67. Heart Failure Flashcards
Heart failure: 3 components involved
structural or functional abnormalities of CV
elevated Intracardiac pressures or depressed CO
clinically recognizatble s or s due to elevated IC pressures or depressed output
HF with reduced EF defn
<40%
HF midrange Ef
40-50%
HF preserved EF
> 50%
Risk factors for HF
age
obesity
htn
dm
tobacco smoking
dld
low ses
ischemic heart disease
CO equation
CO = heart rate x edv x ef
which really means chrontropy (speed) x lusitropy (rate of myocardial relaxation) x inotrophy (squeeze amount)
What does the Frank Starling mechanism do?
talk about relationship between stroke volume (squeeze amount each beat) and EDV (heart ability to relax to fill)
Frank Starling: in an ideal scenario how do sv and edv work together?
EDV increasing leads to increasing SV because of the stretch, allows for greater contraction
ie preload under ideal conditions
Repeated exposures to increased LVEDV (and resultant LVEDP) cause fibrosis and myocardial hypertrophy that ultimately lead to a what kind of ventricle?
stiff
noncompliant
ultimately diastolic dysfunction
What other organ systems and processes can influence HF - ie decreased cardiac output and incr filling pressures?
- Vascular: incr systemic artery tone, loss of laminar flow and impaired ventricular vascular coupling
Microvascular and coronary dysfunction, ischemia - Volume distribution or retension can lead to reduced capacitance of venous reservoirs
- Neurochem/autonomic activity at the brain
- Endocrine responses to stress
- Pulmonary: resp failure, decreased endc organ o2 delivery, impaired RV/PA coupling
- Renal dysfunction and diuretic R
- Coagulaopthy - abnormal RBC mass
What ventricular changes may ensue specifically from diastolic dysfunction? (specific to other heart functions)
decreased myocardial oxygen reserve, abnormalities in nitric oxide signaling, decreased aortic and pulmonary artery compliance, decreased ventricular volume, right ventricular dysfunction, and worsening interventricular and ventricular-circulatory coupling, resulting in depressed tolerance of increased preload and afterload
How does the heart compensate for its diastolic dysfunction (change in EDV) - effects what other CO parameter?
HR - to a degree
hence at certain point even further tachy is detrimental because the heart cannot go any further
Natriuretic peptides are upregulate in heart failure - why?
due to changes in FS curve so that they induce natriuresis and diuresis, vasodilation and antifibrotic effects to remodel to heart
How do the major classes of therapies for Acute HF work?
either by moving the Starling curve left- ward with diuretics or venodilators (decr preload), moving the curve upward to a higher level of efficiency for a given EDV with inotropes or arterial vasodilators (SV), or both
Simple but useful hemodynamic classifcation of hF in the ED - is it a c__ problem or a v___ problem
cardiac (ie, primary pump failure predominates) and vascular (ie, acutely increased preload or afterload predominates) phenotypes of AHF
Central congestion defn Ac HF
true vol overload with excessive intake effecting vena cava/great arteries or proximal organs vs retension - typically via poor pump)
What is one of the largest critical venous reservoirs?
splanchnic circulation
What 3 endocrine/systems may cause the splanchnic circulation to dilate/contract?
central circulation baroreceptors
sympathetic tone
Renin angiotensin aldosterone system
What, under normal circumstances, can act like a buffer to maintain central volume in the splanchnic circulation?
hepatic veins
Hepatic veins, under normal circumstances, can act like a buffer to maintain central volume in the splanchnic circulation - how does this change in HF?
neurohormonal mediators are chronically activated, leading to basal splancnic vasoconstriction and a reduction in the buffer capacity – so fluid shifts can happen more acutely with a “lesser” stress than normal
Afterload: what is this?
pressure at which ventricle must contract to eject blood
ie aortic and pulmonary a pressure for LV and RV respectively
Afterload: What ventricle is more sn to presure and volume tolerant?
RV
