PATHOPHYSIOLOGY OF CVS 1) Write causes which can lead to chronic left/sided heart overload by high volume.

(Left sided heart failure)  ventricle/volume overload (regurgitate overload) seen at valvular regurgitate at mitral or aortic seen as high output state as anemia or hyperthyroidism & as a result of long severe physical work.  ischemic heart disease  aortic stenotic & incompentence  mitral incompentence  inadequately treated systemic hypertension  cardiomyopaties 2) Write causes which can lead to chronic right/sided heart overload by high pressure. (right sided heart failure)         pressure overload - belong to hypertonic disease or aortic stenosis left side failure chronic lung disease (cor pulmonale) tricuspid/ pulmonary valve disease left to right shunts (eg; ventricular septal defects) mitral valve disease with secondary pulmonary hypertension pulmonary embolism isolated right-sided cardiomyopathy (rare)

3) How does the stroke vol (or heart contractility) change when Starling curve shifts to d right (or to the left)? when Starling curve shifts to d right when Starling curve shift to d left SV decrease (< 80 ml)

SV increase (> 80 ml)

* refers to the Frank Sterling curve 4) Which of cardiac indices must be used for best quantitative evaluation of heart work? chronic heart failure = decrease cardiac output ( bcoz decrease contractility of myocardium) 5) What formula can be used to calculation of Stroke volume Cardiac Output Heart index Ejection fraction = EDV (end-diastolic volume) ESV (end- systolic volume) = SV (stroke volume) heart rate = CO/ body surface area = (SV/ EDV) 100

6) What ion has direct relation to a heart muscle contraction - Calcium 7) Describe the mechanism of tachycardia in case of heart failure      Decrease in SV (stroke volume) Decrease in excitation of pressure receptor in sinus carotid Decrease in pulsation nerves depression Decrease in parasympathetic but increase in sympathetic Tachycardia

8) Name the 3 successive stages of cardiac hypertrophy. i) stage of energetic ii) stage of resistance (compensative) iii) stage of decompensative

9) How does the level of Ca ions change in hypertrophied cardiomyocytes? - increase level of Ca ions

10) How does the relative myocardial fiber surface change in the hypertrophied cardiomyocytes? - decrease relative myocardial fiber surface

11) How do cardiac index, venous pressure, peripheral vessel resistance, aldosteron production change at congestive heart failure? - decrease cardiac index, increase of venous pressure, increase peripheral vessel resistance, increase aldosteron production

12) Describe the atriopeptide role in mechanisms of chronic congestive heart failure development polypeptide hormone involved in the homeostatic control of body water, sodium, and adiposity released by atrial myocytes Atrial streching, increase in blood pressure in atrium Release of atriopeptide Decrease of water, sodium, free fatty acid in circulation system Returning blood pressure to normal level

13) What is the best mechanism for compensation for chronic heart insufficiency? a) increase in the activity of the sympathetic nervous system ex. Catecholamine cause more forceful contraction of the heart muscle and increase in heart rate remodeling of heart muscle b) c) hypertrophy cardiac dilatation frank sterling law cardiac failure progress increase end diastolic pressure individual cardiac muscle fibers stretch increase contraction increase cardiac output 14) Describe the mechanism of secondary aldosteronism by congestive heart failure. Secondary aldosteronism Mechanism Decrease left ventricular output Decrease perfusion of the kidneys Local activation of rennin angiotensin system Release of aldosterone Renal tubules reabsorb sodium and water increase total plasma volume of extracellular fluid hypertrophy, dilatation

15) Describe the ECG patch of the right bundle branch block - changes can be seen in lead V1,V6 - no conduction occurs down the right bundle branch therefore septum is depolarized from the left side R wave in V1 Small Q wave in V6 - excitation spreads to the left ventricle S wave in V1 R wave in V6 - excitation to the right ventricle takes longer time R wave in V1 Wide and deep S wave in V6

16) Write the risk factors (5) of myocardial infarction. a) b) c) d) e) hypertension hypercholestremia smoking diabetes mellitus hereditary

17) Write the pathogenetic principles of acute myocardial infarction therapy (5) a) b) c) d) e) analgesics nitrates to dilate coronary vessels thrombolytics anticoagulants antiaggregants

18) Give an ECG description of an acute left side transmural myocardial infarction. Acute: raised ST segment (ischemical injury) Transmural : absence of R wave, only pathological QS wave Left side: determined by identifiying the above signs in V1 and V2 chest leads.

19) Explain the mechanism of T coronary wave formation in case of subepicardial (or transmural) and subendocardial ischemia (make a picture) Mechanism: a) subendocardial

Ischemia in this area prolongs local recovery time. Since repolarization normally proceeds in an epicardial-toendocardial direction, delayed recovery in the subendocardial region due to ischemia does not reverse the direction of repolarization but merely lengthens it. This generally results in a prolonged QT interval or increased amplitude of the T wave or both as recorded by the electrodes overlying the subendocardial ischemic region. b) subepicardial

Transmural ischemia is said to exist when ischemia extends subepicardially. This process has a more visible effect on recovery of subepicardial cells compared with subendocardial cells. Recovery is more delayed in the subepicardial layers, and the subendocardial muscle fibers seem to recover first. Repolarization is endocardialto-epicardial, resulting in inversion of the T waves in leads overlying the ischemic regions.

20) Explain QS complex formation in case of transmural myocardial infarction -from endocardium to epicardium -absent vector, back to base line -formation of QS complex with absent of R wave

21) What kind of myocardial infarction are represented by following   ST segment increase, pathological Q wave in V1-V3 leads  ACUTE MYOCARDIAL INJURY ST on baseline, pathological on Q wave in II, III aVF leads, coronary downwards T wave  ISCHEMIA

22) Write the 4 possible mechanism of heart fibrillation  Digoxin effect  Independent contraction of heart  Systemic disease/metabolic abnormalities 23) In what phase cardiac work does coronary flow most occur End systolic phase ????? 24) Write the 2 main factors that can influence on average pressure in aorta  Systolic blood pressure  Diastolic blood pressure 25) Write the formula for calculation of average arterial pressure in patients.

Old : Based on the normal blood pressure curve configuration, the functional MAP is lower than the arithmetic one (pulse pressure/2). For many years, MAP has been calculated by blood pressure cuff measurements using an empiric formula, which states that the MAP equals one third of the distance between the systolic pressure (SP) and the diastolic pressure (DP). New: new and more accurate heart rate-corrected MAP formula from central aorta pressure determinations in a large number of patients: MAP = DP + [0.33 + (HR 0.0012)] [PP] where SP and DP are systolic and diastolic pressure and HR is heart rate.

26) What are the main target organs at hypertonic disease? Heart,Kidney,Brain & Arterial blood vessels.

27) What humoral substances are vasodilatators and vasoconstrictor? Vasodilators: Adrenalin&noradrenalin(only in skeletal muscle,but vasoconstrictor in other places),PAF, Prostacyclin,Histamine Vasoconstrictor:Anti histamine,Adrenaline,catecholamines,norepinephrin,thromboxane

28) Activation of what humoral systems is associated with increase of arterial blood pressure? catecholamines, angiotensin II and arginine-vasopressin

29) Describe the pathogenesis of cyanosis at heart insufficiency Cyanosis Occur when blood from the right side of the heart enters the left side (right-to-left shunt), cyanosis develops because there is diminished pulmonary blood flow and poorly oxygenated blood enters the systemic circulation 30) Why does left ventricle more often involve in ischemic process Because left ventrical need more oxygen to pump blood to whole body.Increase workload,increase oxygen demand

31) Write causes and consequences of the lung vessels hypertension Causes of lung vessels hypertension:

y y y y y

Use of appetite suppressants, especially fenfluramine and dexfenfluramine Chronic use of cocaine or amphetamines HIV infection Liver disease Connective tissue diseases, such as scleroderma or lupus erythematosus

Consequences:

y y y

The muscles within the walls of the arteries may tighten up. This makes the inside of the arteries narrower. The walls of the pulmonary arteries may thicken as the amount of muscle increases in some arteries. Scar tissue may form in the walls of arteries. As the walls thicken and scar, the arteries become increasingly narrow. Tiny blood clots may form within the smaller arteries, causing blockages.

32) 3 main organ-targets to angiotensin 1. 2. 3. Kidney (adrenal cortex)- Angiotensin II acts on the adrenal cortex, causing it to release aldosterone, a hormone that causes the kidneys to retain sodium and lose potassium. Lung - Angiotensin I is converted to angiotensin II through removal of two terminal residues by the enzyme Angiotensin-converting enzyme (ACE, or kininase), which is found predominantly in the capillaries of the lung. Heart -angiotensin II could be a cause of vascular and cardiac muscle hypertrophy

33) Describe the Starling law

The more the ventricle is filled with blood during diastole (end-diastolic volume), the greater will be during the resulting systolic contraction (stroke volume).

the volume of ejected blood

For example, during venoconstriction the end diastolic volume increases, increasing preload, this will increase stroke volume. The heart will pump what it receives. 34) How much time must coronary flow increase in order to teach it maximum in comparison with normal at rest (coronary reserve) ? - 5 times 35) What difference can be noticed between indexes of central venous pressure in two patient ,when one has cardiogenic shock and another hypovolumic shock? - Cardiogenic shock increase CVP, hypovolumic shock decrease CVP 36) How will change the indexes of pulmonary capillary pressure after successful treatment of left ventricular failure? Index of pulmonary capillary pressure decreases after successful treatment of left ventricular failure 37) Define & calculate: stroke volume (SV) = End diastolic vol (EDV) End systolic vol (ESV) ~ 80ml ejection fraction (EF) = SV x 100% ~ > 50% EDV

cardiac output (CO) i) CO = SV x heart rate ii) CO = O2 (ml) absorbed / min O2 art O2 ven (vol %) ~ 3.1 -3.2 l/min/m cardiac index = CO surface of body coefficient of O2 utilization = Arterial O2 Vein O2 Arterial O2 = 19 vol % - 13 vol % 19 vol %
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