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Shock (Circulatory shock)
This document provides an overview of shock, including: 1. Definitions of shock and classifications according to etiology and pathophysiology. Shock results from inadequate oxygen delivery to tissues. 2. Descriptions of the pathophysiology of shock at the cellular, microvascular, and systemic levels, including metabolic changes, inflammation, and compensatory responses. 3. Clinical features of shock ranging from mild to severe based on degree of blood or fluid loss. Monitoring includes vital signs, urine output, and invasive monitoring like Swan-Ganz catheter. 4. Treatment principles for different types of shock including fluid resuscitation and management of underlying causes like bleeding control or cardiac dysfunction. Outcomes can include
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Shock (Circulatory shock)
- 1. By Dr.Amith WA 1yr PG (OMFS) RRDCH SHOCK
- 2. INDEX Introduction Definitions Historical background Classification Pathophysiology General clinicalfeatures Each type of shock in detail: 1. Pathophysiology 2. Compensatory mechanisms 3. Clinical feature 4. Clinical monitoring 5. Treatment Conclusion References
- 3. INTRODUCTION “Shock isthe most common and therefore the most important cause of death of surgical patients” Death may occur rapidly because of a profound state of shock , or delayed due to consequences of of organ ischemia and reperfusion injury It is therefore important for us to understand the pathophysiology , diagnosis and priorities in management of shock
- 4. DEFINITIONS Shock isa life threatening situation due to poor tissue perfusion with impaired cellular metabolism, manifested in turn by serious patho- physiological abnormalities. (Bailey and Love) Shock may be defined as inadequate delivery of oxygen and nutrients to maintain normal tissue and cellular function. (Schwartz)
- 5. True shock isa circulatory imbalance between oxygen supply and oxygen demand at the cellular level and is also called as circulatory shock ( Harsh Mohan)
- 6. HISTORICAL BACKGROUND ClaudeBernard suggested in the mid-nineteenth century that the organism attempts to maintain constancy in the internal environment against external forces that attempt to disrupt the milieu interieur Walter B. Cannon introduced the word homeostasis During WW2 , Alfred Blalock proposed four categories of shock: hypovolemic, vasogenic, cardiogenic, and neurogenic.
- 7. CLASSIFICATION (BAILEY ANDLOVE) Hypovolemic shock Cardiogenic shock Obstructive shock Distributive shock a. Anaphylactic shock b. Neurogenic shock c. Septic shock Endocrine shock
- 8. CLASSIFICATION Classification basedon the eitiology of shock (Harsh Mohan) 1.Hypovolemic shock
- 9.
- 10. CLASSIFICATION 3. Septic shock a.Gram negative septicemia ( endotoxic shock) ex. E.coli , proteus, klebshiella b. Gram positive septicemia ( exotoxic shock) ex. Streptococci , pneumococci 4. Other types a. Traumatic shock b. Neurogenic shock c. Hypoadrenal shock
- 11. TYPES OF SHOCK– ACC TO S.DAS Hematogenic shock Traumatic shock Neurogenic shock a. Vasogenic shock b. Psychogenic shock Cardiogenic shock Septic shock Miscellaneous a. Anaphylactic shock b. Insulin shock
- 12. PATHOPHYSIOLOGY BASIC FEATURES INPATHOGENESIS OF SHOCK : a. Reduced effective circulatory volume b. Reduced supply of oxygen to cells and tissues with resultant anoxia c. Inflammatory mediators and toxins induced from shock induced cellular injury
- 13. Pathophysiology: Cellular: Cells switchfrom aerobic to anaerobic metabolism Decreased ATP, Lactic acid production Metabolic acidosis Glucose exhausts and anerobic respiration ceases Na+/K+ pump impaired Lysosomes release autodigestive enzymes Cell lysis Cell death
- 14. Micro vascular: tissue ischemia activation of immune and coagulation systems hypoxia and acidosis ,activate complement and neutrophils generation of oxygen free radicles and cytokine release damaged and leaky endothelium fluids leak out and oedema ensues
- 15. Systemic: Cardiovascular: Decrease of preloadand afterload Baroreceptor response – increased sympathetic activity Release of catecholamines Tachycardia and vasoconstriction(except in septic ) Respiratory: Metabolic acidosis Increased respiratory rate and excretion of carbon dioxide Results in compensatory resp. alkalosis
- 17. Renal: decreased urineoutput stimulation of renin angiotensin and aldosterone axis. Increased sodium and water retention Endocrine release of vasopressin from hypothalamus. resulting vasoconstriction and increase water resorption in renal collecting system. Cortisol released from adrenal cortex contributes to sodium and water resorption
- 18. GENERAL CLINICAL FEATURES The classical features of decompensated shock are characterised by the depression of 4 vital processes Reduced blood pressure Feeble pulse Shallow breathing Subnormal temperature
- 19. Stage 1 Initial shock/ Non progressive/ Compensated reversible shock Stage 2 Progressive shock/ Decompensated shock Stage 3 Irreversible shock/ Decompensated shock
- 22. HYPOXIC ENCEPHALOPATHY Compensated Shockresults in cerebral ischemia which produce altered state of consciousness. However, if blood pressure falls below 50 mmHg as occurs in systemic hypotension in prolonged shock & cardiac arrest, brain suffers from serious ischemic damage with loss of cortical functions, coma, & vegetative state.
- 23. Caused by rapidloss of intravascular fluid CLASSIFICATION 1. Hemorrhagic Trauma GI bleeding 2. Non-hemorrhagic External fluid loss Diarrhea Vomiting Poly-urea Burns Anaphylaxis HEMATOGENIC SHOCK
- 25. PATHOPHYSIOLOGY OF HYPOVOLEMICSHOCK Hemorrhage from small venules & veins Decreased filling of right heart Decreased filling of pulmonary vasculature Decreased filling of left atrium & ventricle Left ventricular stroke volume decreases (Frank-Starling mech. ) Drop in arterial blood pressure & tachycardia Poor perfusion to pulmonary arteries Cardiac depression & pump failure
- 26. COMPENSATORY MECHANISM 1. Adrenergicdischarge 2. Hyper ventilation 3. Vasoactive hormones: Ex. Angiotensin ,Vasopressin, Epinephrine 4. Collapse 5. Re-absorption of fluid from interstitial tissue to extracellular space 6. Renal conservation of body water & electrolyte.
- 27. CLINICAL FEATURES OFHYPOVOLEMIC SHOCK Clinical features of hypovolemic shock depend on the degree and loss of blood and duration of shock 1. Mild shock – loss of less than 20% of blood . caused by adrenergic constriction of blood vessels. There is collapse of subcutaneous veins of extremities, pale feet, sweat in forehead ,hand and feat. Urine output, pulse, B.P normal 2. Moderate shock – loss of blood volume from 20 - 40%. Oliguria present, pulse increased 3. Severe shock – loss of blood volume above 40% Pallor present, low urinary output, rapid pulse , low blood pressure
- 29. CLINICAL MONITORING Bloodpressure Respiration Urine output Central venous pressure ECG Swan- Ganz Catheter * cardiac output * mixed venous oxygen level * vascular pressure Pulmonary artery wedge pressure Swan Ganz Catheter
- 30. TREATMENT 1. Resuscitation Itbegins immediately as the patient is admitted Establishment of clear airway ,maintain adequate ventilation and oxygenation Lower head to prevent airway obstruction , in patients with airway obstruction – intratracheal intubation and mechanical ventilation Positive pressure ventilation improves patients cardiovascular status 2. Immediate control of bleeding – achieved by elevating the footend of the body and compression tamponade to the external hemorrhage
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- 32. 3. EXTRACELLULAR FLUIDREPLACEMENT : A non sugar , non protein crystalloid solution with a sodium conc. approx. that of plasma is preferable for the initial stage of the treatment. The solution can be ringer lactate, ringer acetate or normal saline supplemented with 1 or 2 ampules of sodium bicarbonate The solution can be Ringer lactate, ringer acetate should not be used in pts with liver disease. The solution is run at rapid speed so that in 45 mins between 1000 and 2000 ml solution is given iv To know how much fluid should be given, blood pressure, pulse rate , urine output, CVP and other lab tests should be performed . If there is blood loss , it is best replaced with blood , if blood is available blood substitutes are avoided
- 33. Ischemia reperfusion syndrome: Itis the injury that occurs once the normal circulation is restored to the tissues Cause: Acid and potassium load built up leads to myocardial depression vascular dilatation and hypotension Neutrophils are flushed back into the circulation causes further injury to the endothelial cells of lungs and kidneys. Resulting in : Acute lung and renal injury Multiple organ failure Death
- 34. TRAUMATIC SHOCK Peculiarity ofthis shock is that traumatised tissues activate the coagulating system and release micro thrombi into the circulation Differentiating features from hypovolemic shock: Presence of peripheral & pulmonary edema. Infusion of large amount of fluid which is adequate in hypovolemic shock is inadequate here.
- 35. PATHOPHYSIOLOGY OF TRAUMATICSHOCK Traumatic tissue activates the coagulation system Release of micro-thrombi into circulation Obstruction parts of pulmonary microvascular system Increased pulmonary vascular resistance Increased right ventricular diastolic & right atrial pressure Humoral products of thrombi induce increase in capillary permeability Loss of plasma into interstitial tissue Depletion of Vascular volume
- 36. TREATMENT OF TRAUMATICSHOCK 1. Resuscitation – mechanical ventilator support 2. Local treatment of trauma & control of Bleeding , surgical debridement of ischemic & dead tissue & immobilization of fracture. 3. Fluid replacement with Ringers lactate ,Ringers acetate , Normal saline. 4. Anticoagulation with one intravenous dose of 10,000 units of heparin
- 37. CARDIOGENIC SHOCK It isusually due to primary dysfunction of one ventricle or the other Dysfunction may be due to > Myocardial infarction > Chronic congestive heart failure > Cardiac arrhythmias > Pulmonary embolism > Systemic arterial hypertension
- 38. CARDIOGENIC SHOCK CAUSEDBY : Dysfunction of right ventricle right heart unable to pump blood in adequate amount into lungs,filling of Left heart decreases , so left ventricular out put decreases. Dysfunction of left ventricle left ventricle unable to maintain adequate stroke volume , left ventricular output & systemic arterial blood pressure decreases ,there is engorgement of the pulmonary vasculature due to normal right ventricular output,but failure of left heart
- 39. CARDIOGENIC COMPRESSIVE SHOCK Ariseswhen heart is compressed from outside to decrease cardiac output , the cause may be * Tension Pneumothorax * Pericardial Tamponade * Diaphragmatic rupture with herniation of the bowel into the chest
- 40. CLINICAL FEATURES Skinis pale & Urine out put is low. Pulse becomes rapid & the systemic blood pressure is low. Right ventricular dysfunction , neck veins are distended & liver is enlarged. Left ventricular dysfunction , there are broncheal rales & third heart sound heard. Gradually, the heart also becomes enlarged.
- 42. MANAGEMENT . Air waymust be cleared . In case of pulmonary embolus it should be treated with large doses of Heparin, intravenously. . Pain if present should be controlled with sedatives like , morphine. . Fulminant pulmonary edema should be controlled with diuretics. . Drugs Inotrophic agents Chronotropic agents Vasodilators, Beta-Blockers.
- 44. PATHOPHYSIOLOGY Dilatation of thesystemic vasculature ↓ Decreased systemic arterial pressure ↓ Pooling of blood in systemic venules & small veins ↓ The right heart filling & stroke volume decreases ↓ Decreased pulmonary blood volume & left heart filling ↓ Discharge of angiotension & vasopressin though they fail to restore the cardiac output to normal
- 45. CLINICAL FEATURES 1. Warmskin, pink & well perfused in contradiction to hypovolemic shock 2. Urine output may be normal 3. Heart rate is rapid 4. Blood pressure is low
- 46. MANAGEMENT 1. Assuming Trendelenburgposition—displaces blood from systemic venules into right heart & increases cardiac output. 2. Administration of fluids- not so important as in hypovolemic shock 3. Vasoconstrictor drugs : Phenylephrine & Metaraminol It is the only type of shock safely treated with vasoconstrictor .Its prompt action saves patient from immediate damage to important organs like brain , heart & kidney.
- 47. SEPTIC SHOCK Most oftendue to gram-negative than gram-positive bacteria Septic shock is seen in : Severe septicemia, Cholangitis, Peritonitis, Meningitis, etc. The common organisms that are concerned with septic shock are E.coli, klebsiella aerobactor, proteus, pseudomonas, bacteroides, etc.
- 48. GRAM POSITIVE SEPSIS& SHOCK It is usually caused by dissemination of a potent exotoxin liberated from gram positive bacteria without evidence of bacteremia. It is usually seen in Clostridium Tetany or Clostridium Perfringes infection. It is basically caused due to massive fluid losses. Arterial resistance falls but there is no fall in cardiac output. Urine output ususally remains normal.
- 49. GRAM NEGATIVE SEPSIS& SHOCK The most common cause of this infection is genito-urinary infection. Persons who have had operations of the genito- urinary tract are also susceptible. It may also be seen in patients who have undergone tracheostomy or those with gasterointestinal system infections. The severity may vary from mild hypotension to fulminating septic shock which has a poor prognosis. The prognosis is more favorable when the infection is accessible to surgical drainage.
- 50. CLINICAL FEATURES Theclinical manifestations of septic shock may be fulminating and rapidly fatal. It is recognized initially by the development of chills & fever of over 100 degrees. Two types are clearly defined a. Early warm shock. b. Late cold shock.
- 51. EARLY WARM SHOCK oIn this type there is cutaneous vasodilatation. o Toxins increase the body temperature. To bring this down vasculature of the skin dilates. This increases the systemic vascular resistance. o Arterial blood pressure falls but the cardiac output increases, because the left ventricle has minimal resistance to pump against. o Adrenergic discharge further Increases the cardiac output. The skin remains pink, warm & well perfused. o The pulse is high & the blood pressure low. o There are intermittent spikes of fever with bouts of chills.
- 52. LATE COLD SHOCK There is increased vascular resistance due to release of toxic products. This leads to hypovolemia with decrease in right heart filling. There is decreased flow to pulmonary vasculature so the left heart filling & the cardiac output decreases. The knowledge of existence of a septic focus is the only factor that differentiates septic shock from traumatic & hypovolemic shock.
- 53. Treatment: The only wayto reduce mortality in septic shock is by prompt diagnosis and treatment It can be divided into two groups. • Treatment of the infection. • Treatment of the shock. It consists of: 1. Fluid replacement. 2. Debridement & drainage of the infection. 3. Administration of the antibiotics. 4. Mechanical ventilation. 5. Steroids. 6. Vasoactive drugs. 7. Specific gamma globulins to bind the endotoxins. 8. The antibiotic polymixin E also absorbs some of the endotoxin.
- 54. ANAPHYLACTIC SHOCK Etiology : Themost common cause of anaphylaxis is the administration of penicillin. The other causes include anesthesia, dextrans, serum injections, stings, consumption of shell fish. Pathophysiology: The antigen combines with Ig E on the mast cell & basophils releasing large amounts of histamine and slow releasing substances of anaphylaxis. Clinical features: It manifests as bronchospasm, laryngeal edema, respiratory distress, hypoxia, massive vasodilatation, hypotension and shock.the mortality rate is 10%. In the dental office this reaction can occur during or immediately following the administration of penicillin or LA to a previously sensitized patient.
- 56. MANAGEMENT Immediate & aggressivemanagement is imperative if the patient is to survive. Step 1: Position the patient Place the patient in a supine position with the legs slightly elevated. Step 2: A-B-C Open the airway by tilting the head. Breathing & circulation should be established carrying BLS as needed. Step 3: Definitive care As soon as a systemic allergy is suspected emergency medical help is sought.
- 57. (A). Administration ofepinephrine subcutaneously. 0.3ml of 1:1000 for adults, 0.15 for children,0.075ml for infants. With decreased perfusion the absorption of epinephrine will be delayed. In such situations it can be administered sublingually or intralingually. if the respiratory or cardiovascular regions fail to improve within 5 minutes of administration, a 2nd dose should be given. Subsequent doses can be given away 5-10 minutes as needed provided the patient is properly monitored. (B). Administration of oxygen. Deliver oxygen at a flow of 5-6 liters per minute by nasal hood or full face mask at any time during the episode.
- 58. (C). Monitoring ofvital signs. Monitoring the patients cardiovascular & respiratory status continuously. Record blood pressure & carotid heart rate at least every 5minutes & start closed chest compression if cardiac arrest occurs. (D). Additional drug therapy. After the administration of epinephrine, the other drugs to be administered are • Antihistamines. • Corticosteroids. These drugs are administered only after clinical improvement is noted & are not be given during the acute phase as they are too slow in onset.
- 59. Prognosis of shock: 1.The prognosis varies with the origin of shock and its duration. 2. 80%-90% of young patients survive hypovoelemic shock with appropriate management. 3. cardiogenic shock associated with extensive myocardial infraction -(mortality rate up to 75%) 4. Septic shock – (mortality rate up to 75%)
- 60. CONCLUSION Shock canpresent as a consequence of multiple causes & affect the body at cellular ,visceral & systemic levels. Regardless of source ,the fundamental primary treatment of shock remains recognition & prompt fluid replacement. The search for the underlying cause of the shock is only initiated after stabilization.