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Pharmacology II > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

What is a syndrome that exists when the heart is unable to pump sufficient blood to meet the metabolic needs of the body?

A

Heart failure

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2
Q

What are the characteristics of heart failure?

A

Characterized by elevated cardiac filling pressures (preload) and/or inadequate oxygen delivery, at rest or during stress, caused by cardiac dysfunction

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3
Q

What is an impairment of the contraction of left ventricle such that stroke volume (SV) is reduced for any given end-diastolic volume (EDV) or filling pressure?

A

Systolic dysfunction

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4
Q

What is the left ventricular ejection fraction?

A

SV/EDV
Normal: 50 - 70%
Objective measure of systolic function

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5
Q

What is left ventricular ejection fraction measured by?

A

ECHO (Echocardiogram)
RNV (Radionuclide ventriculogram)
cardiac catherization

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6
Q

What is characterized by ventricular filling rate (increased HR) and the extent of filling are reduced (decreased EDV) or a normal extent of filling associated with an inappropriate rise of ventricular diastolic pressure, but a normal EF is maintained?

A

Diastolic dysfunction

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7
Q

Why is normal EF maintained during diastolic dysfunction?

A

Because the left ventricle is still functioning so the ejection fraction but the ability to fill is affected.

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8
Q

What is cardiac output?

A

Heart rate (HR) x Stroke volume (SV)

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9
Q

What is heart rate controlled by?

A

By ANS (SNS and PNS), typically under vagal (PNS) tone

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10
Q

What is SV dependent on?

A

Preload, afterload, and contractility

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11
Q

What is preload?

A

=Left ventricular end-diastolic pressure (LVEDP)
Represented clinically by pulmonary capillary wedge pressure (PCWP)
Pre-filling pressure determines by venous return and atrial contraction

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12
Q

What is afterload?

A

=Systemic vascular resistance (SVR)

aka afterload resistance to ejection, regulated by wall tension,

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13
Q

What are the causes of ischemic heart failure?

A

Coronary Artery Disease
Myocardial ischemia
Myocardial infarction

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14
Q

What are the causes of non-ischemic heart failure?

A 
HYPERTENSION
Primary myocardial muscle dysfunction
Valvular abnormalities 
Structural damage and/or damage to myocardial walls
Dilated Cardiomyopathy
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15
Q

What are the compensatory mechanisms of heart failure?

A
  • -Increased SNS activity: Increase HR and SVR which increases BP
  • -Frank-Starling mechanism: Increased LVEDP = Increased SV
  • -Activation of Renin-angiotensin-aldosterone system (RAAS)
  • -Myocardial Remodeling:Concentric hypertrophy, Eccentric hypertrophy
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16
Q

What are the components of neurohormonal mechanism of CHF?

A 
Endothelin
Vasopressin (ADH)
Atrial Natriuretic Peptide
Endothelium-derived Relaxing Factor
RAAS
SNS
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17
Q

What are the direct toxic effects of NE and AT2?

A

Arrhythmias

Apoptosis

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18
Q

What is the neurohormonal mechanism of CHF effects?

A
  • -Impaired diastolic filling
  • -Increased myocardial energy demand
  • -Increased pre- and afterload
  • -Platelet aggregation
  • -Desensitization to catecholamines (don’t respond as well to NE and EP)
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19
Q

What happens when the heart starts failing?

A

The body starts to try and compensate making it worse and something has to be done or the patient will die.

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20
Q

What are the symptoms of LVF?

A

SOB, DOE, orthopnea, cough, PND, fatigue and weakness, memory loss and confusion, anorexia

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21
Q

What are the signs of LVF?

A

tachy, rales, diaphoresis, S3 and S4 gallops

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22
Q

What are the symptoms of RVF?

A

weight gain, transient ankle swelling, abdominal distention, anorexia, nausea

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23
Q

What are the signs of RVF?

A

JVD. Edema, hepatomegaly, ascites, (+) hepatojugular reflux

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24
Q

What NYHA function classification class involves no limitations of activity; ordinary activity does not cause symtoms?

A

Class I

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25
Q

What NYHA function classification class involves limitation of activity; ordinary activity results in symptoms?

A

Class II

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26
Q

What NYHA function classification class involves marked limitations of activity; less than ordinary activity results in symptoms?

A

Class III

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27
Q

What NYHA function classification class involves being unable to carry on any physical activity without discomfort; symptoms at rest?

A

Class IV

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28
Q

What is class I ACC/AHA CHF guidelines?

A

Conditions for which there is evidence and/or general agreement that a given procedure/therapy is useful and effective.

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29
Q

What is class II ACC/AHA CHF guidelines?

A

Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of performing the procedure/therapy

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30
Q

What is class IIa ACC/AHA CHF guidelines?

A

Weight of evidence/opinion is in favor of usefulness/efficacy

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31
Q

What is class IIb ACC/AHA CHF guidelines?

A

Usefulness/efficacy is less well established by evidence/opinion

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32
Q

What is class III ACC/AHA CHF guidelines?

A

Conditions for which there is evidence and/or general agreement that a procedure/therapy is not useful/effective and in some cases may be harmful.

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33
Q

What are the three levels of evidence that the ACC/AHA CHF guidelines?

A

Level A if the data were derived from multiple randomized clinical trials
Level B when data were derived from a single randomized trial or nonrandomized studies
Level C when the consensus opinion of experts was the primary source of recommendation

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34
Q

What are the class I ACC/AHA guidelines for diuretics?

A

Class I: diuretics and salt restriction are indicated in patients with current or prior symptoms of HF and reduced LVEF who have evidence of fluid retention (Level of Evidence: C)

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35
Q

What is useful to decrease preload?

A

Thiazides can be used if GFR>30ml/min: Distal tubule
Loop diuretics- DOC: Ascending Loop of Henle, Dose BID or daily
Resistance: use combo therapy
Monitor K+, Mg2+, BUN, SCr

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36
Q

What are the class IIa ACC/AHA guidelines for diuretics?

A

Class IIa-Digitalis can be beneficial in patients with current or prior symptoms of HF and reduced LVEF to decrease hospitalization for HF (Level of evidence: B)

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37
Q

What is used for class IIa?

A

Digoxin

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38
Q

Digoxin- hemodynamic effects in HF

A 
Increased CO
Decreased PCWP (wedge pressure)
Increased LVEF (left ventricular ejection fraction)
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39
Q

Digoxin- neurohormonal effects

A 
Vagomimetic action
Improved baroreceptor sensitivity
Decreased NE serum concentration
Decreased activation of RAAS
Direct sympathoinhibitory effect
Increased sympathetic CNS outflow at high doses
Decreased cytokine concentration
Increased release of ANP and BNP
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40
Q

Digoxin- electrophysiological effects

A

SA node: slowing of sinus rate
AV node: slowed conduction
Atrium: No effect or decreased refractory period
Ventricles and Purkinje fibers: no effect at low therapeutic doses

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41
Q

Digoxin- adverse effects

A

Inotropic (increase stroke volume) effect seen at low concentrations
Women may not derive benefit
Conditions likely to alter SDC (metabolism of digoxin) or predispose to toxicity:
Changing renal function
Drug interactions
hypokalemia

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42
Q

Digoxin- drug interactions

A
  • -Amiodarone and quinidine decrease digoxin clearance
  • -Empirically decrease digoxin dose by 50%
  • -Diltiazem, verapamil, Abx, azole antifungals, propafenone decrease digoxin clearance
  • -LASIX(furosimide)
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43
Q

What is most likely to make a patient on digoxin toxic?

A

Hypokalemia

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44
Q

Digoxin- toxicity

A

EKG changes: ventricular arrhythmias, heart block

Visual changes, anorexia, N/V/D, abdominal pain, confusion, HA

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45
Q

What do you treat digoxin toxicity with?

A

Digoxin Immune Fab (Digibind)

Binds with molecules of digoxin; excreted via kidneys

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46
Q

What is the ACC/AHA guidelines for ACEI for Class I?

A

Class I: ACEI are recommended for all patients with current or prior symptoms of HF and reduced LVEF, unless contraindicated. (Level of Evidence: A)

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47
Q

Why are ACEI so beneficial?

A

Because the body is trying to use angiotensin II to compromise and making it worse

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48
Q

What are the ACE inhibitors?

A 
Enalapril
Captopril
Lisinopril
Quinapril
Ramipril
Fosinopril
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49
Q

What was the results from the ATLAS study comparing “high” and “low” dose lisinopril for effects on mortality?

A

No difference in mortality

High-dose reduced hospitalizations for any cause (-13%) and for HF (-24%); p<0.05

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50
Q

ACEI- monitor

A

See patients in 1-2 weeks to monitor SCr, K+, BP and symptoms

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51
Q

ACEI- drug interactions

A

Aspirin may interfere with efficacy, recommend low-dose ASA (<160mg) if necessary (good to know when patient is on both drugs, good for them to stick with the lowest dose of ASA)

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52
Q

ACEI- side effects

A

Renal impairment
Hyperkalemia
Hypotension
COUGH

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53
Q

ACEI- intolerance

A

Cough ~5-10% in caucasians of European descent; ~50% in Chinese
Angioedema in 0.3mg/dL) with severe HF, 5-15% with mild to moderate symptoms
–Decrease diuretic dose?
–Decrease dose of ACEI or d/c??

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54
Q

What is the class I alternative for ACEI- intolerance?

A

ARBs approved for treatment of HF (valsartan, candesartan, losartan) in patients with current or prior symptoms of HF and reduced LVEF who are ACEI-intolerant (Level of Evidence: A)

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55
Q

What is the class IIb alternative for ACEI-intolerance?

A

A combo of isosorbide dinitrate & hydralazine might be reasonable in patient with current or prior symptoms of HF and reduced LVEF who can’t take ACEI or ARB because of drug intolerance, hypotension, or renal insufficiency (Level of Evidence: C)- this should not be the first thing you think about doing for patients.

Not generally something you should do

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56
Q

What are the ARD drugs?

A

Candesartan
Losartan
Valsartan

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57
Q

What are the nitrates/hydralazines?

A

Isosorbide dinitrate
Hydralazine
Bidil

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58
Q

Nitrates/hydralazines- monitor

A

f/u 1-2 weeks post-initiation and with each dose increase to check BP and HR

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59
Q

Nitrates/hydralazines- adverse effects

A

HA, dizziness

60
Q

What are the effects of chronic adrenergic activation (compensation for CHF)?

A
  • -Myocardial remodeling
  • -Direct toxic effects of NE  apoptosis
  • -Arrhythmias
  • -Impaired diastolic filling
  • -Increased myocardial energy demand
61
Q

What are the ACC/AHA HF guidelines for beta blockers for class I?

A

beta-blockers (bisoprolol, carvedilol, sustained release metoprolol succinate) are recommended for all patients with current or prior symptoms of HF and reduced LVEF, unless contraindicated. (Level of Evidence: A)

62
Q

What are the beta blockers used for CHF?

A

Bisoprolol
Carvedilol
Metoprolol CR/XL

63
Q

Beta blockers- contraindications

A
  • -Documented allergy
  • -RAD (renal artery dz)
  • -Symptomatic brady or > 1st degree heart block unless has pacemaker
  • -Evidence of fluid overload or recent requirement for IV inotropic agents
64
Q

Beta blockers- monitoring

A

F/U in 2 weeks to assess tolerability
Monitor HR, BP, weight, symptoms
Hold titration if symptomatic hypotension or bradycardia, worsening symptoms (increased SOB, edema, DOE, dizziness)
–Consider decreasing dose if symptoms severe
–Separate dosing from other BP meds

65
Q

What are the hemodynamic effects of aldosterone?

A
  • Na and water retention
  • Increased plasma fluid volume
  • Elevated BP
66
Q

What are the non-hemodynamic effects of aldosterone?

A
  • -Myocardial and vascular fibrosis
  • -Impaired arterial compliance
  • -Baroreceptor dysfunction
  • -Excretion of K+ and Mg++
  • -Elevated ANP (this can be misleading for these patients)
  • -Parasympathetic inhibition
67
Q

What is aldosterone “synthesis escape” during ACEI and ARB therapy?

A

Aldosterone is still something the body is able to make in lesser amounts even through you bypass the main pathway. Even if you have a pt on ACEI or ARB you still get aldosterone negative effects.

68
Q

What are the ACC/AHA HF guidelines for aldosterone antagonists for class I?

A

Class I: Addition of an aldosterone antagonist is reasonable in selected patients with moderately severe to severe symptoms of HF and reduced LVEF who can be carefully monitored for preserved renal function and normal K+ (Level of Evidence: B)

69
Q

Can you combine an aldosterone and ACEI?

A

Yes, but not in HTN

70
Q

What are the aldosterone antagonists?

A

Spironolactone

Eplerenone

71
Q

Aldosterone antagonists- uses

A

Use only if:

SCr30 ml/min

72
Q

What is a SE of spironolactone?

A

Gynecomastia

73
Q

Aldosterone antagonists- monitor

A

K+ and renal function (BUN/SCr) at 3 days, 1 week, and monthly for first 3 months

74
Q

What are the ACC/AHA guidelines for ACEI + ARB for class IIB?

A

Addition of ARB may be considered in persistently symptomatic patient with reduced LVEF who are already being treated with conventional therapy. (Level of Evidence: B)

75
Q

What are the ACC/AHA guidelines for ACEI + ARB for class III?

A

Routine combined use of ACEI, ARB, and aldosterone antagonist is not recommended for patients with current or prior symptoms of HF and reduced LVEF. (Level of Evidence: C)

76
Q

Do you ever combine ACEI, ARB, aldosterone antagonists?

A

NO NEVER

77
Q

What are the ACC/AHA guidelines for nitrates and hydralazine for class IIA?

A

Addition of combination of hydralazine and a nitrate is reasonable for patients with reduced LVEF who are already taking an ACEI and beta-blocker for symptomatic HF and who have persistent symptoms. (Level of Evidence: A)

78
Q

What are the ACC/AHA guidelines for nitrates and hydralazine for class IIA?

A

Addition of isosorbide dinitrate and hydralazine to a standard medical regimen for HF, including ACEIs and beta-blockers, is resonable and can be effective in blacks with NYHA functional class III or IV HF. Others may benefit, but not yet tested. (Level of Evidence: A)

79
Q

What do antiplatelet & anticoagulants target?

A

Thromboxane A2

80
Q

ASA- uses?

A

ASA reduces risk of CV events in patients without CHF but this has not been demonstrated in CHF patients
Concern that ASA may interfere with benefits of ACEIs
If ASA needed (ischemic pt), dose </= 160mg/d

81
Q

What are anticoagulants reserved for?

A

Reserved for patients with Afib or previous TE (transient ischemic episode) (risk of TE low:1-3%/yr)

82
Q

What are the anticoagulants?

A

Heparin

Onoxapirin

83
Q

What are medications to avoid in CHF?

A

Class III; Level of Evidence: A
—-All antiarrhythmics, except amiodarone and dofetilide, should be avoided because of increasing mortality
CCB (calcium channel blockers), only vasoselective (amlodipine) agents have not adversely effected survival
–NSAIDs promote sodium retention, inhibit renal blood flow
This opposes what you want to do therefore are contraindicated except low dose ASA if the patient is ischemic

84
Q

What is the current treament for CHF?

A
  • -ACEI for all patients (NYHA-FC I-IV) (no matter how bad sx are, can sub with ARB)
  • -Beta-blockers for all patients (be careful when they get worse, if they progress to the worst sx then beta blockers can end up making it worse): Use in NYHA I-III, carefully in IV, Use either metoprolol XL, bisprolol, or carvedilol
  • -ARBs for intolerant patients: Use candesartan or valsartan
  • -Nitrates and Hydralazine for patients intolerant to ACEIs and ARBs (or added to patients that are worse)
85
Q

What is the current treament for CHF (continued)

A
  • -Spironolactone for NYHA III/IV on standard therapy: Provided they have adequate renal function and can be monitored closely (BUN/SCr and K+), Eplerenone for post-MI patients with LV dysfunction or those with gynecomastia from spironolactone
  • -Addition of ARB to ACE inhibitor and beta-blocker: Consider if patient with consistent symptoms, Do not use combine ACEI + Aldosterone antagonist + ARB. NO DATA!
86
Q

What is acute decompnesation of chronic heart failure (ADHF)?

A

Occurs in patients with prior history of LV dysfunction

87
Q

What are the signs/symptoms acute decompnesation of chronic heart failure (ADHF)?

A

Increased dypsnea on exertion (DOE) or at rest, increased fatigue, PND, orthopnea
Physical exam- increased lower extremity pitting edema, hepatomegaly, JVD, (+) HJR, rales/crackles, tachycardia, gallops

88
Q

BNP for ADHF?

A

> 100pg/mL, 90% sensitivity and 76% specificity for dx of ADHF

89
Q

After initial hospitalization _____% with ADHF are readmitted within 6 months?

A

50%

90
Q

What are the causes of ADHF?

A 
Non-compliance- medical, nutrition
Adverse drug effects- NSAIDS, decongestants, Alka-selzer, beta agonists
Undertreatment of HF
Progression of disease
Acute MI- check ECG and cardiac enzymes
91
Q

Control of normal cardiac contractility is done by?

A
  • -Calcium entry from outside the cell triggers release of&raquo_space; calcium from SR
  • -Increased intracellular calcium initiates the contractile process
  • -Calcium is removed by reuptake into SR and extrusion from cell via Ca++/Na+ exchange
  • -Sodium balance is restored by Na+/K+ ATPase
92
Q

What are the three compensatory mechanisms involved in HF?

A

–Increased sympathetic activation
–Fluid retention
–Myocardial dilation and hypertrophy
Initial chamber dilation improves contractility
Excessive elongation => weaker contraction
Wall hypertrophy impairs filling

93
Q

What is impaired ventricular contraction?

A

Systolic HF

94
Q

What is impaired ventricular relaxion that has impaired relaxation and filling?

A

Diastolic HF

95
Q

What is cardiac output?

A

CO = heart rate (HR) x Stroke Volume (SV)
Amount of blood ejected from the left ventricle
Normal CO = 4-8 L/min

96
Q

What is cardiac index (CI)?

A

CI = CO/BSA

Normal CI = 2.8-4.2 L/min/m2

97
Q

What is pulmonary artery wedge pressure?

A

Estimate of left-ventricular end-diastolic pressure
LVEDP = LVED volume = preload
Normal PAWP = <12 mmHg

98
Q

What is systemic vascular resistance (SVR)?

A

Pressure the left ventricle must overcome to eject its blood volume = afterload
Normal value = 900-1400 dynes/sec/cm-5

99
Q

What is the pulmonary artery catheterization (PAC)?

A
  • -Swan-Ganz® catheter
  • -Used for diagnosis, monitoring, and goal-directed therapy
  • -It is a soft, flow-directed catheter with a balloon at the tip used for measuring various pressures
  • -It is introduced typically into the right IJ or the left subclavian vein and is guided by blood flow into the subclavian, then superior vena cava through the venous system to the right atrium and ventricle then into the pulmonary artery
  • -A monitor at the distal lumen tip provides measurement of pulmonary artery pressure and PAWP as well as CO
100
Q

If adaptive mechanisms adequately restores CO is it compensated or decompensated?

A

Compensated

101
Q

If adaptive mechanisms fail to maintain CO is is compensated or decompensated?

A

Decompensated

102
Q

What are the compensatory mechanisms involved with increased sympathetic activity in ADHF?

A
  • -Activation of baroreceptors, responding to low blood pressure
  • -Increased Beta-response leads to increased HR, increased contractility
  • -Alpha1-response results in increased vasoconstriction increased venous return and increased cardiac preloadincreased work load adding to CHF
103
Q

What are the compensatory mechanisms involved with fluid retention in ADHF?

A

As a response to decreased blood flow to the kidney increased release of renin, resulting in synthesis of angiotensin II and aldosterone. This in turn leads to increased PVR, retention of Na+ & H20 leading to edema  increased work load on the heart.

104
Q

What are the compensatory mechanisms involved with myocardial hypertrophy in ADHF?

A
  • -Heart muscles stretch, the walls of the ventricles thicken and the ventricles dilate to compensate for the extra work put on the heart (Saggy, baggy heart).
  • -Systolic failureexcessive elongation of fibers so ventricle unable to contract effectively
  • -Diastolic failurehypertrophy of ventricles affects ability to relax, does not fill properly.
105
Q

What are the therapeutic goals of ADHF?

A
  • -Improve signs and symptoms: Decrease SOB, weight, BNP levels, Increase oxygenation
  • -Stabilize the hemodynamic condition: Decrease PCWP, Increase cardiac output
  • -Decrease mortality
106
Q

What are the loop diuretics?

A

Furosemide
Bumetanide
Torsemide

107
Q

What are loop diuretics used for?

A

To reduce pulmonary and systemic congestion

108
Q

Loop diuretics- ROA, MOA, monitor

A

Administered IV, can be through continuous infusion
Act through both venodilation as well as Na+ and H2O excretion
Monitoring: K+ and Mg2+, BUN/Cr, blood pressure

109
Q

What is the first line choice for a “wet patient”?

A

Loop diuretics IV

110
Q

Sequential nephron blockade (add thiazide diuretic)?

A

Metolazone

Cchlorothiazide

111
Q

What are the positive inotropes?

A

Dobutamine
Dopamine
Inamrinone and Milrinone
Amiodarone

112
Q

Dobutamine-MOA

A

Potent beta1 and beta2 receptor agonist, weak alpha1 agonist
Predominate effect is (+) inotropy (is the big effect) and chronotropy which increases cardiac output and vasodilation which decreases SVR

113
Q

Dobutamine- monitoring

A

vitals, urine output; K+, telemetry (arrhythmias) (concern is development for arrhythmias)

114
Q

Dopamine- MOA

A

Effects beta, alpha and dopaminergic (DA1) receptors

115
Q

What do low DA1 doses cause?

A

increase renal flow and urinary output (decreased SVR, but not really given with <3 failure)

116
Q

What do medium doses of dopamine cause?

A

beta1 effects, which increases CO, some mild alpha1 effects may increase SVR (big reason why you give this)

117
Q

What do high doses of dopamine causes?

A

mcg/kg/min alpha1 effects predominate and increase vasoconstriction (SVR)

118
Q

Dopamine- monitoring

A

vitals, urine output, K+, telemetry (arrhythmias)

119
Q

What are the B-adrenergic agonists?

A

Dobutamine

Dopamine

120
Q

What are the phosphodiesterase inhibitors?

A

Inamrinone
MILRINONE
Amiodarone

121
Q

Inamrinone and milrinone- MOA

A
  • -Increase intracellular cAMP which increases intracellular calcium which increases contractility and cardiac output
  • -Slower onset than dopamine and dobutamine, require loading dose
  • -Longer t1/2 (2-4 hours) therefore titration more difficult
122
Q

Inamrinone and milrinone- monitoring

A

vitals, urine output, K+, telemetry (arrhythmias)

123
Q

Amiodarone

A

Clinical trials have shown that it does not reduce incidence of sudden death or prolong survival in patients with CHF

124
Q

What are the other IV inotropes?

A

Epinephrine
Norepinesphrine
Isoproterenol

125
Q

Epinephrine and Norephinephrine-MOA

A

beta1, beta2 and alpha1 receptor agonists

Increase CO and SVR

126
Q

Isoproterenol- MOA

A

Beta1 and beta2 agonists therefore increases CO and decreases SVR

127
Q

Epinephrine, norepinephrine, isoproterenol- monitoring

A

vitals, urine output, K+, telemetry (arrhythmias)

128
Q

Nitroprusside and nitroglycerin- MOA

A

Venodilators

  • -Reduce preload and therefore PCWP
  • -Nitroglycerin is preferred when CO is not severely compromised or when other inotropic agents are administered
  • -Nitroprusside is also an arterial vasodilator and is preferred in patients with an increased SVR
129
Q

Nitroprusside and nitroglycerin- adverse effects

A

HA, dizziness, reflex tachycardia, hypotension, thiocyanate toxicity (for nitroprusside)

130
Q

Nitroprusside and nitroglycerin- monitor

A

Vitals

131
Q

When should you decrease the dose of nitroglycerin?

A

If SBP decreased below 90-100 mmHG

132
Q

Why should you taper nitroprusside?

A

To avoid rebound HTN

133
Q

What are the vasodilators?

A

Nitroglycerin
Nitroprusside
Morphine
Nesiritide (Natrecor)

134
Q

Morphine- MOA

A 
Reduces preload (via venodilation) and therefore PCWP
Reduces heart rate
135
Q

Morphine- uses and ROA

A

Typically used in the early stage of treatment particularly if patient has associated anxiety
ROA- IVP (IV push)

136
Q

Morphine- Monitor

A

vitals (monitor RR, used a lot in beg and end)

137
Q

Nesiritide (Natrecor)- MOA

A
  • -Recombinant B-type natriuretic peptide
  • -Increases intracellular cGMP which leads to smooth muscle relaxation
  • -Promotes vasodilation, natriuresis, and diuresis
  • -Reduces PCWP, SVR, and increase CO
138
Q

Nesiritide (Natrecor)- Adverse effects

A

hypotension (contraindicated if SBP < 90 mmHg)

139
Q

Nesiritide (Natrecor)- monitor

A

Vitals

140
Q

What is the current controversy with nesiritide?

A

Trials show that they worsen renal function and increased mortality

141
Q

If a patient presents warm and dry what is the treatment goal and what is the treatment?

A

Tx goal- Initiate or titrate CHF therapy

Tx- ACEI, BB +/- digoxin, +/- spironalactone

142
Q

If a patient presents cold and dry what is the treatment goal and what is the treatment?

A

Tx goal- increase CO

Tx- Fluids, +/- IV inotropes, +/- mechanical assistance (IABP, LVAD)

143
Q

If a patient presents cold and wet what is the treatment goal and what is the treatment?

A

Tx goal- increase CO and relieve congestion
Tx- Adequate BP, nitrates or nesiritide, +/- IV diuretics, +/- ionotropes.
Low BP- IV ionotropes, + IV diuretics, +/- mechanical assistance

144
Q

If a patient presents warm and wet what is the treatment goal and what is the treatment?

A

Tx goal- relieve congestion

Tx- IV diuretics, +/- nitrates or nesiritide, +/- IV diuretics

145
Q

Patients in decompensation are at risk for clots what should you add to their tx?

A

Anticoagulation

146
Q

What is used for the prophylaxis of venous thromboembolism?

A 
Heparin
LMWH (do not use if CrCl <30 ml/min)

Pharmacology II (23 decks)

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