Heart failure Flashcards
Top offenders cardio disease
- CAD
- HTN
HF is a secondary disease
HF, any change in demand can =
some reasons…
decompensation
: dysrhthmias, ischemia, fluid imbalance, not adhering to Na restrict, not compliant with meds
Systolic HF
- EF < 40-45% (tells you where the HF is coming from)
- strength of vent contraction is attenuated (reduce force) (inotropy)
- Vent end-diastole vol and pressures increase
- cardiomyocytes become elongated with little or no change in diameter
- increase LV vol, and no change in LV thickness
- Eccentric remodeling, LV mass is increased but no increased in wall thickness
Diastolic HF
- Preserved EF, normal >40%
- concentric (muscle shorten) remodeling and hypertrophy of LV
- increased wall thickness and/or left vent
- increased ration of myocardial mass to cavity vol
- cardiomyocytes increase in diameter but not length
- impared rate and extent of LV filling
- stiff, cant relax
- increased diastolic LV, LA and pulm venous pressures
New york heart association classification
- disease with no limitations (asymptomatic)
- slight limit with physical activity. ok at rest (with mod exertion)
- symptoms with minimal exertion. ok still at rest
- Symptoms at rest
Patho of systolic HF
- decreased LV contractility
- increases preload and increased afterload
- = pulmonary and systemic edema
- thickened alveolar/cap membrane
- decreased arterial and O2 content and saturation
Demand:
- increased HR, WOB, stress
Patho diastolic HF
- inability of the heart to relax
- decreased vent filling
- = flash pulm edema
- low CO and increased afterload
-increased afterload, again increases pulm edema
stenosis
- narrowing of the valve opening
- prevents adequate outflow of blood
- thickening/calcify of leaflets and limits the EF
- aortic common
*aortic effects: dyspnea, exercise intolerance, syncopy, angina, HF
Regurgitation
- cant close and the end of systole
- blood backflows
- mitral* regurg common and associated with HF d/t volume and pressure changes from the chambers
- LV hypertrophies to make room and causes regurg
- sometimes not the cause of HF but the result
- mitral effects: weak and fatigue, dyspnea, palpatations, LV failure
Pathophysiology path of HF
- Heart fails –> decreased CO and BP –> Barroreceptors activated from decreased pressure –> to vasomotor regulatory centers in the medulla –> activate SNS –> release catecholimines (Epi/Norepi) –> causes vasoconstrict and increased HR –> this causes increased demand and consumption and the heart works harder to compensate and the compensatory mechanisms keep trying to help and causes cardiac hypertrophy = increased myocardial O2 consumption
how does HF contribute to A.Fib
the increased preload causes atrial dilation and stretch and disrupts the conduction system
Chronic HF PTs also have : myocardial ischemia, electrolyte imbalance r/t diuretics, chronic SNS stimulation which can all contribute to A.Fib
NSAIDs can cause
fluid retention and are nephrotoxic
Labs for HF
**BNP- secreted from Left vent in response to over-stretching caused by excess preload
confirms HF
- Trop is for ACS but can also be elevated in acute HF. Too much preload
- Hgb- possible decrease d/t chronic illness suppresses bone marrow production of RBC
- BUN and Cr: can be elevated from decreased perfusion (pre-renal). Or chronic even higher elevation in Cr suggesting intrarenal
- Glucose- high. could be from stress response or possible glucose intolerance
- K+, Mg, Na - can be low if PT on diuretics
What is TEE?***
what other test is done
Trans-thoracic Echo Gold standard
reports:
- EF
- < 40% mod, < 25% severe LV dysfunction - LV diameter
- LV mass
- Valve structure
- coronary angio- to determine if ischemia is caused by HF
- 12 lead ECG
- CT angio
LV diameter
Boot
- dilation
- increases risk for emboli, dysrhythmia, and mitral regurg
- need anticoags
