Pathophysiology of cardiovascular system
.pdfc) Catecholamines have a vasoconstrictor action of pumps (an increase in OPS and post-loading)
2) glucocorticoids enhance the effects of catecholamines, the load on the heart increases due to the active stimulation of beta-1-adrenoreceptors
62. Suggest the therapy to the patient with acute Myocardial Infarction. Pathogenetic therapy:
-pain syndrome relief
-prescribe the nitrates (nitroglycerin) to dilate the coronary vessels
-oxygenotherapy
-thrombolytic therapy to recover the magistral bloodflow
-prevention of thromb formation (anticoagulants and antiaggregants)
-decrease the need in oxygen in myocardium
-limitation of the size of infarction by early revascularization
-prevention of dangerous arythmias
-treatment with metabolic cardioprotectors, which improve the metabolic processes in heart
63. Write the pathogenetic principles of acute myocardial infarction therapy (5). Pain relief,
-thrombolytics (if not passed 6 hours from the beginning of them, otherwise we will make even worse, because there will be reperfusion damage to myocardium).
-IAPF, it is possible to give beta-blockers in order to avoid early complications in the form of ventricular fibrillations,
-AT2 blockers,
-nitrates,
-antiarrhythmics
64. Explain the mechanism of T-coronary wave formation in case of transmural (or subepicardial) and subendocardial ischemia (+ make a picture).
Ischemia is localized in subendocardial departments. A wave of repolarization moves from epicarda to the endocardium. -> the vector is directed to the positive pole -> a positive wave
65.Explain pathological Q wave or QS-complex formation in case of nontransmural or transmural myocardial infarction (+ make a picture).
In the first half of the excitement, the area of necrosis is not excited and EMF (ЭДС) does not occur in it. The total instant vector of QRS will be directed towards the negative points of the assignments in which a negative deviation is fixed - exhausted (уширенный) Q. In the next stage of depolarization, the excitation wave covers non-affected subepicardinal departments over the necrosis zone, the excitation as in the norm applies to epicarda, and the total instant vector is
directed toward Positive electrodes. A positive deviation is recorded R. Thus, the main feature is the presence of an increased Q in leads, which are positive electrodes of which lie above the necrosis area.
66. Explain depression or elevation of S-T – segment formation in case of nontransmural or transmural myocardial ischemic injury (+ make a picture).
The damaged zone becomes less negatively charged (more positively charged) in comparing to the surrounding parts of myocardium. So there forms the EMF of the current of damage, where the vector goes from – to + charge. When we have the
subendocardial zone damage -> depression of ST segment, if subepicardial zone damage -> elevation of ST segment
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67. Write causes (1,2,3) and consequences (1,2,3) of the lung vessels hypertension.
Causes:
-left ventricle insufficiency
-parenchymatous lung diseases
-connective tissue diseases Consequences:
-lung edema
-afterload of RV -> hypertrophy -> dilatation -> heart insufficiency with edema of legs, ascites, hydrothorax
-disruption of bronchial vessels -> bleeding and hemoptysis
68.Write the 2 main factors that can influence on the average pressure in aorta. Cardiac output
- Total peripheral resistance
69.Write the formula for calculation of average arterial pressure in patients. Mean arterial pressure = Cardiac output x Total peripheral resistance
70.What humoral substances are vasodilators (a) and vasoconstrictors (b) in systemic blood circulation?
a) * NO
*Bradykinin (Kinins)
*Prostacycline
*Prostaglandine E
*НУФ
LOCALLY:
* Metabolites ( CO2, lactate, adenosine)
*Acetocholine
*Mediators of damage ( histamine, bradykinin, substance P)
b)* Angiotensine 2
*Catecholamines
*Antidiuretic hormone
*Endotelines
*Tromboxane
*Some prostaglandines
*Superoxide anion
Опосредованно: альдостерон, глюкокортикоиды
71. Enumerate neuro-hormonal systems that take part in increase (a) or decrease
(b) systemic arterial pressure.
a) * Urgent reflectory mechanisms - receptors of aortic arch and carotid sinus ( 1- decrease of exatation of baroreceptors, 2 - exatation of chemoreceptors, 3 - Ischemic reaction of the heart = activation of vasomotor center)
*Mechanisms of intermediate duration of action ( 1 - RAS system activation, 2
-Vasopressin secretion н + на всякий случай ещё stretching of resisting vessels
+translocation of the intercellular liquid to the capillaries)
*Late mechanisms of long duration ( 1 - Aldosterone system, 2 - Vasopressin
system + на всякий случай kidney volume-pressure mechanisms) + Angiotensine, Catecholamines, Antidiuretic hormone, Endotelines , Tromboxane, Some prostaglandines, Superoxide anion
b) * Urgent reflectory mechanisms - activation of baroreceptors of carotid sinus and arch of aorta
*Mechanisms of intermediate duration of action - Atrial NatriUretic peptide
*Late mechanisms of long duration - NO ,Bradykinin (Kinins), Prostacycline , Prostaglandine E, NatriUretic peptide
72.Give the classification of hypertension disease due to pathogenesis.
* Essential = primary - chronic disease with unclear etiology ( appear when genetic and external factors meat each other) characterized by stable increase of AP and NO organic violation of regulating AP organs and systems
* Symptomatic = secondary ( Kidney, Endocrine, Cardiovascular, Neurogenic forms)
73. Point out the characteristics of the stages of arterial hypertension disease. 1 - first stage - no objective signs of damage of target organs, AP does not reach high numbers
2 - second stage - one or several signs of target-organs violation WITHOUT deterioration of their function - only hypertrophy of LV albuminuria and narrowing of retinal vessels, atherosclerotic changes in big vessels
3 - exposed clinical picture of target organs damage ( Heart - IHD and infarct, Brain - insult, encephalopathy, Kidney - insufficiency and azotemia, Vessels - delamination of atherosclerotic plaque, occlusive changes, Retina - retinopathy)
74. Enumerate the pathogenic factors that take part in development of essential hypertonic disease.
1- Internal
*genetic
*violation of transmembrane transport of ions
*congenital defect of kidney Na excretion regulation
*Violations in kidney activities
*Obesity and hypodinamia
2 - external factors
*exessive consumption of NaCl
*Not enough administration of Ca and Mg with food
*Smoking
*alcochol
*stress situations
*bad social and economic state
75. What are the main target organs at hypertonic disease? heart
*peripheral arteries
*kidneys
*vessels of retina
*Brain
76.Enumerate the principles of therapy for patient with arterial hypertension disease.
1 - Diuretics
2 - inhibitors of ACE
3 - Antagonists of Ca
4 - beta - Adrenoblockers
+
5 - Agonsts of imidazoline receptors
6- Peripheral vasodilators
7- alrpa -1-adrenoblockers
8- diet without salt
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77. Write the 4 possible mechanisms of heart fibrillation.
из русского файла
1 - electric nonhomogenicity of the miocardium
2 - formation of ectopic foci
3 - electric disbalance of the myocardium ( loss of K and Mg by cardiomyocetes) 4 - change of electrophisiologic properties of the heart due to necrosis
НО Богуш на паре говорила про экстрасистолы вот так...
1- electric nonhomogenicity of the miocardium
2 - unequal speed of impulse conduction
3 - unidirectional blockades
4 - increase amplitude of trace potentials
5 - asynchronic repolarization of separate regions of myocardium
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78.What difference can be noticed between indexes of central venous pressure in two patients, when one has cardiogenic shock and another – hypovolemic shock?
*Central venous pressure is high in cardiogenic and low in hypovolemic * In hypovolemic venous return is decreased
* In cardiogenic cardiac output decreases, ESV, EDV, EDP increase
79.How will change the indices of pulmonary capillary pressure ( ) after successful treatment of left ventricular failure?
Decrease till 5 - 13 mm (наверное)
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80. The student should be able to define and calculate such indices of cardiac functions as stroke volume, ejection fraction, cardiac output (2 formulas), cardiac index, coefficient of O2 utilization, estimate the proper volume of circulating blood.
*Stroke volume - volume of the blood , ejected by the left ventricle to the aorta, right ventrcle - pulmonary artery during one contraction= EDVESV
*Ejection frction = SV/EDV
*Cardiac output - volume of the blood that is ejected by the LV to the aorta or by RV in pulmonary artery in 1 min.
CO= HR*SV
CO= common amount of consumpted O2in 1 min (ml/min)/ O2aort.-O2 venous in ml/l of blood
*CI= CO l/min / Area of the body m"2
*Utilization O2 coef. = O2 aort. - O2venous / O2 aort.
*Proper Volume of circulating blood
1- Common volume of plasma = dye in mg / concentration of dye mg/l
2- Common volume of plasma * 100 / 100 - 0,87 Ht