Heart Failure Flashcards

1
Q

Heart failure results from…

A

the inability of the heart to pump sufficient blood to meet the metabolic needs of the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Systolic Dysfunction

A

reduced contractility and reduced ejection fraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Diastolic dysfunction

A

stiffening and loss of adequate relaxation, which reduces filling and CO

ejection fraction may be normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Systolic etiologies

A
  • ischemic heart disease
  • chronic HTN
  • dilated cardiomyopathy
  • myocarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Diastolic etiologies

A
  • HTN with LV Hypertrophy
  • restrictive and hypertrophic cardiomyopathies
  • fibrosis
  • amyloidosis
  • sarcoidosis
  • constrictive pericarditis
  • hemochromatosis
  • valvular disease
  • aging
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

You will hear an S3 gallop in ______ heart failure

A

systolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

You will hear an S4 gallop in ______ heart failure

A

diastolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

_______ limits diastolic filling time and coronary flow, further stressing the heart.

A

Tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Primary and signs and symptoms of all types of heart failure

A
  • tachycardia
  • decreased exercise tolerance
  • shortness of breath
  • cardiomegaly
  • peripheral and pulmonary edema are often but not always present
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

ACC/AHA Stage A HF

A

Patients at high risk for developing heart failure

Ex: HTN, ASCVD, DM, obesity, metabolic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

ACC/AHA Stage B HF

A

pts w/structural heart dz but no HF signs or symptoms

Ex: Previous MI, LVH, LV systolic dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

ACC/AHA Stage C HF

A

pts w/structural heart disease and current or previous symptoms

Ex: LV systolic dysfunction & symptoms like dyspnea, fatigue, and reduced exercise tolerance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ACC/AHA Stage D HF

A

refractory HF requiring specialized interventions

Ex: pts with treatment refractory symptoms at rest despite maximal medical therapy: pts requiring recurrent hospitalization or who cannot be discharged without mechanical assist devices or inotropic therapy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

NYHA Class I

A

no limitation of physical activity

ordinary physical activity does not cause symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

NYHA Class II

A

slight limitation of physical activity

comfortable at rest

ordinary physical activity causes symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

NYHA Class III

A

marked limitation of physical activity

comfortable at rest

less than ordinary activity causes symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

NYHA Class IV

A

severe limitation and discomfort with any physical activity

symptoms present even at rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Goals of pharmacologic therapy of HFrEF

A

improve symptoms (risk of hospitalization)

slow or reverse deterioration in myocardial function, and reduce mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Improvement in symptoms is achieved by which drugs?

A
  • diuretics
  • BB
  • ACE-I
  • ARBs
  • ARNI (angiotensin receptor-neprilysin inhibitor)
  • hydralazine plus nitrate
  • digoxin
  • aldosterone antagonists
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Prolonged survival rate has been documented with which drugs?

A
  • Beta Blockers
  • ACE-I
  • ARNI
  • hydralazine plus nitrate
  • aldosterone antagonists
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

T/F: drug therapy should be titrated as tolerated to target ranges for optimum clinical benefit

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

T/F: benefits observed from aggressive monitoring strategies suggest treatment beyond clincial congestion may improve outcomes

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What medications would you use for Stage A HF pts?

A

ACE-I or ARB or BB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What meds would you use for Stage B pts with HF

A

ACE-I or ARB as appropriate

BB as appropriate

In select patients:

  • ICD
  • Revascularization or valvular surgery as appropriate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What meds would you use in patients with **Stage C** HF
**HFrEF:** - diuretics - ACE-I or ARB - BB - Aldosterone antagonists - Ivabradine - Sacubitril/Valsartan **In select pts:** - hydralazine/isosorbide dinitrate - Digitalis - CRT - ICD - Revascularization or valvular surgery as appr. **HFpEF:** - Diuresis - Guidelines driven indications for comorbidites - **Aldosterone antagonism** to reduce HF hospitalizations
26
What meds would you give pts with **Stage D HF**?
- advanced care measures - heart transplant - temporary or permanent MCS (mechanical circulatory support) - Experimental surgery or drugs - Palliative care and hospice
27
**MOA:** **Decreases NaCl, KCl, Calcium, Magnesium reabsorption** in **thick ascending limb** of the loop of Henle in the nephron What drug is this?
Furosemide
28
Effects of this drug: - increased **excretion of salt and water** - reduces **cardiac preload & afterload** - reduces **pulmonary and peripheral edema** **What drug is this?**
Furosemide
29
Clinical applications of Furosemide
* **Acute and chronic heart failure** * severe hypertension * edematous conditions
30
Toxicity: hypovolemia, hypokalemia, orthostatic hypotension, ototoxicity, sulfonamide allergy
Furosemide
31
**MOA:** Decreases NaCl reabsorption in the **distal convoluted tubule** **What drug?**
Hydrocholorothiazide (HCTZ)
32
Clinical applications of Hydrocholorothiazide (HCTZ)
* **mild chronic HF** * mild-moderate hypertension * hypercalciuria * **has not been shown to reduce mortality**
33
Toxicity: - hyponatremia - hypokalemia - **hyperglycemia** - **hyperuricemia** - **hyperlipidemia**
Hydrocholorothiazide
34
**MOA:** blocks cytoplasmic **aldosterone receptors** in **collecting tubules** of nephron, possible membrane effect What drug?
Spironolactone (Aldosterone Antagonist)
35
Effects: **- increased salt and water excretion** **- reduces remodeling** - reduces mortality
Spironolactone (Aldosterone Antagonist)
36
Clinical applications of **Spironolactone**
- **Chronic heart failure** **-** aldosteronism (cirrhosis, adrenal tumor) - hypertension - **has been shown to reduce mortality**
37
Toxicity: **Hyperkalemia:** risk increases if Creatinine \>1.6 mg/dL Avoid is Baseline K+\> 5 mEq/L - **Antiandrogen actions**
Spironolactone
38
What is the #1 recommended strategy to reduce the risk for hyperkalemia with aldosterone antagonists?
counsel pts to: - **limit intake of high potassium-containing foods and salt substitutes** - Avoid the use of over the counter NSAIDS
39
**MOA:** Inhibits angiotensin converting enzyme **Effects:** **- ateriolar and venous dilation** **-** reduces **aldosterone secretion** - reduces cardiac remodeling
ACE-I (angiotensin antagonists) ## Footnote **Lisinopril**
40
Clinical applications: - **chronic heart failure** - diabetic renal disease - **has been shown to reduce mortality**
ACE-I (Angiotensin Antagonists) ## Footnote **Lisinopril**
41
Toxicity: - **cough** - **hyperkalemia** - angioedema Interactions: additive w/other angiotensin antagonists
ACE-I (Angiotensin Antagonist) ## Footnote **Lisinopril**
42
**MOA:** Antagonize AII effects at AT1 receptors
Losartan
43
**Clinical applications:** **-chronic heart failure** - hypertension - diabetic renal disease - **has been shown to reduce mortality** - **used in pts intolerant to ACE-I**
**Losartan (ARB)**
44
Can you use ACE-I and ARB together?
NO
45
Toxicity: - hyperkalemia - angioneurotic edema Interactions: - additive with other angiotensin antagonists
**Losartan (ARB)**
46
MOA: **neprilysin blocker**/ARB
ANRi: Sacubitril/valsartan
47
T/F: **discontinue ACE inhibitors** at least 3**6 hours before** initiating **sacubitril/valsartan** treatment
TRUE
48
MOA: competitively **blocks B-1 and A-1 receptors**
**Carvedilol** (Beta Blockers)
49
Effects: - slowsl heart rate - reduces blood pressure - poorly understood effects - reduces heart failure mortality
**Carvedilol** (Beta Blockers)
50
Clinical Applications: - slows progression of **chronic heart failure** - reduces mortality in moderate and severe heart failure
**Carvedilol (**Beta Blockers)
51
**Toxicity:** - bronchospasm - bradycardia - AV block - Acute cardiac decompensation
**Carvedilol** (Beta Blockers)
52
Select group of B blockers that have been shown to reduce heart failure mortality
Metoprolol Bisoprolol
53
Which beta blocker is effective in both **systolic (HFrEF)** and **diastolic (HFpEF)** failure?
Nebivolol
54
**MOA:** - **Releases Nitric Oxide (NO)** - activates guanylyl cyclase
Isosorbide dinitrate
55
**Effects:** - **Venodilation:** reduces preload and ventricular stretch
**Isosorbide dinitrate (Vasodilator)**
56
Clinical applications: - **acute and chronic heart failure** - angina **Toxicity:** - **postural hypotension, tachycardia, headache** **Interactions:** - additive with other vasodilators - **synergistic with phosphodiesterase type 5 inhibitors**
**Isosorbide Dinitrate (Vasodilators)**
57
Clinical applications: - **chronic failure in African Americans** **\*\***Indicated in conjunction with standard heart failure therapy to improve survival and reduce hospitalizations in self identified African American patients
**Hydralazine**- Isosorbide Dinitrate
58
MOA: **increases NO synthesis** in endothelium
**Hydralazine (Aterilar Dilators)**
59
Effects: - **reduces blood pressure and afterload** - **increases Cardiac Output**
**Hydralazine (Arteriolar dilators)**
60
Clinical applications of Hydralazine
**Hydralazine plus nitrates** have reduced mortality
61
Toxicity: - Tachycardia - Fluid retention - **Lupus-like syndrome**
Hydralazine (Arteriolar dilator)
62
MOA: rapid, powerful **vasodilation reduces preload and afterload**
**Nitroprusside**
63
**Clinical application:** acute severe decompensated failure
Nitroprusside
64
P-kinetics: - IV only - Duration: a few minutes
Nitroprusside
65
**Thiocyanate and cyanide toxicity**
Nitroprusside
66
**MOA:** Na+/K+ -ATPase inhibition results in reduced CA2+ expulsion and **increased Ca2+ stored in sarcoplasmic reticulum**
Digoxin
67
**Effects:** - increases cardiac contractility **\*\*cardiac parasympathomimetic effect (slowed sinus heart rate, slowed AV conduction)**
Digoxin (cardaic glycoside)
68
Clinical applications: - chronic symptomatic **heart failure** **- rapid ventricular rate in A-fib** **-** has not been definitively shown to reduce mortality with HFrEF
Digoxin (cardiac glycoside)
69
Toxicity: - **narrow margin of safety** **- nausea, vomiting, diarrhea, cardiac arrhythmias**
Digoxin (Cardiac Glycoside)
70
MOA: **Beta 1 selective agonist** - increases cAMP synthesis
**Dobutamine** (Beta-adrenoceptor agonist)
71
Effects: increases cardiac contractility, output
Dobutamine (Beta-adrenoceptor agonist)
72
Clinical Applications: - **acute decompensated heart failure** - intermittent therapy in chronic failure reduces symptoms
Dobutamine (Beta-adrenoceptor agonists)
73
**P-kinetics, Toxicities, Interactions:** - IV only - Duration a few minutes **Toxicity:** arrhythmias **Interactions:** additive with other sympathomimetics
Dobutamine
74
**MOA: dopamine receptor agonist, higher doses activate B and Alpha adrenoceptors** **Effects:** increases renal blood flow, higher doses increase cardiac force and blood pressure **Clinical applications: acute decompensated heart failure, shock** **\*\*IV only** **Toxicity:** arrhythmias **Interactions:** additive with sympathomimetics
Dopamine (Beta-adrenoceptor agonists)
75
**Mechanism of Action:** Phosphodiesterase type 3 inhibitors decrease cAMP breakdown **Effects:** vasodilators, lower peripheral vascular resistance increase cardiac contractility **Clinical Applications:** acute decompensated heart failure increase mortality in chronic failure **Toxicity:** arrhythmias **Interactions:** additive with other arrhythymogenic agents
Inamrinone, Milrinone
76
MOA: activates BNP receptors, increases cGMP Effects: **vasodilation + diuresis** Clinical Applications: acute decompensated failure, **has not been shown to reduce mortality** **\*\*IV only** **Toxicity:** renal damage, hypotension, may increase mortality
**Nesiritide (Natriuretic Peptide)**
77
**MOA: prolongs diastolic time** by selectively and specifically **inhibiting the If current** within the HCN channel, **reducing heart rate.** **Indication:** symptoms of heart failure that are **stable,** a **normal heartbeat** with a resting heart rate of atleast **70 beat**s per minute, **taking a beta blocker** at the **highest dose tolerated** **\*\*hopefully reduces the risk of being hospitalized for worsening heart failure\*\***
Ivabradine
78
**Interactions:** avoid concomitant use with strong **CYP3A4 inhibitors**
Ivabradine
79
T/F: In patients with NYHA class II and III HF and iron deficiency (ferritin \<100 or 100-300 if transferrin saturation is \<20), IV iron replacement may be reasonable to improve functional status.
TRUE
80
In patients with HF and anemia, ________________ shoud not be used to improve morbidity and mortality
erythropoeitin-stimulating agents
81
In patients with HF, the optimal blood pressure in those with HTN shoud be less than \_\_\_\_\_\_
130/80
82
In pts with CVD and OSA, ______ may be reasonable to improve sleep quality and daytime sleepiness
CPAP
83