Acute HF Flashcards
Epidemiology of Acute HF (8)
Approximately ¾ of patients present to ED
Average age is 72.4 years
Over 1 million hospitalizations each year
75% due to insult in exisiting HF patient
25% de novo HF
5% due to disease progression
Average length of stay is 4 - 5 days
Rehospitalization occurs in 50% of patients!
Cardiac Index (CI)
CI = CO/m2
CI is expressed at L/min/m2
Normal range 2.5-4 L/min/m2
Utility: determinant of O2 delivery and perfusion
You would predict that CI is __low____ in patient with ADHF
Cardiac Output
volume of blood ejected from left ventricle during systole (L/min)
Pulmonary capillary wedge pressure (PCWP)
pulmonary artery occlusion pressure (PAOP)
Normal range 8-12 mmHg
Indirectly measures end diastolic volume
Utility: determinant of patient’s preload / volume status
You would predict that PCWP is __high__in patient with ADHF
Arginine Vasopressin (AVP)
Hormone secreted by posterior pituitary to maintain water homeostasis Also known as antidiuretic hormore Actions Inhibits renal excretion of free water Potent vasoconstriction
Elevated AVP levels in heart failure
Diagnostic value of BNP
100-500 pg/ml has a high sensitivity towards “cardiac issues”
A clinician will use this to differentiate between cardiac and non-cardiac causes of pulmonary congestion/edema
Also, in a patient with a baseline of BNP, any sharp increase is an indicator of a worsening of their HF
Acute decompensated heart failure
There has been an insult/problem to the body (NSAIDS, cocaine, trauma, excess salt) where there is not enough blood being distributed through the body
- Cyanotic, fluid edema, pulm edema
3 ADHF compensatory mechanisms
ET-1
AVP
BNP/ANP
Endothelin-1 (ET-1)
Actions Potent vasoconstriction Induces cardiac remodeling Decreases renal blood flow (GFR) Also acts to further stimulate the RAAS and SNS systems
Elevated ET-1 levels in heart failure and other diseases
Atrial Natriuretic Peptide (ANP)
B-type Natriuretic Peptide (BNP)
ANP is released from atrial myocardium in response to atrial dilation and stretch
BNP is released from ventricular myocardium in response to elevated end diastolic volume (preload)
Both ANP and BNP are elevated in ADHF patients
Actions: vasodilation, natriuresis, diuresis
BNP “helps us”; it balances ET-1 and AVP
Used as a diagnostic tool, very valuable from differentiating between ADHF and PNA
Two main reasons how ADHF occurs
Decreased CO/CI
Sodium/H2O retention
Neurohormonal Actions of ANP and BNP
Antagonizes RAAS
Inhibits SNS
Antagonizes ET-1
Results in peripheral and coronary vasodilation
Renal Actions of ANP and BNP
increases GFR
diuresis
natriuresis
Non-drug related precipitating factors for ADHF
Ischemia Arrhythmias Uncontrolled HTN Dietary indiscretion (high Na diets) Pulmonary embolism Valvular dysfunction Disease progression Thyroid disorders Electrolyte abnormalities Anemia Infection Worsening renal function Non compliance
Drugs that cause water and Na retention (4)
Corticosteroids
NSAIDs (ibuprofen, naproxen)
Thiazolidinediones (pioglitazone, rosiglitazone)
Some antibiotics
Drugs that decrease cardiac contractility
Alcohol Beta blockers Non-dihydropyridine CCB Some antiarrhythmics Some chemotherapy agents (doxorubicin)
ADHERE registry
Factors for in-hospital mortality include
BUN ≥ 43 mg/dL
SBP < 115 mmHg
SCr ≥ 2.75 mg/dL
Mortality is 20%
Mortality correlated with number of factors
None = low risk, 2% mortality 1 = moderate risk, 6% mortality 2 = high risk, 13% mortality 3 = very high risk, 20% mortality
Goals of Therapy for AHF (4)
General approach to therapy varies depending on patient presentation
Goals of therapy for all ADHF patients
Relieve congestion and optimize volume status
Treat symptoms of low CO
Minimize risks associated with drug therapy
Avoid future hospitalization by optimizing chronic therapies and providing patient education
3 Types of AHF
Warm&Wet–> MC
Cold& Wet
Cold& Dry
“Warm & Wet”, subset II
Adequate perfusion Volume overload This is the patient that has chronic HF who has a super bowl party and is fluid overloaded- diuretics/vasodilators Signs and symptoms of pulmonary congestion and/or systemic congestion
PCWP > 18 mmHg
CI > 2.2 L/min/m2
Diuretics and vasodilators that we use— furosemide and nitro are the MC combo
“Cold & Dry”, subset III
Hypoperfusion
Good volume status
This is the patient who has chronic HF and super vigilant about Na and H2O who gets slightly dehydrated with cardiac arrhythmias, lower BPs (systolic low 90s)- gentle rehydration/inotropes
Signs and symptoms of hypo perfusion
Gently rehydrate and use dobutamine to increase inoptrops
“Cold & Wet”, subset IV
Hypoperfusion
Volume overload
This patient is almost in cardiogenic shock; ? MI, possible too high dose of BB- diuretic/inotropes/occasional vasodilators
Signs and symptoms of pulmonary and/or systemic congestion
Signs and symptoms of hypoperfusion
ACE- I
Cornerstone of HF management
Maintain home dose if possible, consider increasing to goal dose if BP allows
Most likely used in “warm and wet” while the other types of ADHF doesn’t have the BP tolerance
3 Meds of Loop Diuretics
Furosemide (Lasix)
Bumetanide (Bumex)
Torsemide (Demadex)
MOA of Loop Diuretics and Onset/Duration of the Med
Mechanism of action:
Increases Na excretion at the loop of Henle
Onset and duration of action:
Oral: onset 30 minutes, duration 6 hrs
IV: onset 5 minutes, duration 2 hrs
Adverse Drug Reactions of Loop Diuretics
Electrolyte abnormalities Hyponatremia Hypokalemia Hypomagnesemia Renal dysfunction Hypotension
Diuretic Resistance
Failure to respond to several IV bolus doses of loop diuretics
Occurs in 1 of 3 pts taking diuretics at home
Ultrafiltration
Also known as aquapheresis Modality for fluid removal Removes a predicable amount of Na and H2O Rate is slow, minimal drop in BP Niche: Diuretic resistance Severe renal impairment
3 Vasodilators
Nitroglycerin
Nitroprusside (Nipride™)
Nesiritide (Natrecor™)
Nitroprusside
Mechanism of action:
potent, balanced vasodilator
acts directly on vascular smooth muscle (nitric oxide donor)
also used for hypertensive crisis
Notes:
ordered as mcg/kg/minute infusion
protect from light
breaksdown to thiocyanate/cyanide (orange dark brown blue solution)
Methods for overcoming diuretic resistance:
Increase loop diuretic dose Start loop diuretic infusion Add thiazide diuretic for synergy Ultrafiltration Ad vasodilator if tolerated
Adverse Effects for Nitroprusside
Hypotension
Coronary steal syndrome
worse outcomes in s/p MI patients who are NOT in heart failure
Metabolized to cyanide and thiocyanate, increased risk of toxicity in patients with renal dysfunction or if high dose for prolonged period
antidote (sodium thiosulfate)
Nitroglycerin
Mechanism of action
primarily a venous vasodilator
Acts as a nitric oxide donor
Notes IV infusion, short-term useful in heart failure with myocardial ischemia Risk of tachyphylaxis Other side effects: HA, hypotension
Nesiritide
Brand name: Natrecor®
Mechanism of action:
Recombinant B-type Natriuretic Peptide
reduces sympathetic stimulation
inhibits renin-angiotension-aldosterone system
Results in vascular smooth muscle relaxation, balanced vasodilator AND diuresis
Adverse Effects of Nesiritide
hypotension, especially if on ACE-I
worsens renal function
Increased mortality
Advantages and Disadvantages for Nesiritide
Advantages:
increases sodium excretion and urine output without excessive hypokalemia
Disadvantages: No more effective than standard of care but thousands $$$ more!!!! How bad drugs get approved!
Note: IV infusion, short term use only
Inotropic Therapy
Dopamine
Dobutamine
Milrinone
Dopamine
Has inotropic and vasopressor activities
Dobutamine/milrinone just have inotropic activities with no vasopressor properties
Dopamine is converted into NE
Activates alpha, beta and dopaminergic receptors
Typically used in “cold”—-almost cardiogenic shock
Dobutamine
Mechanism of action – β-agonist:
Binds to beta 1 receptor and increases calcium influx during systole
Pharmacologic effect:
Increase contractility increase CO/CI
Place in therapy:
acute CHF: “cold” patients
2 Adverse Effects of Dobutamine
Tachycardia
Arrythymogenic
increase mortality in long term
Milrinone
Mechanism of action: Phosphodiesterase inhibitor (PDE3) Increases intracellular cAMP which increases intracellular calcium
Pharmacologic effect:
increased contractility
Vasodilatory effects
Adverse Effects of Milrinone
Arrythymogenic
May decrease BP and result in reflex tachycardia
Hypotension
Thrombocytopenia
Hospital Discharge for ADHF
Opportunity to initiate/maximize chronic heart failure regimen, consider at least: Ace Bb Diuretic EF documentation Smoking cessation HF clinic
