Heart Failure Flashcards
where can you best auscultate murmurs
mid clavicular line 5th ICS at apex
cardiac output
- CO = stroke volume x HR
- 4-6L/min
heart failure
- inadequate cardiac output
- myocardium unable to pump enough blood to meet O2 requirements
- impaired cardiac pumping/filling
mortality rate of HF
- 33% in first year of dx
preload
- volume of blood in ventricles at end of diastole (filling)
afterload
- resistance left ventricle must overcome to circulate blood
- increased after load = increased cardiac workload
what causes increased preload
- hypervolemia
- regurgitation of cardiac valve
- HF
what causes increased after load
- HTN
- vasoconstriction
causes of HF (8)
- HTN
- congenital heart defects
- structural defects
- arrhythmia, previous MI, anemia, pulmonary disease, liver failure, renal failure, hypervolemia
- ineffective endocarditis, cardiomyopathies
- stress
- obesity
- smoking
what is backflow
- 100cc comes in RA then RV
- compromised heart only giving half a squeeze pumping out 70cc
- have 30cc remaining in RV
- but another 100cc is coming into RA then RV
- heart will try to grow and stretch to increase space for fluid resulting in backflow and symptoms
how can previous MI lead to HF
- necrotic/scar tissue = improper electrical current and contraction
4 compensatory mechanisms
1) frank starlings law (dilation)
2) ventricular hypertrophy
3) sympathetic nervous system activation
4) neurohormonal response
frank starlings law
- ventricles stretch to accommodate contraction issues
- after time elasticity is lost = improper recoil and boggy heart
ventricular hypertrophy
- increasing size/strength of heart muscle to increase force of contraction
- over time muscle gets too big = smaller ventricle space = decreased CO
sympathetic nervous system
- decreased CO = tells heart to pump harder and faster
- fight or flight response (E and NE) = increasing HR = increased O2 demands
- lead to ventricular hypertrophy
neurohormonal response
- decreased CO = decreased O2 to kidney = renin-angiotensin-aldosterone system
- activation of angiotensin II = vasoconstriction increasing BP
- aldosterone = retain Na = retain H2O = increased volume
decompensated HF
- when compensatory mechanisms are no longer working/useful
ventricular remodelling
- when heart starts to reshape to accommodate extra fluid and ineffective pumping
right sided HF
- blood starts backing up out of RA into vena cavas
- systemic S&S
right sided HF symptoms
- dependent edema
- bilateral pitting edema
- ascites (edema around abdomen)
- weight gain
- distended jugular vein
- fatigue
- enlarged liver & spleen
- anorexia/GI complaints
symptoms of ascites
- N&V
- GI distress
- decrease appetite
- all from pressure on abdomen
other term for rt sided HF
cor pulmonale
jugular venous pressure (JVP)
- to assess rt sided HF
- pt at 45 degrees
- looking for pulsation in internal jugular and measure up
- <2 is ok
- > 3 = rt sided HF
left sided HF
- blood backs up into Lt and Rt pulmonary veins
- respiratory symptoms
left sided HF symptoms (11)
- pulmonary congestion
- tripod
- confusion/altered LOC (less blood/O2 to brain)
- exertion dyspnea
- cyanosis
- tachycardia (brain telling heart not enough blood so pump faster/harder)
- orthopnea
- paroxysmal nocturnal dyspnea
- chest discomfort (less blood to coronary arteries)
- nocturia
- increased pulmonary capillary wedge pressure
cardinal sign of left sided HF
- orthopnea
- difficulty breathing why lying down
symptoms of pulmonary congestion
- bilateral crackles
- bilateral wheezes
- cough
- blood-tinged sputum
- tachypnea
ejection fraction
- % of blood pumped out of LV during contraction
- amount of blood pumped out/amount of blood in chamber
- decreased EF = decreased CO
ejection fraction numbers
- 50-70% = normal (anything less = compromised LV)
- 41-49% = borderline
- <40% = reduced
diagnostic tests for HF
- S&S + pt hx
- CXR (to see boggy heart)
- Echo
- EF
- BNP
- ABGs (blood saturation with O2)
- liver and kidney function tests
echocardiogram
- measures myocardial thickness
- view BF to determine backflow
- view valves to see if they are shutting properly
valves and ventricular remodelling
- valves can’t grow and stretch so when heart does they pull apart and then cant close properly
BNP
- b type peptide
- hormone released when heart is working really hard
- quick to check if Lt HF or lung issue
BNP values
- <100ng/L = HF improbable
- 100-500ng/L = HF probable
- > 500ng/L = HF very probable
liver function test
- Rt sided because of backflow
- de O2 blood sitting in liver = atrophy and necrotic tissue
- prevents liver from excreting toxins
- albumin made in liver for oncotic pressure, low albumin = fluid seeping out into interstitial spaces
kidney function test
- Lt sided because of lack of forward flow
- kidneys don’t do well without blood/O2
- worried about kidney failure
- BUN, creatinine
complications of HF
- pleural effusion
- dysrhythmias
- LV thrombus
- hepatomegaly
- renal failure (decreased BF)
pleural effusion complication
- fluis in visceral pleura
- blood backs up and moves into lower pressure system
- fluid surrounding lungs preventing full expansion
- increased pressure in lungs
dysrhythmia complication
- heart stretches = altered electrical conduction
- a fib is common
LV thrombus
- clot in LV
- from stagnant blood
- can pump out and get stuck = stroke, PE, MI
hepatomegaly
- Rt HF
- non-efficient drainage of BF
- accumulation of de O2 blood
- atrophy, necrosis of liver
pharmacological management of HF (10)
- ACE inhibitors
- ARBs
- angiotensin-receptor neprilysin inhibitors
- beta blockers
- diuretics
- opioid
- vasodilators
- inotropes
- antidysrhythmic agents
- anticoagulants
ACE inhibitors
- lower BP
- capoten, vasotec, altace, zestril
ARBs
- lower BP, dont effect HR
- atacand, cozaar, diovan
angiotensin receptor neprilysin inhibitors
- lower BP, dont affect HR
- sacubitil/valsartan
beta blockers
- decrease BP, HR, CO
- metoprolol, coreg
diuretics
- to decrease BV
- aldosterone antagonist (K sparing) - aldactone
- loop diuretic (K wasting) - furosemide
- thiazide (K wasting) - hydrochlorothiazide
opioids
- vasodilation
- helps with oxygenation
- morphine
vasodilators
- decrease vascular resistance
- nitrates, nitroprusside
inotropes
- increase contractility of the heart without increasing O2 demands
- cardiac glycoside - digoxin
- beta adrenergic agonist - dopamine
- phosphodiesterase inhibitors - milrione
goals for treating HF (8)
- improve myocardial function
- reduce circulating BV
- reduce venous return
- reduce afterload
- reduce myocardium demands
- improve cardiac function
- improve gas exchange and oxygenation
- decrease anxiety
digoxin
- cardiac glycoside that increases contractility
- apical pulse for 60 secs as it decreases HR
- 1.8-2.3 therapeutic range
- risk of toxicity increases with hypokalemia
- digoxin binds to K+ so if there is none then digoxin is free floating
digoxin toxicity symptoms
- see yellow
- flu like symptoms
- decreased HR
- blurred vision
nursing management of HF
- hemodynamic monitoring
- daily weights
- ins/outs
- diet (Na restrictive, H2O follows Na)
- lab values
- respiratory, cardio, integument, abdominal, neurological assessments
daily weights
- morning before breakfast
- >2kg over 2-5 days means peripheral edema and they are retaining too much fluid
chronic HF
- chronic progressive state
- medically managed at home
- Telehealth home monitor
- at home monitoring
biventricular pacing
- boggy heart and electric conduction affected
- pacemaker implanted to send current to make heart contract
implantable cardio-defibrillators
implanted defibrillator
intra-aortic balloon pump (IABP)
- balloon inserted in aorta
- balloon inflates when heart is at rest to increase pressure and fill ventricle more
- push blood into coronary arteries
- balloon deflates on contraction
- can increase CO by 40%
ventricular assistive device (VADs)
- LVAD inserted in LV
- external pump takes blood from LV and forces it into aorta
- bypasses LV
artificial heart
- cut off ventricles and put in 2 artificial pumps that take over for ventricles
