion needs, limited exercise capacity
what are the 2 types of heart failure?
- forward or low output heart failure
- congestive heart failure
forward/low output HF
CO not meeting perfusion needs of tissues and limited exercise capacity
congestive HF
elevated venous pressures lead to congestion of organs and fluid accumulations (edema/effusion)
what are the 4 congestion quadrants?
- warm and dry: best
- warm and wet: lungs wet- need diuretics, vasodilators, inotropy
- cold and wet: inotropy, vasopressors, diuresis when perfusion is reformed
- cold and dry: congested and low output failure. worse scenario. inotropy and vasopressors. want to use diuretics but are having a problem perfusing; so don’t want to reduce preload so much
acquired causes of HF in cats
HCM
what are compensatory mechanisms for HF (buffering decrease in CO and help preserving perfusion)
- frank starling mechanism
- neurohormonal alterations (nervous system, RAAS, ADH)
- development of ventricular hypertrophy + remodeling
frank starling mechanism
- increased stretch on myofibers induces a greater stroke volume on subsequent contraction
- helps empty large ventricle and preserve forward CO
- beneficial compensatory mech except limited effect in severe HF. only works to a point
CO-HR equation with units
CO (mL/min) = HR (beats/min) x SV (mL/beat)
acquired causes of HF in dogs
- degenerative mitral valve disease (most common)
- DCM
RAAS
- short term RAAS activation: retains Na/H2O for increased SV. vasoconstriction (Increased SVR) short term
- long term RAAS activation: myocardial O2 demand increased: hypertrophy, fibrosis, arrhythmias
short term SNS stimulation
- increased HR, contractility, vasoconstriction, RAAS
useful! but not long term
ventricular remodelign
- heart dealing with inc pressure/volume = secondary remodeling to compensate to maintain CO
- causes: pressure/volume, genetics (sarcomere mutations), thryoid hormone (hyperthyroidism)
- chornic HF: neurohormonal activation promote hypertrophy and fibrosis
long term SNS activation
- maladaptive
- increased myocardial oxygen demand (MVO2)
- chronic RAAS activation
= cardiac fibrosis, arrhythmias. not helpful longterm when your heart is failing
**T/F: with stimulation of the RAAs, systemic vasodilation will occur
false: vasoconstriction
B-blockade in HR?
- mainly a human thing, improves survival
- in dogs and cats: need to be careful because the heart has compensatory mechanisms to keep CO maintained, so if you are blocking Beta as you are in heart failure it can make it worse
- no consensus for B-blockade in HR in dogs and cats, differences in processes between them and humans
**T/F: activation of the RAAS is stimulated by increased perfusion sensed in the renal artery
false- decreased perfusion
clinical manifestations of HF depend on
what side of the heart is affected: R vs L, biventricular
clinical manifestations of HF
dexercise intolerance, weakness, syncope, pale or grey mm, decreased arterial pulse quality, cool periphery, arrhythmias
cardiac cachexia: R CHF > L
how does left sided CHF lead to pulmonary edema?
- increased LA pressure and increased hydrostatic pressure in pulmonary veins
- ex: DMVD, DCM, HCM, subaortic stenosis
