Abhishek Shukla (A-10) Pathology Shock.pptx

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1. Shock Abhishek Shukla A-10

2. Contents : Introduction Types of Shock Clinical Features and Prognosis Stages of Shock Compensatory Mechanism Management of Shock References

3. What is Shock? Shock is a state of circulatory failure that impairs tissue perfusion and leads to cellular hypoxia . At the outset cellular injury is reversible however prolonged shock eventually leads to irreversible tissue injury and can be fatal . Shock may complicate severe heamorrhage extensive trauma or burns,myocardial infarction ,pulmonary embolism and microbial sepsis …(1)

4. Types of Shock Distributive Shock - Septic Shock - Neurogenic Shock - Anaphylactic Shock Obstructive Shock Hypovolemic Shock - Haemorrhagic Shock - Traumatic Shock - Surgical Shock - Dehydration Shock Cardiogenic Shock

5. Hypovolemic Shock Hypovolemic Shock results from Low cardiac output due to low blood volume in the vascular system . Important Haemodynamic changes are Low cardiac Output Low Central Venous pressure Increased systemic resistance Some clinical features are - [ Cold Pale Cyanosed skin ] [ Increased sweating Hypotension] [Lactic acid accumulation ( due to anaerobic glycolysis ) ]

6. It is of 4 types - Haemorrhagic Shock It is the most common cause of Hypovolemic Shock . It is produced due to excessive bleeding . It then results in reduced Venous return due to blood loss and so the cardiac output falls The heart rate starts to increase and the blood pressure starts falling . Traumatic Shock Occurs due to injury causing severe damage to muscle and bone

7. 3) Surgical Shock It occurs as a result of external or internal blood loss caused by rupture of blood vessels during any kind of surgical procedure . 4) Dehydration Shock It results as a result of fluid loss from GIT (prolonged vomitting,diarrhoea) , Kidney ( in case of diabetes) . Fluid loss also ccurse from the skindue to burns …(2)

8. 2) Distributive Shock It occurs as a result of fluid loss from GIT (prolonged vomiting, diarrhea), kidney (diabetes mellitus, diabetes insipidus). Fluid loss also occurs from the skin due to burns (burn shock) which is characterized by hemoconcentration. In burn shock, the most important abnormality is loss of plasma as exudate from the burned surfaces. Here the plasma is lost rather than the whole blood. So hematocrit rises and results in hemoconcentration…(2)

9. Septic Shock It is defined as Life thretening organ dysfu nction caused by dysregulated host response to infection in which particularly profound circulatory, metabolic abnormalities are associated with greater risk or mortality It is most frequently triggered by G+ve Bacteria followed by G-ve Bacteria and fungi It is caused by systemic inflammatory response to infection …(1)

10. Pathoge nesis of septic shock

11. During anaphylaxis (exaggerated allergic reaction to antigen) shock occurs due to release of histamine or histamine like results substances. These substances increase the capacity of vascular system by vasodilatation and by increasing the permeability of capillaries. When capillary permeability increases, there is loss ofproteins and water from the blood into the interstitial space resulting in shock due to reduced cardiac output and venous return …(2) Anaphylactic Shock

12. Neurogenic Shock Neurogenic shock is characterized by sudden depression of nervous system due to loss of vasomotor tone which leads flow to vasodilatation. Some causes of Neurogenic shock are- Deep General Anesthesia often depresses the vasomotor center enough to cause vasomotor paralysis . Spinal Anesthesia often blocks the sympathetic nervous outflow and can be potential cause of shock . Brain Damage is often a cause of vasomotor paralysis .Many patients who have had brain contusion and concussion experience profound neurogenic shock …(2)

13. 3) Cardiogenic Shock When the pumping function of heart is impaired , blood flow to the tissues is no longer adequate to meet resting metabolic demands This results in Cardiogenic Shock . It is caused most commonly due to infarction of left ventricle . It occurs mainly in Myocardial Infarction , Congestive Heart Failure and Arrhythmias . Certain chemicals released from ischemic tissues stimulate ventricular receptors and cause reflex inhibition of vasomotor center producing bradycardia and hypotension making the shock worse …(2)

14. 4) Obstructive Shock Obstructive Shock is due to obstruction to the flow of blood which reduces the perfusion to the tissues . Obstruction in flow of blood maybe caused due to several reasons - ..(2) Pulmonary Embolism Cardiac Tumor Cardiac Tamponade Tension Pneumothorax

15. Clinical Features and Prognosis In Hypovolemic and Cardiogenic shock, patients exhibit hypotension, a weak rapid pulse, tachypnea, and cool, clammy, cyanotic skin. In Septic shock, the skin may be warm and flushed owing to peripheral vasodilation. The primary threat to life is the underlying initiating event (e.g., myocardial infarction, severe hemor- rhage, bacterial infection). However, the cardiac, cerebral, and pulmonary changes rapidly aggravate the situation. Prognosis varies with the origin of shock and its duration. Thus, more than 90% of young, otherwise healthy patients with hypovolemic shock survive with appropriate management; by comparison, septic or cardiogenic shock is associated with substantially poorer outcomes …(1)

16. Stages of Shock Shock - Progressive Disorder - Leads to death if underlying problems not corrected…(1) 3 Stages : 1) Non Progressive Stage Reflex Compensatory Mechansims Activated like baroreceptor reflexes, release of catecholamines and antidiuretic hormone, activation of the renin-angiotensin-aldosterone axis, and generalized sympathetic stimulation. Net effects produced - Tachycardia, peripheral vasoconstriction and Renal Fluid Conservation

17. Compensatory Mechansims Short Term Mechanism Baroreceptor Reflex Chemoreceptor Reflex RAAS Increased Vasoconstriction Activity Increased ACTH and Aldosterone Secretion Constriction of Afferent And Efferent Arterioles to reduce GFR and prevents Renal failure Long Term Mechanism Increases Thirst , Salt Craving and water absorption from Renal tubules and GIT Preformed albumin starts entering circulation from extravascular Stores Increased formation of RBC Increased 2,3 DPG content shifts curve to right so more O2 is released into tissues

18. 2) Progressive Stage - Widespread Tissue Hypoxia, Anaerobic glycolysis, Metabolic Lactic acidosis, Arterioles Dilate - Peripheral pooling of blood Net effects produced - Vital organs affected and begins to fail 3) Irreversible Stage - Widespread Cell Injury - Lysosomal Enzyme leakage, Myocardial Contractile function worsens - increased NO synthesis, Renal Failure occurs Net effects produced- Death

19. Management Of Shock Non Drug Therapy …(2) Head-Low Position The patient should be placed in horizontal /oblique position with the head at least 12 inches lower than the feet . It promotes venous return and may help in increasing the cardiac output. Oxygen Supplement Since the central problem of shock is the lack of oxygen supply giving the patient supplemental oxygen is logical . However if the blood flow is severely affected this oxygen supplementation is of little use .

20. Replacement Therapy (To Replace the Lost Blood Volume) Intravenous Fluids (Saline , Dextrose + Saline , Ringer Lactate ) Plasma Expanders ( ‘dextran’ is a Plasma Expander . It is a large polysaccharide polymer of glucose . It exerts colloid osmotic pressure so that fluid from out of vessels can be pulled into vessels .This increases circulating blood volume . Blood/ Plasma Transfusion

21. Drug Therapy Most important life saving drugs are Sympathomimetic Drugs . They have their actions similar to sympathetic stimulation. Eg. Adrenaline Antihistaminic Drugs and Steroids may be useful in some types of Shock particularly Anaphylactic Shock

22. References : Robbins and Cotran ,Pathologic Basis of Disease 10th Edition, p134-138 Guyton and Hall , Textbook of Medical Physiology 3rd South Asian Edition, p319-325

23. Thank You