Вы находитесь на странице: 1из 4

PATHOPHYSIOLOGY

ETIOLOGY Unknown/idiopathic Familial history of hypertension Gender: Male Age: 74y/o PREDISPOSING FACTORS sedentary lifestyle alcohol intake high fat diet cigarette smoking high salt intake

Fragmentation of elastics increased fat stores Of blood vessels And Increased collagen deposits

vasoconstriction cellular retention of Na

Loss of elasticity and hardening Of blood vessel

fats are deposited on the blood vessels

water retention, with increased ECF volume

Inability of blood vessels to dilate

atherosclerosis on the blood vessels

Narrowed blood vessels

Release of Na transport inhibitor Into the blood Disruption of Na K pump Net increased of intracellular Sodium and calcium Increased reactivity to vasoconstrictive Stimuli vasoconstriction

increased fluid volume

increased preload increased in cardiac output

increased peripheral resistance

blood pressure elevation rapid blood flow

increased pressure on the endothelial lining of blood vessel endothelial injury

decreased tissue perfusion release of renin from the kidneys Angiotensin (liver)

inflammation stimulation of biochemical mediators (histamine, leukotrienes, prostaglandins)

angiotensin I ACE (lungs) angiotensin II

Increased vascular permeability aldosterone

Fever

direct pressor properties and release of Cathecolamines

stimulates release of

vasoconstriction Increased Na, Increased Ca, water, proteins, humoral susbtances

sodium retention water retention

Ca increases smooth muscle contraction increased vasoconstriction

blood vessel thickening

increased cardiac output

increased peripheral resistance

further increase in BP prolonged vasoconstriction and increased pressure stimulates arterial smooth muscle hypertrophy and hyperplasia decreased arterial lumen size increased afterload increased systemic vascular resistance increased force of left ventricular contraction increased cardiac workload activation of myocardial cell grwoth myocyte hypertrophy increased in Left ventricle thickness and mass LEFT VENTRICULAR HYPERTROPHY Ineffective cardiac contraction Decreased cardiac output Decreased systemic tissue perfusion Stimulation of baroreceptors SNS activation Increased heart rate and increased myocardial contractility Activation of neurochemical pathways to increase circulating blood volume increased catecholamines Arrhythmias narrowing of the coronary arteries increased left ventricle wall tension decreased coronary blood flow during diastole imbalance between blood supply and myocardial demand decreased tissue perfusion decreased oxygen in the heart muscles anaerobic metabolism increased lactic acid CHEST PAIN

Increased myocardial oxygen demand Further imbalance between oxygen supply and demand Ischemia Further stress on ventricular wall muscles and Dilatation leading to worsening of ventricular function (Remodeling) Further heart failure

Further decrease in cardiac output RAAS activation Na and water retention Decreased urine production Oliguria Inadequate tissue perfusion peripheral cyanosis, Cold clammy extremities, Slow capillary refill

Thickening of left ventricular wall decreased left ventricular compliance and filling Increased left ventricular filling pressure Separation of mitral valve leaflets Blood dams back to the left atrium Increased Left atrial pressure Blood dams back to the pulmonary veins and capillaries Increased pulmonary capillary pressure Exceeding hydrostatic and osmotic pressure in the pulmonary capillaries Fluid shifts from blood vessels into the interstitium, bronchioles and alveoli Fluid trapped in the pulmonary trees Pulmonary congestion Pulmonary edema Crackles, pink frothy sputum, nocturnal dyspnea, orthopnea, exertional dyspnea, weakness and easy fatigability