Department of pathological physiology-2018
Pathological physiology of blood circulatory system
Classification of insufficiency of blood circulatory system
According to the origin
Heart
Vessel
Mix
According to the compensation
level görə
Compensatory
Decompensatory
According to the course
acute
chronic
According to the manifestation level
of signs
I degree
IIdegree
IIIdegree
Main clinical manifestations of blood circulatory insufficiency
Clinical manifestationsTachycardia
Dyspnea
Cyanosis
Edema
Cardial cirrhosis of liver
Polycythemic hypervolemy
Nicturia
Hemodynamic indices of blood circulatory insufficiency
Systolic and minute volume
Ejection fraction of
blood
Rate of blood flow
Oxygen utilization coefficient
Circulatory blood volume
Systolic index Cardiac index
Arterial pressure
Venous pressure
Cardiac insufficiency
According to the origin
myocardial
Increasing the work of
heart
pericardial mix
According to the localization
Left-ventric
ular
Right-ventricular
total
Emergency
Heterometric
Homeometric
Chronoinotrop
Prolong term
Hypertrophy of myocardium
Compensation mechanisms during cardiac insufficiency
Hypertrophy of myocardium
Emergency stage
Relative-stable hyperfunction and ending
of hypertrophy
Progressive cardiosclerosis and decompensation
Vascular insufficiency
Vascular insufficiency
Acute
shock
collapse
syncope
Chronic Arterial hypotension
Insufficiency of coronary vessels
Types Developmental reasons
AbsoluteRelative
Obturation
compressionangiospazm
Ischemic diseases of heart
Angina pectoris
Pre-infarct state
Myocardial infarction Cardiosclerosis
Risk factors: hypercholesterolemia; obesity; arterial hypertension; diabetes mellitus; hypodynamy; bad habits, ets.
Angina pectoris
ECG:negative T wave and depression of ST interval
Stable (typical)angina pectoris
Prinsmetal angina pectoris
Non-stable angina pectoris
It is ischemic necrosis of myocardium, developing as a result of acute coronary
insufficiency
Atherosclerosis of coronary artery
Emboli of coronary artery
Congenital defects of coronary
vessels
Prolonged term spasm of coronary
vessels
Another nature damages of
coronary vessels
Typical form
Anginoz variant
Atypical form
Asthmaticvariant
Abdominal variant
Arythmik variant
Serebro-vascular variant
Less symptom variant
RESORBTİON-NECROTİC SYNDROME
It is develops as a result ofabsorption of products ofnecrotic tissue into blood duringmyocardial infarction. Signs:- fever- neutrophil leukocytosis- increasing of ESR- enzymemia- hypermyoglobulinemia- determination of non-enzyme nature specific proteins (cardial troponin-TnT və TnI)
- Dressler syndrome
Changes in ECG during myocardial infarction
Ischemic zone
Damage zone
Necrotic zone
Ischemia-negative T wave
Damage-elevation of ST interval
Necrosis- deep Q wave
Restoration-normalization of ST interval
Early complications
• Cardiogenic shock• Acute cardiac
insufficiency• Acute aneurism of heart• Tamponage of heart• Thromboembolia
• Disturbance of cardiac rhythm and conductivity,
ets
Late complications
• Dressler syndrome• Chronic aneurism of heart
• Chronic cardiac insufficiency, ets
Complications of myocardial infarction
ATHEROSCLEROTIC
After myocardial infarction
Myocarditic
Arrhythmia• Arrhythmia, connecting with
disturbance of automatism;• Arrhythmia, connecting with
disturbance of excitation;• Arrhythmia, connecting with
disturbance of conductivity;• Arrhythmia, connecting with
simultaneously disturbance of excitation and conductivity;
• Arrhythmia, connecting with disturbance of contraction in the heart.
• a
Arrhythmia, connecting with disturbance of automatism
Homotop rhythms:• Sinus tachycardia• Sinus bradicardia• Sinus arrhythmia• Syndrome of weakness
of sinus node
Heterotop rhythms:• Slow atrial rhythm• Atrioventricular rhythm • Migration of pacemaker• İdioventricular rhythm
Arrhythmia, connecting with disturbance of
excitation in the heart
Ekstrasystole Paroksizmal tachycardia
Atrial extrasystole
Atrial-ventricular extrasystole
Ventricular extrasystole
Arrhythmia, connecting with disturbance of conductivity in the heart
Weakening of conductivity• Sinoauricular blokage• Intra-atrial blockage• Atrioventricular blockage• Intra-ventricular blockage
Acceleration of conductivity• Volf-Parkinson-Wayt
syndrome (WPW)• Klerk-Levi-Kristesko
syndrome
ATRİO-VENTRİCULAR BLOKAGE
I degree atrioventricular blockage
Venkebach-Samoylov periods during II degree blockage
Complete transverse blockage
Arrhythmia, connecting with simultaneously disturbance of excitation and conductivity of heart
• Frequency of impulses in one minute is 250-400
Flutter of atria
• Frequency of impulses in one minute is 400-600
Fibrillation of atria
• Frequency of impulses in one minute is 150-300
Ventricular flutter
• Frequency of impulses in one minute 300-500
Ventricular fibrillation
Atrial fibrillation
Ventricular flutter and fibrillation
Atherosclerosis
Difference of atherosclerosis from Menkebergarteriosklerosis
Indices Atherosclerosis Menkebergarteriosclerosis
Localization of damage İntima Media
Predominant processes İnfiltrationand prolipheration
Degeneration andsklerosis
Precipitated elements Lipids (cholesterol) Calcium salts
Manifestations stenosis of arteries Decreasing elasticity of arterial wall
Results Ischemia of orqan andtissues
Aneurism of vessels
Factors, acting to the vascular tone
PRESSOR FACTORS• sympatoadrenal system; • renin-angiotensin system; • aldosteron-vasopressin
system; • glucocorticoids; • tromboxan-A2; • endotelin, ets.
DEPRESSOR FACTORS• Impulses, passing from
aortal curve and sinocarotid zone;
• A, E prostaglandins; • prostacyclin (PGI2); • kallikrein-kinin system; • Atrial sodium-uretic
hormone; • Relax factor (NO) , ets.
ARTERIAL HYPERTENSION
• essential• symptomatic
NORM ARTHERIOSCLEROSISHypertrophy and hyperplasia of smooth muscular cells
Fibrosis
Damage of endothelium
• as a result of weakening of cardiaccontraction;
• as a result of decreasing of circulatingblood volume;
• as a result of decreasing of tone ofresistive vessels.