Congestive Heart Failure Flashcards
1
Q
congestive heart failure (CHF)
A
- heart not pumping blood adequately to lungs, chambers or into aorta and body
- results in cardiac, pulmonary and systemic congestion (blood pools)
- end point of cardiovascular diseases
- syndrome (b/c you can identify it based on its mnfts)
- complex & leads to systemic effects and multi-organ failure
- example of cardiogenic shock
- results in progressively dec Fx
2
Q
etiology
A
- CAD (atherosclerosis)
- uncontrolled HTN
- cardiomyopathy
- valvular disease
3
Q
risk factors for HF (most important targets for prevention of CHF)
A
- HTN
- ischemic heart disease
- DM Type 2 & metabolic syndrome
- hyperlipidemia
- smoking
- diff risk factors than CVD, but some overlap
4
Q
in a healthy person, the workload of the heart can inc…
A
5-fold:
- “cardiac reserve”
- used when external factors create an inc demand for blood and O2 (such as exercise)
- someone w/ CHF does not have same adaptability (cardiac reserve already used up at rest –> inc metabolic demand –> heart not able to cope)
5
Q
L and R sided HF
A
- often times L vent fails –> dec CO to systemic circuit
- results in congestion within pulm circuit
- now R vent must work harder to pump blood to lungs and hypertrophy occurs within R vent myocardium
- pumping against resistance results in residual vol within R vent, backing up into R atrium and eventually into systemic circuit (edema)
- R sided failure usually follows L sided failure if L sided failure occurs first (R sided failure does not cause L sided failure)
6
Q
L sided HF pathophysiology
A
- L sided failure –> insufficent CO –> residual vol in L vent –> L atrium pumps harder to empty –> not enough space for L atrium to empty = residual vol in L atrium –> L atrium unable to receive full pulm return –> inc CHP in pulm circuit
- -> pulm congestion & pulm edema in IS space and then into alveoli –> inc workload of R vent –> hypertrophy of R vent, but still cannot empty fully –> R sided failure
- failure to eject blood into systemic circuit = pooling in pulm circuit
7
Q
L sided HF manifests as…
A
- pulm congestion
- pulm edema
8
Q
R sided HF pathophysiology
A
- R sided HF –> failure to eject blood into pulm circuit = pooling in systemic circuit
9
Q
R sided HF manifests as…
A
- peripheral edema
- abd organ distention
10
Q
compensation mechanisms for CHF
A
- V dilation (Frank-Starling Law)
- SNS
- RAAS
- natriuretic peptides (ANP & BNP)
- endothelins
- hypertrophy & remodelling
- heart failing but body accomodating so pt clinically asymptomatic at first
- compensatory mechanisms work for a while but will eventually fail
11
Q
V dilation (Frank-Starling Law) compensation
A
- the more stretched the heart is, the more blood is filled, which inc venous return = inc EDV = inc preload = inc CO
- if heart persistently stretched, it will lose contractility –> dec CO
- w/ dec CO, there is an inc in O2 requirement for the heart, initiating SNS
12
Q
SNS compensation
A
- response to dec CO
- aims to inc CO by causing tachycardia, systemic vasoconstriction, inc contractility
- CO inc but inc workload w/ ATP & O2 demand –> advances HF
13
Q
RAAS compensation
A
- triggered by dec in CO and renal perf –> angiotensin II formed
- angiotensin II –> vasoconstriction –> inc TPR –> inc BP –> inc CO
- releases aldosterone & ADH –> fluid retention –> inc blood vol –> inc vasoconstriction –> inc CO
14
Q
ANP & BNP compensation
A
- causes potent diuresis & natriuresis (secrete water and sodium in excess) –> dec blood vol –> dec workload of heart –> dec BP
- affects vascular SM –> vasodilation
- does opposite action of SNS and RAAS
15
Q
endothelins compensation
A
- vasoconstrictors released by epithelial and cardiac muscle cells and released in vessel walls –> inc BP
- release GFs that ause cardiac hypertrophy –> larger muscles require more resources –> if O2 demand not met, they die
