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- 1. APPROACH TO SHOCK Presented by: Farahin
- 2. Outlines ◦ Definition ofShock ◦ Pathophysiology of shock ◦ Classification of Shock ◦ Hypovolemic Shock ◦ Cardiogenic Shock ◦ Obstructive Shock ◦ Distributive Shock
- 3. Definition of Shock ◦Life threatening emergency ◦ Reversible in appropriately recognized and treated ◦ Inadequate perfusion of tissue, such that the oxygen and blood volume delivery fails to meet the cellular metabolic and consumption need.
- 4. Pathophysiology: Cellular Insufficient delivery of oxygenand glucose Cells switch from aerobic to anaerobic metabolism If perfusion is not restored in a timely fashion, cell death ensues
- 5. Pathophysiology: Microvascular Tissue ischemia activation of the immune and coagulation systems Hypoxia and acidosis activate complement and neutrophils generation of O2 free radicals and cytokine release This leads to injury of the capillary of endothelial cells Damaged endothelium loses its integrity and becomes ‘leaky’. This allows fluid to leaks out and tissue edema ensues
- 6. Pathophysiology: Systemic Cardiovascular • ↓preload and afterload compensatory baroreceptor response ↑ sympathetic activity, release of catecholamines • This results in tachycardia and vasoconstriction (except in septic) Respiratory • As there is metabolic acidosis and ↑ sympathetic response ↑ in RR ↑ excretion of CO2 • This produce a compensatory respiratory alkalosis Renal • ↓ perfusion pressure ↓ glomerular filtration ↓ urine output stimulates renin- angiotensin- aldosterone axis • This leads to further vasoconstriction and ↑ water and sodium reabsorption in the kidney Endocrine • Due to preload, ADH secreted by by pituitary resulting in vasoconstriction and ↑ resorption of water from kidney. • Adrenal cortex will release cortisol and contributes to sodium and water reabsorption and sensitizing the cells to catecholamines
- 7. STAGES OF SHOCK Early compensated shock Progressive/ decompensate d shock Irreversible state
- 9. HISTORY ◦ May bedifficult or impossible due to altered mental status ◦ Prior medication and history may help ◦ Possibility of trauma in unconscious patient without witness PHYSICAL EXAMINATION ◦ Physical examination of patient in shock must be done thoroughly ◦ ABCDE approach helps to efficiently evaluate patient while balancing management priorities
- 10. ED EVALUATION ◦ Vitalsigns are important indicators of the patient’s physiologic status
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- 12. Classification of Shock ◦ TYPESOF SHOCK HYPOVOLAEMIC (Intravascular volume loss) • Haemorrhagic (Trauma) • Non-haemorrhagic (DKA/AGE/Dengue fever) CARDIOGENIC (Ineffective pumping due to heart damage) • Myocardial infarction • Arrhythmias • Mechanical • Cardiomyopathy DISTRIBUTIVE (Abnormal blood flow in the small vessels caused by generalized peripheral dilatation due to inflammatory causes) • Septic shock • Anaphylactic shock • Neurogenic shock OBSTRUCTIVE (Blood flow to and from the heart is blocked due to obstructive presure) • Pulmonary embolism • Cardiac tamponade • Tension pneumothorax
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- 14. HYPOVOLAEMIC SHOCK ▪ Themost common form of shock and to some degree is a component of all other forms of shock. ▪ Can be divided into two: ▪ Hemorrhagic ▪ Non-hemorrhagic
- 17. HISTORY ◦ History oftrauma, recent surgery, evidence of bleeding, vomiting, diarrhea or GI illness point to fluid loss PHYSICAL EXAMINATION ◦ Cold peripheries, low pulse volume, prolonged CRT. Pallor in setting of bleeding INVESTIGATION FBC – Haemoglobin and haematocrit Electrolytes – Potassium, Calcium Acid/base – Lactate, acidosis/alkalosis Renal function – BUN: creatinine ratio > 20 Coagulation study – Prolonged due to coagulopathy Imaging – CXR, FAST scan, CT scan, Angiography TREATMENT
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- 19. 2. CARDIOGENIC SHOCK •Result from failure of the cardiac “pump” to forward delivery of blood and, therefore, oxygen to the tissues, leading to shock. • Pressure in one or both ventricles may elevate due to inefficiencies in the right or left side of the heart. • When pressure elevate on the left side, pulmonary oedema may occur causing right heart dysfunction and leads to systemic congestion. • In response to reduction in cardiac output, systemic vascular resistance increase in response to catetholamine stimulation and angiotensin II.
- 21. HISTORY ◦ Classically presentswith crushing substernal pain, upper extremity, back, epigastric or jaw pain. Atypical chest pain in women and patients with neuropathic changes in heart innervation (eg diabetic) PHYSICAL EXAMINATION ◦ New or changing murmur in valvular disruption ◦ Signs of elevated filling pressure increase JVP in right heart failure, bibasal crepitation on auscultation of the lung in left heart failure ◦ Cool and mottled extremities ◦ Vital signs: INVESTIGATION TREATMENT HR – ↑/normal/↓ BP – normal or ↓ RR – ↑ SpO2 – ↓ ◦ ECG ◦ Cardiac enzymes – troponin, CK,CKMB ◦ CXR ◦ Echocardiography ◦ Optimization of intravascular volume with caution ◦ Medication administration – dual anti platelet when necessary ◦ Vasopressor support to MAP 65mmHg – noradrenaline and dopamine ◦ Fibrinolytic therapy and/pr percutaneous coronary intervention (PCI) ◦ Admission to coronary care unit
- 22. DRUGS RECEPTOR EFFECTDOSE DILUTION IONOTROPES ADRENALINE ɑ1 and ß receptors • Low dose : Beta effects predominate o Increasing CO and Vasodilatation • Higher dose : Alpha 1 effects predominate o Increasing Systemic vascular resistance • Also causes splanchnic vasoconstriction, hyperglycemia, increased myocardial O2 consumption and lactate production 2-10mcg/min 1-2mcg/kg/min 3mg/3cc dilute in 50cc NS DOPAMINE ɑ1, ß1, ß2 & dopamine receptors • Low dose : Dopamine effects predominate o Increased splanchnic and renal perfusion • Higher dose : Alpha 1 and Beta 1 effects predominate o Results in vasoconstriction and increased CO 5-20mcg/kg/min 1amp : 5cc : 200mg dilute in 45mls NSD5 DOBUTAMINE ß1 and ß2 receptors • Beta 1 : Increased HR and force of contraction • Beta 2 : Peripheral Vasodilatation • Useful in low CO state (Eg : Post MI) • Frequently use with Noradrenaline (Peripheral vasoconstriction to maintain Systemic vascular resistance) Run at 2.5-25mcg/kg/min 250-500mg in 50cc NS VASOPRESSOR NORADRENALI NE ɑ1 receptors • Causes peripheral vasoconstriction • Excessive use can increase afterload and reduce CO, reduce renal perfusion, reduce splanchnic blood flows, and impair peripheral perfusion Run at 0.05-1mcg/kg/min • 4mg in 50cc D5% (single strength) • 8mg in 50cc D5% (double strength)
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- 24. 3. OBSTRUCTIVE SHOCK •Impediment to the flow of blood in the cardiopulmonary circuit
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- 27. 4. Distributive Shock ◦This shock describes the pattern of cardiovascular responses characterising a variety of conditions. ◦ This include: ◦ Septic shock. ◦ Anaphylaxis shock. ◦ Spinal cord injury. ◦ Characteristic of distributive shock Vasodilation ◦ Anaphylaxis Vasodilatation due to histamine release. ◦ Spinal cord injury There is failure of sympathetic outflow and adequate vascular tone. ◦ Septic shock Less clear but it is related to the release of bacterial products (endotoxin) and the activation of the immune systems.
- 28. Septic Shock: TheEvolving Changes: 2016 Update: Sepsis 3.0 ◦ In sepsis 2.0, SIRS criteria was still used for sepsis and SOFA criteria was predominantly used for severe sepsis. ◦ Due to new evidences of poor specificity of SIRS score, the Sepsis Task Force again updated the definition in 2016. ◦ Under this new definition, the term “severe sepsis” is redundant. ◦ Septic shock was defined as the subset of sepsis with profound circulatory, cellular, and metabolic dysregulation, and associated with a much higher mortality of 40%, compared with the 10% mortality observed with sepsis. ◦ The use of qSOFA (Quick Sequential Organ Failure Assessment Screening Tool).
- 29. qSOFA Score ◦ TheSOFA score is cumbersome to calculate and requires laboratory values that are not readily available especially outside ICU setting. ◦ The qSOFA score was introduced and its use is suggested for non ICU patient. ◦ Studies have shown that predicted mortality was similar to those patients identified using the full SOFA score.
- 31. Septic Shock: ClinicalManifestation
- 32. Septic Shock: GeneralManagement 1. Establishment of Diagnosis • FBC, RP, LFT, UFEME, blood cultures and urine cultures. • Imaging: CXR (pneumonia), CT abdomen (diverticulitis, abscess). • Role of serial procalcitonin if taken early can guide to abx cessation. 2. Antibiotics and Source Control • Early initiation of abx preferably within 1 hours with blood cultures taken prior to that • Initiate broad spectrum (according to local guidelines and considering comorbidities) that cover both gram +ve and –ve organisms. • If suspecting intraabdominal sepsis, anaerobic coverage is indicated. • In patients with immunodeficiencies, consider covering with antifungal. • Always keep in mind regarding localised source infected pressure ulcer or erythematous vascular catheter site. Management may include removal of invasive devices (eg, dialysis catheters, infected orthopedic hardware, or pacemakers) or surgical evacuation of abscess.
- 33. Septic Shock: Management 3.Fluid Resuscitation • Studies have shown that reducing the duration of hypotension in sepsis is associated with decreased mortality in septic shock. • Most of the guidelines suggest an initial fluid bolus of 30 mL/kg. • Studies have shown that excess volume administration is associated with worsened mortality, which may be due to associated pulmonary edema requiring prolonged mechanical ventilation and worsened kidney injury. • Responsiveness can be best assessed with bedside usg/echocardiography, pulse-pressure variations.
- 34. Septic Shock: Management 4.Target blood pressure • Many guidelines recommend a target MAP of at least 65. • The only large randomized trial of 2 blood pressure targets in patients with septic shock attempted to compare the effect of lower MAP target (65–70) compared with higher target (80–85) and did not demonstrate a mortality benefit of one versus the other. 5. Vasopressor • Historically, dopamine was recommended as theinitial blood pressure agent of choice in septic shock. However, randomized trials comparing the use of dopamine versus norepinephrine as an initial agent showed higher incidences of tachyarrhythmia and worsened mortality with dopamine compared with norepinephrine. Hence, the current recommendationnis that norepinephrine be used as a first-line agent. • Epinephrine has been compared with norepinephrine as an initial agent and did not reveal a mortality difference; however, epinephrine was associated with greater tachycardia and lactic acidosis.
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- 37. Anaphylactic Shock Common identifiedcauses of anaphylaxis: • food (e.g. nuts) - the most common cause in children • drugs • venom (e.g. wasp sting) Allergic reaction immune system overreacts to a harmless substance known as an allergen. Anaphylaxis o Allergic reaction involve more than one systems (SKIN + CVS/GIT/CNS) Anaphylactic Shock o Anaphylaxis + Shock Immediate hypersensitivity reaction (Type I), mediated by interaction of IgE on mast call and basophils triggers release of histamine, leukotrienes, and other mediators that cause diffuse smooth muscle contraction (eg, resulting in bronchoconstriction, vomiting, or diarrhea) and vasodilation with plasma leakage (eg, resulting in urticaria or angioedema). Primary Mediatiors: Histamine, serotonin, eosinophil Secondary Mediators: Bradykinin, prostaglandins
- 39. ● Early signsof impending anaphylaxis ○ Nasal itching/ stuffiness ○ Stridor/ hoarseness ○ SOB/ tachypnea ○ Nausea/vomiting/ diarrhea ○ Tingling of face (esp mouth), upper chest, palames, soles ● Severe anaphylaxis ○ Angioedema of tongue, soft palate, larynx ○ Tachycardia, hypotension, altered mental status, dizziness, wheezing → Cardiac arrest
- 40. Allergic Reaction : IVHydrocortisone 200mg / 4mg/kg (Paeds) IV Piriton 10mg / 0.1mg/kg (Paeds) Anaphylaxis : IM Adrenaline 0.5mg (Paeds : 10mcg/kg) repeat every 5 minutes as needed IV Hydrocortisone 200mg (Paeds 4mg/kg) IV Piriton 10mg (Paeds 0.1mg/kg) Neb Salbutamol (Wheezing/rhonci) Anaphylactic Shock : ABCDE IV Adrenaline 0.1mg (1:10000) slow bolus over 5-10mins (Paeds 0.01mg/kg) -1 amp =1mg/ 1:1000, dilute 1 amp in 10cc NS , give 1cc= 0.1mg IVI Adrenaline 3mg in 50cc NS run at 3mls/Hour IM/ s/c Adrenaline: 0.5mg (1:1000) Adult / Paeds 0.01mg/kg IVD 1-2L Bolus IV Hydrocortisone 200mg IV Piriton 10mg
- 41. Anaphylactic Shock ◦ Anaphylaxisis one of the few times when you would not have time to look up the dose of a medication . ◦ Adrenaline can be repeated every 5 minutes if necessary. The best site for IM injection is the anterolateral aspect of the middle third of the thigh. Adrenaline Hydrocortisone Chlorpheniramine < 6months 150 micrograms (0.15 ml 1 in 1000) 25 mg 250 micrograms/kg 6 months- 6 years 150 micrograms (0.15 ml 1 in 1000) 50 mg 2.5 mg 6-12 years 300 micrograms (0.3 ml 1 in 1000) 100 mg 5 mg > 12 years 500 micrograms (0.5 ml 1 in 1000) 200 mg 10 mg
- 42. Anaphylactic Shock ◦ Managementfollowing stabilization: • Patients who have had emergency treatment for anaphylaxis should be observed for 6–12 hours from the onset of symptoms, as it is known that biphasic reactions can occur in up to 20% of patients. • Sometimes it can be difficult to establish whether a patient had a true episode of anaphylaxis. Serum tryptase levels are sometimes taken in such patients as they remain elevated for up to 12 hours following an acute episode of anaphylaxis.
Editor's Notes
- #3 Shock is related to the determinant of oxygen delivery: cardiac output, vascular integrity and resistance (SVR) and oxygen content (determined by haemoglobin and oxygen saturation CO and SVR will compensate each other to maintain MAP. Basis of shock physiology as follows
- #7 Shock is a progressive disorder that leads to death if the underlying problems are not corrected. In early compensated shock, various neurohumoral mechanisms help maintain cardiac output and blood pressure such as baroreceptor reflexes, release of catecholamines and ADH, activation of renin-angiotensin-aldosterone-axis and generalized sympathetic stimulation. Net effects are tachycardia, peripheral vasoconstriction and renal fluid conservation As in decompensated shock, characterized by widespread tissue hypoxia Intracellular aerobic respiration is replaced by anaerobic glycolysis with excessive production of lactic acid Lactic acidosis blunts the vasomotor response; arterioles dilate and blood begins to pool in microcirculation Peripheral pooling puts endothelial cells at risk for development of anoxic injury with subsequent disseminated intravascular coagulation. Peripheral pooling also worsen cardiac output. Vital organs affected and begin to fail. In irreversible state, widespread cell injury is reflected in lysosomal enzyme leakage Myocardial contractile function worsens Ischemic bowel may allow intestinal flora to enter the circulation, bacteremic shock may be superimposed multisystem failure
- #9 Approach to patients with hypotension and concern of shock includes evaluation for diagnostic clues to underlying and type of shock Initial part of shock are often compensated and reversible
- #10 Approach to patients with hypotension and concern of shock includes evaluation for diagnostic clues to underlying and type of shock Initial part of shock are often compensated and reversible
- #11 Approach to patients with hypotension and concern of shock includes evaluation for diagnostic clues to underlying and type of shock Initial part of shock are often compensated and reversible
- #15 Recognise : S&S: thirst, muscle cramps, and/or orthostatic hypotension. Physical examination: dry mucous membranes, decreased skin turgor, and no raised jugular venous presssure Tachycardia and hypotension can be seen along with decreased urinary output. Patients in shock can appear cold, clammy, and cyanotic
- #17 ABC Fluid replacement : saline or colloid initially; if bleeding use blood Monitor BP, CVP, urine output Treat underlying causes The main problem is inadequate volume Unless cardiogenic shock is suspected, aggressive fluid resuscitation with 1-2L of crystalloids should be started while assessing for response and to repeat if necessary, further resuscitation with colloids, pack cells or whole blood may be appropriate Ensure adequate fluid resuscitation has taken place before starting vasopressor support Give IV dopamine 5-20mcg/kg/min Add IV Noradrenaline 0.5-1.5mcg/kg/min if necessary Placement of central venous line may be necessary for guiding fluid therapy Correct electrolyte abnormalities
- #21 Sign and sx : Chest pain, Palpitations, Dyspnoea, Nausea and vomiting, Profuse sweating, Confusion/disorientation, Syncope, Severe systemic hypotension, Respiratory distress due to pulmonary congestion Laboured breathing with audible coarse crackles or wheezing. Impaired circulation: Tachycardia (may be absent if patients are on beta blockers), delayed capillary refill, hypotension, diaphoresis, and poor peripheral pulses. End-organ dysfunction (e.g. decreased mental function and urinary output). Jugular venous distension as evidence of right ventricular failure. Pulmonary oedema from left ventricular dysfunction. Loud murmurs may indicate valvular dysfunction. Beck's triad (diagnostic features are jugular venous distension, pulsus paradoxus and muffled Beck's triad (diagnostic features are jugular venous distension, pulsus paradoxus and muffled heart sounds) may be present to suggest tamponade. Gallop (especially the S3 heart sound which is pathognomonic of congestive heart failure).The presence of pulmonary oedema in the setting of hypotension increases the likelihood of cardiogenic shock.
- #25 Cardiac tamponade : clinical syndrome caused by the accumulation of fluid in the pericardial space, resulting in reduced ventricular filling and subsequent hemodynamic compromise. Signs : Beck’s Triad : Hypotension, Muffled heart sound, Distended neck veins, Kussmaul’s signs (increased neck distension upon inspiration & pulsus paradoxus). The definitive treatment of cardiac tamponade involves drainage of the pericardial fluid, preferably by needle pericardiocentesis Tension pneumothorax: Life-threatening condition that develops when air is trapped in the pleural cavity under positive pressure, displacing mediastinal structures and compromising cardiopulmonary function. A needle thoracostomy (e.g. 14G intravenous cannula) can be inserted, typically in the 2nd intercostal space in the midclavicular line, before a larger underwater drain can be inserted Pulmonary embolism: Occurs when a blood clot (thrombus) becomes lodged in an artery in the lung and blocks blood flow to the lung. D-dimers can be useful in low-risk to rule out a VTE. Visualizing the clot using CTPA is the commonest way to make the diagnosis.