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Cardio Final > Treatment of Chronic HF > Flashcards

Treatment of Chronic HF Flashcards

1
Q

Systolic dysfunction =

A

HF with reduced EF (pump problem)
EF less than or equal to 40%
Left ventricular dysfunction
Dilated cardiomyopathy

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2
Q

Diastolic dysfunction =

A

HF with preserved EF (filling problem)
EF greater than or equal to 50
Symptoms of SOB or fatigue are common
Left ventricular hypertrophy or abnormal LV diastolic function

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3
Q

Borderline HFpEF

A

41-49%

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4
Q

Improved HFpEF

A

> 40% but previously had HF with reduced EF

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5
Q

Causes of HF

A 
Drugs
MI
HTN
CAD
Idiopathic
Volume overload
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6
Q

All of the causes of HF cause

A

Decrease CO and Increase sympathetic NS

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7
Q

Increased cardiac output can lead to

A

Increased renin which makes more Ang I and then Ang II which then leads to aldosterone synthesis which causes sodium and water retention and increase preload

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8
Q

Ang II can also cause

A

Increased sympathetic NS and arteriolar constriction

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9
Q

Increased Sympathetic NS causes

A
  1. Increase HR
  2. Increased venous constriction which increases preload
  3. Arteriolar constriction which increases afterload
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10
Q

Beta blockers are used to

A

Decrease HR and sympathetic NS tone

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11
Q

Hydralazine =

A

Potent arteriole dilator which helps decrease afterload

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12
Q

Detrimental effects of increased sympathetic activity are

A

Increase HR which decrease ventricular filling time
Excess catecholamines which can be cardiotoxic and further decrease the hearts function
Cardiac stimulations which can stimulate arrhythmias
Increased afterload which can further decrease SV

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13
Q

Class I

A

No limitation of physical activity

Ordinary physical activity does not cause symptoms of HF

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14
Q

Class II

A

Slight limitation of PA

Comfortable at rest, but ordinary PA results in symptoms

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15
Q

Class III

A

Marked limitation of PA

Comfortable at rest but less than ordinary activity causes symptoms of HF

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16
Q

Class IV

A

Unable to carry on any PA without symptoms of HF or symptoms of HF at rest

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17
Q

Stage A

A

Patients at high risk for developing HF

- HTN, CAD, diabetes, obesity, metabolic syndrome

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18
Q

Stage B

A

Patient with structural hear disease but no HF signs/symptoms
- Previous MI, LV hypertrophy, LV systolic dysfunction

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19
Q

Stage C

A

Patients with structural heart disease and current or previous symptoms
- LV systolic dysfunction and symptoms such as dyspnea, fatigue, and reduced exercise tolerance

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20
Q

Stage D

A

Refractory HF requiring specialized intervention

- Cannot be discharge without medical assist devices or inotropic therapy

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21
Q

Goals of therapy for HFrEF

A

Improve patients quality of life by: reducing symptoms, reduce hospitalization, slow progression, increase exercise tolerance, prolong survival

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22
Q

Treatment Principle: Determine Etiology and/or Precipitating Factors

A

Disease associated with a cause or trigger of HF (obesity, thyroid disorder, DM, acromegaly and growth hormone deficiency, cardiomyopathy, myocarditis)
Nonadherence with drugs and non-drug therapy
Medications: Alcohol, glucocorticoids, smoking

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23
Q

Treatment Principle: ID pts at risk and prevent progression

A 
Treat and control HTN
Manage CAD/dyslipidemia
Control hyperglycemia
Smoking cessation 
Weight loss
Regular exercise (once euvolemia and stable)
Moderate sodium-restricted diet
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24
Q

Role of BNP testing

A

Released when the heart is excessively stretched and it stimulates natriuresis and diuresis
Useful in evaluation of pts presenting to urgent care
Might be useful in establishing prognosis or severity

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25
Q

Diuretics and nitrates therapeutic actions in CHF

A

Decrease Preload

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26
Q

ACEi/ARBs therapeutic actions in CHF

A

Decrease neurohormonal tone
Decreased preload
Decreased afterload

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27
Q

Beta Blockers therapeutic actions in CHF

A

Decrease neurohormonal tone

Decrease chronotrope

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28
Q

Digoxin therapeutic actions in CHF

A

Positive inotrope

Decreased neurohormonal tone

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29
Q

Hydralazine therapeutic actions in CHF

A

Decreased afterload

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30
Q

Aldosterone antagonists therapeutic actions in CHF

A

Decrease prelaod
Decrease neurohormonal tone
Decrease myocardial fibrosis

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31
Q

Diuretics Relieve symptoms of Congestion/edema

A 
Peripheral edema
Pulmonary edema (crackles)
Portal congestion (jugular venous distention, hepato-judular reflex)
Usually used in combination with other agents and Na restriction
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32
Q

Diuretics can improve

A

Cardiac function, symptoms, exercise tolerance

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33
Q

What type of diuretics is more potent than another?

A

Loop is more potent than thiazide

34
Q

Goal with diuretics

A

Eleminate clinical evidence on fluid retention

35
Q

Thiazide Diuretics

A

Relatively week
Good option for HTN and mild fluid retention
May work in early stages of HF but more potent agents are typically needed for congestion
Sometimes in combo with loops

36
Q

Loop diuretics

A

May lower BP acutely
Remain effective with impaired renal function
PO is usually less potent then IV
Use dosages that maintain patient at a stable weight

37
Q

Loops for chronic use

A

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

38
Q

Furosemide (Lasix) dose

A

20-40 mg daily or BID

Max: 160-200 mg

39
Q

Bumetanide (Bumex) Dose

A

0.5-1.0 mg daily or BID

Max single dose 4-8 mg

40
Q

Torsemide (Demadex) Dose

A

10-20 mg daily

Max single dose 100-200 mg

41
Q

Diuretic resistance

A

Change to a different loop

Combine with thiazide

42
Q

Diuretics Monitoring Parameters

A 
Symptoms
Weight
PE
In's and Outs in acute settings
Electrolytes (K, Na, Mg, Uric acid, BUN/SCr)
43
Q

Potassium Loss

A

Maximum fall in potassium is usualy reached by the end of the first week

44
Q

Potassium Replacement

A

Dietary supplementation
Potassium sparing diuretics (triamterene/dyrenium, sprinolactone/aldactone, amiloride/midamorc)
Potassium supplements (HCl 20-120 mEq/d)

45
Q

***Diuretic Clinical Pearls

A

Know dry weight and weigh daily
May be used PRN or as a sliding scale
Combine with moderate sodium restriction
May alter the efficacy/toxicity of other agents (NSAIDs, ACEi)
Avoid agents that may block diuresis (NSAIDs, large sodium intake, glucocorticoids)

46
Q

ACEi/ARBs Therapeutics

A 
Provide symptomatic relief (increase QOL)
Decrease hospitalizations 
Improve CO
Improve functional capacity
DECREASE MORBIDITY AND MORTALITY
47
Q

ACEi/ARB Action

A

Decrease preload and afterload
Decrease neurohormonal tone
Increase CI, SV and decrease LV and SVR

48
Q

ACEi/ARB Recommendations for HFrEF

A

All patients with LVD unless contraindicated
Used together with beta-blockers
Use ARBs in those who can’t tolerant ACEi
May be useful to prevent HF in those at high risk
They have long term benefits even if symptoms present

49
Q

SEE LECTURE FOR DOSES

A

SEE LECTURE FOR DOSES

50
Q

ACEi/ARB AE

A 
Hypotension 
Renal insufficiency if pts have sever HF , hypoNa and dehydration
HyperK
Angioedema
Cough (up to 40%)
51
Q

Captopril challenge

A

Patients have reduced EF to begin with so here you give them a very small dose and see how they respond to it

52
Q

***ACEi/ARB Clinical Pearls

A

Use ACEi first
Start low and go slow
Increase as toelrated to target doses

53
Q

Beta-Blocker Therapeutics

A

Recommended for routine use in HFrEF
Improved symptoms
Decreased hospitalizations
Decreased morbidity and mortality

54
Q

Beta Blocker Actions

A

Slow heart rate to allow for adequate filling of LV
Sympathetic NS antagonists (decrease neurohormonal tone)
Anti-arrhythmic
Decrease MVO2, HF and increase EF, CO, SV

55
Q

Beta Blocker Recommendations in HFrEF

A

In all paitnets with current or prior to symptoms and decrease LVEF
Start in stable patients on diuretics
Should be used in combo with ACEi/ARB or diuretic

56
Q

Beta Blocker AE/Monitoring

A

Daily weight
HR and BP (if hypotensive, consider doing ACEi/ARB and beta blocker at different time or decrease diuretic)
Counsel patients on the fact that they might feel worse initially
May need to decrease ACEi or increase diuretic dose initially

57
Q

***Beta Blocker Clinical Pearls

A 
Benefits take 2-3 months
Use drugs with HF data
Start low and go slow
Even if symptoms do not improve, long-term benefits do occur
Avoid abrupt withdraw
58
Q

Aldosterone Antagonists Therapeutics

A

Conisder in HFrEF pts with Class II-IV with recent hospitalization or elevated natriuretic pepetides or patients with LVDF early after MI
Used as add-on to ACEi/ARB and beta blcokers
Use with milder symptom pts
DECREASE MORBIDITY AND MORTALITY
Improves symptoms

59
Q

Aldosterone Antagonists Actions

A

Potassium Sparing Diuretics
Aldosterone receptor antagonists
Decrease Na retention, Mg and K loss, sympathetic activity, PS inhibition, myocardial and vascular fibrosis, baroreceptor dysfunction and vascular damage and impaired arterial compliance

60
Q

Aldosterone Receptor Recommendations

A

Decreased mortality in patients with current or recent Class II-IV
Should be considered in patients with advanced HF

61
Q

Aldosterone Antagonists AE

A

Hyperkalemia (avoid if CrCl is less than 30 or baseline K is greater than 5)
Impotence and gynecomastia in men
Menstrual irregularities in women

62
Q

***Aldosterone Antagonists Monitoring

A 
Renal function (use smaller doses if CrCl is less than 50)
Avoid when SCr is >2.5 in men or >2.0 in females
Chem Chem 7 in 3 days and at 1 week after initiation and at least monthly for first 3 months
63
Q

Aldosterone Antagonists Clinical Pearls

A

After initiating hold K supplement or reduce dose and carefully monitor for hyperkalemia
Hold during an episode of diarrhea or while loop diuretic therapy interrupted
Counsel to avoid foods high in K and to not use NSAIDs

64
Q

Hydrazline MOA

A

Works on arteriolar constriction and decreases afterload

May interfere with progression of HF

65
Q

Isosorbide Dinitrate MOA

A

Works on venous constriction to decrease preload

Decreases dyspnea at night and improves exercise tolerance

66
Q

H/ID Therapeutics

A

First therapy to demostrate reduction in mortality but not hospitalizations
(less effective than ACEi in HF so not first line)
Higher doses of H needed in HF

67
Q

H/ID Recommendations

A

May be considered for patients who can’t deal with ACEi/ARBs
Should not be used in those who haven’t used ACEi/ARBs and are not a substituted for these
Combination (BiDil) has been shown to be beneficial in blacks
As an add on therapy in Class III/IV HF it does decrease mortality, hospitalizations and improved quality of life

68
Q

H/ID AE/Monitoring

A

Headache
Dizziness
GI upset
Na/H2O retention, SLE drug induced with H

69
Q

***H/ID Clinical Pearls

A

Side effects limit drug use
Poor adherence bc it is TID
Consider in blacks

70
Q

Digoxin Therapeutics

A

Improve symptoms and QofL

Decrease hospitalization

71
Q

Digoxin MOA

A

Mild positive inotrope
Increase vagal tone which decreases HR and increases diastolic filling
Vagal effect causes decreased conduction and increase in refractoriness in AV node
Blunt excessive neurohormonal activation

72
Q

Digoxin Recommendations

A

Consider add on in pts with more severe HFrEF (class III-IV) to BB, ACEi, diuretics, ARBs
May improve clinical status of these pts
Consider in HFrEF with HF who have rapid response afib

73
Q

Digoxin AE

A

Anorexia, N/V, visual disturbances, fatigue, weakness, headache
Arrhythmias, bradycardia, heart block

74
Q

Digoxin Monitoring

A

Monitor K, Mg, Ca
Vital signs (HR, BP)
Serum concentration monitoring debatable

75
Q

**Digoxin Clinical Pearls

A

Do not withdraw without a clear indication
If you do monitor, go with lower concentrations
Pts may have toxicity with normal concentrations in the setting of hypoK, hypoMg, and hypothyroidism
Watch for drug intearctions

76
Q

Calcium Channel Blockers Recommendations

A

Not recommended for routine treatment in pts with HFrEF

77
Q

Stage A Treatment

A

ACEi/ARB

78
Q

Stage B Treatment

A

ACEi/ARB and beta-blocker

79
Q

Stage C Treatment

A

ACEi + Beta blocker
Presistent volume overload = diuretics
Persistent HTN = ARB, hydralazine, Amlodipine or felodipine (DHP CCB)
Concomitant angina = Nitrates or amlodipine or felodipine

80
Q

Management based on control of RF associated with progression to systolic dysfunction of which diseases?

A 
Dyslipidemia
Control HTN
HR
Intervention for CAD
Consider beta-blocker use when appropriate

Cardio Final (12 decks)

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