Heart Failure Flashcards
heart failure
•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).
heart failure epidemiology
- 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
two most common underlying causes of HF
- 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
the two presentations of HF in terms of LVEF
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).
HFrEF
- 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
HFpEF
- 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%
other causes of HF
*Genetic defects Most are autosomal dominant
-Genes that encode cytoskeletal proteins
- Alcohol
- Cancer chemotherapeutic agents
-Trastuzumab (Herceptin®)
–Anthracyclines - Adriamycin
•Cocaine
associated disorders
DISEASES OF:
PERICARDIUM
MYOCARDIUM
HEART VALVES
GREAT VESSELS
PERIPHERAL VESSELS
METABOLIC ABNORMALITIES
clinical syndrome
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
All HF Patients, Regardless of EF value, Have the Clinical Syndrome HF
- 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.
The Clinical Manifestations of HF are Similar Regardless of the EF
- Reduced exercise tolerance
- Dyspnea on exertion
- Orthopnea
- Paroxysmal nocturnal dyspnea
- Peripheral edema
- Pulmonary congestion apparent on chest radiographs or computed tomography (CT) scans
HF Classification
- NYHA A functional classification-Sx Classes I-IV
- ACC/AHA Stages using risk factors and structural abnormalities Stages A-D
precipitating causes of HF
PRECIPITATING CAUSES
- Arrhythmias
- Thyrotoxicosis
- Pregnancy
- Myocarditis
- Myocardial infarction
- PE
- Infective endocarditis
- Infection
- Hypertension
- Anemia
- Physical, dietary, fluid, environmental or emotional excesses
HF Neurohumoral activation
- RENIN ANGIOTENSIN ALDOSTERONE ANGIOTENSIN II (Ang II) ALDOSTERONE
- SYMAPATHETIC NERVOUS SYSTEM NOREPINEPHRINE (NE)
- VASOPRESSIN(ADH)
- ENDOTHELIN
- CYTOKINES
- NATRIURETIC PEPTIDES (BNP, NT-pro- BNP)
Indicators of Cardiac Stress, Malfunction & Injury
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
LV REMODELING IN HFrEF
- 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
Determinants of Myocardial Function
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
source of natriuretic peptides
SOURCE
- BRAIN
- HEART
- VASCULATURE
- KIDNEY
action of natriurectic peptides
- VASODILATION
- NATRIURESIS
- RAAS INHIBITION
- SNS INHIBITION
- ANTIPROLIFERATIVE
- ANTIHYPERTROPHIC
BNP
Dx of HF
Association between concentration and severity
Correlates with neurohormonal activation: SNS, RAAS & Endothelin
Assessment of response to therapy
BIOMARKERS OF RESPONSE TO CARDIAC INJURY/ STRESS
NEUROHORMONAL ACTIVATION – NE – ANG II – ADH – ALDOSTERONE – ENDOTHELIN
