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Flashcards in Heart Failure Deck (66)
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1
Q

Characterized by a high risk for HF without structural heart disease or symptoms (i.e. hypertension, atherosclerosis, diabetes, obesity, etc.)

A

Stage A

2
Q

Structural heart disease without the development of HF

-Prior MI, depressed LV ejection fraction, LVH

A

Stage B

3
Q

Characterized by structural heart disease with current or prior symptoms

A

Stage C

4
Q

Classified as end-stage HF

A

Stage D

5
Q

The fraction of blood ejected by the ventricle relative to its end diastolic volume

A

Ejection Fraction

6
Q

How do we find ejection fraction?

A

EF = (SV / LVEDV) * 100

7
Q

Normally, ejection fraction is greater than

A

50-60%

8
Q

Preload is the myocardial stretch, which can be found as

A

Preload = EDV / /EDP

9
Q

Force of myocardial contraction and is independent of preload or afterload

A

Contractility

10
Q

Characterized by decreased capacity to eject blood due to decreased contractility

-LVEF is usually less than 40-50%

A

HF with Reduced EF

11
Q

Characterized by abnormal diastolic function due to increased stiffness

-LVEF is greater than 50%

A

HF with preserved EF

12
Q

Ventricles fill at higher than normal pressures with

A

HF w/ preserved EF

13
Q

When the RV becomes thin-walled and more compliant leading it to accept a wide range of volume w/out change in filling pressures

A

RV Failure

14
Q

The most common cause of RV failure is

A

LV failure

15
Q

If RV failure is due to lung process, we call it

A

Cor Pulmonale

16
Q

Has a limited benefit in severely decreased contractility

A

Frank-Starling Mechanism

17
Q

Serves to maintain perfusion to vital organs by increasing SVR and increasing intravascular volume

A

Neuro-Hormonal Activation

18
Q

The acute effects are beneficial but the chronic effects are deleterious

A

Neuro-Hormonal Activation

19
Q

Characterized by increasing sympathetic and decreasing parasympathetic output to the heart and periphery

A

Neuro-hormonal activation

20
Q

Cleaves angiotensinogen to AN-I

A

Renin

21
Q

Cleaves AN-I to AN-II

A

ACE

22
Q

A potent vasoconstrictor that stimulates thirst and increases aldosterone and Na retention, which thus increases volume

A

AN-II

23
Q

Secreted by the posterior pituitary and functions to increase water retention in distal nephron

A

ADH/Vasopressin

24
Q

Beneficial hormones that respond to stretch and increase Na+ and water retention

A

Natriuretic peptides (ANP and BNP)

25
Q

ANP and BNP promote

A

Vasodilation

26
Q

ANP and BNP inhibit

A

Renin secretion

27
Q

Used in diagnosis of HF

A

BNP levels

28
Q

Ventricular remodeling and hypertrophy reduces wall stress and maintains

A

Contractility

29
Q

Characterized by cardiac cachexia, tachypnea, and tachycardia with rales and decreased BS

A

Left sided HF

30
Q

We will see a diffuse apical impulse and a weak pulse with

A

Left sided HF

31
Q

Characterized by increased JVD and hepatic enlargement with ascites and leg edema

A

Right sided HF

32
Q

What labs suggest chronic HF?

A

Decreased Na and Hgb w/ increased creatinine

33
Q

Function in water and Na+ elimination which decreases intravascular and diastolic volumes

A

Diuretics

34
Q

The most potent diuretics are

A

Loop diuretics

35
Q

Less potent, but additive diuretics

A

Thiazides

36
Q

Venous vasodilators used to increase venous capacitance and decrease LV preload

A

Nitrates

37
Q

Arteriolar vasodilators used to decrease SVR which increases CO and thus increases BP

A

Hydralazine and Prazosin

38
Q

Balanced venous and arterial vasodilators

A

ACE inhibitors and ARBs

39
Q

Decrease AN-II and aldosterone while increasing bradykinins

A

ACE inhibitors

40
Q

Limit maladaptive remodeling and improves survival

A

ACE inhibitors

41
Q

Complete AN-II inhibition w/ no effect on bradykinins

A

ARBs

42
Q

Similar efficacy and survival benefit as ACE inhibitors, but can be an alternative if patient gets ACE-induced cough

A

ARBs

43
Q

Improve survival, especially in AA

-Alternative if ACE inhibitor/ARB intolerant

A

Hydralazine/Nitrates

44
Q

Phosphodiesterase inhibitor used to increase ventricular contractility

A

Milrinone

45
Q

Blunts sympathetic drive and slows AVN conduction

A

Digoxin

46
Q

Inhibits Na+/K+ ATPase which increases intracellular Ca2+

A

Digoxin

47
Q

Improves symptoms and reduces hospitalizations, but has no effect on survival

A

Digoxin

48
Q

How do we treat patients with HF w/ reduced EF

A

Aldosterone Antagonists

49
Q

What are two examples of aldosterone antagonists?

A

Spironoloactone and eplerenone

50
Q

Blunt cardiac fibrosis and remodeling

A

Spironolactone and eplerenone

51
Q

In patients taking the aldosterone antagonists, we need to monitor

A

K+ levels

52
Q

When we have LVEF that is less than 35%, what can we use for SCD prevention?

A

AICD

53
Q

We want to avoid overdiuresis with

A

Right-sided HF

54
Q

The majority of patients with acute decompensated HF have what is classified as

A

Wet and Warm HF (Normal perfusion at rest w/ presence of congestion)

55
Q

The number one goal to treat wet and warm is

A

Diurese

56
Q

We want to keep wet and warm patients on

A

Beta-blockers

57
Q

May be added to diuretic therapy w/ wet and warm in absence of symptomatic hypotension and still w/ severe HF

A

Vasodilators

58
Q

Causes rapid improvement in congestion and is useful in pulmonary edema and severe hypertension

A

Vasodilators

59
Q

Peripheral edema means that the

A

Right side of heart is affected

60
Q

A low EF and low output syndrome w/ marginal BP and unresponsiveness to vasodilators

A

Wet and Cold HF

61
Q

Shows a poor response to diuretics and worsening renal function

A

Wet and Cold HF

62
Q

How do we treat patients w/ wet and cold HF?

A

IV inotropes

63
Q

Usually do not get admitted unless they are in end-stage

A

Patients with Dry and cold HF

64
Q

For dry and cold HF, what do we give if:

  1. ) BP is ok?
  2. ) BP is low?
A
  1. ) Vasodilators

2. ) Inotropes

65
Q

Characterized as stable and chronic HF

A

Dry and Warm HF

66
Q

In patients w/ advanced HF w/ reduced EF, are used in conjunction with ACE inhibitors

A

Beta-Blockers