HEART FAILURE, CARDIOMYOPATHIES Flashcards
HF definition
inability of the heart to fill with or eject blood at a rate appropriate to meet tissue requirements
s/s HF
dyspnea
fatigue
s/s circulatory congestion OR s/s end-organ hypoperfusion
causes of HF
- impaired myocardial contractility
- cardiac valve abnormalities
- systemic HTN
- pericardial diseases
- pulmonary HTN (cor pulmonale)
systolic vs. diastolic HF
systolic = decreased ventricular systolic wall motion diastolic = abnormal ventricular relaxation & reduced compliance
acute vs. chronic HF
acute = change in the s/s HF that requires emergency therapy (hypotension)
- worsening chronic HF
- new onset HF (ie valve rupture, MI, severe HTN)
- terminal HF (refractory to therapy)
chronic = long-standing cardiac disease; venous congestion, but BP is maintained
left vs. right HF
left = high LVEDP –> pulmonary congestion
right = high RVEDP –> systemic congestion (usually a product of LVF)
compensatory mechanisms to HF to help maintain a normal CO
- frank starling relationship
- SNS activation
- alterations of inotropy, HR, afterload
- humoral-mediated responses
preoperative evaluation & management of the pt w HF
HF = single most important risk factor for predicting perioperative cardiac morbidity & mortality
- all precipitating factors should be noted & aggressively treated pre-op
intraoperative management of pt w/ HF (not IHSS)
High/normal HR, high/normal preload, low afterload, increase contractility
- opioids
- PPV (decrease pulmonary congestion)
- art line
- CVP +/- or PA cath
- TEE
- regional = usually helpful bc decreases SVR, but can also be unpredictable/hard to control
hypertrophic cardiomyopathy: definition & pathophysiology
def = LV hypertrophy in absence of other cardiac disease
- myocardial hypertrophy
- LV outflow tract obstruction (assymetrical hypertrophy, anterior movement of the MV & MR)
- diastolic dysfunction
- myocardial ischemia
- dysrhythmias
hypertrophic cardiomyopathy: what increases outflow obstruction?
- increased myocardial contractility (B stim, dig)
- decreased preload (hypovolemia, vasodilators, tachycardia, PPV)
- decreased afterload (hypotension, vasodilators)
hypertrophic cardiomyopathy: what decreases outflow obstruction?
- decreased myocardial contractility (BB, volatiles, CCB)
- increased preload (hypervolemia, bradycardia)
- increased afterload (HTN, a stim)
hypertrophic cardiomyopathy: anesthetic management goals
minimized LV outflow tract obstruction
- low contractility
- high preload
- high afterload
hypertrophic cardiomyopathy: induction
- avoid sudden decreases in SVR (will compensate w/ increased HR/contractility)
- modest myocardial depression is good
hypertrophic cardiomyopathy: anesthetic management (maintenance)
- keep full, low inotropy (volatile good)
- be careful w/ PPV (decreases preload) - try high rr, low Tv, avoid PEEP
- consider TEE
- tx hypotension w/ alpha-agonist (avoid beta stim = inotropy)
- promptly replace fluid/blood loss
- no vasodilators if hypertensive
dilated cardiomyopathy: definition
LV or biventricular dilation
systolic dysfunction
normal LV wall thickness
dilated cardiomyopathy: anesthetic management
same as HF (since it is a cause of HF)
- normal/high HR
- normal/high preload
- low/normal afterload
- increase contractility
cor pulmonale: definition
- RV enlargement (hypertrophy and/or dilation) that may progress to RVF
- caused by dz that induces pulmonary HTN
preoperative management of cor pulmonale
- eliminate & control acute & chronic pulmonary infections
- reverse bronchospasm
- improve clearance of airway secretions
- expand collapsed or poorly ventilated alveoli
- hydration
- correct electrolyte imbalances
intraoperative management of cor pulmonale
- avoid bronchospasm (make sure they’re deep before DL)
- use a volatile (good bronchodilator); avoid large doses of opioids (vent depression post-op)
- avoid histamine releasers (sux, some NDNMR)
- PPV
effects of SNS activation in HF
- arteriolar constriction = maintains BP despite CO decrease, redirects BF to coronary & cerebral systems
- venous constriction = increases preload, helps maintain CO (Frank)
- RAAS activation 2/2 decrease in RBF –> increased blood volume & ultimately CO
- HR increases
clinical features of HF
- dyspnea (orthopnea, PND)
- fatigue
- weakness at rest
- tachycardia
- oliguria
- edema
- afib (2/2 dilation)
- tachypnea
- lung rales
- S3 gallop
- hypotension
- JVD
pathogenesis of HF
- decreased contractility
- ventricle dilated to increase contractility from stretched muscle fibers
- increase ventricular radius = increased cardiac work
- increased O2 consumption & increased cardiac work
- CO falls
- increased SNS outflow to increase HR/SVR
- SV falls
