Heart Failure Flashcards

1
Q

heart failure

A

•Heart failure is a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood.

A CLINICAL DIAGNOSIS All HF patients, regardless of ejection fraction status (EF value), have the clinical syndrome of heart failure (HF).

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2
Q

heart failure epidemiology

A
  • In the US 6.5x 10⁶ have it
  • Over age 65 years incidence: 10 per 1000
  • > 68,000 die per year with HF as 1⁰ Dx
  • 2.4-3.6 X 10⁶ hospitalized per year
  • 40—50% annual mortality rate
  • Women: More have it and more die of it than men
  • blacks have the highest risk for HF
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3
Q

two most common underlying causes of HF

A
  • coronary artery disease
  • hypertension
  • CORONARY ARTERY DISEASE 60-75%
  • HYPERTENSION IN 75% INCLUDING THOSE WITH CAD
  • CAD, HTN AND DIABETES INTERACT TO AUGMENT RISK
  • 20-30% of cases of HFrEF cause is unknown = nonischemic or dilated or idiopathic cardiomyopathy
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4
Q

the two presentations of HF in terms of LVEF

A

LV EJECTION FRACTION = SV/EDV

HFrEF EF ≤ 50%

HFpEF EF ≥ 50% I

t is only in HFrEF that evidence - based pharmacotherapy has been demonstrated to confer morbidity and mortality benefits (M&M).

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5
Q

HFrEF

A
  • EF≤ 40%
  • Also referred to as systolic HF.
  • Trials of pharmacotherapy have mainly enrolled subjects with HFrEF, and it is only in these patients that therapies with morbidity/ mortality benefits have been shown
  • coronary artery disease
  • HTN –> LVH –> increased O2 demand
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6
Q

HFpEF

A
  • EF ≥ 50% Most common EF normal, SV low - not filling up enough, reduced preload
  • Also referred to as diastolic HF.
  • Various criteria have been used to further define HFpEF.
  • The diagnosis is one of exclusion of other potential noncardiac causes of symptoms suggestive of HF.
  • To date efficacious therapies have not been identified
  • hypertension –> LVH –> less room
  • aortic stenosis
  • hypertrophic cardiomyopathy
  • restrictive cardiomyopathy
  • ABOUT 50% OF PERSONS WITH HF
  • RELATIVELY NORMAL LV FUNCTION
  • DIASTOLIC HF
  • CARDIAC OUTPUT LIMITED BY:
  • ABNORMAL LV FILLING
  • DISORDERED VENTRICULAR RELAXATION DURING EXERCISE
  • VENTRICULAR PRESSURES ELEVATED FOR A GIVEN VOLUME WITH: PULMONARY CONGESTION DYSPNEA PERIPHERAL EDEMA
  • OLDER WOMEN WITH

a-FIBRILLATION

  • HTN

–DM

-OBESITY CKD

• HYPERTENSION THE CAUSE IN ~ 60% TO 89%

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7
Q

other causes of HF

A

*Genetic defects Most are autosomal dominant

-Genes that encode cytoskeletal proteins

  • Alcohol
  • Cancer chemotherapeutic agents

-Trastuzumab (Herceptin®)

–Anthracyclines - Adriamycin 

•Cocaine

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8
Q

associated disorders

A

DISEASES OF:

 PERICARDIUM

 MYOCARDIUM

 HEART VALVES

 GREAT VESSELS

 PERIPHERAL VESSELS

 METABOLIC ABNORMALITIES

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9
Q

clinical syndrome

A

 DYSPNEA

 FATIGUE EXERCISE INTOLERANCE

FLUID RETENTION

Sx 2 0 to impaired LV function

ECHO evidence of systolic and / or diastolic dysfunction

Pulmonary/splanchnic congestion & Peripheral edema

Exercise intolerance little fluid retention

Others c/o edema, dyspnea or fatigue

 No single diagnostic test

 A clinical Dx based on Hx & PE

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10
Q

All HF Patients, Regardless of EF value, Have the Clinical Syndrome HF

A
  • Abnormal left ventricular (LV) filling dynamics
  • Elevated LV diastolic pressure
  • LV systolic and diastolic dysfunction
  • Neurohormonal activation
  • Impaired exercise tolerance, frequent hospitalization, and reduced survival.
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11
Q

The Clinical Manifestations of HF are Similar Regardless of the EF

A
  • Reduced exercise tolerance
  • Dyspnea on exertion
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
  • Peripheral edema
  • Pulmonary congestion apparent on chest radiographs or computed tomography (CT) scans
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12
Q
A
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13
Q
A
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14
Q
A
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15
Q

HF Classification

A
  • NYHA A functional classification-Sx Classes I-IV
  • ACC/AHA Stages using risk factors and structural abnormalities Stages A-D
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16
Q

precipitating causes of HF

A

PRECIPITATING CAUSES

  • Arrhythmias
  • Thyrotoxicosis
  • Pregnancy
  • Myocarditis
  • Myocardial infarction
  • PE
  • Infective endocarditis
  • Infection
  • Hypertension
  • Anemia
  • Physical, dietary, fluid, environmental or emotional excesses
17
Q

HF Neurohumoral activation

A
  • RENIN ANGIOTENSIN ALDOSTERONE ANGIOTENSIN II (Ang II) ALDOSTERONE
  • SYMAPATHETIC NERVOUS SYSTEM NOREPINEPHRINE (NE)
  • VASOPRESSIN(ADH)
  • ENDOTHELIN
  • CYTOKINES
  • NATRIURETIC PEPTIDES (BNP, NT-pro- BNP)
18
Q

Indicators of Cardiac Stress, Malfunction & Injury

A

 Inflammation – TNF, Interleukins & CRP

 Oxidative stress – Oxidized low density lipoproteins

 Neurohormonal pathway activation – NE, Ang II, Aldosterone, ADH & Endothelin

 Extracellular matrix remodeling – Matrix metalloproteinases

 Myocyte injury – cardiac specific troponins ***diagnosis

 Myocyte stress – Brain natriuretic peptide (BNP) & N-terminal pro-BNP (NT pro-BNP)

***diagnosis and monitoring

19
Q

LV REMODELING IN HFrEF

A
  • LV remodeling develops in response to a series of complex events that occur at the cellular and molecular levels. These changes include:
  • (1) Myocyte hypertrophy
  • (2) Alterations in the contractile properties of the myocyte
  • (3) Progressive loss of myocytes through necrosis, apoptosis, and autophagic cell death
  • (4) β-adrenergic desensitization
  • (5) Abnormal myocardial energetics and metabolism
  • (6) Reorganization of the extracellular matrix
20
Q

Determinants of Myocardial Function

A

Preload - determines volume and therefore sarcomere length

Contractility – determined by Ca²⁺ availability

Afterload - determines how much work the heart must do to successfully eject blood

Heart rate - contributes to Ca²⁺-loading of SR and therefore contractility

21
Q

source of natriuretic peptides

A

SOURCE

  • BRAIN
  • HEART
  • VASCULATURE
  • KIDNEY
22
Q

action of natriurectic peptides

A
  • VASODILATION
  • NATRIURESIS
  • RAAS INHIBITION
  • SNS INHIBITION
  • ANTIPROLIFERATIVE
  • ANTIHYPERTROPHIC
23
Q

BNP

A

 Dx of HF

 Association between concentration and severity

 Correlates with neurohormonal activation: SNS, RAAS & Endothelin

 Assessment of response to therapy

24
Q

BIOMARKERS OF RESPONSE TO CARDIAC INJURY/ STRESS

A

NEUROHORMONAL ACTIVATION – NE – ANG II – ADH – ALDOSTERONE – ENDOTHELIN

25
Q

Activation of the SNS

A
26
Q

HF PATHOPHYSIOLOGY NOREPINEPHRINE

A
  • ↑CONTRACTILITY & HEART RATE
  • ↑VENTRICULAR PRELOAD & AFTERLOAD
  • CONSTRICTION AFFERENT GLOMERULAR ARTERIOLE
  • ↑RENIN
  • ↑PROXIMAL TUBULAR Na⁺ REABSORPTION
  • ↓REGULATION OF β-1 RECEPTORS
27
Q

activation of the RAS

A
28
Q

HF PATHOPHYSIOLOGY ANGIOTENSIN II

A

Angiotensin II actions are similar to those of norepinephrine and also include:

  • Increase in CNS sympathetic outflow
  • Enhancement of peripheral noradrenergic (norepinephrine) neurotransmission
  • Release of aldosterone
  • Actions on myocytes and other cells to alter cardiovascular structure and function = remodeling
29
Q

HF PATHOPHYSIOLOGY ALDOSTERONE

A

Aldosterone, released from the adrenal cortex and produced locally, has actions that include:

  • Increase in renal reabsorption of Na+ and H2O and increased renal excretion of K+ /H⁺
  • Stimulation of collagen synthesis causing fibrosis (remodeling)
30
Q

HF PATHOPHYSIOLOGY ANTIDIURETIC HORMONE (VASOPRESSIN)

A

Antidiuretic hormone: release occurs as a consequence of baroreceptor activation by low cardiac output. The actions which serve to increase blood pressure and cardiac preload include:

  • Vasoconstriction with increase in systemic vascular resistance
  • Stimulation of thirst
  • Increase in water reabsorption in the renal collecting ducts
31
Q

functional modifications of neurohormonal activation in HF

A
  • increased inotropy - maintaining CO
  • increased heart rate - maintaining CO
  • vasoconstriction - maintains BP
  • salt and water retention -preload increase, maintaining CO

this leads to …

  • increased energy demand
  • altering loading conditions
  • altered vascular/diastolic properties
  • proarrhythmogenic effect
32
Q

structural modifications of neurohormonal activation in HF

A
  • hypertrophy
  • increased nonmuscular tisue
  • increased expression of adult cardiac genes

this leads to …

  • increased energy demand
  • altering loading conditions
  • altered vascular/diastolic properties
  • proarrhythmogenic effect
33
Q

Homeostatic Responses to Impaired Cardiac Performance (Due in part to activation of the renin-angiotensin-aldosterone system (RAAS) and of the sympathetic nervous system).

A