Heart Failure Flashcards

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

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2
Q

Structural heart disease without the development of HF

-Prior MI, depressed LV ejection fraction, LVH

A

Stage B

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3
Q

Characterized by structural heart disease with current or prior symptoms

A

Stage C

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4
Q

Classified as end-stage HF

A

Stage D

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5
Q

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

A

Ejection Fraction

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6
Q

How do we find ejection fraction?

A

EF = (SV / LVEDV) * 100

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7
Q

Normally, ejection fraction is greater than

A

50-60%

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8
Q

Preload is the myocardial stretch, which can be found as

A

Preload = EDV / /EDP

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9
Q

Force of myocardial contraction and is independent of preload or afterload

A

Contractility

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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

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11
Q

Characterized by abnormal diastolic function due to increased stiffness

-LVEF is greater than 50%

A

HF with preserved EF

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12
Q

Ventricles fill at higher than normal pressures with

A

HF w/ preserved EF

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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

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14
Q

The most common cause of RV failure is

A

LV failure

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15
Q

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

A

Cor Pulmonale

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16
Q

Has a limited benefit in severely decreased contractility

A

Frank-Starling Mechanism

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17
Q

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

A

Neuro-Hormonal Activation

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18
Q

The acute effects are beneficial but the chronic effects are deleterious

A

Neuro-Hormonal Activation

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19
Q

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

A

Neuro-hormonal activation

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20
Q

Cleaves angiotensinogen to AN-I

A

Renin

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21
Q

Cleaves AN-I to AN-II

A

ACE

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22
Q

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

A

AN-II

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23
Q

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

A

ADH/Vasopressin

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24
Q

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

A

Natriuretic peptides (ANP and BNP)

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25
ANP and BNP promote
Vasodilation
26
ANP and BNP inhibit
Renin secretion
27
Used in diagnosis of HF
BNP levels
28
Ventricular remodeling and hypertrophy reduces wall stress and maintains
Contractility
29
Characterized by cardiac cachexia, tachypnea, and tachycardia with rales and decreased BS
Left sided HF
30
We will see a diffuse apical impulse and a weak pulse with
Left sided HF
31
Characterized by increased JVD and hepatic enlargement with ascites and leg edema
Right sided HF
32
What labs suggest chronic HF?
Decreased Na and Hgb w/ increased creatinine
33
Function in water and Na+ elimination which decreases intravascular and diastolic volumes
Diuretics
34
The most potent diuretics are
Loop diuretics
35
Less potent, but additive diuretics
Thiazides
36
Venous vasodilators used to increase venous capacitance and decrease LV preload
Nitrates
37
Arteriolar vasodilators used to decrease SVR which increases CO and thus increases BP
Hydralazine and Prazosin
38
Balanced venous and arterial vasodilators
ACE inhibitors and ARBs
39
Decrease AN-II and aldosterone while increasing bradykinins
ACE inhibitors
40
Limit maladaptive remodeling and improves survival
ACE inhibitors
41
Complete AN-II inhibition w/ no effect on bradykinins
ARBs
42
Similar efficacy and survival benefit as ACE inhibitors, but can be an alternative if patient gets ACE-induced cough
ARBs
43
Improve survival, especially in AA -Alternative if ACE inhibitor/ARB intolerant
Hydralazine/Nitrates
44
Phosphodiesterase inhibitor used to increase ventricular contractility
Milrinone
45
Blunts sympathetic drive and slows AVN conduction
Digoxin
46
Inhibits Na+/K+ ATPase which increases intracellular Ca2+
Digoxin
47
Improves symptoms and reduces hospitalizations, but has no effect on survival
Digoxin
48
How do we treat patients with HF w/ reduced EF
Aldosterone Antagonists
49
What are two examples of aldosterone antagonists?
Spironoloactone and eplerenone
50
Blunt cardiac fibrosis and remodeling
Spironolactone and eplerenone
51
In patients taking the aldosterone antagonists, we need to monitor
K+ levels
52
When we have LVEF that is less than 35%, what can we use for SCD prevention?
AICD
53
We want to avoid overdiuresis with
Right-sided HF
54
The majority of patients with acute decompensated HF have what is classified as
Wet and Warm HF (Normal perfusion at rest w/ presence of congestion)
55
The number one goal to treat wet and warm is
Diurese
56
We want to keep wet and warm patients on
Beta-blockers
57
May be added to diuretic therapy w/ wet and warm in absence of symptomatic hypotension and still w/ severe HF
Vasodilators
58
Causes rapid improvement in congestion and is useful in pulmonary edema and severe hypertension
Vasodilators
59
Peripheral edema means that the
Right side of heart is affected
60
A low EF and low output syndrome w/ marginal BP and unresponsiveness to vasodilators
Wet and Cold HF
61
Shows a poor response to diuretics and worsening renal function
Wet and Cold HF
62
How do we treat patients w/ wet and cold HF?
IV inotropes
63
Usually do not get admitted unless they are in end-stage
Patients with Dry and cold HF
64
For dry and cold HF, what do we give if: 1. ) BP is ok? 2. ) BP is low?
1. ) Vasodilators | 2. ) Inotropes
65
Characterized as stable and chronic HF
Dry and Warm HF
66
In patients w/ advanced HF w/ reduced EF, are used in conjunction with ACE inhibitors
Beta-Blockers