congestive heart failure Flashcards

1
Q

CHF is the end point of

A

cardiovascular diseases

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2
Q

CHF is complex and leads to

A

multi-organ failure

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3
Q

CHF is an example of what shock

A

cardiogenic- shock induced by an alternation in cardiac function

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4
Q

heart is not pumping adequately to lungs, throughout chambers, into aorta and body, this results in:

A

cardiac (within heart chambers), pulmonary, and systemic congestion
-blood POOLS, still flows but not adequately

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5
Q

etiology of CHF

A
  • CAD (atherosclerosis)
  • cardiomyopathy
  • uncontrolled HTN
  • valvular disease
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6
Q

risk factors for HF (A LOT)

A
  • htn
  • ischemic heart disease
  • type 2 diabetes and metabolic syndrome
  • hyperlipidemia
  • smoking
  • obesity
  • older age
  • sex
  • ethnicity
  • physical inactivity
  • excessive ETOH, salt
  • cardiotoxic agents
  • family hx/genetics
  • low EF, impaired diastolic
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7
Q

basically CHF can be produced by any condition that…

A

reduces pumping ability of heart

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8
Q

in a health person the heart workload can increase 5-fold but in CHF…

A

heart does not have the same adaptability—> cardiac reserve is used up at rest, so if there is increased metabolic demand, heart will NOT cope

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9
Q

often times which part of heart fails?

A

left ventricle, which results in decreased CO to systemic circuit
-results in residual volume in chamber

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10
Q

failure of the left ventricles results in…

A

congestion within the pulmonary circuit, then the right ventricle must work harder to pump blood to lungs and HYPERTROPHY occurs within RV myocardium

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11
Q

summarize what happens in left-sided failure

A
  • insufficient CO—> residual volume in left ventricle —> left atrium pumps harder to empty —> notenough space for left atrium to empty, so residual volume in left atrium
  • left atrium unable to receive full pulmonary return—> increased CHP in pulmonary circuit—> pulmonary congestion (edema in interstitial spaces and alveoli)—> increased workload of right ventricle—> hypertrophy of right ventricle —-> right sided failure (usually)
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12
Q

summarize what happens in right-sided failure

A

failure to eject blood into pulmonary circuit= pooling in systemic circuit (manifests as peripheral edema and abdominal organ distention)

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13
Q

general rule of HF

A

ANY CHAMBER being pumped to NOT getting enough blood and any chamber RECEIVING blood is congested

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14
Q

why is the patient asymptomatic at the beginning of CHF?

A

the patient has compensation mechanisms that are kicking in! 6

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15
Q

name the SIX compensatory mechanisms for CHF

A
  • frank-starling law
  • SNS
  • RAAS
  • ANP and BNP
  • endothelins
  • cardiac hypertrophy and remodelling
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16
Q

what is the frank-starling law?

A

-more the heart is stretched, the more blood is filled, which increases venous return= increased end-diastolic volume= increased preload= increased cardiac output
BUT, if heart is consistently stretched, it will lose contractility… decreases CO and when there is decreased CO, more O2 is needed… SNS kicks in

17
Q

SNS does what..

A

aims to increase cardiac output by causing tachycardia and systemic vasoconstriction (BV not affected)
-but, increased contractility, increased workload and O2 demand can advance the heart failure

18
Q

RAAS is triggered by…

A

the decrease in CO and renal perfusion—> angiotensin II= patent vasoconstrictor, increases BP and increases CO
-releases ADH and aldosterone—> fluid retention (increased BV, CO)

19
Q

what are ANP and BNP

A

both are natriuretic peptides
anp= atrial natriueretic peptide, secreted by heart muscle cells
bnp= brain natriuretic peptide, released by ventricles of heart in response to excessive stretching of heart muscle cells

20
Q

what do ANP and BNP cause…

A

potent diuresis and natriuresis (secrete H20 and NA)—> decrease blood volume, decrease workload of the heart—-> decreased BP

  • VASODILATOR
  • OPPOSITE of SNS and RAAS
21
Q

endothelins do what?

A

vasocsontrictors released by epithelial and cardiac muscle cells in wall of vessels—> increase BP
-release growth factors that cause vascular and cardiac muscle hypertrophy—> larger muscle require more resources (more O2 or die)

22
Q

cardiac hypertrophy and remodelling?

A
  • increased workload causes hypertrophy—> eventually decreased contractility—> requires more O2—> myocardial dysfunction, EVENTUALLY
  • compensation leads to DECOMPENSATION and FAILURE
23
Q

manifestations of CHF?

A
  • vary depending on severity and type, signs and symptoms are related to effects of impaired pumping
  • hypoperfusion, hypoxia, acidosis all due to congestion
24
Q

symptoms in compensatory phase?

A

ASYMPTOMATIC

25
Q

diagnosis of CHF?

A

EASY and comprehensive: history—> look at risk factors, lab values—-> anemia, electrolyte, renal fx, hematology (liver fx)

  • ECG- possibly persistent in acute
  • echocardiogram: shows hemodynamics
26
Q

treatment of CHF?

A
  • acute: stabilize pt and correct the cause (MI—> anticoagulant, thrombolytic, antiarrhythmic, O2, morphine)
  • chronic: symptomatic management; decrease risks, increase functioning, rest
27
Q

what is systolic HF and how do u treat it?

A

EF is less than 40: treat with ace inhibitor and beta blocker to increase EF

28
Q

if EF is 40% or more than…

A

treat cause (eg. diabetes), ace inhibitor w/ or w/o beta blocker

  • angiotensin receptor blocker if pt has symptoms with activity
  • diuretic is pt has symptoms at rest
29
Q

surgery for HF?

A

stenting, fix valvular defect