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Pharm II > Acute Decompensated HF > Flashcards

Acute Decompensated HF Flashcards

1
Q

What is the definition of Acute Decompensated HF?

A

It’s an injury/insult to the body where not enough blood is being pumped into the heart, causing acute fluid overload

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2
Q

Approx. how many pts will present to the ED with ADHF?

A

75% of pts

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3
Q

What is the average age for ADHF?

A

72.4 yrs

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4
Q

Why would a 40 yr old present to with ADHF?

A

Malignant/ untreated HTN, drug/ EtOH abuse, SLEEP APNEA

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5
Q

What % of pts will be hospitalized d/t an insult in existing HF?

A

75%

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6
Q

What % of pts will be hospitalized d/t de novo HF?

A

25%

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7
Q

What % of pts will be hospitalized d/t disease progression?

A

5%

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8
Q

Approx how many hospitalizations per year are d/t HF?

A

Over 1 mill.

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9
Q

What is the avg length of hospital stay in ADHF?

A

4-5 days

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10
Q

What % will re-hospitalization occur in ADHF pts?

What is the problem with this?

A

50%

Readmission for the same Dx w/in 30 days = no compensation from insurance companies

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11
Q

What is the formula for Cardiac Index?

What is the normal range?

A

CI = CO m^2
Expressed in L/min/m^2
Nml range: 2.5 - 4 L/min/m^2

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12
Q

What is the definition of Cardiac Output?

A

The volume of blood ejected from the LV during systole (expressed in L/ min)

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13
Q

What is the utility of Cardiac Index?

A

To determine O2 delivery and perfusion: is there enough oxygenated blood being delivered to the periphery

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14
Q

Would CI be high or low in a pt w/ ADHF?

A

LOW –> low-normal

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15
Q

What is Pulmonary capillary wedge pressure (PCWP) aka pulmonary artery occlusion pressure (PAOP)? What is its utility?

A

It indirectly measures end diastolic volume to determine pt’s preload (EDV) / volume status; i.e. pulmonary edema, LV dysfunction
(Amount of blood @ end of diastole)

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16
Q

How is PCWP measured? What are its limitations?

A

With a Swan-Ganz catheter: starting in the SVC, catheter is threaded thru RA –> RV –> PA –> lungs
Dangerous: risk vs. benefit analysis – should mostly be used if they’re refractory to all meds
Doesn’t change the outcome: finding the same signs on physical exam

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17
Q

What is the normal range for PCWP?

A

8 - 12 mmHg

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18
Q

Would PCWP be high or low in a pt w/ ADHF?

A

HIGH d/t fluid backup

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19
Q

What is the most common type of ADHF?

A

Warm and wet

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20
Q

How would you predict CI and PCWP for a pt in “warm and wet” AHF?

A
  • CI: preserved, slightly depressed (CO is okay - dec.)

- PCWP: high

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21
Q

What would a physical exam of a “warm and wet” AHF pt reveal?

A

Warm: stable BP, good perfusion, extremities are warm
Wet: pulm edema: auscultation, CXR, cough; peripheral edema: palpated in legs

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22
Q

Give examples of how “warm and wet” HF occurs

A
  • Valve dysfunction
  • Post holiday/ weekend w/ high-Na+/ fat foods; tOH
  • Drugs: B-Blocker (dec. CO); adding steroids for COPD exacerbation
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23
Q

What are 3 compensatory mechanisms against ADHF?

A
  • Endothelin-1 (ET-1)
  • Arginine Vasopressin (AVP)
  • B-type Natriuretic Peptide/ Atrial Natriuretic Peptide (BNP/ ANP)
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24
Q

What are the 4 major actions of ET-1?

A
  • Potent vasoconstriction (to inc BP, inc perfusion)
  • Induces cardiac remodeling
  • Dec renal blood flow (GFR)
  • Acts to further stimulated RAAS and SNS systems (inc volume)
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25
Q

Will ET-1 levels be high or low in HF?

A

High

ET-1 “hurts us”

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26
Q

What is AVP?

A

aka antidiuretic hormone

A hormone secreted by the post. pituitary to maintain water homeostasis

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27
Q

What are 2 actions of AVP?

A
  • Inhibits renal excretion of free water (inc. volume)

- Potent vasoconstriction (inc. BP)

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28
Q

Will AVP levels be high or low in HF?

A

High

AVP “hurts us”

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29
Q

What triggers the release of ANP?

A

In response to atrial dilation and stretch, ANP is released from atrial myocardium

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30
Q

What triggers the release of BNP?

A

In response to elevated end diastolic volume (preload), BNP is released from ventricular myocardium

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31
Q

Will ANP/BNP levels be high or low in HF?

A

High

BNP “helps us” as it balances ET-1 and AVP

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32
Q

What are the 3 major actions of ANP/BNP?

A
  • Vasodilation: peripheral & coronary
  • Natriuresis
  • Diureses
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33
Q

Used as a diagnostic tool, ANP/BNP levels are useful in differentiating between which conditions?

A

ADHF (cardiac origin) and pneumonia/ COPD (pulmonary congestion/ edema)
-Suggestive of CHF; compare with baseline

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34
Q

If someone with CHF with an elevated baseline BNP comes in with an increased BNP, what would that suggest?

A
  • Renal insufficiency: the kidneys can’t clear the BNP

- Worsening HF

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35
Q

What values would be indicative of NO HF vs. inconclusive vs. Cardiac issues?

A

No HF: < 100 pg/mL
Inconclusive: >100 - < 500 pg/mL
Cardiac issues (highly sensitive): > 500 pg/mL

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36
Q

What are the 3 neurohormonal actions of ANP & BNP?

A
  • Antagonist to RAAS
  • Inhibits SNS
  • Antagonist to ET-1
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37
Q

What are 3 renal effects of ANP & BNP?

A
  • Increases GFR
  • Inc diuresis
  • Inc natriuresis
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38
Q

What are the 2 main causes of ADHF?

A
  1. Decreased CO/ CI

2. Sodium / H2O retention

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39
Q

What are 3 prognostic factors for in-hospital mortality according to the ADHERE registry?

A
  1. BUN >/= 43 mg/dL
  2. SBP < 115 mmHg (< 90 = cardiogenic shock)
  3. SCr >/= 2.75 mg/dL
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40
Q

What is the mortality correlated with the number of prognostic factors according to the ADHERE registry?

A 
0 = low risk, 2% mortality
1 = mod risk, 6% mortality
2 = high risk, 13% mortality
3 = very high risk, 20% mortality
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41
Q

What are the 4 goals of therapy for all ADHF pts?

A
  1. Relieve congestion and optimized volume status
  2. Treat symptoms of low CO
  3. Minimize risks associated with drug therapy
  4. Avoid future hospitalization by optimizing chronic therapies & providing pt education –> B-Blockers, ACEis; counseling
42
Q

What is the diagnosis of ADHF based on?

A

Primarily based on pt’s signs & symptoms

43
Q

What are some signs of congestion?

A
    • CXR
  • Auscultation
  • Observe breathing
  • Cough
44
Q

What are some signs of hypoperfusion?

A
  • Looking hemodynamically unstable
  • Gasping
  • Cyanosis
  • Asking family members if they look normal
  • Borderline hypotension: NOT in shock SBP > 90 mmHg, compare it to baseline
45
Q

Which 3 drugs increase Cardiac Index?

A
  • Dobutamine (IV, pure B1 agonist)
  • Dopamine (watch out for inc. BP)
  • Milrinone/ Amrinone (inc CO)
46
Q

Which 2 factors encompass the “warm and wet” subset of AHF?

A
  • Adequate perfusion

- Volume overload: systemic or pulmonary

47
Q

Visually how would a “warm and wet” pt present?

A
  • Non-cyanotic, stable, nml BP

- Sxs of pulmonary congestion, systemic congestion e.g. if 200 lbs on Sat, 215 lbs on Tues –> need diuretic

48
Q

What are some precipitating events for a “warm and wet” pt?

A
  • A pt with chronic HF who has a part w/ high Na+/ EtOh

- Too high of a B-Blocker dose (dec. CO) i.e. Atenolol

49
Q

How would you treat a “warm and wet” pt?

A
  • Diuretics: Lasix
  • Vasodilators: Nitroglycerine
  • MC drug combination
50
Q

Is C.I. high or low in a “warm and wet” pt?

PCWP high or low?

A
  • C.I. is high

- PCWP is high

51
Q

Which 2 factors encompass the “cold and dry” subset of AHF?

A
  • Hypoperfusion

- Good volume status

52
Q

Visually how would a “cold and dry” pt present

A

-Cyanotic, dec. BP (not hypotensive)

53
Q

What are some precipitating events for a “cold and dry” pt?

A
  • A pt with chronic HF and is really vigilant with Na+/ H2O restriction (slightly dehydrated); compliant w/ Lasix
  • Cardiac arrhythmias
  • Lower BP (systolic low 90s)
54
Q

How would you treat a “cold and dry” pt?

A
  • GENTLE rehydration

- Inotropes (e.g. dobutamine)

55
Q

Why wouldn’t you use a vasodilator for a “cold and dry” pt?

A

Don’t need to lower their blood pressure, borderline hypotensive

56
Q

Is C.I. high or low in a “cold and dry” pt?

PCWP high or low?

A

C.I is low

PCWP is low

57
Q

Which 2 factors encompass the “cold and wet” subset of AHF?

A
  • Hypoperfusion

- Volume overload

58
Q

Visually how would a “cold and wet” pt present?

A
  • Almost in cardiogenic shock; cyanosis

- Wet lungs on auscultation; cough w/ sputum; peripheral edema

59
Q

What are some precipitating events for a “cold and wet” pt?

A
  • S/p M.I.: acute insult to heart, dec. CO, borderline shock d/t BP
  • Possible too high dose of B-B i.e. Labetolol, Carvedilol (a & B blocker)
60
Q

How would you treat a “cold and wet” pt?

A
  • Diuretics
  • Inotropes (Dobutamine)
  • Occasional vasodilators unless BP is too low
61
Q

Is C.I. high or low in a “cold and wet” pt?

PCWP high or low?

A

C.I is low

PCWP is high

62
Q

For ADHF, how would you manage a pt’s ACEi dose?

A

Maintain home dose if possible (5-10 mg Lisinopril), consider INCREASE dose to goal if BP allows

63
Q

What is the most likely subset of HF that would require an ACEi?

A

“Warm and wet” (other subsets usually won’t have the BP tolerance)

64
Q

What are the 2 most common Loop Diuretics used in “wet” HF pts?

A

Furosemide (Lasix) – IV

Bumetanide (Bumex)

65
Q

What is the MOA of Loop diuretics?

A

Increases Na+ excretion at the loop of Henle

66
Q

What is the onset & duration of action for both PO and IV Loop Diuretics?

A

PO: onset 30 min, duration 6 hrs
IV: onset 5 min, duration 2 hrs

67
Q

If a patient is already taking 20mg PO Lasix and they are fluid overloaded by 5kg, how would you proceed?

A

Give more Loop! Not getting enough response

68
Q

What is the dose conversion of Loops from PO to IV?

A

40 mg PO QD –> 20 mg IV infusion

69
Q

What are the two possible options w/in the IV route for Loops? Which is better?

A

IV Bolus

Continuous IV infusion: less stress on kidneys

70
Q

What are the 3 main ADRs with Loop Diuretics?

A
  • Electrolyte abnormalities: dec. Na+, K+, and Mg++
  • Renal dysfunction: strains kidney; want to see diuresis w/ stable SCr
  • Hypotension
71
Q

What is diuretic resistance? How often does it occur?

A
  • Failure to respond to several IV bolus doses of Loops

- Occurs in 1 in 3 pts taking diuretics at home

72
Q

What are the 5 possible methods for overcoming diuretic resistance?

A
  • Give an increased dose
  • Add a thiazide for synergistic action (except in renal dysfunction)
  • Start a Lasix infusion at 10mg/hr
  • Ultrafiltration
  • Add a vasodilator if tolerated (more volume to excrete)
73
Q

What is the purpose of ultrafiltration? What are the indications?

A
  • Modality for fluid removal, removes a predictable amt of Na+/ H2O; rate is slow –> minimal drop in BP
  • For diuretic resistance, severe renal impairment
74
Q

What are 3 potent vasodilators used in ADHF?

A

Nitroglycerine (MC)
Nitroprusside (pts w/ NTG intolerance)
Nesiritide (restricted use)

75
Q

What is the MOA of Nitroprusside?

A
  • Potent, balanced vasodilator (dec. BP)

- Acts directly on vascular smooth muscle –> NO donor

76
Q

What is another use for Nitroprusside besides HF?

A

-Also used in HYPERTENSIVE CRISIS

77
Q

What are some main take away points for Nitroprusside?

A
  • Ordered as mcg/kg/min infusion
  • Protected from light
  • Byproduct is cyanide so it CANNOT be used in RENAL DYSFUNCTION/ prolonged high dose –> inc risk for toxicity
78
Q

What are 2 other adverse effects associated with Nitroprusside?

A
  • Hypotension
  • Coronary steal syndrome (diverting blood away from coronary arteries) –> worse outcome s/p M.I. in pts who are NOT in heart failure
79
Q

What is the MOA of Nitroglycerine?

A
  • Venous vasodilator

- Acts as a NO donor

80
Q

What is another use for Nitroglycerine besides HF?

A

Useful in HF with myocardial ischemia

81
Q

What are some take away points for NTG?

A
  • Given as IV infusion, short-term

- Risk for tachyphylaxis (dec. response)

82
Q

What are 2 main side effects of NTG?

A

H.A

Hypotension

83
Q

What is the MOA of Nesiritide?

A
  • Reduces SNS stimulation

- Inhibits RAAS

84
Q

What effects are seen with Nesiritide?

A
  • Vascular smooth muscle relaxation
  • Balanced vasodilator
  • Diuresis
85
Q

Which subset of HF would Nesiritide be useful for? Limitation?

A

“Warm and wet” pts, esp those who have failed Nitro/Lasix combo: USED AS A LAST RESORT

  • Expensive
  • May increase mortality for some pts; no more effective than traditional standard of care
86
Q

What are 3 major ADRs for Nesiritide?

A
  • Hypotension, esp. with ACEi
  • Worsens renal function (inc. SCr)
  • Possible increased mortality
87
Q

What are some advantages of using Nesiritide?

A

-Increases Na+ excretion & urine output WITHOUT excessive hypokalemia

88
Q

What are 3 inotropic agents used in ADHF?

A
  • Dopamine
  • Dobutamine
  • Milrinone
89
Q

Which subsets of pts would inotropic agents be best for?

A

Cold & wet

Cold & dry

90
Q

What is the MOA behind Dopamine?

A
  • Has inotropic & vasopressor activities

- Converted into NE and activates alpha, Beta & dopaminergic receptors –> vasoconstriction

91
Q

What is the general MOA behind dobutamine & milrinone?

A

Inotropic activities

NO vasopressor properties (unlike Dopamine)

92
Q

In what setting would Dopamine be used? Not used?

A
  • Typically for COLD patients, almost cardiogenic shock

- A pt w/ preserved SBP, shouldn’t get dopamine d/t peripheral vasoconstriction –> dec. capillary perfusion

93
Q

What is the specific MOA of Dobutamine?

A

-B - agonist, binds to receptor & inc. Ca++ influx during systole

94
Q

What is the pharmacologic effect of dobutamine?

A
  • Increases contractility (CO/ CI)

- Blood pressure neutral

95
Q

What is the place in therapy for dobutamine?

A

-Acute CHF –> “cold” pts (w/ dec. CO)

96
Q

What are adverse effects of dobutamine?

A
  • Tachycardia (B1 receptor)
  • Arrhythmogenic
  • Increase in mortality w/ long term use: typical 4-5 day stay for “cold” inpts; stage D: w/ pump @ home
97
Q

What is the specific MOA of Milrinone?

A
  • Phosphodiesterase inhibitor (PDE3) – inodilator

- Increases intracellular cAMP –> inc. intracellular Ca++

98
Q

What is the pharmacologic effect of milrinone?

A
  • Increased contractility

- Vasodilatory effects – inodilator

99
Q

What are some adverse effects of milrinone?

A
  • Arrhythmogenic
  • May DEC. BP and result in reflex tachycardia
  • Hypotension
  • Thrombocytopenia
  • Inc in mortality
100
Q

What are 3 main drug classes to consider when discharging an inpatient and initiating/ maximizing a chronic HF regimen?

A

ACEi
B-Blocker (Toprol 200 mg QD)
For systolic HF; inc. 1 drug dose Q 2-4 wks
-Low dose diuretic

101
Q

What are 3 other important aspects to consider when discharging an inpatient and initiating/ maximizing a chronic HF regimen?

A
  • Ejection fraction documentation
  • Smoking cessation counseling
  • HF clinic esp if they don’t have a cardiologist
102
Q

For a pt with chronic heart failure (diagnosed 1 yr ago) and this is their 2nd admission, they are already on ACEi/ B-B, what is the next best step?

A
  • Spironolactone (K+ sparing)
  • SHORT COURSE digoxin to inc CO
  • Hydralazine/ nitrates for an African Am or C/I to ACEi) req. inc frequency, dec. BP

Pharm II (5 decks)

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