Heart Failure Flashcards
T or F: Heart failure is an event.
FALSE
heart failure
inability of the myocardium to pump enough blood to meet the needs of the body
Heart failure involves impaired
a) pumping
b) filling
c) both
c) both
Common causes of HF (many)
CAD/MI
hypertension
valvular disease - rheumatic fever
R sided pulmonary hypertension
PE
infiltrative disorders
pericardial disease (restrictive)
inflammatory (myocarditis)
cardiomyopathy
dysrhythmias
medication non-compliance
Top 3 causes of HF
1) CAD/MI
2) hypertension
3) valvular disease
Effects of valves not closing all the way
NOT going to have a CLOSED SYSTEM (isovolumetric)
leakage
Effects of valve stenosis
have to pump harder
Impacts on the cardio system
affects preload, filling, afterload
decreased filling time
decreased time in diastole
increased HR
increased BP
Pathophysiology - 3 major systems
1) SNS
-bad
2) RAAS
-bad
3) Natriuretic Peptide system
-good
SNS chemicals
catecholamines
E and NE
SNS effects
VASOCONSTRICTION
-increased HR
-decreased filling time
-increased BP
-increased afterload
-increased oxygen needs and demand on heart
Receptors that activate the CNS
baroreceptors
sense low BP
Med that targets SNS
beta-blockers
RAAS chemicals
angiotensin II
aldosterone
RAAS effects
VASOCONSTRICTION
-increased BP
-increased afterload
Na+/water retention
-increased BP
Meds that target RAAS
ACE inhibitors
ARBs
diuretics
Mineralocorticoid Receptor Antagonist
What secretes ADH?
posterior pituitary
stimulates by low perfusion
What does ADH do?
acts on DISTAL tubules to increased reabsorption of water
Frank Starling Mechanism
heart’s SV increases in response to an increase in the volume of blood in the ventricles at the end of diastole
eventually overstretch will result in ineffective contaction
Chemicals of the Natriuretic Peptide System
ANP
BNP
ANP released from the…
atria
BNP released from the…
ventricles
In heart failure, levels of ANP and BNP are:
a) elevated
b) lowered
a) elevated
What increases levels of ANP and BNP?
STRETCH
Effects of ANP and BNP
diuretic
natriuretic
hypotensive
inhibits RAAS and SNS
Main compensation mechanisms (4)
1) SNS
2) neural-hormone/RAAS
3) dilation of ventricle
-Frank-Starling
4) ventricular hypertrophy
Acute HF
sudden onset
NO compensatory mechanisms
over days or hours
e.g. MI
Chronic HF
ongoing process
months to years
progressive worsening of ventricular function
chronic neuro-hormonal activation that results in ventricular remodelling
Left-sided HF
left ventricular dysfunction
disturbance of the contractile function of the left ventricle, resulting in a low cardiac output state
Right-sided HF
ineffective right ventricular contractile function
backwards flow
Most common HF:
a) left
b) right
a) left
What is right-sided HF most often a result of?
left-sided HF
Systolic HF
PUMPING problem
decreased contractility
Diastolic HF
FILLING problem
Ejection fraction is determined by:
a) % of blood being pumped out
b) volume of blood being pumped out
a) % of blood being pumped out
EF can look normal because it’s not showing volume
EF may be normal in:
a) systolic HF
b) diastolic HF
b) diastolic HF
less volume, but normal %
How is EF calculated?
echo (cardiac ultrasound)
left ventricle
Clinical heart failure syndromes (3)
1) HFrEF
2) HFpEF
3) HFpEF
Complications of HF (many)
pleural effusions
dysrhythmias
left ventricle thrombus
hepatomegaly
renal failure (pre-renal)
Diagnosis of HF
history and physical exam
chest x-ray
ECG
BNP levels
echo
may do imaging, catheterization, stress testing etc.
Big consideration with assessment
what has CHANGED
Signs of worsening HF (many)
hypotension
worsening renal function
altered mentation
dyspnea at REST**
worsening congestion
weight gain*
electrolyte disturbance
defib - repeating firings
afib
Conditions associated with worsening HF (many)
pneumonia
PE
diabetic ketoacidosis
ACS
Abnormal heart sounds associated with HF
murmur
S3 and S4
-resistance to filling
Grade I HF
normal
EF: > 50%
Grade II HF
mild
EF: 41 - 49%
Grade III HF
moderate
EF: 30 - 41%
Grade IV HF
severe
EF: < 30%
Lab work (many)
BNP
CBC
-anemia
-polycythemia
-leukocytosis
Electrolytes
Renal function
Liver function
-enzymes will be elevated
Troponin, CK
Glucose
Thyroid
Blood gases
Consideration for hypertension management
don’t want it to be too high OR too low
need to fine tune meds
Considerations for nutrition
decreased appetite and nausea
small, frequent meals
sodium and fluid restriction
Sodium restriction values
<2 to 3 g/day
Severe: 1.5 g/day
Fluid restriction values
1.5 - 2L/day
Concerning weight gain
2 - 3 lbs in a day
5 lbs in a week
Considerations for activity
cluster care
allows adequate rest
restrict during periods of exacerbation
according to tolerance
Principles of pharmacologic therapy
start low, go slow
1 med at a time
reassess
patient-specific parameters*
Medication therapy main goals (2)
1) HR < 70 bpm
2) restore normal sinus rhythm
Med that you may start first
ACE inhibitor or ARB
Meds for REDUCED EF HF
ACE inhibitor/ARB
Beta-blocker
MRA
Meds for PRESERVED EF HF
Beta-blocker/Ca+ channel blocker
Nitrates
Diuretics
“New” meds
Neprilysin inhibitor
ARB + neprilysin
Which drug is neprilysin contraindicated with?
ACE inhibotor
What does Ivabradine (Lancora) act on?
If channel in the SA node
does NOT lower BP
in conjunction with other meds
SGLT2 Inhibitor MOA
reduces reabsorption of
glucose from tubular lumen
more glucose excreted
pulls water with it (diuretic)
Digoxin MOA
acts by INHIBITING the Na-K-ATPase pump
decreases HR
increases contractility
Consideration for Digoxin
last resort
bad side effects like bradycardia
usually only used for patients with high HRs
Venous Thromboembolism Prophylaxis med
heparin
Criteria for taking heparin
afib
EF: <35%
Side effects of metal valves
blood clots
have to be on anticoagulants for life
Side effects of tissue valves
no blood clots
but don’t last as long
Most patients will have a change in symptoms at least __ to ___ days before ER visit
2 to 3 days
What medication is typically given at the hospital for HF exacerbations?
diuretics
Most common symptoms during palliation (3)
1) dyspnea
2) pain
3) fatigue