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NSCC 7320 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Acute heart failure

A

is characterized by a sudden onset of symptoms.
imbalance between oxygen supply and demand and hemodynamic deterioration. Acute heart failure
can be the result of acute myocardial infarction or acute myocarditis, or it can happen as an acute deterioration of chronic heart failure

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2
Q

Chronic heart failure

A

heart failure that has been adequately treated with appropriate self-management techniques and medical therapies to optimize cardiac output. Not rapidly changing

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3
Q

Sysstolic dysfunction

A

is the more common type of heart failure. Systolic dysfunction is a problem with pumping
and ventricular emptying and is associated with reduced left ventricular (LV) contractility
and subsequently reduced cardiac output and ejection fraction (EF). The ventricle becomes
large, dilated, congested, and overloaded. Hemodynamically, there is a low cardiac output, an elevated ventricular end-diastolic volume (preload), and an elevated systemic vascular
resistance (afterload).

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4
Q

Dobutamine

A

Dobutamine is a synthetic catecholamine with mainly beta 1 receptor agonism and some
beta 2 receptor activity, which make Dobutamine an “inotropic vasodilator”

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5
Q

Heart failure

A

abnormal heart function results in, or increases risk of, clinical symptoms and signs of low cardiac output

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6
Q

Milrinone

A

phosphodiesterase III inhibitor. Inhibition of phosphodiesterase III results in elevated levels of cyclic adenosine monophosphate in the myocardium and smooth
muscle, which leads to increased cardiac contractility and vasodilation. Milrinone produces
hemodynamic changes similar to those of Dobutamine, but because it works differently, it can be effective if the patient has previously been on beta blockers, a situation where Dobutamine likely will not.

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7
Q

New York Heart Association (NYHA) classification

A

is a classification system with four levels. Level one ranges from cardiac disease that is
asymptomatic with physical activity to level four, cardiac disease that is symptomatic at
rest.

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8
Q

Self-management strategies for heart failure

A

daily weight,

dietary management-including fluid and sodium restrictions, exercise
Pharmaceutical

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9
Q

Systolic dysfunction

A

is the more common type of heart failure. Systolic dysfunction is a problem with pumping
and ventricular emptying and is associated with reduced left ventricular (LV) contractility
and subsequently reduced cardiac output and ejection fraction (EF). The ventricle becomes
large, dilated, congested, and overloaded. Hemodynamically, there is a low cardiac output,
an elevated ventricular end-diastolic volume (preload), and an elevated systemic vascular
resistance (afterload)

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10
Q

Digoxin function in Heart failure

A

Digoxin acts to enhance inotropy of cardiac muscle and also reduces activation of the SNS and RAAS

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11
Q

DIURETICS function in Heart failure

A

Diuretics such as furosemide relieve fluid retention (pulmonary congestion and peripheral edema) and improve exercise tolerance

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12
Q

ACE inhibitors function in Heart failure

A

ACE inhibitors such as captopril and enalapril block the conversion of angiotensin I to angiotensin II, which reduces activation of the RAAS

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13
Q

Angiotensin receptor blockers function in Heart failure

A

Angiotensin receptor blockers such as valsartan, losartan, and candesartan are used in patients who cannot tolerate ACE inhibitor therapy and work directly on the angiotensin receptors that are the final downstream target of the RAAS pathway

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14
Q

Beta-Blockers function in Heart failure

A

β-Blocking agents such as carvedilol and metoprolol is used to protect the heart and vasculature from the deleterious effects of overstimulation of the SNS and to help slow the heart down to allow for more efficient contraction

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15
Q

Aldosterone antagonists function in Heart failure

A

Aldosterone antagonists such as spironolactone also directly inhibit the RAAS

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16
Q

INOTROPES function in Heart failure

A

Inotropic agents such as milrinone provide direct stimulation of the myocardium to increase contractility.

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17
Q

alveolar gas exchange in heart failure

A

systolic heart failure (because of the ever increasing preload), blood will eventually “back up” into the lungs and systemic circulation.
In pulmonary edema, the alveolar capillary membrane will be thickened due to the presence of fluid. Thickening of the alveolar capillary membrane results in a reduction of diffusion of gases across the membrane.

V/Q matching.

Shunt- Pulmonary edema
Dead space- Decreased cardiac output

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18
Q

SNS impact in CHF

A

epinephrine and norepinephrine, catecholamines from the sympathetic nervous system, cause excessive vasoconstriction and an increased afterload

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19
Q

aldosterone causes

A

salt and water retention and increased preload.

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20
Q

Vasodilators function in Heart failure

A

The venodilating effects increase venous capacitance and venous pooling, which effectively redistributes fluid and thus reduces preload.

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21
Q

Natriuretic Peptides

A

because they are produced by the heart in response to atrial and ventricular stretch, and act to offset the sodium retention and vasoconstriction central to ADHF.

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22
Q

CPAP and Bipap in HF

A

Short-term positive pressure is an important treatment for
pulmonary edema associated with ADHF.

positive airway pressure pushes the intra-alveolar
fluid out of the alveoli and creates more alveolar surface area for gas exchange.

positive intrathoracic pressure inherent in these therapies
acts to decrease venous return to the heart and reduce preload.

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23
Q

Systolic HF: Effects on CO

A

↓ Contractility + ↑ Compliance = ↑ Preload
↓ Contractility + ↑ Preload = a compensatory ↑ Afterload
↓ Contractility + ↑ Preload + ↑ Afterload = ↓ CO

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24
Q

Systolic HF

A 
Ventricles become large, dilated,
overloaded
Increased LVEDV (increased preload) and LVEDP
HFrEF (<40%)
S3 gallop
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25
Q

Systolic Heart Failure – Oxygen Demand

A 
Increased oxygen demand:
• Increased heart rate
• Increased workload of heart
• Decreased lung compliance
• Physiological stress
• Emotional stress
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26
Q

Diastolic HF

A

Ventricles are thick/stiff and non-compliant
• Cardiomyocytes increase in diameter, not length.
• Concentric remodeling and
hypertrophy of LV
• Possible causes: HTN, hypertrophic cardiomyopathy, aging, etc.
• Decreased LVEDV (preload) but increased LVEDP
• Increased LA volumes and pressures
• HFpEF (>50%)
• S4
• High BP

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27
Q

Diastolic HF: Functional Alterations

A
  • Slowed, delayed and incomplete relaxation of the myocardium
  • Impaired rate and extent of LV filling
  • Increased diastolic LV, LA, and pulmonary pressures
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28
Q

Diastolic HF: Effects on CO

A

↑ Afterload – original issue and/or compensation from ↓CO
Contractility – unable to stretch
Preload – ventricles are non-compliant – an increase in preload cannot be accommodated
Contractility* + Preload* + ↑ Afterload = ↓ CO
* Usually just okay, but cannot improve if need to.

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29
Q

Cardiomyocytes in systolic HF

A

Elongated, diameter the same

30
Q

Cardiomyocytes in diastolic HF

A

Length the same, thicker diameter

31
Q

Preload in systolic HF

32
Q

Afterload in systolic HF

33
Q

Contractility in systolic HF

34
Q

Preload in diastolic HF

A

decreased because there isn’t room to fill

35
Q

Afterload in diastolic HF

36
Q

Contractility in diastolic HF

A

normal (but it is not pumping large volumes)

37
Q

Heart failure (diastolic and systolic) causes Increased Diastolic Pressures In

A

LV, LA, pulmonary vessels

38
Q

Blood movement through the heart and body

A 
BODY
Right atrium
R ventricle
Lungs
L atrium 
L ventricle 
Body
39
Q

____ sided heart failure causes ____ sided heart failure

A

Left-sided heart failure causes right-sided heart failure

40
Q

Why do the ventricles become like that?

A

ventricular remodeling is due to prolonged COMPENSATORY MECHANISMS

41
Q

Heart failure and the SNS

A 
↓ CO 
Stimulation of baroreceptors 
Activation of SNS Release of catecholamines
Stimulation of α and β receptors
Vasoconstriction and ↑HR
↑ Afterload
42
Q

Neural hormonal mechanisms

A

SNS-increased HR and contractility and causes vasoconstriction

RAAS Vasoconstriction & Na+/H2O Retention

Vasopressin- vasoconstriction and H2O retention

43
Q

HF and RAAS

A 
↓ CO 
Poor kidney perfusion
Activation of RAAS
Angiotensin II & Aldosterone
Vasoconstriction & Na+/H2O Retention
↑ Afterload and Preload
44
Q

HF and Ventricular Remodeling

A

LONG TERM compensation occurs because neurohormones genetically modify cardiomyocytes

45
Q

Valvular stenosis

A

cant open- obstructed flow

46
Q

Valvular regurgiation

A

doesn’t close so flow backs up

ie mitral valve regurgitation results in blood going back into Left atrium

47
Q

Heart failure treatment

A

Reduce or redirect Preload
Improve arterial oxygen saturation
Optimize Oxygen transport

48
Q

Endothelin

A

Produced by endothelin cells in the endothelium of vessels
• Potent vasoconstrictor
• Effects
• Vasculature: Vasoconstriction (systemic and pulmonary arteries)
• Myocardium: Possibly inotropic, hypertrophic, proarrhythmic
• Renal: Renal vasoconstriction and Na+ retention

49
Q

Vasopressin (ADH)

A

↑ Preload & Afterload

d/t H2O reabsorption

50
Q

Apoptosis

A

Compensatory neurohormones also promote apoptosis
• Decreases the number and/or strength of cardiomyocytes
• ACEI and β-blockers help to slow this down

51
Q

Cause of Arrhythmias and HF

A

Catecholamines can also lead to arrhythmias
• Remodeling/stretch/cell changes → Changes in conduction pathways
• Electrolyte imbalances
• MI – acute or chronic; scar tissue
• Chronic SNS stimulation

  • EF<30% and a history of ventricular arrhythmias
  • Good predictor of sudden death

Atrial fibrillation – common in HF
V. Tach & V. Fib – common causes of death

52
Q

Ventricular Remodeling and Natriuretic Peptides

A

THE GOOD GUYS

Promote balanced vasodilation by:
• ↓ Preload ↓ sodium/water retention
• ↓ Afterload ↓ production & action of
vasoconstrictor peptides
• Inhibit sympathetic tone
53
Q

How do people get Chronic HF

A

common medical issues that lead to chronic HF such as CAD or HTN

result in compensatory mechanisms ( RAAS SNS activation etc.)

these lead to :
Myocyte Changes
Ventricular Remodeling
Apoptosis

54
Q

Chronic HF to acute

A 
Noncompliant with meds
Dysrhythmia
Embolic event
Ischemia
↑ Na+ intake
55
Q

Pulmonary edema is caused by

A

Unable to pump blood forward
Blood backs up into pulmonary system
Increased hydrostatic pressure in pulmonary capillaries
Fluid shifts into alveoli

56
Q

BNP Assays

A

Brain Natriuretic peptide-secreted by left ventricle in response to over-stretching caused by excessive
preload
● Confirms HF in patients presenting with dyspnea when clinical diagnosis remains uncertain
● BNP levels > 80 pg/ml confirms HF
● BNP increases with severity
● Age dependent

57
Q

Troponins

A 
Often elevated in Acute HF
○ Correlates with severity of HF and poorer prognosis
○ Possibly d/t:
■ Ventricular remodeling
■ CAD
■ Microcirculation abnormalities
■ Reduced coronary reserve
■ Ventricular strain
58
Q

Reduce or redirect Preload in HF

A

Preload: need to ↓ so that ↓overstretching to improve contractility (Starling’s Law); ↓hydrostatic pressure to improve oxygenation &ventilation
1. diuretics (e.g. furosemide IV push/continuous) - ↓total
circulating vol, ↓preload, ↓pulmonary edema
2. vasodilators (e.g. nitroglycerine IV - ↑venous capacitance, ↑ venous pooling, ↓preload

59
Q

Improve arterial oxygen saturation in HF

A
  • Oxygen therapy
  • CPAP or BIPAP
  • Positioning (high Fowler’s)
  • Diuretic therapy
60
Q

Optimize Oxygen transport in HF

A

Hemoglobin level

• Oxyhemoglobin dissociation curve

61
Q

Reducing O2 demand in HF

A

Morphine – to reduce anxiety and Perception of dyspnea

62
Q

Improving contractility (if still hemodynamically unstable after addressing preload)

A

Dobutamine - inotropic vasodilator
(Beta 1 receptor agonist, some Beta 2)

Milrinone – phosphodiesterase III inhibitor
with vasodilation effect

Digoxin – use for heart rate control in acute HF
- as an inotrope for chronic HF

63
Q

Dobutamine

A

inotropic vasodilator

Beta 1 receptor agonist, some Beta 2

64
Q

Milrinone

A

phosphodiesterase III inhibitor

with vasodilation effect

65
Q

Digoxin

A

use for heart rate control in acute HF

- as an inotrope for chronic HF

66
Q

Embolitic events in HF

A

With chronic atrial fibrillation - stasis of blood in the atria
• With heart failure - sluggish blood flow thru a dilated poorly
contractile ventricle
• With valve disease – calcific embolization
• Rx with anticoagulation or anti-platelet drugs

67
Q

Short-term Device Management

A

Intra Aortic Balloon Pump (IABP)
Impella
Extracoporeal Membrane Oxygenation (ECMO)

68
Q

Chronic heart failure drugs

A

● Beta Blockers - “lols” (Bisoprolol, Metoprolol)
● ACE Inhibitors - “prils” (Captopril, Rampril)
● Angiotensin Receptor Blocker (Candesartan, Valsartan)
● Aldosterone Antagonist (Spironolactone)
● Vasodilator: Isosorbide dinitrate, Hydralazine

69
Q

LONG TERM MANAGEMENT: Drug Therapy

A

Used in NYHA Class 2 or 3 (symptomatic)
● Used in patients who have had an MI
● Used in patients with EF<40%
● ACEI + BB TOGETHER SLOW VENTRICULAR REMODELLING AND
PROGRESSION OF HF
● If needed-Digoxin, long acting nitrates or hydralyzine

70
Q

Surgical Interventions

A

CABG
Remodel the heart
Valve Replacement Surgery-repair or replace old valve
Transcatheter Valve Procedures (minimally invasive)
Heart Transplant

NSCC 7320 (9 decks)

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