PATHOPHYSIOLOGY OF CARDIOVASCULAR SYSTEM Case 1. y y y y y y y 84 years old man with an attack of cardiac fibrillation in severe state.

Had pulmonary edema,tachyarrhytmia(130/min),HR=96/min,atr hypotension=85/60mmHg ECG showed atrial fibrillation,cicatricial alteration of inferior wall of left ventricle Antiarrhythmic therapy ineffective and transthoracic atrial defibrillation was given Sinus rhythm restored=94/min Symptoms of acute left ventricular failure decreased within 15 min Art pressure increased to 120/70 mmHg

Question: 1. Why did the attack of paroxysmal tachycardia make the state of the patient worse? y Fibrillation - occurs when the heart muscle begins a quivering motion due to a disunity in contractile cell function. y Absent of P wave>absent normal systole of atrium>increase blood volume>increase volume of blood in left ventricle>decrease stroke volume>heart failure 2. y How and why did the end-systolic volume change during the attack of tachyarrhythmia? Decrease ESV becoz regular impulses produced by the sinus node to provide rhythmic contraction of the heart are overwhelmed by the rapid randomly generated electrical discharges produced by larger areas of atrial tissue. What factors can contribute to the development of arrhythmia in myocardial infarction? increase formation of automaticity increase level of potassium in myocard re-entry mechanism activation of sympathetic nervous system dilation of myocardium Why did atrial defibrillation make the state of the patient better? defibrillation inhibit multi re-entry and restore sinoatrium mechanism increase stroke volume(patient feel better)

3. I. II. III. IV. 4. y

Case 2 A 36 year old woman was admitted to the hospital with the complaints of dyspnea, tachycardia, pedal edema ,ascites , anasarca. From history : she has rheumatic heart disease and mitral stenosis. Physical examination : the skin is cold sweaty and cyanotic , the sclera of the eyes is yellow, the liver is increased and extended 8cm below the costal margin. The heart is increased (hypertrophy of RV and LV), atrial fibrillation , heart rate-110-120/min. Ejection fraction of LV-29%. Pressure blocks the blood flow in lung capillaries in 33mmHg. The level of albumin in blood decreased. Norepinephrine in blood -600pg/ml. Diuresis 300ml/day. Question: 1. What form of heart pathology does the patient have? Congenital heart disease 2. Explain the mechanism of the symptoms y Increase hydrostatic pressure y Decrease oncotic pressure y Increase permeability of vessels wall. Insufficiency of lymph circulation y Edema Portal cirrohosis- Increase blood volume to liver in big circulation Destroyed fret of liver- sclera eyes are yellow. 3. y y y y y 4. Estimate the hemodynamic parameters. Hypertrophy of myocardium Decrease ejection fraction of LV 67-70 (normal) Pressure tat blocks the blood flow in the lung capillaries is 33mg (5-13 mmg normally) Increase hydrostatic pressure in left atrium Diuresis decrease due to activation of RAAS What pathogenetic therapy can you suggest in this case. Therapy with RAAS

Case 3 A 68-year-old man developed symptoms of angina pectoris. Over the previous week the number of attacks had increased to 10-15 daily. The attacks stopped after administration of nitroglycerine and taking off the load. The day, when the patient was admitted to the hospital, the attack of angina pectoris had developed during walking and couldn't be blocked with nitroglycerine. Physical examination : the patient was pale, frightened, complained of severe chest pain. Arterial pressure was 90/60 mm Hg, HR - 100/min. ECG showed elevation of ST segment in the leads I,aVL,V, - V4, coronary T-waves were in V, - V4. Sonogram showed a thinning of the left ventricle wall and an area of akinesia. In blood: increased level of myoglobin, troponine, creatinphosphokinase, neutrophilia. Body temperature - 38,4 C. Questions: 1. What pathology did the patient have? Myocardial ischemia injury 2. What is the cause of the disease?

Fixed atherosclerotic narrowing of coronary artery leads to atrophy of LV insufficiency of heart pumping. 3. What are the mechanisms of severe chest pain? Obstruction of coronary artery myocardial O2 demand maybe adequate under basal condition(rest),but cant be augmented sufficiently to meet requirement .(physical exercise,heavywork) 4. What are the mechanisms of neutrophilia, fever, tachycardia, biochemical changes in the blood. Neutrophilia,fever,tachycardia--All are symptoms of Acute Phase Response(APR) Injury of myocardial site-- troponin & myoglobin. 5. What pathogenetic therapy can you suggest in this case? B- adrenal blockers,atherosclerotic therapy,anti coagulant & antiaggregation,nitroglycerine,vasodilator drug,rest.

1)palpitation 2)severe headache 3)vomiting 4)disturbance of eyesight He took hypotension tablets periodically Had night attacks of asphyxia for 3 yrs prior to admission examination : i. patient was pale ii. puffy iii. talkative iv. his memory was decrese v. HR was 64-68/min vi. pulse was tense vii. BP changed from 200/120 to 180/90mmHg ECG::prolonged QRS complexes,hypertrophy of left ventricle. Examination of eye fundus showed the narrow arterioles of the retina with thickening of its walls and numerous hemorrhages. The patient had albuminuria-0.06% Question: 1) Classify this hypertension according to the level of arterial pressure - severe arterial hypertension - because:systole arterial pressure > 180 mmHg diastole > 110 mmHg 2) Name the disease stages rd - 3 stage (clinical sign appear at target organ) 3) Calculate the average arterial pressure Average arterial pressure = Diastolic arterial press + 1/3 arterial press pulse (PP) = 120 + 1/3 (200 120) [PP = Sys AP Dias AP] = 120 + 6.667 = 126.667 mmHg 4) Point out the target organs in this patient - heart, kidney, vessels of eyes 5) What is the recommendations for the treatment can you give? y antihypertensive drug Commonly used drugs include: y ACE inhibitors such as captopril, enalapril, fosinopril (Monopril), lisinopril (Zestril), quinapril, ramipril (Altace) y Angiotensin II receptor antagonists: eg, irbesartan (Avapro), losartan (Cozaar), valsartan (Diovan), candesartan (Atacand) y Alpha blockers such as doxazosin, prazosin, or terazosin y Beta blockers such as atenolol, labetalol, metoprolol (Lopressor, Toprol-XL), propranolol. y Calcium channel blockers such as amlodipine (Norvasc), diltiazem, verapamil y Diuretics: eg, bendroflumethiazide, chlortalidone, hydrochlorothiazide (also called HCTZ) y Combination products (which usually contain HCTZ and one other drug)

Case 4 58 yr old man complaints:::