CARDIO1 - PATHOPHYSIOLOGY OF HEART FAILURE Flashcards

(20 cards)

1
Q

causes of heart failure

A
  • hypertension
  • valvular disease
  • coronary artery disease
  • idiopathic cardiomyopathy
  • congenital heart disease
  • metabolic/endocrine
  • infective
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2
Q

precipitating factors of heart failure

A
  1. INCREASED CARDIAC OUTPUT: infection, pregnancy, anemia and hyperthyroidism
  2. CARDIOVASCULAR EVENTS: arrhythmia, myocardial ischemia
  3. CONCOMITANT MEDICATION:
    - sodium retention: NSAIDS, Steroids
    - negative inotropes
    -antiarrythmic drugs - calcium channel blockers
    alcohol
    trycyclic antidepressants
  4. NON COMPLIANCE:
    - Diet - increased sodium
    - excesssive fluid intake
    - missed medication
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3
Q

compensatory mechanisms? - sympathetic nervous system

A
  • 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
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4
Q

B1 adrenergic activation beneficial and adverse effects?

A

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

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5
Q

compensatory mechanism for HF: RAAS

A
  • low renal artery pressure
  • check on google
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6
Q

actions of angiotensin 2

A
  • 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
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7
Q

other activated compensatory systems : CYTOKINES

A
  • ↑ Tumor necrosis factor
    → oxidative stress
    → inducible nitric oxide
    synthase (increase NO)
    →cachexia
  • platelet derived growth factor
  • fibroblast growth factor
  • transforming growth factor Beta
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8
Q

explain the concept of oxidative stress

A
  • Oxidant metabolites exert toxic effects: ↑ production, ↓ protection, induction of apoptosis
  • oxygen free radicals :
    • Xanthine oxidase
      - Activated neutrophils
      • catecholamine autoxidation

ANTIOXIDANTS:
- Superoxide dismutase, Catelase, Gluthione peroxidase, Vitamin E, Vitamin C, cysteine

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9
Q

explain the 4 mechanisms of heart failure

A
  1. Myocardial ischemia
    - Altered contractility and relaxation
    - depletion of energy stores
    - reduced sensitivity of contractile proteins to calcium
    hibernating myocardium
  2. Myocardial infarction
    - myocyte necrosis
    - remodelling
    - myocytes replaced by fibrous tissue
  3. myocyte destruction of unkown origin - cardiomyopathy
  4. known toxic agents: alcohol, cytotoxic drugs
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10
Q

CLINICAL PRESENTATION: SYMPTOMS

A
  • 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
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11
Q

PHYSICAL FINDINGS

A
  1. EVIDENCE OF ↑ ADRENERGIC ACTIVITY
    - tachycardia
    - peripheral vasoconstriction : pallor and cold extremities
  2. SYSTEMIC VENOUS HYPERTENSION:
    - ↑ JVP
    - hepatojugular reflex
    - hepatomegaly
    - Ascites
    - leg oedema
  3. PULMONARY VENOUS HYPERRTENSION
    - basal inspiratory crackles
    - pleural effusion
  4. CARDIAC
    - cardiomegaly - displaced apex bbeat
    - added sounds: S3 and S4
    - murmurs
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12
Q

INVESTIGATIONS

A

→ 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

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13
Q

INVESTIGATIONS (bnp)

A
  • 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
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14
Q

BNP & pro-BNP uses

A
  • differentiating between dyspnoea due to cardiac/respiratory causes
  • assessing prognosis
    -titrating anti-failure therapy
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15
Q

ACC/AHA Classification of heart failure Stage A

A
  • at high risk, no structural heart disease:
    • hypertentsion
    • lipid disorders
    • type 2 DM
      treat underlying condition
      lifestyle modification
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16
Q

ACC/AHA CLASSIFICATION OF HEART FAILURE: STAGE B

A
  • asymptomatic structural heart disease
  • valve lesion
  • congenital heart disease:
    • ACE Inhibition B-blockade
17
Q

ACC/AHA CLASSIFICATION OF HEART FAILURE: STAGE C

A
  • structural heart disease
  • previous or current heart failure symptoms
  • diuretics
  • ace inhibition
    salt restriction
18
Q

ACC/AHA CLASSIFICATION OF HEART FAILURE: STAGE D

A
  • refractory heart failure: mechanical assist devices
  • IV inotropic support
  • heart transplantation
    hospice care
19
Q

heart failure : treatment

A
  • 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