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Cardiovascular System
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Principles of Circulatory Failure
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Principles of Circulatory Failure
Heart Failure Acute Heart Failure Chronic Heart Failure Circuit Failure Vessels (increased capillary permeability (maldistributive shock) Blood (loss of fluid from the vascular system (hypovolemic shock)
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CAUSES OF CARDIOVASCULAR DYSFUNCTION
Cardiac arrhythmia Obstructed flow Regurgitant flow Contractile dysfunction (systolic failure) Inadequate filling (diastolic failure) Anatomic abnormalities
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Compensatory Mechanisms
Physiologic Pathologic
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Compensatory Mechanisms
Increase in heart rate Increase in stroke volume Increase in oxygen extraction Redistribution of blood
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Stroke Volume Ventricular distending or filling pressure (preload)
Contractility of the myocardium (inotropic state) The tension that the ventricular myocardium must develop during contraction and early ejection (afterload) The sequence of atrial and ventricular depolarization
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Decreased renal perfusion results in the release of renin by the juxtaglomerular cells in the kidney and the activation of the renin-angiotensin-aldosterone system. Renin causes the conversion of angiotensinogen to angiotensin I, and angiotensin I in turn is converted to angiotensin II in the lungs. Angiotensin II is a powerful vasoconstrictor that promotes the effect of norepinephrine. Angiotensin II also stimulates the release of aldosterone from the adrenal cortex, which acts to increase sodium retention by the kidney with consequent expansion of the interstitial fluid and blood volumes.
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Chronic (Congestive) Heart Failure CHF
Valvular Diseases Myocardial Diseases Pericardial Diseases Hypertension Pressure Load (After Load) Volume Load (Flow Load) (Pre Load) Pumping Defects (Systolic Failure) Filling Defects (Diastolic Failure)
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Valvular Disease • Endocarditis resulting in either valvular stenosis or valvular insufficiency • Congenital valvular defects, most commonly valvular stenosis • Rupture of valve or valve chordae
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Myocardial Disease • Myocardial degeneration: nutritional or toxic
• Myocarditis: bacterial, viral, parasitic, or toxic • Myocardial degeneration: nutritional or toxic • Congenital or hereditary cardiomyopathy • Toxins affecting cardiac conduction
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Congenital Anatomic Defects Producing Shunts
• Cardiac defects, such as ventricular or atrial septal defects, tetralogy of Fallot • Vascular abnormalities producing shunts, such as patent ductus arteriosis
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Hypertension • Pulmonary hypertension: high altitude disease, cor pulmonale • Systemic hypertension: undocumented cause of congestive heart failure in large animals
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Pressure Load Pressure loads occur with lesions that produce an obstruction to outflow, such as aortic or pulmonary valve stenosis, during which the heart is required to perform more work to eject an equivalent amount of blood. Generally, the left ventricle can tolerate a pressure load to a much greater extent than the right ventricle without overt signs of cardiac insufficiency.
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Volume Load Volume loads (flow loads) are common with both acquired and congenital heart defects. In aortic valve and mitral valve insufficiency the volume of blood delivered to the tissues does not differ significantly from normal. However, to achieve a normal cardiac output, the forward stroke volume of the ventricle is markedly increased and the heart is much more inefficient for the same amount of effective work. Generally, the right ventricle is more capable of sustaining a flow load than the left ventricle.
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Pumping Defects (Systolic Failure)
Cardiac insufficiency may occur without any increase in workload if there is a primary weakness in the myocardium or defect in its rhythmic and coordinated contraction.
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Filling Defects (Diastolic Failure)
Pericardial diseases such as pericarditis and pericardial tamponade can result in cardiac insufficiency by interfering with diastolic filling. Filling of the ventricle is determined by the complex interaction of a number of factors, including: mean circulatory filling pressure, meanright atrial pressure, stiffness of the ventricular chamber
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Heart Failure Right side congestive heart failure
Anasarca Ascites Hydrothorax Hydropericardium Left side congestive heart failure Pulmonary Congestion Pulmonary Edema
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Treatment Diuretics (Furosemide) Stall Rest
Positive inotropic agents, Cardiac Glycosides (Digoxin)
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Acute Heart Failure Disorders of filling Tachyarrhythmia Bradycardia
Increase in workload
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Disorders of filling • Pericardial tamponade: atrial and ventricular rupture • Aortic and pulmonary artery rupture
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Tachyarrhythmia • Myocarditis, e.g., encephalomyocarditis virus, foot-and-mouth disease • Nutritional deficiency myopathy, e.g., copper or selenium deficiency • Plant poisoning, e.g., Phalaris spp., • Electrocution and lightning strike
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Bradycardia • Iatrogenic, e.g., IV calcium gluconate or borogluconate administration, xylazine, tolazoline, concentrated solutions of potassium chloride. • Plant poisoning, e.g., Taxus spp.
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Increase in workload • Rupture of aortic valve • Acute anaphylaxis
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