Pathophysiology
Lecture Cardiovascular 4; Porth, Chapter 19
HEART FAILURE
Several types of cardiac dysfunction that result in inadequate tissue perfusion
Left Heart Failure Right Heart Failure
High Output Failure
LEFT HEART FAILURE (congestive heart failure)
Cardiac Output
Stroke Volume
Heart Rate
Contractility Preload
Afterload
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LEFT HEART FAILURE: Changes in Myocardial Contractility
Myocardial Infarction Myocarditis Cardiomyopathies Decreased contractility Myocardial remodeling
Decreased Stroke Volume ; Increased LVEDV
Increased Preload Decreased Cardiac Output Further decrease in contractility
LEFT HEART FAILURE: Changes in Afterload
Increased PR (hypertension) (valvular disease) Hypertrophy of the ventricle Increased work for left ventricle
Increased oxygen demand of ventricular tissue
Ventricular remodeling
Increased connective tissue (collagen)
Decreased Cardiac Output
Vicious Cycle of Decreased CO in heart failure
Decreased Cardiac Output
Baroreceptor response
Decreased renal perfusion
ADH response Increased Peripheral Resistance (Increased afterload) Increased Plasma Volume (Increased Preload)
Activation of reninangiotensin system
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Effect of Heart Failure on Myocardial Oxygen Supply
Increased Preload
Increased force of contraction Decreased lumen size of coronary arteries
Decreased Ejection fraction
Increased metabolic O 2 demand
Decreased O2 supply to coronary arteries
Myocardial Ischemia
Chemical responses to CHF
Catecholamines raised by Sym. NS Increase fC & PR Toxic affects at high levels Downregulation of receptors Arrhythmias
CHF
Edema (inflammation)
Atrial Naturetic Peptides: Decrease blood volume
Arginine vasopressin (ADH) Hyponatremia & edema Increased Angiotensin II Increased pre-, afterload Toxic affects at high levels
Endothelin: poor prognosis Endotoxins: due to myocyte apoptosis
Interleukins (IL6):
Myocyte remodeling Decreased NO Weight-loss Weakness
DIASTOLIC HEART FAILURE
Myocardial remodeling
Can occur with Systolic Can occur independently: Pulmonary congestion despite normal CO More common in women
LV hypertrophy
Decrease Compliance of LV
Normal LVEDV Increased LVEDP
Dyspnea Fatigue Pulmonary Edema (rales, pleural effusions) Management: Increase ventricular compliance; diastolic filling time
Pulmonary Edema
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RIGHT HEART FAILURE
Left Heart failure Back-up pulmonary circ. Pulmonary disease: COPD, Cystic Fibrosis, ARDS
Diffuse hypoxic pulmonary vasoconstriction
Increased Afterload on Right Heart
Right Heart dilates and fails (poor adaptability)
Peripheral Edema
HIGH-OUTPUT FAILURE
Inability of heart to supply nutrients even in presence of normal CO and contractility
Anemia
Metabolic acidosis
Bacterial toxins Sepsis
Decreased systemic Fever
Impaired resistance O 2 delivery
Tissue hypoxia
Increased fC & SV
Hyperthyroidism
Increased BMR
Increased O 2 demand of tissue
Increased CO
DYSRHYTHMIAS: Sinus Bradycardia
Sinus Bradycardia: P rate < 60 PR interval normal QRS for each P SA Node Effects: Increased preload Decreased MAP Causes: Hyperkalemia - slows depolarization Vagal hyperactivity
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DYSRHYTHMIAS: Sinus tachycardia
Sinus Tachycardia: P rate >100 PR interval normal QRS for each P SA node
Effects: Decreased filling times Decreased MAP Increased myocardial demand Causes: Catecholamines (raised resting potential) Fever Early heart failure/lung disease (hypoxic cell metabolism) Hypercalcemia
DYSRHYTHMIAS: Premature Ventricular Contractions
PVCs: QRS in absence of P QRS occasionally inverted
Effects: Decreased CO due to lack of contribution of atrial filling Ventricles depolarize independently and more slowly (normal conductive tissue not used) > 3 PVC in a row considered ventricular tachycardia Causes: hypoxia Anesthesia Age
DYSRHYTHMIAS: Ventricular Tachycardia
VT: P absent QRS widened (>0.11) QRS rate >100
Effects: Decreased CO due to lack of contribution of atrial filling Ventricles depolarize independently and more slowly (normal conductive tissue not used) Can be life threatening if prolonged Causes: Hypoxia Anesthesia
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DYSRHYTHMIAS: Ventricular Fibrillation
VF: P absent QRS >300 and usually not observable
Effects: No cardiac output Not compatible with life Causes: Rapid effusion of K + Impulse originates in cells outside normal conduction pathways and spreads through intercalated disks
DYSRHYTHMIAS: Atrial Fibrilla...