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ht failure--systolic dysfunction
lacks sufficient force pump all blood (decreased CO) to meet body's O2 demands (decreased tissue perfusion)
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ht failure--diastolic dysfunction
filling disfunction (vent dev a stiffness and fails to relax enough between contractions
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(HF) When CO fails--compensatory mechanisms activated to maintain tissue and organ perfusion:
- hr and stroke vol increase
- arterial and venous vasoconstriction--increasing venous return
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Fall in CO activates what?
renin-angiotensin-aldosterone system
- -vasoconstriction and salt and H2O retention
- -salt and H2O help restore CO
- -overtime--mus cells enlarge--vent hypertropy and HF
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Biventricular failure
- both vents function inadequately
- little to no cardiac reserve
- pr awakes at night SOB;eduma during day is reabsorbed into circulation at night and gives fluid overload and pulm congestion
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Atrial Natriuretic Factor (Peptide)
- synthesized in atrial muscle
- used to preduct CHF (chronic= decreased) (acute= increased)
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Brain Natiuretic Peptide
- Neurohormone secreted primarily by bets d/t vol expansion and pressure overload
- MORE SENSITIVE than ANF/ANP
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Hemodynamic monitoring
- pg 98
- assess CV function and response to treatment
- norm: 2-8 cm
- eval fl balence, vent function, and effects of interventions (drugs)
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Peripheral arterial line
measures arterial BP
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(HF) morphine
- acute pulm edema
- reduces anxiety, improves breathing and vasodilation
- reduces venous return and lowers rt atrial pressure
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(HF) digitalis glycosides
pos inotropic agents and neg chronotropic
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(HF) sympathomimetic agents
Dopamine (inotropin)
- low dose 1-4 mcg/min>>>> increased renal bl flow
- 5-10 mcg/min>>>>> increased contractility
- over 10 mcg/min>>>>>> increased contractility and caused vasoconstriction (inc afterload)
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(HF) sympathomimetic agents (2)
- Dobutamine (Dobutrex)
- preferred over dopamine
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phosphodiesterase inhibitors
inhibits phosphodiesterase to improve myocardial contractility and vasodilate
- Amrinone (Inocor)
- Milrinone (Primacor)
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Atrial Natiuretic peptide hormone
Nesiritide (Natrecor) /Vasodilator
used for serious, acutely decompensated HF
increased Na+ loss
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Angiotensin-converting enzyme inhibitor
- inhibits formation of angiotensin II (potent vasoconstrictor) and blocks release aldosterone (so increase Na+ excretion and K+ retention)
- end in "pril"
- improves CO and tissue perfusion
- lowers peripheral resistance= decreased afterload
- inc renal perfucion
- increased tolerance to activity
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Side effects of ACEI
- chronic cough, swelling face/eyes/throat (angioedema, neutropenia)
- initial dose may cause hypotension, dizziness, tachycardia, and faiting--lay down is they occur--do not DC bc this is normal for 1st dose
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Angiotensin II receptor antagonists (blocker) ARBS
- end in "sartan"
- try ARB after ACE
- Valsartan (Diovan) approved for pt who can't tolerate ACE inhibitors
- losartan (corzaar)
prevent release aldosterone (Na+ retaining hormone) and block angiotensin II from receptors in many tissues. Causes vasodilation and dec afterload
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Beta-Adrenergic Blocking Agents
- Inhibit cardiac response to sympathetic nerve stimulation
- Dec renin-angiotensin-aldosterone system which would cause inc vasoconstriction and Na retention
- commonly used w ACEI
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Diet and Activity w HF
Restricted Na+ 1.5- 2 g/day
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Dynamic cardiomyoplasty
- improved functioning in existing heart
- -wrapping skeletal muscle graft around ht to support
- -grafted skeletal muscle stimulated to contract w heart muscle--more forceful contraction and inc CO
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Cardiac transplant
type 1
type 2
1-heart removed and replaced w donor heart
2. piggyback transplant--ht left in place and donor ht sutured to it. both function but most work done by donor heart.
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