CARDIO1 - PATHOPHYSIOLOGY OF HEART FAILURE Flashcards
(20 cards)
causes of heart failure
- hypertension
- valvular disease
- coronary artery disease
- idiopathic cardiomyopathy
- congenital heart disease
- metabolic/endocrine
- infective
precipitating factors of heart failure
- INCREASED CARDIAC OUTPUT: infection, pregnancy, anemia and hyperthyroidism
- CARDIOVASCULAR EVENTS: arrhythmia, myocardial ischemia
- CONCOMITANT MEDICATION:
- sodium retention: NSAIDS, Steroids
- negative inotropes
-antiarrythmic drugs - calcium channel blockers
alcohol
trycyclic antidepressants - NON COMPLIANCE:
- Diet - increased sodium
- excesssive fluid intake
- missed medication
compensatory mechanisms? - sympathetic nervous system
- increased activity
- vascular alpha-adrenergic receptors : increased venous return and increased arterial resistance
- Myocardial B-adrenergic receptors: increased heart rate and increased myocardial contractility
- increased energy consumption
-increased actin-myosin crossbridging - increased calcium delivery to myofibrils
- increased intra-cellular cAMP ( myocyte destruction and apoptosis)
- catecholamine metabolism _ free radicals
B1 adrenergic activation beneficial and adverse effects?
beneficial : increased myocardial contractility and increased cardiac output
adverse: increased myocardial oxygen consumption
- increased cAMP - increased intracellular calcium, calcium overload, myocardial necrosis
- increased vasoconstriction - peripheral tissue anoxia
- arrythmogenesis
compensatory mechanism for HF: RAAS
- low renal artery pressure
- check on google
actions of angiotensin 2
- direct vasoconstrictor effect on vessels
- ↑ nor adrenaline release → vasoconstriction
- Endothelin 1 formation - potent vasoconstrictor , cardiac hypertrophy
- mild inotropic effect via ↑ calcium influx
- release of growth factors from vascular smooth muscle cells PDGF, TGF B1, FGF
- activates proto-ocogens like c-fos
- Phospholipase C activation : stimulation of cell growth, collagen synthesis by fibroblasts
other activated compensatory systems : CYTOKINES
- ↑ Tumor necrosis factor
→ oxidative stress
→ inducible nitric oxide
synthase (increase NO)
→cachexia - platelet derived growth factor
- fibroblast growth factor
- transforming growth factor Beta
explain the concept of oxidative stress
- Oxidant metabolites exert toxic effects: ↑ production, ↓ protection, induction of apoptosis
- oxygen free radicals :
- Xanthine oxidase
- Activated neutrophils- catecholamine autoxidation
- Xanthine oxidase
ANTIOXIDANTS:
- Superoxide dismutase, Catelase, Gluthione peroxidase, Vitamin E, Vitamin C, cysteine
explain the 4 mechanisms of heart failure
- Myocardial ischemia
- Altered contractility and relaxation
- depletion of energy stores
- reduced sensitivity of contractile proteins to calcium
hibernating myocardium - Myocardial infarction
- myocyte necrosis
- remodelling
- myocytes replaced by fibrous tissue - myocyte destruction of unkown origin - cardiomyopathy
- known toxic agents: alcohol, cytotoxic drugs
CLINICAL PRESENTATION: SYMPTOMS
- Exertional dyspnoea NYHA FC 2-4: 2 degree to pulmonary capillary hypertension, increased LA & LV filling pressures
- Paroxysmal Nocturnal Dyspnoea
- Orthopnea : increased pulmonary venous congestion
- fatigue and weakness
- cough: dry, productive, pink frothhy sputum
- leg oedema
– abdominal distention - anorexia and weight loss
PHYSICAL FINDINGS
- EVIDENCE OF ↑ ADRENERGIC ACTIVITY
- tachycardia
- peripheral vasoconstriction : pallor and cold extremities - SYSTEMIC VENOUS HYPERTENSION:
- ↑ JVP
- hepatojugular reflex
- hepatomegaly
- Ascites
- leg oedema - PULMONARY VENOUS HYPERRTENSION
- basal inspiratory crackles
- pleural effusion - CARDIAC
- cardiomegaly - displaced apex bbeat
- added sounds: S3 and S4
- murmurs
INVESTIGATIONS
→ ELECTROCARDIOGRAM:
- Rhythm, rate, R wave, ST depression/elevation Q waves
→ECHOCARDIOGRAM
- structural and functional information, chamber size, LVEF, valve morphology and severity of dysfunction
- pericardium: effusion/constriction
→ CHEST XRAY
→ LABORATORY INVESTIGATIONS: biochemistry
INVESTIGATIONS (bnp)
- BNP: 32 amino acid polypeptide
- NT-proBNP: 76 amino acid inactive pro- hormone
- Poduced in the heart (ventricles), brain, in response to wall stretch
- inhibit RAAS, partially inhibit SS
- Functions: diuretic, natriuretic, hypotensive
BNP & pro-BNP uses
- differentiating between dyspnoea due to cardiac/respiratory causes
- assessing prognosis
-titrating anti-failure therapy
ACC/AHA Classification of heart failure Stage A
- at high risk, no structural heart disease:
- hypertentsion
- lipid disorders
- type 2 DM
treat underlying condition
lifestyle modification
ACC/AHA CLASSIFICATION OF HEART FAILURE: STAGE B
- asymptomatic structural heart disease
- valve lesion
- congenital heart disease:
- ACE Inhibition B-blockade
ACC/AHA CLASSIFICATION OF HEART FAILURE: STAGE C
- structural heart disease
- previous or current heart failure symptoms
- diuretics
- ace inhibition
salt restriction
ACC/AHA CLASSIFICATION OF HEART FAILURE: STAGE D
- refractory heart failure: mechanical assist devices
- IV inotropic support
- heart transplantation
hospice care
heart failure : treatment
- valve repair/replacement
- angioplasty
- CABG
- Correction of congenital diseases
*FOR HIDDEN CONDITIONS
- aortic stenosis, mitral stenosis, ASD , Ischaemic heart disease with silent ischemia
- exercise echocardiogram
- dobutamine stress echocardiogram