Pathophysiology of cardiovascular

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Pathophysiology of Hypertension Classification of blood pressure Category Systolic blood pressure (mmHg) Diastolic blood pressure >140/90 Optimal blood pressure Normal blood pressure High-normal blood pressure Grade 1 Hypertension (mild) <120 <130 130-139 140-159 160-179 >180 140-159 >160 <80 (mmHg) Hypertension <85 85-89 90-99 100-109 >110 <90 <90 Grade 2 Hypertension (moderate) Grade 3 Hypertension (severe) Isolated Systolic Hypertension (Grade 1) Isolated Systolic Hypertension (Grade 2) BHS classification Types of Hypertension  Essential (primary): 90-95% of cases. (cause unknown)  Secondary: 5-10% Renal disorders Endocrine disorders Pregnancy induced Vascular Medicines: steroids, OCPs Risk factors for primary HBP        Genetic- familial: heritability Obesity Smoking Males Alcohol High Na++ Low K+ Ca++ Mg ++ Pathophysiology of HBP BP = CO X (SV x HR) X PVR PVR Pathophysiology: A. Volume overload B. Increase in PVR A. Volume overload: i. salt water retention (renin-angiotensinaldosterone system) ii. Changes in ANP activity/production iii. Change on adrenomedullin activity iv. Disorder in endothelial function v. Insulin resistance B. Increase PVR i. increase sympathetic tone ii. Remodeling of peripheral vessels. Investigations Urine dipstick Chest x ray ECG, Echo Blood tests: sugar, electrolytes, kidney function, lipids, thyroid function. Specific tests for secondary causes. Principles of treatment Reduce volume overload: Salt restriction, diuretics Reduce peripheral resistance: Vasodilators Prevent angio II induced remodeling of vessels and heart: ACEI, Angio II blockers Reduce heart rate: Beta-blockers Central acting drugs: Methyldopa. End (target) organ damage in HBP Hypertension Heart Brain Kidneys Arteries LVH Ischemia Proteinuria Retinopathy PVD CAD CHF Stroke Kidney failure Pathophysiology of Congestive heart failure  Poor pumping by the heart: inadequate cardiac output  Cardiac output depends upon 1. initial stretch (Starlings law); myocardial contractility 2. preload (venous return) 3. after load (resistance) 4. heart rate  Positive and negative inotropism  Factors affecting: * O2 * nerve supply: symphathetic +ve; parasymph: -ve * hormones: catechols; thyroxine * drugs: digoxin; dobutamine for +ve inotropism  Common causes of CHF 1. IHD (most common and important) 2. Hypertension 3. Valvular heart disease Increased pre-load or after load Dilatation/hypertrophy myocardial ischemia Ventricular remodeling Poor contractile function Decreased CO poor kidney perfusion RAAS activation Increase ED volume Fluid retention by kidneys Catecholamines, angio II, aldo, ADH, TNF alpha, endothelin play part in the above. Role of sympathetic activity in CCF CHF Myocardial contractility Baroreceptors Contractility & HR Reflex symphathetic activation disadvantage advantage Peripheral resistance O2 consumption In already damaged heart Helps maintain CO for some time Work load of heart Overall situation worsens CHF Kidney helps to retain fluid & electrolytes Sympathetic excitation Both together initially help to maintain CO But later worsens failure Because O2 consumption increases further  Symptoms and signs • • • • • • • • Breathlessness (dyspnoea) Cough Fatigue Edema Cyanosis in severe cases Raised JVP. Fast low volume pulse Low BP.  Investigations ECG, CXR, electrolytes Echo.  Principles of treatment Reduce preload: Reduce blood volume; salt restriction, Diuretics Reduce after load: Angio II blockers Improve symptoms: O2 when required, B-blockers Increase contractility: inotropic drugs; digoxin  Principles of nursing Help to relief symptoms Maintain urine output chart Diet; Low salt/ salt free  Pulmonary edema Acute left ventricular failure after: i. a myocardial infarction ii. left ventricular hypertrophy hypoxia of myocardium Inability of LV to pump blood-accumulates in lungs Severe breathlessness (air hunger or paroxsymal nocturnal dyspnea) moist lung sounds (rales) Other causes: valvular heart disease, cardiomyopathies  Right Heart (ventricular) failure. Causes:  Secondary to Left heart failure.  Lung disease: chronic bronchitis/ emphysema Pathophysiology: inflow of blood into lungs is blocked back pressure on the venous circulation accumulation of fluid. Symptoms: Pitting Edema, Raised JVP, Ascites, liver enlargement  HIGH out put failure: CO increases  Causes - severe anemia - hyperthyroidism - septicemia Valvular Heart Disease Normal structure and function of heart valves i. separate atria and ventricles ii separate the great arteries from the ventricles iii. ensure one way flow between atria and ventricles iv. prevent backflow into atria during ventricular contraction v. generation of heart sounds vi. help generate required pressures Alteration in valve function 1) Stenosis (narrowing)  hypertrophy and dilatation of chamber behind the stenosed valve i) Aortic stenosis: Left ventricular hypertrophy Left ventricular failure Pulmonary congestion, back pressure Backpressure on left atrium - Stagnation of blood Right side chambers Raised JVP, enlarged liver, peripheral pitting edema ; Cyanosis ii) Mitral stenosis. Common variety of stenosis Common cause is Rheumatic heart disease. Backpressure on left atrium - Stagnation of blood Pulmonary congestion, back pressure Right side chambers Raised JVP, enlarged liver, peripheral pitting edema ; Cyanosis 2) Regurgitation (incompetence, insufficiency)  Continuous leak back into ventricles  Leading to hypertrophy and failure  Effect of back pressure  Heart sound Murmurs are abnormal heart sounds. Could be systolic or Diastolic. S1 S1 S2

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