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45 Cards in this Set
- Front
- Back
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scope of the HF problem
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6 million in US
700,000 new cases nearly 300,000 deaths 4% in hospital mortality |
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pathophysiology of acute HF
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inciting event in est HF
or new onset HF stable HF w/0 identifiable cause- progression increased elevated filling pressure in V decline in CO LV dilatation, worsening Mitral regurg - trigger neurohormonal cascade - this is the main maladaptive - tachycardia, fluid retention, worsening end organ damage, hypotension, |
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percipitants of HF exacerbations
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patient related factors:
non- adherence to meds, lifestyle, diet, salt and fluids, ingestion of toxins, alcohol, cocaine Cardiac arrhythmias: atrial or ventrial bradycardias, heart block HTN, ischemia, MI, valvular disease non cardiac: PE,anemia, bleeding, systemic infection, thyroid adverse meds |
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diagnosing ADHF
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no single finding definitive
Hx, px, labs, ECF, CXR |
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findings of ADHF
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HF history
SOB- related to volume overload orthopnea, PND fatigue- low CO increasing weight, edema, abdominal girth physical exam: elevated JVP peripheral edema, ascites rales, hypoxia, Inc RR tachypnea, tachycardia - to maintain CO |
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history
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past hx of HF
most specific sx: PND sensitive: SOBOE |
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volume overload and congestion- sx
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predominant symptom in ADHF
PND- waking at night SOB, orthopnea- SOB lying flat cough, dry cough, edema - weight gain, abdominal girth, nausea, GI symptoms- congestion of intestine and stomach |
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reduced CO sx
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fatigue, day time somnolence, cold intolerance
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On exam
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vitals
BP- hypertensive usually HR- high requires supplemental O2 3rd heart sound JVP |
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JVP
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height of column of JVP from sternal notch
<4-5 cm normal measure of right atrial pressure double waveform non- palpable occludable changes with inspiration |
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CXR congestion
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pulmonary vascular redistribution
interstial/alveolar edema pleural effusion |
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EKG
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atrial fib - can quickly make patients decompensated
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BNP
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diagnositic test- usually helpful in acute situations
blood test- <100 can rule out diagnosis of ADHF natriuretic hormone- from ventricle prohormone plasma levels increased in HF >400 HF 100-400 gray zone Afib also associated with high BNP useful when Dx is in question |
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hospitalization guideline
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recommended if
hypotensive, worsening renal failure, alteration in mentation- low output, hypoxia, dyspnic at rest, resting tachypnea, arrhythmia- new onset A fib ACS |
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when is hospitalization considered
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worsened congestion even without dyspnea- peripheral edema
sx of pulmonary or systemic congestion - w or wo weight gain major electrolyte disturbance associated co-morbid conditions- DKA, pneumonia, PE, TIA, stroke repeated ICD firings undiagnosed, new onset HF |
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tx options
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pharm:
diuretics vasodilators- oral: ACE ARB, nitrates IV: Nitroglycerin, nitroprusside, nesiritide inotropes: IV nonpharm O2, non- invasive positive pressure ventilation narcotics- morphine etc - venodilation properties- reduce preload- relieve SOB, reduce filling pressure |
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diuretics
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mainstay
loop better best given IV 2 or more times daily- peak and trough effect bolus high dose bolus - better outcome acutely reduce filling pressures - pathophysiologic problem monitor kidney, electrolytes diuretic resistance; use thiazide or switch strategies |
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loop diuretics ex
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furosemide (lasix)
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general guideline of dosing diuretics in AHF
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normal kidney function- new HF- 20-40 mg BID or TID
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vasodilators
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nitroglycerin
nitroprusside nesiritide |
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IV nitroglycerin
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venous and arterial dilator
provides acute reduction in filling pressure in venous reduces congestion, augments diuresis arteriodilator - at higher doses- decreases afterload, inc SV and CO want to lower BP to a point to allow CO to increase useful with concomittant MI TACHYPHYLAXIS- after 5-6 days of continuous NG- not doing anything HA and hypotension adverse effects |
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nitroprusside
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V and A dilator
drug of choice in HTN crisis or severe valvular regurg need continuous arterial BP monitoriing A line can cause coronary steal phenomenon- percipitate anginal thiocyanite toxicity |
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NEsiritide
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recombinant B type NP,
vasodilator and provides diuresis as well still need diuretics |
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Inotropes
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increases contractility
Dobutamine milrinone dopamine these also have vasodilation qualities use only for short term chronic admin is associated with worse outcome |
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Dobutamine
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stimulates both B1 and B2 receptors
increases CAMP by upregulating adenyl cyclase- increases contractility also causes mild arteriolar vasodilation causes tachycardia, tachyarhythmias tachyphylaxis with chronic tx |
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milrinone
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inhibits PDEInhibitory- prevents breakdown of CAMP
increases CAMP- contractility does not act on beta receptors increased CAMP- vasodilation- decreases afterload and preload may cause severe and sustained hypotension potent vasodilator no tachyphylaxis long half life- problem if poor renal function |
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dopamine
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beta and alpha receptor
also stimulates dopaminergic receptors at lower doses- vasodilatory effect higher doses- B and A stimulation causes tachycardia modest ionotropy and vasodilation- more potent iontorope than dobutamine cardiogenic shock- dopamine best choice- b/c bp support and ionotropy support |
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do you withdraw beta blockers in an acute exacerbation of HF
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no - do worse
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refractory HF
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if not on ionotropes- start them on it
dont need to have low BP to start ionotropes |
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what is the most common indicator for someone needing ionotropes
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worsening renal function indicative of poor CO
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other tx modalities
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non-invasive positive pressure ventilation - constant hypoxia
narcotics venodilate alleviate feeling of suffocation |
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identify the triggers for HF
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ischemia, arrhythmias, non compliace, progression of the disease, concurrent medical condition
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what are the two main problems in HF patients
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congestion
perfusion (CO) one or the other or mxture of both |
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dry and warm
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not congested well perfused
normal people |
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dry and cold
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not congested but low output symptoms
usually not admitted unless End stage |
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wet and warm
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most common presentation
volume overloaded but perfusion is normal diureses these patients and inc est. oral vasodilators- ACE or ARB - to reduce after load if they fail diuretics: inc dose, salt and fluid restrictionm diuretic infusion, 2nd type of diuretic ultrafiltration IV vasodilators if symptomatic hypotension, and still severe HF causes rapid improvement in congestion. useful in pulmonary edema and severe HTN |
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wet and cold
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least common
volume overloaded and low output end stage HF diuretics, inc vasodilators first - IV ionotropes used when low EF wtih Low output - bp in 80s 90s not responsive to vasodilators, diuretics worsening renal function |
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PA catheter
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sits in pulmonary artery- diagnostic tool to help guide tx
used when: refractory to initial tx patients with cardiogenic shock unclear volume status and filling pressures significant hypotn, worsening renal function considering for Heart transplant |
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clinical monitoring
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daily:
weight (diuresing well), outputing more than taking in, symptoms, JVP renal function and electrolytes vital signs - few times a day |
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tx goals
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improve symptoms
volume status oral therapy identify etiology assess for revascularizatio or device |
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discharge criteria
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near optimal volume status, oral therapy,
assess ambulation, exacerbating factors early follow up- 7-10 days referral for disease management |
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refractory HF
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mechanical circulatory support
ECMO LVAD BVAD fialing med therapy bridge to recovery/tranplant Heart transplant |
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ECMO
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full cardiac and pulmonary support
acute patient in cardiogenic shock if heart recovers - good if it doesnt- transplant |
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indications for transplant
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persisitently severe symptomatic HF
freq hosp, renal , arrhythmias absence of contraindications poor one year survival failure to respond to meds/ device based tx |
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contraindications of transplant
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no other disease - limiting survival
active infection psychosocial drug and alcohol noncompliance recent cancer body size obesity cachexia |
