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38 Cards in this Set
- Front
- Back
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heart failure defn
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syndrome resulting from inability of heart to pump sufficient blood for body's peripheral requirements in O2 and cell nutrients, at rest and effort
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epidemiology of CHF
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1% over 65
4% over 70 only CVD increasing in prevalence and incidence causes 9% of all deaths in canada cost for CHF 2X of all cancers disease mostly of old age |
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prognosis
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5 year mortality - 50%
hospitalized 1 yr mortality - mild to moderate - 10-20% severe symptoms 40-60%ca |
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causes of readmissions
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diet non-compliance- salt
tx- non-compliance inappropriate tx- NSAIDS- Na retention and fluid retention |
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why increase in numbers with CHF
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aging population 80s 90s
better survival with CAD and HTN paradox HF patietns becoming older, frailer |
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evolution of CHF clinical stages
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normal no symptoms, normal LV funcitions
asymtomatic LV dysfunction- no symptoms dilated CM compensated heart failure - symptoms only on exertion decompensate HF- symptoms at rest or with minimal activity Refractory CHF: end stageq |
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Causes of HF
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IPVVHT
ischemia - (EF lowers) post partum: best prognosis Viral: Dilate CM valve problems: AS (can b fixed) HTN: toxins |
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heart failure pathophysiology
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myocardial injury for whatever injury:
Low ejection fraction, weak LV several system activated RAAS (most imp) CNS system endothelium activation of all these causes Peripheral vasoconstriction: causes hemodynamic alteration and worsening LV dysfunction. Ang and aldosterone can cause direct myocardial toxicity leading to worsening LV function which again activates these systems leading to a vicious circle |
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classification of CHF
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systolic: doesnt squeeze well
diastolic: does not relax well - (HTN, HTCM) low cardiac output: HA not working well High output cardiac failure: hyperthyroid, anemia left sided: MI or AS on LV- can lead to RHF RHF: severe pulmonary HTN, pulmonary stenosis acute: ruptured papilary muscle- mitral valve blown wide open chronic: |
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difficulty in diagnosing CHF
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wide range of symptoms
overlap with COPD, obesity, nephrotic syndrome, drug induced edema, cirrhosis and sleep apnea |
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symptoms of HF
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compensated - no symptoms unless exert themselves
ucompensated: symptoms fatigue dyspnea orthopnea- pillows PND- fluid redistribution after a few hours ankle edema weight gain- weigh every day at the same day patients with very low EF may not have any symptoms |
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NYHA classifications
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Class I- asymptomatic
CII: symptoms with moderate exertion CIII:symptoms with minimal exertion CIV: symptoms at rest |
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asymptomatic LV dysfunction causes
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LVH
diabetes HTN CAD |
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evaluation of the patient
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HX and physical
CXR EKG- blood work BNP Echo - single most useful dx text cardiac cath- if risk for CAD |
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physical exam signs
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elevated JVP
crackles, rales- not present with low EF (normal capillary pressure - 12) S3- almost pathgnomonic for HF. can be physiological for young until ascites lower extremity edema |
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CXR findings
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vascular redistribution- can be seen in normal patietns after lying down
cardiomegaly kerly b lines bronchial cuffing cephalization of vessels |
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ejection fraction
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percent of blood pumped out during each beat
normal heart 50-70% HF : <40% |
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EF severity
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EF>50 normal
35-49 mild 25-34 moderate <30 severe |
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BNP
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BNP released in response to heart stretch
from ventricular myocardium due to vetricular overload in PE; get strain on Right side of heart - some elevation very high only in CHF |
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diagnostic algorithm
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initial evaluation
BNP proper management |
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therapy approach
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consider etiology- ex valvular disease- fix valve
identify triggers exclude ischemia general measures symptomatic tx prognostic tx |
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non pharm management
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physical activity
need exercise stress test low salt test- salt retains water-increases peripheral edema weight 1.5-2 L fluid restrictions quit alcohol - can cause cardiac dysfunction in genetically suspceptible |
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main drugs used in CHF
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ACE/ARB
beta blockers diuretics digoxin |
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ACE inhibition
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works as antiischemic- stimulate endothelial NO production- vasodilator
reduce myocardial o2 consumption prevent Chol buildup reduces PVR and mean BP "prils" |
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contraindications for ACE
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angioedema , renal failure
bilateral renal artery stenosis pregnancy- placenta insufficiency hyperkalemia >5.5 severe hypotension |
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beta blockers
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decrease in neurohormonal activation- catecholamines are high in HF
make sure patient is euvolemic may feel worse before start feeling better metoprolol |
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contraindications for b-blockers
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true asthma
advanced Heart block |
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aldosterone blocks
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for CLass III or IV HF
can cause hyperkalemia can dev gynecomastia - spironolactone |
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digoxin
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does not change survival
decrease symptoms and hospitalization |
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nitrates + hydralizine
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in people that cant tolerate ACE
use combo of N and H also benefit in AAmericans |
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tx of HF
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anyone with EF<40 ACE an BB
Class II and III- spironolactone continues to be symptomatic digoxin |
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additional tx options
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Devices:
defibs: prevents SCD biventricular pacemakers: surgery: revascularizations valvular reconstruction ventricular support: LVAD/ iantra aortic balloon pump transplatnt |
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ICD
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like a pacemakers- puts a lead into venous circulation RV- if patient develops VF or VT- that device tx
indications: low EF dilated CM Class III and IV with low EF <35% |
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SCD
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caused by electrical problems
SCD= causes 450,000 deaths in US HF patients 6-9X more likely to dev SCD |
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biventricular pacing
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like an ICD- lead into RA and third lead goes into coronary sinus.
In LV dysfunction- heart does not contract at same time- attempts to synchronize improve EF and survivial and symptoms use in moderate to severe symptoms EF<30 evidence of conduction delay |
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LVAD
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left ventricle assist device
takes over function of damaged ventricle bridge to transplant |
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VAD candidates
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decompensated end stage CHF
subacute rapidly deteriorating CHF post surgical shock acute myocarditis post AMI cardiogenic shock |
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Heart transplant
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160 in canada
not enough donors exclusion: PHTN, DM and end organ damage, renal, infection, techinical issues, psychosocial malignancy |
