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Shock

This document provides an overview of shock, including its history, definition, pathogenesis, stages, classification, and treatment. It discusses the various types of shock - hypovolemic (hemorrhagic), cardiogenic, obstructive, and distributive (septic, anaphylactic, neurogenic). For hypovolemic shock, it outlines the stages, compensatory mechanisms, assessment including vital signs and labs, and classification based on percentage of blood loss. Treatment of hypovolemic shock involves initial and late resuscitation, with goals of hemodynamic stabilization while avoiding over-resuscitation and permissive hypotension when possible.

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SHOCK DR. KANIKA CHAUDHARY 1
2 OVERVIEW • HISTORY • DEFINITION • PATHOGENESIS AND ORGAN RESPONSE • STAGES OF SHOCK • CLASSIFICATION • HYPOVOLEMIC SHOCK:-  HEMORRHAGIC SHOCK • CARDIOGENIC SHOCK • OBSTRUCTIVE SHOCK • DISTRIBUTIVE SHOCK:-  SEPTIC SHOCK  ANAPHYLATIC SHOCK  NEUROGENIC SHOCK • REFERENCES
HISTORY • Despite recognition of a post traumatic syndrome by Greek physicians such as Hippocrates and Galen, the origin of the term shock is generally credited to the French surgeon Henri Francois Le Dran, who in 1737 defined the same as “A treatise of reflections drawn from experience with gunshot wounds” and coined the term “choc” to indicate a severe impact . • An inappropriate translation by the English physician Clare, in 1743, led to the introduction of the word “shock” to the English language to indicate the sudden deterioration of a patient’s condition when major trauma has occurred. 3
• “The state in which profound and wide spread reduction of effective perfusion leads first to reversible, and then, if prolonged, to irreversible cellular injury – IJA,Shock review ,2003 • Shock is characterized by systemic hypoperfusion of tissues; it can be caused by diminished cardiac output or by reduced effective circulating blood volume. The consequences are impaired tissue perfusion and cellular hypoxia –Robbin’s basic pathology 9th ed • Shock is the clinical syndrome that results from inadequate tissue perfusion- Harrison’s 19th ed DEFINITION 4
5 PATHOGENESIS AND ORGAN RESPONSE 1. CELLULAR RESPONSE:- Inadequate tissue perfusion Reduced amount of both oxygen and substrate Shift from aerobic to anerobic metabolism Lactic acid accumulation , fall in pH metabolic acidosis Cell membrane dysfunction and associated increase in intracellular sodium and water
6 Swelling of mitochondria and other intracellular organelles including lysosomes If this process continues cell membranes break down and enzymes are released, causing destruction of the cell and local tissue damage Proteolytic enzymes released from damaged cells initiate formation of plasma kinins, activation of intravascular coagulation and activation of complement Kinins increase capillary permeability, dilate small blood vessels and depress myocardial function
7 2. MICROCIRCULATION:- • Innervated by the sympathetic nervous system and has a profound effect on the larger arterioles. Following hemorrhage, larger arterioles vasoconstrict; however, in sepsis or neurogenic shock, these vessels vasodilate • Vasopressin, angiotensin II, and endothelin-1, also lead to vasoconstriction to limit organ perfusion to organs such as skin, skeletal muscle, kidneys, and the gastrointestinal (GI) tract to preserve perfusion of the myocardium and CNS • Impairment of the microcirculation derangement of cellular metabolism organ failure
8 • Failure of the integrity of the endothelium of the microcirculation capillary leakintracellular swelling the development of an extracellular fluid deficitdecreased capillary hydrostatic pressure loss of extracellular fluid volume • Capillary dysfunction also occurs secondary to activation of endothelial cells by circulating inflammatory mediators generated in septic shock exacerbates endothelial cell swelling and capillary leak, as well as increases leukocyte adherencecapillary occlusion
9 3. NEUROENDOCRINE RESPONSE:- • Hypotension disinhibits the vasomotor center increased adrenergic output and reduced vagal activity. • Release of norepinephrine peripheral and splanchnic vasoconstriction • Reduced vagal activity increases the heart rate and cardiac output • Loss of vagal activity  upregulate the innate immune inflammatory response • Epinephrine increased glycogenolysis and gluconeogenesis and reduced insulin release
10 4. CARDIOVASCULAR RESPONSE Hypovolemia Decreased ventricular preload  decreased stroke volume Increased catecholamine release from adrenal medulla Increased heart rate and contractility
11 5. PULMONARY RESPONSE:- • Stimulation of pulmonary J receptors and carotid body chemoreceptors, hypo-perfusion of the medullary respiratory center increased minute volume (tachypnea, hyperpnea), hypocapnia and primary respiratory alkalosis. • Increased minute volume and decreased cardiac output  increased V/Q ratio • With increased workload, respiratory and diaphragmatic muscle impairment caused by hypoperfusion respiratory failure. If shock is not promptly reversed and the initiating condition controlled adult respiratory distress syndrome (ARDS) may develop
12 6. RENAL RESPONSE:- Hypoperfusion Decreased renal blood flow, particularly blood flow to cortex Activation of RAAS Aldosterone release by adrenal cortex and vasopressin by posterior pituitary Reduced GFR +increased aldosterone and vasopressin= OLIGURIA
13 • The net effect is a decreased glomerular filtration rate. The three pathologic changes seen are (a) Tubular necrosis (b) Tubular obstruction by casts or debris and (c) Tubular epithelial damage
14 7. GASTROINTESTINAL:- • Ileus, erosive gastritis,pancreatitis, acalculous cholecystitis and colonic submucosal hemorrhage • Enteric bacteria and antigens translocate from the gut lumen into the systemic circulation during gut ischemia causing irreversible shock 8. LIVER:- • Centrilobular injury with mild increases of transaminases and lactate dehydrogenases usually peaks in 1-3 days of ischemic insult and resolves over 3-10 days • Shock liver associated with massive ischemic necrosis and a major elevation of transaminases is atypical in the absence of extensive hepatocellular disease
15 9. HEMATOLOGICAL DISTURBANCES:- Trigger Coagulation activation Intravascular coagulation Consumption of clotting factors & platelets Fibrin deposition Fibrinolysis Fibrin degradation products HAEMORRHAGE Microvascular thrombosis ORGAN DYSFUNCTION
16 10. METABOLIC DISTURBANCES:- • Disruption of the normal cycles of carbohydrate, lipid, and protein metabolism • Anaerobic metabolism lactate • Increased hepatic gluconeogenesis • Hepatic lipogenesis Increased Triglycerides • Protein catabolism Muscle wasting
17 11. INFLAMMATORY RESPONSES:-
18 STAGES OF SHOCK • An initial nonprogressive stage, during which reflex compensatory mechanisms are activated and vital organ perfusion is maintained • A progressive stage, characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic derangement, including acidosis • An irreversible stage, in which cellular and tissue injury is so severe that even if the hemodynamic defects are corrected, survival is not possible
19 NON PROGRESSIVE SHOCK COMPENSATORY MECHANISM 1.Baroreceptor reflexes sympathetic stimulation of the circulation. 2.Central nervous system ischemic response:-Not activated significantly until the arterial pressure falls below 50 mm Hg. 3.Reverse stress-relaxation of the circulatory system, which causes the blood vessels to contract around the diminished blood volume so that the blood volume that is available more adequately fills the circulation 4.Increased secretion of renin by the kidneys and formation of angiotensinII, constricts the peripheral arteries and decreased output of water and salt by the kidneys
20 5.Increased secretion by the posteriorpituitary vasopressinconstricts the peripheral arteries and veins and increases water retention by the kidneys 6.Increased secretion by the adrenalmedulla of epinephrine and norepinephrine constricts the peripheral arteries and veins and increases the heart rate 7.Compensatorymechanisms that return the bloodvolume back toward normal:-absorption of large quantities of fluid from the intestinal tract, absorption of fluid into the blood capillaries from the interstitial spaces of the body
21 PROGRESSIVE SHOCK
CLASSIFICATION • A classification based on cardiovascular characteristics, which was initially proposed in 1972 by Hinshaw and Cox, is the most accepted one amongst many others that have been given. • Four major categories: 1. Hypovolemic shock 2. Cardiogenic shock 3. Obstructive shock 4. Distributive shock 22
1.Hypovolemic Shock:- • loss in circulatory volume decreased venous return, decreased filling of the cardiac chambers decreased cardiac output • The haemodynamic profile on monitoring of flow pressure variables shows  low central venous pressure (CVP)  low pulmonary capillary wedge pressure (PCWP)  low cardiac output (CO) and cardiac index (CI) and high SVR  The arterial blood pressure may be normal or low 23
24 CAUSES:-
Baskett’s Classification of Hemorrhagic Shock CLASS I CLASS II CLASS III CLASS IV BloodLoss (ml) % <750 15% 750-1500 15%-30% 1500-2000 30-40% >2000 >40% HR <100 >100 >120 >140 BP normal normal decrease decrease PP normal decrease decrease decrease RR 15-20 20-30 30-40 >35 UOP >30 20-30 5-15 negligible CNS Normal mildly anxious anxious confused confused lethargic 25 Baskett PJ. ABC of major trauma. Management of hypovolaemic shock. BMJ. 1990;300;1453-1457.
Stages of Shock - Events
27 ASSESSMENT IN HEMORRHAGIC SHOCK INITIALASSESSMENT:-  Mentation  Skin perfusion  Pulse  Blood pressure  Pulse pressure  Shock index  ROPE  Urine output INVESTIGATION:-  Hb  HCT  pH  Serum lactate  Base deficit  Others
28 INITIALASSESSMENT  Changing mentation is an indicator of perfusion, it is affected by drugs, alcohol,head injury  Pulse:- • lacks specificity alone, • Pulse & character together are more reliable • “Any patient who is cool and tachycardic is in shock until proven otherwise”(ATLS) • Relative bradycardia (paradoxical bradycardia):- pulse<90/min with SBP <90mmhg,occurs in 45% of all hypotensive trauma  Skin perfusion:- pale, cool, mottled(vasoconstriction)  Capillary refill:- unreliable to measure, normal: <2 sec
BP Estimation from Pulse 60 70 80 80 • If you can palpate this pulse, you know approximately the SBP 29
30  Systolic BP drop a late signt  olic BP does not fall until: • Adults 30% blood loss • Pediatrics 40-45% blood loss  SBP < 90 mm Hg: mortality approaches 65%  Narrow pulse pressure suggest significant blood loss- results from increased diastolic blood pressure from compensatory increase in catecholamine release  Shock index(SI) = HR / SBP i Elevated early in shock ii Normal 0.5 - 0.7 iii SI > 0.9 predicts: 1. Acute hypovolemia in presence of normal HR & BP 2.Marker of injury, severity & mortality
31 ROPE ROPE* : Pulse Rate over Pulse Pressure Evaluation as a method of predicting decompensation in patients with compensated haemorrhagic shock. PULSE RATE ÷ PULSE PRESSURE A ROPE value of >3.0 had a positive predictive value of < 3.0 had a negative predictive for the development of decompensated shock**. **Campbell, Roderick MBChB; Ardagh, Michael W. PhD; Than, Martin MBBS: Validation of the pulse rate over pressure evaluation index as a detector of early occult hemorrhage: A prospective observational study:, Journal of Trauma and Acute Care Surgery: July 2012 –vol.73-issue1-p286-288 *Michael W Ardagh, Timothy Hodgson et al., Pulse rate over pressure evaluation (ROPE) is useful in the assessment of compensated haemorrhagic shock: Emergency Medicine (2001) 13, 43–46
32 Hemoglobin / Hematocrit • Unreliable estimation acute blood loss • Lag time of several hours • Baseline value for comparison only Hemoglobin — is not a good indicator of the depth of hemorrhage, because it expresses a concentration of red cells, which will not change in a patient who is losing whole blood. Haematocrit – During loss of whole blood the proportion of RBC to plasma volume remains unchanged.
33 Arterial pH Acidosis - Serum pH < 7.20 Ongoing Marker of Severe Physiologic Derangement • Decreased cardiac contractility • Decreased cardiac output • Vasodilation and decreased BP • Decreased hepatic and renal blood flow
34 Base Deficit Sensitive measure of inadequate perfusion Normal range -3 to +3 Worsening BD: ◦ Inadequate volume replacement It is a reliable marker for shock and the need for transfusion.
35 Lactate  Indirect marker of tissue hypoperfusion, cellular oxygen debt and severity of hemorrhagic shock  Normal value= 0.56-1.39 mmol/L  Lactate value>5 indicative of increased mortality
36  Traditional measurement of platelets, international normalized ratio, and partial thromboplastin time may not reflect the coagulopathy of trauma or response to therapy effectively  Recently, thrombo- elastography (TEG) has been used as a quicker, more comprehensive determination of coagulopathy and fibrinolysis in the injured patient Others:-
37 TREATMENT…..
38 Class 1 Class 2 Class 3 Class 4 Blood loss(ml) UPTO 750 750-1500 1500-2000 >2000 Blood loss (%blood volume) UPTO 15% 15-30% 30-40% >40% Pulse rate <100 >100 >120 >140 Blood pressure NORMAL NORMAL DECREASED DECREASED Pulse pressure NORMAL OR ↑ DECREASED DECREASED DECREASED Respiratory rate 14-20 20-30 30-40 >35 Urine output(ml/hr) >30 20-30 5-15 NEGLIGIBLE CNS/Mental status SLIGHTLY ANXIOUS MILDLY ANXIOUS ANXIOUS CONFUSED CONFUSED LETHARGIC Fluid replacement CRYSTALLOID CRYSTALLOID CRYSTALLOID & BLOOD CRYSTALLOID & BLOOD Baskett PJ. ABC of major trauma. Management of hypovolaemic shock. BMJ. 1990;300;1453-1457.
39 INITIAL RESUSCITATION….
40 Resuscitation should be considered in the following two phases: • Early: While active bleeding is still ongoing • Late: Once all hemorrhage has been controlled
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43 HEMOSTATIC RESUSCITATION….
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48 •Assess for coagulopathy early •Control bleeding and follow A,B,C protocol. •LR is fluid of choice in trauma •If cross matched blood is available it should be used as a initial resuscitation fluid. •Haemostatic resuscitation is at 1: 1: 1 ratio (PRBC: FFP: PLATELET). •Avoid aggressive resuscitation and maintain Permissive Hypotension. •Serial sampling of ABG and lactate level and correct acidosis. •Start appropriate antibiotics, adequate analgesia, and early repair of injury.
49 2. CARDIOGENIC SHOCK • Cardiogenic shock (CS) is a state of end-organ hypoperfusion due to acute catastrophic failure of left ventricular pump function • The definition of CS (AHA) includes hemodynamic parameters: i. Persistent hypotension (systolic blood pressure <80 to 90 mm Hg or mean arterial pressure 30 mm Hg lower than baseline) ii. Severe reduction in cardiac index (<1.8 L · min−1 · m−2 without support or <2.0 to 2.2 L · min−1 · m−2 with support) iii. Adequate or elevated filling pressure (eg, left ventricular [LV] end-diastolic pressure >18 mm Hg or right ventricular [RV] end-diastolic pressure >10 to 15 mm Hg).
50 CAUSES:-
51 PATHOPHYSIOLOGY OF CARDIOGENIC SHOCK
52 DIAGNOSIS:- • Due to the unstable condition of these patients, supportive therapy must be initiated simultaneously with diagnostic evaluation • A focused history and physical examination should be performed, blood specimens sent to the laboratory, and an electrocardiogram (ECG) and chest x-ray obtained
53 CLINICAL FEATURES:- • Dyspnea • Pale, apprehensive, and diaphoretic, and mental status may be altered • Pulse is weak and rapid, 90–110 beats/min, or severe bradycardia due to high-grade heart block may be present • Systolic BP is reduced (<90 mmHg or ≥30 mmHg below baseline) with a narrow pulse pressure (<30 mmHg) • Tachypnea, and jugular venous distention may be present • Acute, severe MR and VSR usually are associated with characteristic systolic murmurs Rales are audible in most patients with LV failure
54 INVESTIGATIONS:- 1. Laboratory findings:- • WBC is elevated with a left shift • Renal function is initially unchanged, but blood urea nitrogen and creatinine rise progressively • Hepatic transaminases may be markedly elevated due to liver hypoperfusion. The lactic acid level is elevated • ABG:-hypoxemia and anion gap metabolic acidosis, which may be compensated by respiratory alkalosis • Cardiac markers, creatine phosphokinase and its MB fraction, and troponins I and T are markedly elevated.
55 2.Electrocardiogram:- In CS due to acute MI with LV failure, Q waves and/or >2-mm ST elevation in multiple leads or left bundle branch block are usually present. More than one-half of all infarcts associated with shock are anterior 3.Chest roentgenogram :-Pulmonary vascular congestion and often pulmonary edema, but these findings may be absent in one-third of patients • The heart size is usually normal when CS results from a first MI but is enlarged when it occurs in a patient with a previous MI 4.Echocardiogram:- Doppler mapping demonstrates a left-to-right shunt in patients with VSR and the severity of MR • Proximal aortic dissection with aortic regurgitation or tamponade may be visualized, or evidence for pulmonary embolism may be obtained
56 Fig 326-2 harrison,pg no. 1761
57 3. OBSTRUCTIVE SHOCK • Obstructive shock is due to a decrease in venous return or cardiac compliance due to an increased left ventricular outflow obstruction or marked preload decrease • Cardiac tamponade and tension pneumothorax are common causes • Several hemodynamic patterns may be observed, depending on the cause, from decrease in filling pressures (as in mediastinal compressions of great veins); to trends towards equalization of pressures in the case of cardiac tamponade; or to markedly increased right ventricular filling pressures with low PCWP in the case of pulmonary embolism. Cardiac output is usually decreased with increased SVR.
58 CAUSES:-
59 • The diagnosis of obstructive shock is based on clinical findings, the chest radiograph, and an echocardiogram • Pericardial tamponade:-confirmed by echocardiography, and treatment consists of immediate pericardiocentesis or the creation of an open subxiphoid pericardial window • Tension pneumothorax:-Chest decompression must be carried out immediately and, ideally, should occur based on clinical findings rather than awaiting a chest radiograph. Release of air and restoration of normal cardiovascular dynamics are both diagnostic and therapeutic MANAGEMENT:-
60 4. DISTRIBUTIVE SHOCK • This type of shock is associated with not only poor vascular tone in the peripheral circulation but maldistribution of blood flow to organs within the body also • The CO varies, but is usually raised • Haemodynamic profile :-  low or normal PCWP  high CO  low arterial blood pressure  low SVR.
61 CAUSES:-
62 SEPTIC SHOCK…..
63 NEW DEFINATIONS*:- *Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016;315(8):801-810. doi:10.1001/jama.2016.0287 **qSOFA:- Quick sequential organ failure assessment • Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection • Patients with suspected infection who are likely to have a prolonged ICU stay or to die in the hospital can be promptly identified at the bedside with qSOFA**, i.e, alteration in mental status, systolic blood pressure ≥100 mm Hg, or respiratory rate ≥22/min • Organ dysfunction can be identified as an acute change in total SOFA score ≥2 points consequent to the infection. The baseline SOFA score can be assumed to be zero in patients not known to have preexisting organ dysfunction. • A SOFA score ≥2 reflects an overall mortality risk of approximately 10% in a general hospital population with suspected infection.
64 • Septic shock is defined as a subset of sepsis in which underlying circulatory and cellular metabolism abnormalities are profound enough to substantially increase mortality • Patients with septic shock can be identified with a clinical construct of sepsis with persisting hypotension requiring vasopressors to maintain MAP ≥65 mm Hg and having a serum lactate level >2 mmol/L (18mg/dL) despite adequate volume resuscitation. Terms like septicemia / severe sepsis / SIRS has been REMOVED *Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016;315(8):801-810. doi:10.1001/jama.2016.0287
65 CAUSES:- 1.Peritonitis caused by spread of infection from the uterus and fallopian tubes, sometimes resulting from instrumental abortion performed under unsterile conditions. 2.Peritonitis resulting from rupture of the gastrointestinal system, sometimes caused by intestinal disease and sometimes by wounds. 3.Generalized bodily infection resulting from spread of a skin infection such as streptococcal or staphylococcal infection. 4.Generalized gangrenous infection resulting specifically from gas gangrene bacilli, spreading first through peripheral tissues and finally by way of the blood to the internal organs, especially the liver. 5.Infection spreading into the blood from the kidney or urinary tract, often caused by colon bacilli.
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67 CLINICAL MANIFESTATIONS :- • The manifestations of the septic response are superimposed on the symptoms and signs of the patient’s underlying illness and primary infection • Some patients with sepsis are normo- or hypothermic; the absence of fever is most common in neonates, in elderly patients, and in persons with uremia or alcoholism • Hyperventilation, producing respiratory alkalosis, is often an early sign of the septic response • Disorientation, confusion, and other manifestations of encephalopathy may also develop early, particularly in the elderly and in individuals with preexisting neurologic impairment
68 • Hypotension and DIC predispose to acrocyanosis and ischemic necrosis of peripheral tissues, most commonly the digits • Cellulitis, pustules, bullae, or hemorrhagic lesions may develop when hematogenous bacteria or fungi seed the skin or underlying soft tissue • Gastrointestinal manifestations such as nausea, vomiting, diarrhea, and ileus may suggest acute gastroenteritis. Stress ulceration can lead to upper gastrointestinal bleeding. Cholestatic jaundice, with elevated levels of serum bilirubin (mostly conjugated) and alkaline phosphatase, may precede other signs of sepsis
69 DIAGNOSIS:- • There is no specific diagnostic test for sepsis • Definitive etiologic diagnosis requires identification of the causative microorganism from blood or a local site of infection  At least two blood samples should be obtained (from two different venipuncture sites) for culture; in a patient with an indwelling catheter, one sample should be collected from each lumen of the catheter and another via venipuncture
70 MANAGEMENT……
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72 2016 Surviving sepsis Campaign Guidelines:- A. INITIAL RESUSCITATION AND INFECTIOUS ISSUES B. HEMODYNAMIC SUPPORT AND ADJUNCTIVE THERAPY C. OTHER SUPPORTIVE THERAPY OF SEVERE SEPSIS
73 A. INITIAL RESUSCITATION AND INFECTIOUS ISSUES • Sepsis and septic shock are medical emergencies, and we recommend that treatment and resuscitation begin immediately • In the initial resuscitation from sepsis- induced hypoperfusion, at least 30 mL/kg of intravenous crystalloid fluid be given within the first 3 hours • Following initial fluid resuscitation, additional fluids be guided by frequent reassessment of hemodynamic status • A target mean arterial pressure of 65 mmHg in patients with septic shock requiring vasopressors • Targeting resuscitation to normalize lactate in patients with elevated lactate levels as a marker of tissue hypoperfusion
74 • A fluid challenge technique be applied where fluid administration is continued as long as hemodynamic factors continue to improve • Crystalloids as the fluid of choice for initial resuscitation and subsequent intravascular volume replacement in patients with sepsis and septic shock
75 ANTIMICROBIAL THERAPY • Appropriate routine microbiologic cultures (including blood) be obtained before starting antimicrobial therapy in patients with suspected sepsis and septic shock if it results in no substantial delay in the start of antimicrobials (i.e, <45 minutes) • Administration of intravenous antimicrobials be initiated as soon as possible after recognition and within 1hour for both a) septic shock and b) sepsis without shock • Empiric broad-spectrum therapy with one or more antimicrobials for patients presenting with sepsis or septic shock to cover all likely pathogens (including bacterial and potentially fungal or viral coverage) • If combination therapy is used for septic shock, de-escalation is recommended, with discontinuation of combination therapy within the first few days in response to clinical improvement and/or evidence of infection resolution. This applies to both targeted (for culture-positive infections) and empirical (for culture-negative infections) combination therapy
76 • Antimicrobial treatment duration of 7‒10 days is adequate for most serious infections • Daily assessment for de-escalation of antimicrobial therapy in patients with sepsis • Measurement of procalcitonin levels can be used to shorten the duration of antimicrobial therapy in sepsis patients • Prompt removal of intravascular access devices that are a possible source of sepsis or septic shock after other vascular access has been established
77 B. HEMODYNAMIC SUPPORT AND OTHER ADJUNCTIVE THERAPY • If hypotension persists after the initial volume resuscitation, infusion of a vasoconstrictor drug (vasopressor) like norepinephrine or dopamine should begin. Vasoconstrictor drugs must be infused through a central venous catheter, and the goal is to achieve a mean arterial pressure (MAP) ≥ 65 mm Hg • Norepinephrine as the first-choice vasopressor. For norepinephrine, start with a dose rate of 0.1 μg/kg/min and titrate upward as needed. Dose rates up to 3.3 μg/kg/min are successful in raising the blood pressure in a majority of patients with septic shock • If the desired MAP is not achieved at a dose rate of 3 – 3.5 μg/kg/min, add dopamine as a second vasopressor VASOPRESSOR THERAPY:-
78 • For dopamine, start at a dose rate of 5 μg/kg/min and titrate up- ward as needed. Vasoconstriction is the predominant effect at dose rates above 10 μg/kg/min • .If the desired MAP is not achieved with a dose rate of 20 μg/kg/min, hypotension is refractory to norepinephrine and dopamine, vasopressin may be effective in raising the blood pressure. (Vasopressin is used as an additional pressor rather than a replacement for norepinephrine or dopamine.) The dose range for vasopressin is 0.01–0.04 units/min, but in septic shock is 0.03 units/min
79 Role of Corticosteroids:- • Do not use intravenous hydrocortisone to treat septic shock patients if adequate fluid resuscitation and vasopressor therapy are able to restore hemodynamic stability. If this is not achievable, then intravenous hydrocortisone alone at a dose of 200 mg per day • When low-dose hydrocortisone is given, then use continuous infusion rather than repetitive bolus injections • Corticosteroids should not be administered for the treatment of sepsis in the absence of shock
80 C. OTHER SUPPORTIVE THERAPY OF SEVERE SEPSIS Administration of Blood products:- • Red blood cell transfusion occur only when hemoglobin concentration decreases to <7.0‒7.5 g/dL in adults in the absence of extenuating circumstances, such as myocardial ischemia, severe hypoxemia, or acute hemorrhage • Prophylactic platelet transfusion when counts are <10,000/mm3 (10 x 109/L) in the absence of apparent bleeding and when counts are <20,000/mm3 (20 x 109/L) if the patient has a significant risk of bleeding. Higher platelet counts (≥50,000/mm3 [50 x 109/L]) are advised for active bleeding, surgery, or invasive procedures
81 Mechanical ventilation and weaning • Target a tidal volume of 6 mL/kg predicted body weight in patients with sepsis-induced ARDS vs 12 mL/kg • Upper limit goal for plateau pressures of 30 cmH20 over higher plateau pressures in adult patients with sepsis-induced severe ARDS • Higher positive end expiratory pressure (PEEP) over lower PEEP in adult patients with sepsis-induced moderate to severe ARDS • Using prone over supine position in adult patients with sepsis-induced ARDS and a PaO2/FiO2 ratio <150 • Use of HFOV in adult patients with sepsis-induced ARDS
82 • Mechanically ventilated sepsis patients be maintained with the head of the bed elevated between 30 and 45 degrees to limit aspiration risk and to prevent the development of VAP • Continuous or intermittent sedation be minimized in mechanically ventilated sepsis patients, targeting specific titration endpoints • Use of spontaneous breathing trials in mechanically ventilated sepsis patients with sepsis when they satisfy the following criteria: a) arousable; b) hemodynamically stable (without vasopressor agents); c) low ventilatory and end-expiratory pressure requirements; and d) low FiO2 requirements which can be safely delivered with a face mask or nasal cannula. If the spontaneous breathing trial is successful, extubation should be considered
83 GLUCOSE • Commence insulin dose when two consecutive blood glucose levels are >180 mg/dL • Blood glucose values be monitored every 1 to 2 hours until glucose values and insulin infusion rates are stable, then every 4 hours thereafter in patients receiving insulin infusions
84 VTE Prophylaxis • Pharmacologic prophylaxis (unfractionated heparin [UFH] or low molecular weight heparin [LMWH]) against VTE in the absence of contraindications to the use of these agents • Mechanical VTE prophylaxis when pharmacologic VTE is contraindicated
85 Stress Ulcer prophylaxis • Stress ulcer prophylaxis be given to patients with sepsis or septic shock who have risk factors for GI bleeding • Either proton pump inhibitors (PPIs) or histamine-2 receptor antagonists (H2RAs) when stress ulcer prophylaxis is indicated
86 NUTRITION • Administration of early full enteral nutrition rather than early parenteral nutrition alone or parenteral nutrition in combination with enteral feedings in critically ill patients with sepsis or septic shock who can be fed enterally • Use of prokinetic agents in critically ill patients with sepsis or septic shock and feeding intolerance
87 ANAPHYLACTIC SHOCK….
88 • Anaphylaxis is an acute multiorgan dysfunction syndrome produced by the immunogenic release of inflammatory mediators from basophils and mast cells • The characteristic feature is an exaggerated immunoglobulin E (IgE) response to an external antigen; i.e., a hypersensitivity reaction type I • The manifestations of anaphylaxis typically involve the skin, lungs, gastrointestinal tract, and cardiovascular system • Identical manifestations can occur without the involvement of IgE; these are called anaphylactoid reactions, and are not immunogenic in origin • Common triggers for anaphylactic reactions include food, antimicrobial agents, and insect bites, while common triggers for anaphylactoid reactions include opiates and radiocontrast dyes
89 • Anaphylactic shock is an immediate threat to life, with profound hypotension from systemic vasodilatation and massive fluid loss through leaky capillaries. • The hemodynamic alterations in anaphylactic shock are similar to those in septic shock, but are often more pronounced
90 PATHOPHYSIOLOGY
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92 TREATMENT
93  Volume Resuscitation • Aggressive volume resuscitation is essential in anaphylactic shock because at least 35% of the intravascular volume can be lost through leaky capillaries , which is enough to produce hypovolemic shock Volume resuscitation can begin by infusing 1– 2 liters of crystalloid fluid (or 20 mL/kg), or 500 mL of isooncotic colloid fluid (e.g., 5% albumin), over the first 5 minutes . Thereafter, the infusion rate of fluids should be tailored to the clinical condition of the patient  Refractory Hypotension • Persistent hypotension despite epinephrine infusion and volume resuscitation can be managed by adding glucagon or another vasopressor such as norepinephrine or dopamine
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95 NEUROGENIC SHOCK • Neurogenic shock is a devastating consequence of spinal cord injury (SCI), also known as vasogenic shock. Injury to the spinal cord results in sudden loss of sympathetic tone, which leads to the autonomic instability that is manifested in hypotension, bradyarrhythmia, and temperature dysregulation • Neurogenic shock is most commonly a consequence of traumatic spinal cord injuries, more in cervical spine injuries • Other causes include inadvertent cephalad migration of spinal anesthesia, or devastating head injury, Guillain-Barre syndrome, transverse myelitis
96 DIAGNOSIS • Neurogenic shock is most commonly associated with a blunt cervical spine injury • Neurogenic shock should be considered only after a hemorrhagic shock has been ruled out in a traumatic patient, the presence of vertebral fracture or dislocation raises the concern for neurogenic shock • Bradyarrhythmia, hypotension, flushed warm skin are the classic signs associated with neurogenic shock • The joint committee of the American Spinal Injury Association and the International Spinal Cord Society propose the definition of neurogenic shock to be autonomic nervous system dysfunction that includes symptoms such as orthostatic hypotension, autonomic dysreflexia, temperature dysregulation. A focal neurologic deficit is not necessary for the diagnosis of neurogenic shock
97 TREATMENT • Initial management of neurogenic shock is focused on hemodynamic stabilization. Hypotension should be treated first to prevent secondary injury. The first-line treatment for hypotension is intravenous fluid resuscitation • If hypotension persists despite euvolemia, vasopressors and inotropes are the second lines • Phenylephrine is commonly used as it is a pure alpha-1 agonist that causes peripheral vasoconstriction to counteract the loss sympathetic tone • Epinephrine ,for refractory cases of hypotension • Keep the mean arterial pressure (MAP) at 85–90 mmHg for the first 7 days to improve spinal cord perfusion • Initial spine immobilization is important to prevent further spinal cord injury
98 REFERENCES 1.Guyton & Hall: Textbook of Medical Physiology, 12th ed 2.Robbin’s Basic pathology, 9th ed 3.Harrison’s principle of internal medicine, 19th ed 4.Miller’s Anesthesia, 8th ed 5.Wylie and Churchill-Davidson's A Practice of Anesthesia , 5th ed 6.Marino’s The ICU Book, 4th ed 7.Tintinalli’s Emergency Medicine ,A Comprehensive Study Guide ,8th ed 8.SHOCK – A SHORT REVIEW ,IJA 2003,Dr. A. K. Sethi, Dr. Prakash Sharma, Dr. Medha Mohta, Dr. Asha Tyagi 9.Cardiogenic Shock,Harmony R. Reynolds and Judith S. Hochman,Circulation. 2008;117:686-697, February 4, 2008 https://doi.org/10.1161/CIRCULATIONAHA.106.613596 10.Baskett PJ. ABC of major trauma. Management of hypovolaemic shock. BMJ: British Medical Journal. 1990 Jun 2;300(6737):1453 11.Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, Bellomo R, Bernard GR, Chiche JD, Coopersmith CM, Hotchkiss RS. The third international consensus definitions for sepsis and septic shock (sepsis-3). Jama. 2016 Feb 23;315(8):801-10 12.Rhodes A, Evans LE, Alhazzani W, Levy MM, Antonelli M, Ferrer R, Kumar A, Sevransky JE, Sprung CL, Nunnally ME, Rochwerg B. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock: 2016. Intensive care medicine. 2017 Mar 1;43(3):304-77 13.Dave S, Cho JJ. Shock, Neurogenic. StatPearls ,www.ncbi.nlm.nih.gov/books/NBK459361 .

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Shock

  • 1.
  • 2.
    2 OVERVIEW • HISTORY • DEFINITION •PATHOGENESIS AND ORGAN RESPONSE • STAGES OF SHOCK • CLASSIFICATION • HYPOVOLEMIC SHOCK:-  HEMORRHAGIC SHOCK • CARDIOGENIC SHOCK • OBSTRUCTIVE SHOCK • DISTRIBUTIVE SHOCK:-  SEPTIC SHOCK  ANAPHYLATIC SHOCK  NEUROGENIC SHOCK • REFERENCES
  • 3.
    HISTORY • Despite recognitionof a post traumatic syndrome by Greek physicians such as Hippocrates and Galen, the origin of the term shock is generally credited to the French surgeon Henri Francois Le Dran, who in 1737 defined the same as “A treatise of reflections drawn from experience with gunshot wounds” and coined the term “choc” to indicate a severe impact . • An inappropriate translation by the English physician Clare, in 1743, led to the introduction of the word “shock” to the English language to indicate the sudden deterioration of a patient’s condition when major trauma has occurred. 3
  • 4.
    • “The statein which profound and wide spread reduction of effective perfusion leads first to reversible, and then, if prolonged, to irreversible cellular injury – IJA,Shock review ,2003 • Shock is characterized by systemic hypoperfusion of tissues; it can be caused by diminished cardiac output or by reduced effective circulating blood volume. The consequences are impaired tissue perfusion and cellular hypoxia –Robbin’s basic pathology 9th ed • Shock is the clinical syndrome that results from inadequate tissue perfusion- Harrison’s 19th ed DEFINITION 4
  • 5.
    5 PATHOGENESIS AND ORGANRESPONSE 1. CELLULAR RESPONSE:- Inadequate tissue perfusion Reduced amount of both oxygen and substrate Shift from aerobic to anerobic metabolism Lactic acid accumulation , fall in pH metabolic acidosis Cell membrane dysfunction and associated increase in intracellular sodium and water
  • 6.
    6 Swelling of mitochondriaand other intracellular organelles including lysosomes If this process continues cell membranes break down and enzymes are released, causing destruction of the cell and local tissue damage Proteolytic enzymes released from damaged cells initiate formation of plasma kinins, activation of intravascular coagulation and activation of complement Kinins increase capillary permeability, dilate small blood vessels and depress myocardial function
  • 7.
    7 2. MICROCIRCULATION:- • Innervatedby the sympathetic nervous system and has a profound effect on the larger arterioles. Following hemorrhage, larger arterioles vasoconstrict; however, in sepsis or neurogenic shock, these vessels vasodilate • Vasopressin, angiotensin II, and endothelin-1, also lead to vasoconstriction to limit organ perfusion to organs such as skin, skeletal muscle, kidneys, and the gastrointestinal (GI) tract to preserve perfusion of the myocardium and CNS • Impairment of the microcirculation derangement of cellular metabolism organ failure
  • 8.
    8 • Failure ofthe integrity of the endothelium of the microcirculation capillary leakintracellular swelling the development of an extracellular fluid deficitdecreased capillary hydrostatic pressure loss of extracellular fluid volume • Capillary dysfunction also occurs secondary to activation of endothelial cells by circulating inflammatory mediators generated in septic shock exacerbates endothelial cell swelling and capillary leak, as well as increases leukocyte adherencecapillary occlusion
  • 9.
    9 3. NEUROENDOCRINE RESPONSE:- •Hypotension disinhibits the vasomotor center increased adrenergic output and reduced vagal activity. • Release of norepinephrine peripheral and splanchnic vasoconstriction • Reduced vagal activity increases the heart rate and cardiac output • Loss of vagal activity  upregulate the innate immune inflammatory response • Epinephrine increased glycogenolysis and gluconeogenesis and reduced insulin release
  • 10.
    10 4. CARDIOVASCULAR RESPONSE Hypovolemia Decreasedventricular preload  decreased stroke volume Increased catecholamine release from adrenal medulla Increased heart rate and contractility
  • 11.
    11 5. PULMONARY RESPONSE:- •Stimulation of pulmonary J receptors and carotid body chemoreceptors, hypo-perfusion of the medullary respiratory center increased minute volume (tachypnea, hyperpnea), hypocapnia and primary respiratory alkalosis. • Increased minute volume and decreased cardiac output  increased V/Q ratio • With increased workload, respiratory and diaphragmatic muscle impairment caused by hypoperfusion respiratory failure. If shock is not promptly reversed and the initiating condition controlled adult respiratory distress syndrome (ARDS) may develop
  • 12.
    12 6. RENAL RESPONSE:- Hypoperfusion Decreasedrenal blood flow, particularly blood flow to cortex Activation of RAAS Aldosterone release by adrenal cortex and vasopressin by posterior pituitary Reduced GFR +increased aldosterone and vasopressin= OLIGURIA
  • 13.
    13 • The neteffect is a decreased glomerular filtration rate. The three pathologic changes seen are (a) Tubular necrosis (b) Tubular obstruction by casts or debris and (c) Tubular epithelial damage
  • 14.
    14 7. GASTROINTESTINAL:- • Ileus,erosive gastritis,pancreatitis, acalculous cholecystitis and colonic submucosal hemorrhage • Enteric bacteria and antigens translocate from the gut lumen into the systemic circulation during gut ischemia causing irreversible shock 8. LIVER:- • Centrilobular injury with mild increases of transaminases and lactate dehydrogenases usually peaks in 1-3 days of ischemic insult and resolves over 3-10 days • Shock liver associated with massive ischemic necrosis and a major elevation of transaminases is atypical in the absence of extensive hepatocellular disease
  • 15.
    15 9. HEMATOLOGICAL DISTURBANCES:- Trigger Coagulationactivation Intravascular coagulation Consumption of clotting factors & platelets Fibrin deposition Fibrinolysis Fibrin degradation products HAEMORRHAGE Microvascular thrombosis ORGAN DYSFUNCTION
  • 16.
    16 10. METABOLIC DISTURBANCES:- •Disruption of the normal cycles of carbohydrate, lipid, and protein metabolism • Anaerobic metabolism lactate • Increased hepatic gluconeogenesis • Hepatic lipogenesis Increased Triglycerides • Protein catabolism Muscle wasting
  • 17.
  • 18.
    18 STAGES OF SHOCK •An initial nonprogressive stage, during which reflex compensatory mechanisms are activated and vital organ perfusion is maintained • A progressive stage, characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic derangement, including acidosis • An irreversible stage, in which cellular and tissue injury is so severe that even if the hemodynamic defects are corrected, survival is not possible
  • 19.
    19 NON PROGRESSIVE SHOCK COMPENSATORYMECHANISM 1.Baroreceptor reflexes sympathetic stimulation of the circulation. 2.Central nervous system ischemic response:-Not activated significantly until the arterial pressure falls below 50 mm Hg. 3.Reverse stress-relaxation of the circulatory system, which causes the blood vessels to contract around the diminished blood volume so that the blood volume that is available more adequately fills the circulation 4.Increased secretion of renin by the kidneys and formation of angiotensinII, constricts the peripheral arteries and decreased output of water and salt by the kidneys
  • 20.
    20 5.Increased secretion bythe posteriorpituitary vasopressinconstricts the peripheral arteries and veins and increases water retention by the kidneys 6.Increased secretion by the adrenalmedulla of epinephrine and norepinephrine constricts the peripheral arteries and veins and increases the heart rate 7.Compensatorymechanisms that return the bloodvolume back toward normal:-absorption of large quantities of fluid from the intestinal tract, absorption of fluid into the blood capillaries from the interstitial spaces of the body
  • 21.
  • 22.
    CLASSIFICATION • A classificationbased on cardiovascular characteristics, which was initially proposed in 1972 by Hinshaw and Cox, is the most accepted one amongst many others that have been given. • Four major categories: 1. Hypovolemic shock 2. Cardiogenic shock 3. Obstructive shock 4. Distributive shock 22
  • 23.
    1.Hypovolemic Shock:- • lossin circulatory volume decreased venous return, decreased filling of the cardiac chambers decreased cardiac output • The haemodynamic profile on monitoring of flow pressure variables shows  low central venous pressure (CVP)  low pulmonary capillary wedge pressure (PCWP)  low cardiac output (CO) and cardiac index (CI) and high SVR  The arterial blood pressure may be normal or low 23
  • 24.
  • 25.
    Baskett’s Classification of HemorrhagicShock CLASS I CLASS II CLASS III CLASS IV BloodLoss (ml) % <750 15% 750-1500 15%-30% 1500-2000 30-40% >2000 >40% HR <100 >100 >120 >140 BP normal normal decrease decrease PP normal decrease decrease decrease RR 15-20 20-30 30-40 >35 UOP >30 20-30 5-15 negligible CNS Normal mildly anxious anxious confused confused lethargic 25 Baskett PJ. ABC of major trauma. Management of hypovolaemic shock. BMJ. 1990;300;1453-1457.
  • 26.
  • 27.
    27 ASSESSMENT IN HEMORRHAGICSHOCK INITIALASSESSMENT:-  Mentation  Skin perfusion  Pulse  Blood pressure  Pulse pressure  Shock index  ROPE  Urine output INVESTIGATION:-  Hb  HCT  pH  Serum lactate  Base deficit  Others
  • 28.
    28 INITIALASSESSMENT  Changing mentationis an indicator of perfusion, it is affected by drugs, alcohol,head injury  Pulse:- • lacks specificity alone, • Pulse & character together are more reliable • “Any patient who is cool and tachycardic is in shock until proven otherwise”(ATLS) • Relative bradycardia (paradoxical bradycardia):- pulse<90/min with SBP <90mmhg,occurs in 45% of all hypotensive trauma  Skin perfusion:- pale, cool, mottled(vasoconstriction)  Capillary refill:- unreliable to measure, normal: <2 sec
  • 29.
    BP Estimation fromPulse 60 70 80 80 • If you can palpate this pulse, you know approximately the SBP 29
  • 30.
    30  Systolic BPdrop a late signt  olic BP does not fall until: • Adults 30% blood loss • Pediatrics 40-45% blood loss  SBP < 90 mm Hg: mortality approaches 65%  Narrow pulse pressure suggest significant blood loss- results from increased diastolic blood pressure from compensatory increase in catecholamine release  Shock index(SI) = HR / SBP i Elevated early in shock ii Normal 0.5 - 0.7 iii SI > 0.9 predicts: 1. Acute hypovolemia in presence of normal HR & BP 2.Marker of injury, severity & mortality
  • 31.
    31 ROPE ROPE* : PulseRate over Pulse Pressure Evaluation as a method of predicting decompensation in patients with compensated haemorrhagic shock. PULSE RATE ÷ PULSE PRESSURE A ROPE value of >3.0 had a positive predictive value of < 3.0 had a negative predictive for the development of decompensated shock**. **Campbell, Roderick MBChB; Ardagh, Michael W. PhD; Than, Martin MBBS: Validation of the pulse rate over pressure evaluation index as a detector of early occult hemorrhage: A prospective observational study:, Journal of Trauma and Acute Care Surgery: July 2012 –vol.73-issue1-p286-288 *Michael W Ardagh, Timothy Hodgson et al., Pulse rate over pressure evaluation (ROPE) is useful in the assessment of compensated haemorrhagic shock: Emergency Medicine (2001) 13, 43–46
  • 32.
    32 Hemoglobin / Hematocrit •Unreliable estimation acute blood loss • Lag time of several hours • Baseline value for comparison only Hemoglobin — is not a good indicator of the depth of hemorrhage, because it expresses a concentration of red cells, which will not change in a patient who is losing whole blood. Haematocrit – During loss of whole blood the proportion of RBC to plasma volume remains unchanged.
  • 33.
    33 Arterial pH Acidosis -Serum pH < 7.20 Ongoing Marker of Severe Physiologic Derangement • Decreased cardiac contractility • Decreased cardiac output • Vasodilation and decreased BP • Decreased hepatic and renal blood flow
  • 34.
    34 Base Deficit Sensitive measureof inadequate perfusion Normal range -3 to +3 Worsening BD: ◦ Inadequate volume replacement It is a reliable marker for shock and the need for transfusion.
  • 35.
    35 Lactate  Indirect markerof tissue hypoperfusion, cellular oxygen debt and severity of hemorrhagic shock  Normal value= 0.56-1.39 mmol/L  Lactate value>5 indicative of increased mortality
  • 36.
    36  Traditional measurementof platelets, international normalized ratio, and partial thromboplastin time may not reflect the coagulopathy of trauma or response to therapy effectively  Recently, thrombo- elastography (TEG) has been used as a quicker, more comprehensive determination of coagulopathy and fibrinolysis in the injured patient Others:-
  • 37.
  • 38.
    38 Class 1 Class2 Class 3 Class 4 Blood loss(ml) UPTO 750 750-1500 1500-2000 >2000 Blood loss (%blood volume) UPTO 15% 15-30% 30-40% >40% Pulse rate <100 >100 >120 >140 Blood pressure NORMAL NORMAL DECREASED DECREASED Pulse pressure NORMAL OR ↑ DECREASED DECREASED DECREASED Respiratory rate 14-20 20-30 30-40 >35 Urine output(ml/hr) >30 20-30 5-15 NEGLIGIBLE CNS/Mental status SLIGHTLY ANXIOUS MILDLY ANXIOUS ANXIOUS CONFUSED CONFUSED LETHARGIC Fluid replacement CRYSTALLOID CRYSTALLOID CRYSTALLOID & BLOOD CRYSTALLOID & BLOOD Baskett PJ. ABC of major trauma. Management of hypovolaemic shock. BMJ. 1990;300;1453-1457.
  • 39.
  • 40.
    40 Resuscitation should beconsidered in the following two phases: • Early: While active bleeding is still ongoing • Late: Once all hemorrhage has been controlled
  • 41.
  • 42.
  • 43.
  • 44.
  • 45.
  • 46.
  • 47.
  • 48.
    48 •Assess for coagulopathyearly •Control bleeding and follow A,B,C protocol. •LR is fluid of choice in trauma •If cross matched blood is available it should be used as a initial resuscitation fluid. •Haemostatic resuscitation is at 1: 1: 1 ratio (PRBC: FFP: PLATELET). •Avoid aggressive resuscitation and maintain Permissive Hypotension. •Serial sampling of ABG and lactate level and correct acidosis. •Start appropriate antibiotics, adequate analgesia, and early repair of injury.
  • 49.
    49 2. CARDIOGENIC SHOCK •Cardiogenic shock (CS) is a state of end-organ hypoperfusion due to acute catastrophic failure of left ventricular pump function • The definition of CS (AHA) includes hemodynamic parameters: i. Persistent hypotension (systolic blood pressure <80 to 90 mm Hg or mean arterial pressure 30 mm Hg lower than baseline) ii. Severe reduction in cardiac index (<1.8 L · min−1 · m−2 without support or <2.0 to 2.2 L · min−1 · m−2 with support) iii. Adequate or elevated filling pressure (eg, left ventricular [LV] end-diastolic pressure >18 mm Hg or right ventricular [RV] end-diastolic pressure >10 to 15 mm Hg).
  • 50.
  • 51.
  • 52.
    52 DIAGNOSIS:- • Due tothe unstable condition of these patients, supportive therapy must be initiated simultaneously with diagnostic evaluation • A focused history and physical examination should be performed, blood specimens sent to the laboratory, and an electrocardiogram (ECG) and chest x-ray obtained
  • 53.
    53 CLINICAL FEATURES:- • Dyspnea •Pale, apprehensive, and diaphoretic, and mental status may be altered • Pulse is weak and rapid, 90–110 beats/min, or severe bradycardia due to high-grade heart block may be present • Systolic BP is reduced (<90 mmHg or ≥30 mmHg below baseline) with a narrow pulse pressure (<30 mmHg) • Tachypnea, and jugular venous distention may be present • Acute, severe MR and VSR usually are associated with characteristic systolic murmurs Rales are audible in most patients with LV failure
  • 54.
    54 INVESTIGATIONS:- 1. Laboratory findings:- •WBC is elevated with a left shift • Renal function is initially unchanged, but blood urea nitrogen and creatinine rise progressively • Hepatic transaminases may be markedly elevated due to liver hypoperfusion. The lactic acid level is elevated • ABG:-hypoxemia and anion gap metabolic acidosis, which may be compensated by respiratory alkalosis • Cardiac markers, creatine phosphokinase and its MB fraction, and troponins I and T are markedly elevated.
  • 55.
    55 2.Electrocardiogram:- In CSdue to acute MI with LV failure, Q waves and/or >2-mm ST elevation in multiple leads or left bundle branch block are usually present. More than one-half of all infarcts associated with shock are anterior 3.Chest roentgenogram :-Pulmonary vascular congestion and often pulmonary edema, but these findings may be absent in one-third of patients • The heart size is usually normal when CS results from a first MI but is enlarged when it occurs in a patient with a previous MI 4.Echocardiogram:- Doppler mapping demonstrates a left-to-right shunt in patients with VSR and the severity of MR • Proximal aortic dissection with aortic regurgitation or tamponade may be visualized, or evidence for pulmonary embolism may be obtained
  • 56.
  • 57.
    57 3. OBSTRUCTIVE SHOCK •Obstructive shock is due to a decrease in venous return or cardiac compliance due to an increased left ventricular outflow obstruction or marked preload decrease • Cardiac tamponade and tension pneumothorax are common causes • Several hemodynamic patterns may be observed, depending on the cause, from decrease in filling pressures (as in mediastinal compressions of great veins); to trends towards equalization of pressures in the case of cardiac tamponade; or to markedly increased right ventricular filling pressures with low PCWP in the case of pulmonary embolism. Cardiac output is usually decreased with increased SVR.
  • 58.
  • 59.
    59 • The diagnosisof obstructive shock is based on clinical findings, the chest radiograph, and an echocardiogram • Pericardial tamponade:-confirmed by echocardiography, and treatment consists of immediate pericardiocentesis or the creation of an open subxiphoid pericardial window • Tension pneumothorax:-Chest decompression must be carried out immediately and, ideally, should occur based on clinical findings rather than awaiting a chest radiograph. Release of air and restoration of normal cardiovascular dynamics are both diagnostic and therapeutic MANAGEMENT:-
  • 60.
    60 4. DISTRIBUTIVE SHOCK •This type of shock is associated with not only poor vascular tone in the peripheral circulation but maldistribution of blood flow to organs within the body also • The CO varies, but is usually raised • Haemodynamic profile :-  low or normal PCWP  high CO  low arterial blood pressure  low SVR.
  • 61.
  • 62.
  • 63.
    63 NEW DEFINATIONS*:- *Singer M,Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016;315(8):801-810. doi:10.1001/jama.2016.0287 **qSOFA:- Quick sequential organ failure assessment • Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection • Patients with suspected infection who are likely to have a prolonged ICU stay or to die in the hospital can be promptly identified at the bedside with qSOFA**, i.e, alteration in mental status, systolic blood pressure ≥100 mm Hg, or respiratory rate ≥22/min • Organ dysfunction can be identified as an acute change in total SOFA score ≥2 points consequent to the infection. The baseline SOFA score can be assumed to be zero in patients not known to have preexisting organ dysfunction. • A SOFA score ≥2 reflects an overall mortality risk of approximately 10% in a general hospital population with suspected infection.
  • 64.
    64 • Septic shockis defined as a subset of sepsis in which underlying circulatory and cellular metabolism abnormalities are profound enough to substantially increase mortality • Patients with septic shock can be identified with a clinical construct of sepsis with persisting hypotension requiring vasopressors to maintain MAP ≥65 mm Hg and having a serum lactate level >2 mmol/L (18mg/dL) despite adequate volume resuscitation. Terms like septicemia / severe sepsis / SIRS has been REMOVED *Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016;315(8):801-810. doi:10.1001/jama.2016.0287
  • 65.
    65 CAUSES:- 1.Peritonitis caused byspread of infection from the uterus and fallopian tubes, sometimes resulting from instrumental abortion performed under unsterile conditions. 2.Peritonitis resulting from rupture of the gastrointestinal system, sometimes caused by intestinal disease and sometimes by wounds. 3.Generalized bodily infection resulting from spread of a skin infection such as streptococcal or staphylococcal infection. 4.Generalized gangrenous infection resulting specifically from gas gangrene bacilli, spreading first through peripheral tissues and finally by way of the blood to the internal organs, especially the liver. 5.Infection spreading into the blood from the kidney or urinary tract, often caused by colon bacilli.
  • 66.
  • 67.
    67 CLINICAL MANIFESTATIONS :- •The manifestations of the septic response are superimposed on the symptoms and signs of the patient’s underlying illness and primary infection • Some patients with sepsis are normo- or hypothermic; the absence of fever is most common in neonates, in elderly patients, and in persons with uremia or alcoholism • Hyperventilation, producing respiratory alkalosis, is often an early sign of the septic response • Disorientation, confusion, and other manifestations of encephalopathy may also develop early, particularly in the elderly and in individuals with preexisting neurologic impairment
  • 68.
    68 • Hypotension andDIC predispose to acrocyanosis and ischemic necrosis of peripheral tissues, most commonly the digits • Cellulitis, pustules, bullae, or hemorrhagic lesions may develop when hematogenous bacteria or fungi seed the skin or underlying soft tissue • Gastrointestinal manifestations such as nausea, vomiting, diarrhea, and ileus may suggest acute gastroenteritis. Stress ulceration can lead to upper gastrointestinal bleeding. Cholestatic jaundice, with elevated levels of serum bilirubin (mostly conjugated) and alkaline phosphatase, may precede other signs of sepsis
  • 69.
    69 DIAGNOSIS:- • There isno specific diagnostic test for sepsis • Definitive etiologic diagnosis requires identification of the causative microorganism from blood or a local site of infection  At least two blood samples should be obtained (from two different venipuncture sites) for culture; in a patient with an indwelling catheter, one sample should be collected from each lumen of the catheter and another via venipuncture
  • 70.
  • 71.
  • 72.
    72 2016 Surviving sepsisCampaign Guidelines:- A. INITIAL RESUSCITATION AND INFECTIOUS ISSUES B. HEMODYNAMIC SUPPORT AND ADJUNCTIVE THERAPY C. OTHER SUPPORTIVE THERAPY OF SEVERE SEPSIS
  • 73.
    73 A. INITIAL RESUSCITATIONAND INFECTIOUS ISSUES • Sepsis and septic shock are medical emergencies, and we recommend that treatment and resuscitation begin immediately • In the initial resuscitation from sepsis- induced hypoperfusion, at least 30 mL/kg of intravenous crystalloid fluid be given within the first 3 hours • Following initial fluid resuscitation, additional fluids be guided by frequent reassessment of hemodynamic status • A target mean arterial pressure of 65 mmHg in patients with septic shock requiring vasopressors • Targeting resuscitation to normalize lactate in patients with elevated lactate levels as a marker of tissue hypoperfusion
  • 74.
    74 • A fluidchallenge technique be applied where fluid administration is continued as long as hemodynamic factors continue to improve • Crystalloids as the fluid of choice for initial resuscitation and subsequent intravascular volume replacement in patients with sepsis and septic shock
  • 75.
    75 ANTIMICROBIAL THERAPY • Appropriateroutine microbiologic cultures (including blood) be obtained before starting antimicrobial therapy in patients with suspected sepsis and septic shock if it results in no substantial delay in the start of antimicrobials (i.e, <45 minutes) • Administration of intravenous antimicrobials be initiated as soon as possible after recognition and within 1hour for both a) septic shock and b) sepsis without shock • Empiric broad-spectrum therapy with one or more antimicrobials for patients presenting with sepsis or septic shock to cover all likely pathogens (including bacterial and potentially fungal or viral coverage) • If combination therapy is used for septic shock, de-escalation is recommended, with discontinuation of combination therapy within the first few days in response to clinical improvement and/or evidence of infection resolution. This applies to both targeted (for culture-positive infections) and empirical (for culture-negative infections) combination therapy
  • 76.
    76 • Antimicrobial treatmentduration of 7‒10 days is adequate for most serious infections • Daily assessment for de-escalation of antimicrobial therapy in patients with sepsis • Measurement of procalcitonin levels can be used to shorten the duration of antimicrobial therapy in sepsis patients • Prompt removal of intravascular access devices that are a possible source of sepsis or septic shock after other vascular access has been established
  • 77.
    77 B. HEMODYNAMIC SUPPORTAND OTHER ADJUNCTIVE THERAPY • If hypotension persists after the initial volume resuscitation, infusion of a vasoconstrictor drug (vasopressor) like norepinephrine or dopamine should begin. Vasoconstrictor drugs must be infused through a central venous catheter, and the goal is to achieve a mean arterial pressure (MAP) ≥ 65 mm Hg • Norepinephrine as the first-choice vasopressor. For norepinephrine, start with a dose rate of 0.1 μg/kg/min and titrate upward as needed. Dose rates up to 3.3 μg/kg/min are successful in raising the blood pressure in a majority of patients with septic shock • If the desired MAP is not achieved at a dose rate of 3 – 3.5 μg/kg/min, add dopamine as a second vasopressor VASOPRESSOR THERAPY:-
  • 78.
    78 • For dopamine,start at a dose rate of 5 μg/kg/min and titrate up- ward as needed. Vasoconstriction is the predominant effect at dose rates above 10 μg/kg/min • .If the desired MAP is not achieved with a dose rate of 20 μg/kg/min, hypotension is refractory to norepinephrine and dopamine, vasopressin may be effective in raising the blood pressure. (Vasopressin is used as an additional pressor rather than a replacement for norepinephrine or dopamine.) The dose range for vasopressin is 0.01–0.04 units/min, but in septic shock is 0.03 units/min
  • 79.
    79 Role of Corticosteroids:- •Do not use intravenous hydrocortisone to treat septic shock patients if adequate fluid resuscitation and vasopressor therapy are able to restore hemodynamic stability. If this is not achievable, then intravenous hydrocortisone alone at a dose of 200 mg per day • When low-dose hydrocortisone is given, then use continuous infusion rather than repetitive bolus injections • Corticosteroids should not be administered for the treatment of sepsis in the absence of shock
  • 80.
    80 C. OTHER SUPPORTIVETHERAPY OF SEVERE SEPSIS Administration of Blood products:- • Red blood cell transfusion occur only when hemoglobin concentration decreases to <7.0‒7.5 g/dL in adults in the absence of extenuating circumstances, such as myocardial ischemia, severe hypoxemia, or acute hemorrhage • Prophylactic platelet transfusion when counts are <10,000/mm3 (10 x 109/L) in the absence of apparent bleeding and when counts are <20,000/mm3 (20 x 109/L) if the patient has a significant risk of bleeding. Higher platelet counts (≥50,000/mm3 [50 x 109/L]) are advised for active bleeding, surgery, or invasive procedures
  • 81.
    81 Mechanical ventilation andweaning • Target a tidal volume of 6 mL/kg predicted body weight in patients with sepsis-induced ARDS vs 12 mL/kg • Upper limit goal for plateau pressures of 30 cmH20 over higher plateau pressures in adult patients with sepsis-induced severe ARDS • Higher positive end expiratory pressure (PEEP) over lower PEEP in adult patients with sepsis-induced moderate to severe ARDS • Using prone over supine position in adult patients with sepsis-induced ARDS and a PaO2/FiO2 ratio <150 • Use of HFOV in adult patients with sepsis-induced ARDS
  • 82.
    82 • Mechanically ventilatedsepsis patients be maintained with the head of the bed elevated between 30 and 45 degrees to limit aspiration risk and to prevent the development of VAP • Continuous or intermittent sedation be minimized in mechanically ventilated sepsis patients, targeting specific titration endpoints • Use of spontaneous breathing trials in mechanically ventilated sepsis patients with sepsis when they satisfy the following criteria: a) arousable; b) hemodynamically stable (without vasopressor agents); c) low ventilatory and end-expiratory pressure requirements; and d) low FiO2 requirements which can be safely delivered with a face mask or nasal cannula. If the spontaneous breathing trial is successful, extubation should be considered
  • 83.
    83 GLUCOSE • Commence insulindose when two consecutive blood glucose levels are >180 mg/dL • Blood glucose values be monitored every 1 to 2 hours until glucose values and insulin infusion rates are stable, then every 4 hours thereafter in patients receiving insulin infusions
  • 84.
    84 VTE Prophylaxis • Pharmacologicprophylaxis (unfractionated heparin [UFH] or low molecular weight heparin [LMWH]) against VTE in the absence of contraindications to the use of these agents • Mechanical VTE prophylaxis when pharmacologic VTE is contraindicated
  • 85.
    85 Stress Ulcer prophylaxis •Stress ulcer prophylaxis be given to patients with sepsis or septic shock who have risk factors for GI bleeding • Either proton pump inhibitors (PPIs) or histamine-2 receptor antagonists (H2RAs) when stress ulcer prophylaxis is indicated
  • 86.
    86 NUTRITION • Administration ofearly full enteral nutrition rather than early parenteral nutrition alone or parenteral nutrition in combination with enteral feedings in critically ill patients with sepsis or septic shock who can be fed enterally • Use of prokinetic agents in critically ill patients with sepsis or septic shock and feeding intolerance
  • 87.
  • 88.
    88 • Anaphylaxis isan acute multiorgan dysfunction syndrome produced by the immunogenic release of inflammatory mediators from basophils and mast cells • The characteristic feature is an exaggerated immunoglobulin E (IgE) response to an external antigen; i.e., a hypersensitivity reaction type I • The manifestations of anaphylaxis typically involve the skin, lungs, gastrointestinal tract, and cardiovascular system • Identical manifestations can occur without the involvement of IgE; these are called anaphylactoid reactions, and are not immunogenic in origin • Common triggers for anaphylactic reactions include food, antimicrobial agents, and insect bites, while common triggers for anaphylactoid reactions include opiates and radiocontrast dyes
  • 89.
    89 • Anaphylactic shockis an immediate threat to life, with profound hypotension from systemic vasodilatation and massive fluid loss through leaky capillaries. • The hemodynamic alterations in anaphylactic shock are similar to those in septic shock, but are often more pronounced
  • 90.
  • 91.
  • 92.
  • 93.
    93  Volume Resuscitation •Aggressive volume resuscitation is essential in anaphylactic shock because at least 35% of the intravascular volume can be lost through leaky capillaries , which is enough to produce hypovolemic shock Volume resuscitation can begin by infusing 1– 2 liters of crystalloid fluid (or 20 mL/kg), or 500 mL of isooncotic colloid fluid (e.g., 5% albumin), over the first 5 minutes . Thereafter, the infusion rate of fluids should be tailored to the clinical condition of the patient  Refractory Hypotension • Persistent hypotension despite epinephrine infusion and volume resuscitation can be managed by adding glucagon or another vasopressor such as norepinephrine or dopamine
  • 94.
  • 95.
    95 NEUROGENIC SHOCK • Neurogenicshock is a devastating consequence of spinal cord injury (SCI), also known as vasogenic shock. Injury to the spinal cord results in sudden loss of sympathetic tone, which leads to the autonomic instability that is manifested in hypotension, bradyarrhythmia, and temperature dysregulation • Neurogenic shock is most commonly a consequence of traumatic spinal cord injuries, more in cervical spine injuries • Other causes include inadvertent cephalad migration of spinal anesthesia, or devastating head injury, Guillain-Barre syndrome, transverse myelitis
  • 96.
    96 DIAGNOSIS • Neurogenic shockis most commonly associated with a blunt cervical spine injury • Neurogenic shock should be considered only after a hemorrhagic shock has been ruled out in a traumatic patient, the presence of vertebral fracture or dislocation raises the concern for neurogenic shock • Bradyarrhythmia, hypotension, flushed warm skin are the classic signs associated with neurogenic shock • The joint committee of the American Spinal Injury Association and the International Spinal Cord Society propose the definition of neurogenic shock to be autonomic nervous system dysfunction that includes symptoms such as orthostatic hypotension, autonomic dysreflexia, temperature dysregulation. A focal neurologic deficit is not necessary for the diagnosis of neurogenic shock
  • 97.
    97 TREATMENT • Initial managementof neurogenic shock is focused on hemodynamic stabilization. Hypotension should be treated first to prevent secondary injury. The first-line treatment for hypotension is intravenous fluid resuscitation • If hypotension persists despite euvolemia, vasopressors and inotropes are the second lines • Phenylephrine is commonly used as it is a pure alpha-1 agonist that causes peripheral vasoconstriction to counteract the loss sympathetic tone • Epinephrine ,for refractory cases of hypotension • Keep the mean arterial pressure (MAP) at 85–90 mmHg for the first 7 days to improve spinal cord perfusion • Initial spine immobilization is important to prevent further spinal cord injury
  • 98.
    98 REFERENCES 1.Guyton & Hall:Textbook of Medical Physiology, 12th ed 2.Robbin’s Basic pathology, 9th ed 3.Harrison’s principle of internal medicine, 19th ed 4.Miller’s Anesthesia, 8th ed 5.Wylie and Churchill-Davidson's A Practice of Anesthesia , 5th ed 6.Marino’s The ICU Book, 4th ed 7.Tintinalli’s Emergency Medicine ,A Comprehensive Study Guide ,8th ed 8.SHOCK – A SHORT REVIEW ,IJA 2003,Dr. A. K. Sethi, Dr. Prakash Sharma, Dr. Medha Mohta, Dr. Asha Tyagi 9.Cardiogenic Shock,Harmony R. Reynolds and Judith S. Hochman,Circulation. 2008;117:686-697, February 4, 2008 https://doi.org/10.1161/CIRCULATIONAHA.106.613596 10.Baskett PJ. ABC of major trauma. Management of hypovolaemic shock. BMJ: British Medical Journal. 1990 Jun 2;300(6737):1453 11.Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, Bellomo R, Bernard GR, Chiche JD, Coopersmith CM, Hotchkiss RS. The third international consensus definitions for sepsis and septic shock (sepsis-3). Jama. 2016 Feb 23;315(8):801-10 12.Rhodes A, Evans LE, Alhazzani W, Levy MM, Antonelli M, Ferrer R, Kumar A, Sevransky JE, Sprung CL, Nunnally ME, Rochwerg B. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock: 2016. Intensive care medicine. 2017 Mar 1;43(3):304-77 13.Dave S, Cho JJ. Shock, Neurogenic. StatPearls ,www.ncbi.nlm.nih.gov/books/NBK459361 .

Editor's Notes

  • #26 The classification of hemorrhage into 4 classes based on clinical signs is a useful tool for estimating the percentage of acute blood loss. This classification system is also useful in emphasizing the early signs and pathophysiology of shock.
  • #30 Crude measures such as BP estimation from pulse and mentation from (can the patient talk) test, are useful for both simplicity and accuracy in trauma. They have assisted in r/o shock especially in the military for use on the battlefield and for civilian use in disaster triage scenarios. Now it is also used by prehospital personnel to ID which patients may require an IV and or any fluids.
  • #31 Measurements early in the course of shock are not well correlated with blood flow or cardiac output. Significant hypoperfusion occurs in blunt and penetrating trauma patients despite normal, standard vital signs, especially in young, healthy patients. Compensatory mechanisms allow significant reductions in central circulating blood volume, stroke volume, and cardiac output to occur well before changes in arterial blood pressure. Such physiologic compensations can thus mask the true nature and severity of many traumatic injuries.
  • #33 In real time, laboratory data lag behind the clinical situation. The fastest measure of blood composition to turn around—the hemoglobin—is not a good indicator of the depth of hemorrhage, because it expresses a concentration of red cells, which will not change in a patient who is losing whole blood. Use of the hematocrit to estimate acute blood loss is unreliable and inappropriate”. Changes in hematocrit show a poor correlation with blood volume deficits and red cell volume deficits in acute hemorrhage. In fact, loss of whole blood is not expected to change the hematocrit because the relative proportions of plasma and red cell volume are unchanged. The decrease in hematocrit occurs when the kidney begins to conserve sodium (as described previously), which takes 8 to 12 hours to become evident. Another factor that drops the hematocrit in acute hemorrhage is the administration of intravenous (asanguinous) fluids. The administration of intravenous (asanguinous) fluids is expected to produce a dilutional decrease in the hematocrit, even in the absence of blood loss, and thus a decrease in the hematocrit during volume resuscitation is a dilutional effect, and it is not an indication of ongoing blood loss.
  • #34 If the pH is low (under 7.35) and the bicarbonate levels are decreased (<24 mmol/l), metabolic acidosis is diagnosed. A pH < 7.20 is associated with generalized myocardial depression. Treatment with bicarbonate is rarely advocated, rather fixing the underlying injury is the recommended action. Concerns regarding myocardial contractility with lactic acidosis are often cited as reasons for administration of sodium bicarbonate. There have been several studies of the hemodynamic impact of sodium bicarbonate in human lactic acidosis. Although sodium bicarbonate increased pH and serum bicarbonate concentrations, it did not improve hemodynamics or catecholamine responsiveness. Specifically, the effects of bicarbonate were indistinguishable from saline with regard to heart rate, CVP, pulmonary artery pressure, mixed venous oxyhemoglobin saturation, systemic oxygen delivery, oxygen consumption, arterial blood pressure, pulmonary artery occlusion (wedge) pressure, and cardiac output.
  • #35 Base Deficit is performed on blood gases and it is the amount of base required to titrate whole blood to a normal pH. It is considered a reliable marker for shock and the need for transfusion.
  • #36 Lactate reflects an imbalance between glycolysis and glucose oxidation. Elevated levels are of concern, but the time to clearance of lactate back to normal levels is most predictive of outcome in hemorrhagic shock. Values > 1.0 indicates magnitude of shock Be aware that as under perfused tissue beds become reperfused, the accumulated lactate may be washed into the circulation…..causing a temporary elevation of serum lactate levels. Ability to clear lactate to normal is the most important variable predicting survival after injury