CARDIOVASCULAR DISEASES 1. Consequences of blood loss (acute, chronic) 2. Pathophysiology of the vessels 3. Pulmonary hypertension (causes and consequences) 4. Arterial hypertension 5. Shocks, common features and differences 6. Acute heart failure 7. Congestive (chronic) heart failure 8. Disorders of coronary circulation and clinical forms of ischemic heart disease 9. Congenital heart disease 10. Valvular defects 11. Disturbances in impulse conduction in the heart, cardiac arrhytmias 12. Test of cardiovascular function, ergometry

1. Consequences of blood loss (acute, chronic) Acute blood loss (circulatory shock) Bleeding external, internal Consequences volume dependent according to blood loss Haematocrit haemodynamic changes Signs Stages and mechanisms of progress (compensatory reactions, refractory shock) Management: volume replacement therapy x packed red blood cells

Chronic loss (anemias) - hemolytic (causes, hypersplenism) - chronic posthemorragic (causes, GIT and kidney disorders) Diagnosis, laboratory findings Morfologic classification Symptoms: Therapy:

2. Pathophysiology of the vessels Arteries disorders Local narrowing - anatomical - functional Widening Reduced compliance Conseqences: pressure and flow changes Critical closure pressure

Capillaries disorders Increased permeability – edemas Fragility – bleeding Viscosity x blood flow Plasma skimming

Veins disorders compliant wall contain little smooth muscle, valves constriction – norepinephrin, circulating endotelins Central and peripheral venous pressure (thoracic pump, heart rate, muscle-venous pump) Gas embolism – causes Chronic venous insufficiency – enlargement of superficial veins - varicose veins (lower limbs, esophageal, haemorroids – external, internal)

Risk factors: Complications: Deep vein thrombosis (DVT)– thrombus formation, pulmonary embolism Wirchov´s triad Tromboflebitis x flebothrombosis

3. Pulmonary hypertension (causes and consequences) values of pulmonary pressure pathogenesis – increased resistance x increased blood flow Classification: Acute x chronic Precapillary x postcapillary Acute – pulmonary embolism Chronic - congenital heart defects, obstructive and restrictive pulmonary diseases risk factors origin of an embolus diagnosis and manegement morphologic changes of pulmonary vessels venous cogestion in the lungs – lung edema Cardiac asthma Cor pulmonale (ECG signs)

4. Arterial hypertension normal BP, systolic and diastolic hypertension pathogenesis: BP = CO x TPR primary x secondary

Classification and causes

essential

hyperkinetic circulation?? Na+ excretion??

renal

renovascular, renal parenchyma disorders

cardiovascular

aortic coarctation

endocrine adrenomedular adrenocortical

feochromocytom aldosteron idiopatic adrenal hyperplasia, Cushing´s, enzymatic disorders of synthesis of steroids

neurogenic

CNS, baroreception

during pregnancy isolated systolic hypertension

reduced compliance of elastic arteries

Consequences – myocard, arteries, kidneys, malignant hypertension Principles of treatment possibilities of vasodilation

5. Shocks, common features and differences Circulatory shock Systemic hypoperfusion (ischemia) resulting from decreased venous return, characterized by hypotension. Causes: a) decreased volume of circulating blood (hypovolemic shock) b) increased capacity of vascular bed (distributive shock) Stages of shock: initial (activation of compensatory mechanisms) progressive

hypovolemic shock: hemorrhagic fluid loss - burns - dehydration distributive: anaphylaxis sepsis neurogenic vasodilation Treatment:: differs according to type of shock (volume replacement therapy, sympatomimetics, corticoids)

6. Acute heart failure Acute (cardiogenic shock) – abrupt decrease of CO resulting without immediate intervention in death left ventricular failure, right ventricular failure central venous pressure (CVP) cardiac output (CO) Causes: Acute coronary syndromes extreme changes in the heart rate decrease of contractility tamponade rupture of a papillary muscle increased afterload (pulmonary embolism)

Signs: Diagnostic: Principles of therapy:

7. Congestive (chronic) heart failure Chronic (congestive) hypertension IHD diabetes valvular disorders

systolic dysfunction

SV

diastolic dysfunction

EDP

contractility

systolic dysfunction

BP

GFR

diastolic dysfunction

EDP

edema

RAS

retention of water and electrolytes

Molecular mechanisms: energy Ca2+ remodeling of the heart

Treatment: vasodilation, cardiotonics, diuretics Heart failure with high cardiac output

8. Disorders of coronary circulation and clinical forms of ischemic heart disease Disruption of coronary blood flow: Causes: a) increased resistance of coronaries – functional: vasoconstriction shortening of diastole anatomical: atherosclerosis trombi, emboli combination of previous two b) decreased pressure gradient – decreased aortic diastolic pressure increased right atrial pressure Therapy – vasodilating drugs (stealing phenomenon) - invasive Ischemic heart disease Causes of decreased coronary blood flow Acute coronary syndrome Consequences of ischemia – contractility, arrhytmias, angina pectoris, ECG signs necrosis Symptoms: angina pectoris – stable nonstable vasospastic ECG laboratory Myocardial Infarction – subjective symptoms ECG - STEMI, NSTEMI, inversion T, deep Q laboratory acute heart failure early and later complications Management - PCI, trombolysis, surgery Prevention

9. Congenital heart diseases a) without shunt – coarctation of aorta, valvular disorders b) with shunt – left to right (possible cyanosis) right to left (cyanotic) left to right - high pulmonary blood flow – response of pulmonary vasculature – reversal of the flow right to left – conditions of surviving

Coarktation of aorta

Persisting ductus arteriosus (PDA):

Ventricular septal defect

Fallot´s tetralogy (TOF):

Atrial septal defect

10. Valvular defects valvular anatomy heart sounds fonocardiography echocardigraphy pressure gradients Causes: congenital valvular defects acquired valvular disorders (endocarditis) changes in valvular diameter Stenosis – pressure overload, compensation Insufficiency – volume overload, compensation Pressure - volume curve Starling´s mechanism

Zdroj: http://www.cvphysiology.com Changes of contractility Changes of EDV

11. Disturbances in impulse conduction in the heart, cardiac arrhytmias Definition Clinical signs (subjective, objective) Etiology (extracardial, myocardial) Diagnostics Arrhytmias classification (electric processes, localization, velocity)

Mechanisms, reentry

Consequences Principles of therapy (pharmacology, defibrilation, cardioversion, cardiostimulation)

12. Test of cardiovascular function, ergometry Echocardiography (cardiac echo) importace in diagnostics wall of myocardium valves cinetics disorders Doppler shunts Transesophageal echocardiogram

Holter monitor (continual 24 hours) monitoring of ECG or blood pressure

Exercise stress testing: determination of functional capacity assessment the probability and extent of coronary disease assessment the ffects of cardiovascular interventions and rehabilitation - bicycle (treadmill) ergometry (stress ECG) - spiroergometry (assessment of cardiopulmonary performance) - stress echocardiography (exercise or pharmacologic - dobutamin -stress testing) - 6 min walking test (6-MWT) basic workload, intensification after 2 min exercise induced changes (ECG, blood pressure, heart rate, minute ventilation) maximal heart rate blood pressure amplitude RQ (RER) anaerobic threshold