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Anti- HTN & Chronic HF > Acute HF > Flashcards

Acute HF Flashcards

1
Q

Epidemiology of Acute HF (8)

A

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!

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2
Q

Cardiac Index (CI)

A

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

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3
Q

Cardiac Output

A

volume of blood ejected from left ventricle during systole (L/min)

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4
Q

Pulmonary capillary wedge pressure (PCWP)

A

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

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5
Q

Arginine Vasopressin (AVP)

A 
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

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6
Q

Diagnostic value of BNP

A

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

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7
Q

Acute decompensated heart failure

A

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

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8
Q

3 ADHF compensatory mechanisms

A

ET-1
AVP
BNP/ANP

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9
Q

Endothelin-1 (ET-1)

A 
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

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10
Q

Atrial Natriuretic Peptide (ANP)

B-type Natriuretic Peptide (BNP)

A

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

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11
Q

Two main reasons how ADHF occurs

A

Decreased CO/CI

Sodium/H2O retention

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12
Q

Neurohormonal Actions of ANP and BNP

A

Antagonizes RAAS
Inhibits SNS
Antagonizes ET-1
Results in peripheral and coronary vasodilation

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13
Q

Renal Actions of ANP and BNP

A

increases GFR
 diuresis
 natriuresis

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14
Q

Non-drug related precipitating factors for ADHF

A 
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
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15
Q

Drugs that cause water and Na retention (4)

A

Corticosteroids
NSAIDs (ibuprofen, naproxen)
Thiazolidinediones (pioglitazone, rosiglitazone)
Some antibiotics

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16
Q

Drugs that decrease cardiac contractility

A 
Alcohol
 Beta blockers
 Non-dihydropyridine CCB
 Some antiarrhythmics
 Some chemotherapy agents (doxorubicin)
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17
Q

ADHERE registry

Factors for in-hospital mortality include

A

BUN ≥ 43 mg/dL
SBP < 115 mmHg
SCr ≥ 2.75 mg/dL
Mortality is 20%

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18
Q

Mortality correlated with number of factors

A 
None = low risk, 2% mortality
1 = moderate risk, 6% mortality
2 = high risk, 13% mortality
3 = very high risk, 20% mortality
19
Q

Goals of Therapy for AHF (4)

A

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

20
Q

3 Types of AHF

A

Warm&Wet–> MC
Cold& Wet
Cold& Dry

21
Q

“Warm & Wet”, subset II

A 
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

22
Q

“Cold & Dry”, subset III

A

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

23
Q

“Cold & Wet”, subset IV

A

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

24
Q

ACE- I

A

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

25
Q

3 Meds of Loop Diuretics

A

Furosemide (Lasix)
Bumetanide (Bumex)
Torsemide (Demadex)

26
Q

MOA of Loop Diuretics and Onset/Duration of the Med

A

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

27
Q

Adverse Drug Reactions of Loop Diuretics

A 
Electrolyte abnormalities
Hyponatremia
Hypokalemia
Hypomagnesemia
Renal dysfunction
Hypotension
28
Q

Diuretic Resistance

A

Failure to respond to several IV bolus doses of loop diuretics
Occurs in 1 of 3 pts taking diuretics at home

29
Q

Ultrafiltration

A 
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
30
Q

3 Vasodilators

A

Nitroglycerin
Nitroprusside (Nipride™)
Nesiritide (Natrecor™)

31
Q

Nitroprusside

A

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)

32
Q

Methods for overcoming diuretic resistance:

A 
Increase loop diuretic dose
Start loop diuretic infusion
Add thiazide diuretic for synergy
Ultrafiltration
Ad vasodilator if tolerated
33
Q

Adverse Effects for Nitroprusside

A

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)

34
Q

Nitroglycerin

A

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
35
Q

Nesiritide

A

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

36
Q

Adverse Effects of Nesiritide

A

hypotension, especially if on ACE-I
worsens renal function
Increased mortality

37
Q

Advantages and Disadvantages for Nesiritide

A

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

38
Q

Inotropic Therapy

A

Dopamine
Dobutamine
Milrinone

39
Q

Dopamine

A

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

40
Q

Dobutamine

A

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

41
Q

2 Adverse Effects of Dobutamine

A

Tachycardia
Arrythymogenic
increase mortality in long term

42
Q

Milrinone

A 
Mechanism of action:
Phosphodiesterase inhibitor (PDE3)
Increases intracellular cAMP which increases intracellular calcium

Pharmacologic effect:
increased contractility
Vasodilatory effects

43
Q

Adverse Effects of Milrinone

A

Arrythymogenic
May decrease BP and result in reflex tachycardia
Hypotension
Thrombocytopenia

44
Q

Hospital Discharge for ADHF

A 
Opportunity to initiate/maximize chronic heart failure regimen, consider at least:
Ace
Bb
Diuretic
EF documentation
Smoking cessation
HF clinic

Anti- HTN & Chronic HF (4 decks)

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