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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
Systolic Heart Failure – Oxygen Demand
``` Increased oxygen demand: • Increased heart rate • Increased workload of heart • Decreased lung compliance • Physiological stress • Emotional stress ```
26
Diastolic HF
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
27
Diastolic HF: Functional Alterations
* Slowed, delayed and incomplete relaxation of the myocardium * Impaired rate and extent of LV filling * Increased diastolic LV, LA, and pulmonary pressures
28
Diastolic HF: Effects on CO
↑ 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.
29
Cardiomyocytes in systolic HF
Elongated, diameter the same
30
Cardiomyocytes in diastolic HF
Length the same, thicker diameter
31
Preload in systolic HF
Increased
32
Afterload in systolic HF
increased
33
Contractility in systolic HF
decreased
34
Preload in diastolic HF
decreased because there isn't room to fill
35
Afterload in diastolic HF
increased
36
Contractility in diastolic HF
normal (but it is not pumping large volumes)
37
Heart failure (diastolic and systolic) causes Increased Diastolic Pressures In
LV, LA, pulmonary vessels
38
Blood movement through the heart and body
``` BODY Right atrium R ventricle Lungs L atrium L ventricle Body ```
39
____ sided heart failure causes ____ sided heart failure
Left-sided heart failure causes right-sided heart failure
40
Why do the ventricles become like that?
ventricular remodeling is due to prolonged COMPENSATORY MECHANISMS
41
Heart failure and the SNS
``` ↓ CO Stimulation of baroreceptors Activation of SNS Release of catecholamines Stimulation of α and β receptors Vasoconstriction and ↑HR ↑ Afterload ```
42
Neural hormonal mechanisms
SNS-increased HR and contractility and causes vasoconstriction RAAS Vasoconstriction & Na+/H2O Retention Vasopressin- vasoconstriction and H2O retention
43
HF and RAAS
``` ↓ CO Poor kidney perfusion Activation of RAAS Angiotensin II & Aldosterone Vasoconstriction & Na+/H2O Retention ↑ Afterload and Preload ```
44
HF and Ventricular Remodeling
LONG TERM compensation occurs because neurohormones genetically modify cardiomyocytes
45
Valvular stenosis
cant open- obstructed flow
46
Valvular regurgiation
doesn't close so flow backs up | ie mitral valve regurgitation results in blood going back into Left atrium
47
Heart failure treatment
Reduce or redirect Preload Improve arterial oxygen saturation Optimize Oxygen transport
48
Endothelin
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
Vasopressin (ADH)
↑ Preload & Afterload | d/t H2O reabsorption
50
Apoptosis
Compensatory neurohormones also promote apoptosis • Decreases the number and/or strength of cardiomyocytes • ACEI and β-blockers help to slow this down
51
Cause of Arrhythmias and HF
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
Ventricular Remodeling and Natriuretic Peptides
THE GOOD GUYS ``` Promote balanced vasodilation by: • ↓ Preload ↓ sodium/water retention • ↓ Afterload ↓ production & action of vasoconstrictor peptides • Inhibit sympathetic tone ```
53
How do people get Chronic HF
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
Chronic HF to acute
``` Noncompliant with meds Dysrhythmia Embolic event Ischemia ↑ Na+ intake ```
55
Pulmonary edema is caused by
Unable to pump blood forward Blood backs up into pulmonary system Increased hydrostatic pressure in pulmonary capillaries Fluid shifts into alveoli
56
BNP Assays
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
Troponins
``` 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
Reduce or redirect Preload in HF
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
Improve arterial oxygen saturation in HF
* Oxygen therapy * CPAP or BIPAP * Positioning (high Fowler’s) * Diuretic therapy
60
Optimize Oxygen transport in HF
Hemoglobin level | • Oxyhemoglobin dissociation curve
61
Reducing O2 demand in HF
Morphine – to reduce anxiety and Perception of dyspnea
62
Improving contractility (if still hemodynamically unstable after addressing preload)
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
Dobutamine
inotropic vasodilator | Beta 1 receptor agonist, some Beta 2
64
Milrinone
phosphodiesterase III inhibitor | with vasodilation effect
65
Digoxin
use for heart rate control in acute HF | - as an inotrope for chronic HF
66
Embolitic events in HF
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
Short-term Device Management
Intra Aortic Balloon Pump (IABP) Impella Extracoporeal Membrane Oxygenation (ECMO)
68
Chronic heart failure drugs
● Beta Blockers - “lols” (Bisoprolol, Metoprolol) ● ACE Inhibitors - “prils” (Captopril, Rampril) ● Angiotensin Receptor Blocker (Candesartan, Valsartan) ● Aldosterone Antagonist (Spironolactone) ● Vasodilator: Isosorbide dinitrate, Hydralazine
69
LONG TERM MANAGEMENT: Drug Therapy
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
Surgical Interventions
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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