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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
Diuretics and nitrates therapeutic actions in CHF
Decrease Preload
26
ACEi/ARBs therapeutic actions in CHF
Decrease neurohormonal tone Decreased preload Decreased afterload
27
Beta Blockers therapeutic actions in CHF
Decrease neurohormonal tone | Decrease chronotrope
28
Digoxin therapeutic actions in CHF
Positive inotrope | Decreased neurohormonal tone
29
Hydralazine therapeutic actions in CHF
Decreased afterload
30
Aldosterone antagonists therapeutic actions in CHF
Decrease prelaod Decrease neurohormonal tone Decrease myocardial fibrosis
31
Diuretics Relieve symptoms of Congestion/edema
``` Peripheral edema Pulmonary edema (crackles) Portal congestion (jugular venous distention, hepato-judular reflex) Usually used in combination with other agents and Na restriction ```
32
Diuretics can improve
Cardiac function, symptoms, exercise tolerance
33
What type of diuretics is more potent than another?
Loop is more potent than thiazide
34
Goal with diuretics
Eleminate clinical evidence on fluid retention
35
Thiazide Diuretics
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
Loop diuretics
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
Loops for chronic use
Furosemide (Lasix) Bumetanide (Bumex) Torsemide (Demadex)
38
Furosemide (Lasix) dose
20-40 mg daily or BID | Max: 160-200 mg
39
Bumetanide (Bumex) Dose
0.5-1.0 mg daily or BID | Max single dose 4-8 mg
40
Torsemide (Demadex) Dose
10-20 mg daily | Max single dose 100-200 mg
41
Diuretic resistance
Change to a different loop | Combine with thiazide
42
Diuretics Monitoring Parameters
``` Symptoms Weight PE In's and Outs in acute settings Electrolytes (K, Na, Mg, Uric acid, BUN/SCr) ```
43
Potassium Loss
Maximum fall in potassium is usualy reached by the end of the first week
44
Potassium Replacement
Dietary supplementation Potassium sparing diuretics (triamterene/dyrenium, sprinolactone/aldactone, amiloride/midamorc) Potassium supplements (HCl 20-120 mEq/d)
45
***Diuretic Clinical Pearls
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
ACEi/ARBs Therapeutics
``` Provide symptomatic relief (increase QOL) Decrease hospitalizations Improve CO Improve functional capacity DECREASE MORBIDITY AND MORTALITY ```
47
ACEi/ARB Action
Decrease preload and afterload Decrease neurohormonal tone Increase CI, SV and decrease LV and SVR
48
ACEi/ARB Recommendations for HFrEF
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
SEE LECTURE FOR DOSES
SEE LECTURE FOR DOSES
50
ACEi/ARB AE
``` Hypotension Renal insufficiency if pts have sever HF , hypoNa and dehydration HyperK Angioedema Cough (up to 40%) ```
51
Captopril challenge
Patients have reduced EF to begin with so here you give them a very small dose and see how they respond to it
52
***ACEi/ARB Clinical Pearls
Use ACEi first Start low and go slow Increase as toelrated to target doses
53
Beta-Blocker Therapeutics
Recommended for routine use in HFrEF Improved symptoms Decreased hospitalizations Decreased morbidity and mortality
54
Beta Blocker Actions
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
Beta Blocker Recommendations in HFrEF
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
Beta Blocker AE/Monitoring
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
***Beta Blocker Clinical Pearls
``` 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
Aldosterone Antagonists Therapeutics
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
Aldosterone Antagonists Actions
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
Aldosterone Receptor Recommendations
Decreased mortality in patients with current or recent Class II-IV Should be considered in patients with advanced HF
61
Aldosterone Antagonists AE
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
***Aldosterone Antagonists Monitoring
``` 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
Aldosterone Antagonists Clinical Pearls
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
Hydrazline MOA
Works on arteriolar constriction and decreases afterload | May interfere with progression of HF
65
Isosorbide Dinitrate MOA
Works on venous constriction to decrease preload | Decreases dyspnea at night and improves exercise tolerance
66
H/ID Therapeutics
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
H/ID Recommendations
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
H/ID AE/Monitoring
Headache Dizziness GI upset Na/H2O retention, SLE drug induced with H
69
***H/ID Clinical Pearls
Side effects limit drug use Poor adherence bc it is TID Consider in blacks
70
Digoxin Therapeutics
Improve symptoms and QofL | Decrease hospitalization
71
Digoxin MOA
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
Digoxin Recommendations
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
Digoxin AE
Anorexia, N/V, visual disturbances, fatigue, weakness, headache Arrhythmias, bradycardia, heart block
74
Digoxin Monitoring
Monitor K, Mg, Ca Vital signs (HR, BP) Serum concentration monitoring debatable
75
****Digoxin Clinical Pearls
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
Calcium Channel Blockers Recommendations
Not recommended for routine treatment in pts with HFrEF
77
Stage A Treatment
ACEi/ARB
78
Stage B Treatment
ACEi/ARB and beta-blocker
79
Stage C Treatment
ACEi + Beta blocker Presistent volume overload = diuretics Persistent HTN = ARB, hydralazine, Amlodipine or felodipine (DHP CCB) Concomitant angina = Nitrates or amlodipine or felodipine
80
Management based on control of RF associated with progression to systolic dysfunction of which diseases?
``` Dyslipidemia Control HTN HR Intervention for CAD Consider beta-blocker use when appropriate ```

Cardio Final (12 decks)

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