CIRCULATORY SHOCK Lecture by Dr.Mohammed Sharique Ahmed Quadri Assistant professor,Physiology

بسم الله الرحمن الرحيم

Objectives Define shock. Recognize types of shock – haemorrhagic, anaphylactic, septic, and cardiogenic. Understand the shock by discussing changes occurring in haemorrhagic shock. Explain compensatory response of body to shock. Identify the concept of irreversible (unresponsive) shock.

Circulatory shock Is acute failure of circulatory system to supply the peripheral tissues and organs of the body with adequate blood supply, resulting in cellular hypoxia.

TYPES OF SHOCK HYPOVOLEMIC CARDIOGENIC OBSTRUCTIVE DISTRIBUTIVE 5

6 DISTRIBUTIVE SHOCK

Hypovolaemic Volume Loss Blood loss -Haemorrhage Plasma Loss-Burns ECF Loss- Vomiting & Diarrhoea 7

Hypovolumic shock Is most widely studied shock & often used as prototype in discussion of manifestations of shock Hypovolemic shock is also called "cold shock." It is characterized by – Hypotension; – Rapid, thready Pulse; – Cold, Pale, Clammy Skin; – Intense Thirst; – Rapid Respiration; – Restlessness.

Hemorrhagic shock It illustrate the features of a major form of hypovolemic shock and the multiple compensatory reactions that come into play to defend ECF volume Hemorrhage Decrease arterial pressure Decrease cardiac out put Decrease blood volume Decrease venous return Decrease stroke volume

Compensatory response

Compensatory reactions activated by hemorrhage. – Vasoconstriction – Tachycardia – Venoconstriction – Tachypnea→increased thoracic pumping – Restlessness→increased skeletal muscle pumping (in some cases) – Increased movement of interstitial fluid into capillaries – Increased secretion of norepinephrine and epinephrine – Increased secretion of vasopressin – Increased secretion of renin and aldosterone – Increased secretion of erythropoietin – Increased plasma protein synthesis

Points to Ponder Goal of compensatory mechanisms is to maintain cerebral and cardiac perfusion Vasoconstriction of splanchnic, and renal blood flow Compensatory mechanisms are not effective over the long term and fails when shock state is prolonged. 13

Effect of hemorrhage on mean arterial pressure

Stages of Shock 1.Non progressive stage or Compensated stage: in this circulatory compensatory mechanism cause Full recovery without therapy 2.Progressive stage: Decreased BP AND COP. Here without therapy,shock gets worse. 3.Refractory shock or Irreversible stage : Here patient does not respond to Treatment. 15

Irreversible or refractory shock Factors contributing irreversible shock Cerebral ischemia – Depression of vasomotor and cardiac areas of the brain (vasodilatation, decreased BP, decreased HR) Myocardial depression due to Acidosis causes decreased COP Respiratory failure (ARDS) – triggered not only by shock but also by sepsis, lung contusion, other forms of trauma. – Damage to capillary endothelial cells and alveolar epithelial cells, with release of cytokines.

Cardiogenic Pump Failure May be due to – Inability of heart to Contract or – Inability of heart to pump blood Myocardial damage ( M.I) Arrhythmias Valvular damage Symptoms are those of shock and heart failure ( pulmonary oedema) 17

Distributive Decreased Peripheral Vascular Resistance (blood volume is normal but vascular capacity increases, i.e. relative hypovolemia) Septic Shock (inflammatory mediators) Neurogenic Shock (loss of sympathetic control on vascular tone) ANAPHYLACTIC shock (presence of vasodilator substances like histamine) 18

Anaphylactic Shock Systemic response to the inflammatory mediators released in type I hypersensitivity – Histamine, acetylcholine, kinins, leukotrienes, and prostaglandins all cause vasodilation and increase capillary permeability º What will happen when arterioles vasodilate throughout the body? º What will happen when there is increase vascular permeability – Acetylcholine, kinins, leukotrienes, and prostaglandins all can cause bronchoconstriction

SEPTIC SHOCK Usually due to gram-negative bacteria Endotoxins released by gram-negative Bacteria—cause VASODILATATION(Skin is warm therefore called WARM SHOCK). High fever Increased capillary permeability with loss of fluid in tissues Mortality is 30-50% 20

Neurogenic shock In Neurogenic shock, there is decreased sympathetic activity, therefore, increased vascular capacity. Reason—Sudden loss of Vasomoter Tone resulting in massive dilation of veins therefore Venous pooling of blood and decreased venous return to heart. Causes of Neurogenic shock Brain injury Depressant action of drugs General anesthesia (barbiturate) 21

Fainting and Syncope Fainting--Feeling of dizziness due to decreased cerebral perfusion but not sufficient to cause loss of consciousness. Syncope—Temporary impairment of consciousness due to reduction in cerebral blood flow 22

Vasovagal syncope Vasovagal attacks---Increased Vagal activity,ANS Disturbance -- It causes vasodilatation due to sympathetic inhibition therefore pooling of blood in extermities and Fainting. --Bradycardia --It is short lived and Benign. Causes-----overwhelming Fear, or severPain 23

Fainting/ syncope Other forms of syncope include – postural syncope, due to pooling of blood in the dependent parts of the body on standing from lying down or sitting possition. – Micturition syncope, during urination, occurs in patients of orthostatic hypotension It is due to the combination of the orthostasis and reflex bradycardia induced by voiding in these patients.

Fainting/ syncope – Pressure on the carotid sinus, produced, for example, by a tight collar, can cause such marked bradycardia and vasodilation that fainting results (carotid sinus syncope). – Rarely, vasodilation and bradycardia may be precipitated by swallowing (deglutition syncope). – Cough syncope occurs when the increase in intrathoracic pressure during straining or coughing is sufficient to block venous return

References Human physiology by Lauralee Sherwood, seventh edition Text book physiology by Guyton &Hall,11 th edition Text book of physiology by Linda.s contanzo,third edition