Heart Failure Flashcards
Heart failure definition
when the heart can’t meet the body’s O2 demands
- inability to relax enough to receive SV
- inability to deliver SV
LV is the no 1 cause. LV is also the #1 cause of RVHF
Systolic most common in men. Diastolic most common in women
strongest indicator for perioperative cardiac morbidity and mortality
Acute HF
from structural event like MI that causes a valvular dysfunction or a new RWMA
Poorly tolerated bc no time for compensation
manifested by high ventricular filling pressures, low CO, HTN/HypTN
Use diuretics, vasodilators, inotropic drugs, mechanical assist devices
Chronic HF
remodeling of the heart and RAAS activation
BP is maintained and signs of venous congestion are present
LHF
LVED is elevated and leads to pulmonary congestion
S3 gallop hypotension tachycardia cool/pale extremities anorexia/weight loss
RHF
associated with systemic congestion, edema, hepatomegaly
JVD distensible by pressing on the liver - hepatojugular reflex
ascites
weight gain
peripheral edema
High output failure
when the heart can’t keep up with massively increased metabolic demands (anemia, pregnancy, sepsis)
Low output CO
unable to respond to exercise or stress
commonly encountered when trying to come off CPB in pts with severe systolic HF
Starling curve
SV increases as wall tension is increased by contracting muscle
Venous capacitance vessels constrict to increase preload to contribute to this increased wall tension
When contractility becomes impaired then SV is reduced for any given volume put into the ventricle
HF path
initial cause of HF causes an increase in preload to maintain CO but eventually exercise intolerance dvlps
In late stages, CO is sufficient at rest but pt can’t exercise
Neurohormonal reflexes activated to try to maintain CO and SVR
the RAAS system and ADH starts going overtime to increase tone by increasing fluid volume and resting sympathetic vascular tone
Blood is shifted from the peripheral to central circulation and arteriolar constriction redistributes blood from the kidneys, splanchnic circulation, skeletal muscles, skin
The kidneys’ perceive this decrease in BP and pump out more renin, worsening the cycle
As the heart fails in systolic HF you expect a high resting HR to maintain CO
Heart as an endocrine organ
tries to combat cycle
ANP is released in response to increased stretch of the atria.
BNP is released by the ventricles
This causes diuresis, natriuresis, vasodilation, anti-inflammatory effects , inhibition of the RAAS and SNS, inhibits remodeling
body eventually does not respond to this
CVP has to rise to maintain preload and CO and eventually any increase in preload does not result in increased CO and the cycle leads to decompensation and death
DX HF
ECHO
potential cause - such as valve disorders
concurrent pericardial effusions
establish baselines
HF classification
AHA
A - high risk for HF w/o structure disease or symptoms
B- structural disease w/o s/s
C - Structural disease with HF symptoms
D - Refractory HF requiring specialized interventions
HF classification
NYHA
I - no limitation of physical activity; ordinary activity does not cause HF symptoms
II - slight limitations of physical activity; comfortable at rest, but ordinary physical activity results in HF symptoms
III - marked limitations of physical activity; comfortable at rest, but less than ordinary activity causes HF symptoms
IV 0 unable to carry on any physical activity w/o HF symptoms
Managing systolic HF
BB - combat SNS activation
diuretics - relieve circulatory congestion
digoxin
vasodilators - work well in African Americans (hydralazine, NTG)
statins - anti-inflammatory effects
ACEI - RAAS inhibition. beneficial at any stage of HF
aldosterone antagonists
Managing diastolic HF
lifestyle modifications
low dose diuretics
statins
Definitive treatment for HF
transplant
Total artificial heart
implanted in the chest
pulsatile flow
two pumps that simulate ventricles
bridge to treatment or destination
