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.