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![HYPOVOLEMIC SHOCK
• Encompasses disease processes that reduce CO (and oxygen delivery) via a reduction in
preload
• Elevated SVR and low CVP and PCWP related to decreased intravascular volume.
• most commonly related to hemorrhage
• External (secondary to trauma)
• Internal (most commonly upper or lower gastrointestinal [GI]) bleeding
• Non-hemorrhagic processes
• GI illnesses causing profound emesis or diarrhoea,
• renal losses (osmotic diuresis associated with diabetic ketoacidosis or diabetes insipidus)
• skin loss (severe burns, inflammatory conditions such as Stevens-Johnson)](https://image.slidesharecdn.com/shock-harrison-240901075345-142f5eea/75/shock-harrison-all-types-classification-pathophysiology-pptx-14-2048.jpg)
![PHYSICAL EXAMINATION
• most cases, this is manifest as hypotension
• Systolic blood pressure [SBP] <90 mmHg or mean arterial pressure [MAP] <65 mmHg
• Isolated hypotension is not shock
• Patients with underlying hypertension may develop shock and organ dysfunction at higher
blood pressures.
• Absence of an elevated heart rate does not exclude shock .
• Tachypnea is another vital sign abnormality seen early in shock
• body compensates for a developing metabolic acidosis](https://image.slidesharecdn.com/shock-harrison-240901075345-142f5eea/75/shock-harrison-all-types-classification-pathophysiology-pptx-28-2048.jpg)
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shock - harrison-all types, classification, pathophysiology.pptx
- 1. Approach to thepatient with shock DR.HASHID I DNB RESIDENT
- 2. SHOCK • Shock isthe clinical condition of organ dysfunction resulting from an imbalance between cellular oxygen supply and demand. • The organ dysfunction seen in early shock is reversible with restoration of adequate oxygen supply
- 3. PATHOPHYSIOLOGY OF SHOCK •Cellular oxygen imbalance • Impaired oxygen delivery • Increased oxygen consumption • Impaired oxygen utilization.
- 5. • Maintenance ofthe homeostatic environment of the cell is dependent on an adequate supply of ATP. • ATP-dependent ion pumping systems, such as the Na+/K+ ATPase, consume 20–80% of the cell’s energy • Decreased ATP disrupt the cell’s ability to maintain osmotic, ionic, and intracellular pH homeostasis • Influx of calcium can lead to activation of calcium dependent phospholipases and proteases, causing cellular swelling and death.
- 6. DETERMINANT'S OF OXYGENDELIVERY • Oxygen delivery (DO2) = Cardiac output (CO) Arterial Oxygen content(CaO2) x Heart rate (HR) Stroke volume(SV) x SV depend on Preload Afterload( Systemic vascular resistance (SVR) Cardiac contractility SV Systemic vascular resistance α (Preload × Contractility) CaO2 is composed of oxygen carried by convection with hemoglobin and oxygen dissolved in blood, CaO2 = (Hb × 1.39 × SaO2) + (PaO2 × 0.03)
- 7. Oxygen delivery (DO2)= Cardiac output (CO) Arterial Oxygen content(CaO2) x
- 8. CLASSIFICATION OF SHOCK •Each shock type has a distinct hemodynamic profile
- 9. DISTRIBUTIVE SHOCK • Primaryphysiologic disturbance is a reduction in SVR • The most common cause of distributive shock is sepsis • dysregulated host response to infection resulting in life-threatening organ dysfunction. • accompanied by persistent hypotension requiring vasopressor support (despite adequate volume resuscitation), it is classified as septic shock.
- 10. OTHER PROCESSES • Pancreatitis •Severe burns • Liver failure • Anaphylaxis • Patients with severe brain or spinal cord injury ( Autonomic dysfunction) Adrenal insufficiency • chronic steroid use • Medications(immune checkpoint inhibitor- associated primary adrenal insufficiency) • metastatic malignancy, • Adrenal hemorrhage, • Infection • Autoimmune adrenalitis • Amyloidosis.
- 12. CARDIOGENIC SHOCK • Reductionin CO owing to a primary cardiac problem. • Compensatory increase in SVR in cardiogenic shock • When the cardiac process affects the Left ventricle increase in PCWP , and Right ventricle CVP will be elevated
- 13. • Oxygen delivery(DO2) = Cardiac output (CO) Arterial Oxygen content(CaO2) Stroke volume(SV) Heart rate (HR) SV may be reduced by processes that affect myocardial contractility • Myocardial infarction • Ischemic cardiomyopathies • Primary myocarditis Mechanical valvular disease • Acute mitral insufficiency • Aortic insufficiency • Bradyarrhythmia’s • Tachyarrhythmias (from either an atrial or ventricular source)
- 14. HYPOVOLEMIC SHOCK • Encompassesdisease processes that reduce CO (and oxygen delivery) via a reduction in preload • Elevated SVR and low CVP and PCWP related to decreased intravascular volume. • most commonly related to hemorrhage • External (secondary to trauma) • Internal (most commonly upper or lower gastrointestinal [GI]) bleeding • Non-hemorrhagic processes • GI illnesses causing profound emesis or diarrhoea, • renal losses (osmotic diuresis associated with diabetic ketoacidosis or diabetes insipidus) • skin loss (severe burns, inflammatory conditions such as Stevens-Johnson)
- 16. OBSTRUCTIVE SHOCK • reductionin oxygen delivery related to reduced CO, • etiology of the reduced CO is an extracardiac pulmonary vascular or mechanical process impairing blood flow. • Tension pneumothorax (PTX) • Cardiac tamponade • Restrictive pericarditis • Pulmonary embolism • Venous air embolism • fat embolism (right heart) • Aortic dissection (left heart)
- 18. Mixed Shock • Patientwill present with more than one type of shock • Ex – Septic shock • The initial insult to the physiology Is though distributive shock • Secondarily sepsis induced cardiomyopathy can develop which will cause secondary cardiogenic shock
- 19. Undifferentiated Shock • Patientshave undifferentiated shock in which the shock type and specific disease process are not apparent • Emergency department (ED) of a university hospital in Denmark -2019 • 30.8% hypovolemic shock • 27.2% septic shock • 23.4% distributive non-septic shock • 14% cardiogenic shock • 0.9% obstructive shock. • 90-day mortality of the septic and cardiogenic patients was 56.2% and 52.3 % 2010 study (from eight hospitals) - ICU shock patients • 62% septic shock • 16% hypovolemic shock • 15% cardiogenic shock • 2% obstructive shock
- 20. STAGES OF SHOCK •Compensated shock (pre-shock), shock (decompensated shock), and irreversible shock. COMPENSATED SHOCK SHOCK (decompensated shock) IRREVERSIBLE SHOCK
- 21. COMPENSATED SHOCK • Bodyutilizes a variety of physiologic responses to counteract the initial insult • No overt signs of organ dysfunction • Laboratory evaluation may demonstrate mild organ dysfunction • elevated creatinine or troponin • a mild elevation of lactate. • Specific compensatory response is determined by the initial pathophysiologic defect
- 22. SHOCK (DECOMPENSATED SHOCK) •Host compensatory responses are overwhelmed, the patient transitions into true shock with evidence of organ dysfunction • Appropriate interventions to restore perfusion and oxygen delivery during these initial two phases of shock can reverse the organ dysfunction
- 23. IRREVERSIBLE SHOCK. • Atthis point, the organ dysfunction is permanent and often the patient progresses to Multi-organ failure
- 25. EVALUATION OFTHE PATIENTWITH SHOCK • First aim is confirmation of the presence of shock. • possibility of shock should be considered in all patients presenting with new organ dysfunction or hypotension. • Second aim of the initial is to identify either a specific shock etiology or to determine the type of shock present. • Initiation of therapy should not be delayed while the final diagnosis is being determined.
- 26. HISTORY • Concise, focusedhistory is essential. • Oftentimes a patient with shock will present with nonspecific symptoms such as weakness, malaise, or lethargy. • As the history is being obtained, we must be attentive to any details indicating new organ dysfunction. • most easily identified new organ dysfunction from the history is the • presence of a newly altered mental status or • a decrease in urine output (oliguria)
- 27. • Patients withdistributive shock from sepsis may present with fever and a history suggesting a focal site of infection • Anaphylactic distributive shock may be suggested by the onset of pruritis, hives, dyspnea, and new facial edema after exposure to common allergens. • Cardiogenic shock may be identified by the onset of exertional chest discomfort, palpitations with syncope or presyncope. • Hypovolemic shock may be identified in patients who present with a history of trauma (blunt or penetrating) or GI bleed • preexisting immune dysfunction or medication-induced neutropenia may present with hypoperfusion and new organ dysfunction Septic Shock
- 28. PHYSICAL EXAMINATION • mostcases, this is manifest as hypotension • Systolic blood pressure [SBP] <90 mmHg or mean arterial pressure [MAP] <65 mmHg • Isolated hypotension is not shock • Patients with underlying hypertension may develop shock and organ dysfunction at higher blood pressures. • Absence of an elevated heart rate does not exclude shock . • Tachypnea is another vital sign abnormality seen early in shock • body compensates for a developing metabolic acidosis
- 29. • Central nervoussystem (CNS), kidney, and skin are the organ systems most easily assessed for evidence of organ dysfunction. • Decreased oxygen delivery to the brain is manifest as confusion and encephalopathy. • To assess renal function during the physical examination • the patient’s urine output since the time of presentation. • In patients with normal baseline renal function, oliguria(<0.5 mL/kg per hr)may indicate shock. • Cold and clammy skin , Capillary refill time (CRT) • Examination findings suggestive of high-output shock (distributive) include • warm peripheral extremities • normal capillary refill (<2 s), and • large pulse pressure with low diastolic pressure
- 30. • Low COforms of shock • cool extremities • Delayed capillary refill • weak pulses (with narrow pulse pressure) • Among types of shock with low CO, the examination can be used to distinguish between conditions with • increased intravascular filling pressure (cardiogenic shock, obstructive shock) and • intravascular volume depletion (hypovolemic shock) Elevation of jugular venous pressure (JVP) presence of peripheral edema S3 gallop Reduced (JVP <8 cm) Rales on pulmonary auscultation may be related to in hypovolemic shock Left-sided cardiac dysfunction patients with chronic heart failure do not present with the classical findings of acute heart failure.
- 31. site of anuntreated infection (cellulitis, abscess, infected pressure injury) Sepsis brady- or tachyarrhythmia Cardiogenic large ecchymosis bleed related to trauma or spontaneous retroperitoneal bleeding Pulsus paradox and elevated JVP cardiac tamponade. paucity of breath sounds over the affected side deviation of the trachea away from the affected side Tension pneumothorax
- 32. SHOCK INDEX Shock index= Heart rate Systemic blood pressure • Normal SI being 0.5–0.7. • An elevated SI (>0.9) has been proposed to be a more sensitive indicator of transfusion requirement • SI may also identify patients at risk for postintubation hypotension
- 33. QUICK SEQUENTIAL ORGANFAILURE ASSESSMENT (qSOFA) • rapid assessment scale that assigns a point for • SBP <100 • respiratory rate >22 • Altered mental status (Glasgow Coma Scale <15). • A qSOFA ≥2 (with a concern for infection) is associated with a significantly greater risk of death or prolonged ICU stay.
- 34.
- 35. • Urine electrolyteswith subsequent calculation of the fractional excretion of sodium (FENa) or fractional excretion of urea (FEUrea) may indicate states of hypovolemia or decreased effective circulating volume. • Elevation of alkaline phosphatase may suggest biliary obstruction • Elevation of cardiac enzymes can indicate a primary cardiac problem with myocyte damage related to ischemia, myocarditis, or a pulmonary embolism. • elevation of the white blood cell count may raise suspicion for an infective process, but this is certainly not diagnostic • an accompanying left shift may improve the sensitivity of this measure.
- 36. • Reduction inhemoglobin and hematocrit are seen in patients with hemorrhagic hypovolemic shock. • Extent of acidosis may be determined with a venous blood gas (VBG), if there is accompanying hypoxemia an arterial blood gas should be obtained. • Lactate measurement has a role in the diagnosis, risk stratification, and, potentially, the treatment of shock. • In the setting of reduced oxygen delivery and cellular hypoxia, the amount of lactate produced from these tissues increases. • elevated lactate correlates with a worse outcome • serial lactate measurements in the evaluation of critically ill patients and their response to therapy.
- 37. ELECTROCARDIOGRAM • There maybe a bradycardia or tachycardic arrhythmia causing a reduction in CO. • ST segment elevation • S1 Q3 T3 • Reduced voltage in the presence of electrical alternans raises the possibility of pericardial tamponade.
- 38. CHEST X-RAY • Focalalveolar or interstitial infiltrate • Pulmonary edema • Bilateral cephalization of the pulmonary vasculature • Peri-bronchial cuffing • septal thickening, • intralobular thickening • widened mediastinum raises the possibility of a pericardial effusion.
- 40. Focal oligemia West marksign Hamptons Hump Palla’s sign
- 41. POINT-OF-CARE ULTRASOUND • Severalstructured protocols exist for evaluation of undifferentiated shock including the • Rapid Ultrasound for Shock and Hypotension(RUSH • Abdominal and Cardiothoracic Evaluation with Sonography in Shock (ACES • Sequential Echo graphic Scanning Assessing Mechanism Or Origin of Shock of Indistinct Cause (SESAME). • In a rapid and protocolized manner, views are obtained of the heart, lungs, pleural space, inferior vena cava, abdominal aorta, abdomen, and pelvis
- 42. • POCUS transthoracicechocardiography (TTE) • LV function • Evaluation of LV function through estimation of left ventricular ejection fraction (LVEF) can identify shock with globally reduced LV function or regional wall motion abnormalities. • RV function • RV size and wall thickness , to identify conditions such as elevated pulmonary pressures or suggest pulmonary embolism • Pericardium
- 43. • IVC evaluationto assess intravascular filling • collapsible IVC at the end of expiration suggests reduced intravascular volume • POCUS pleural space evaluation • more sensitive than CXR for identifying a PTX. • Examinations that extend to the proximal deep veins of the lower extremity can identify deep venous thrombosis • One significant limitation of POCUS is that performance and interpretation of testing is operator-dependent.
- 44. INITIAL TREATMENT OFSHOCK • Key principle in shock management is to initiate treatment for circulatory shock simultaneous with efforts to elucidate shock etiology . • If initial evaluation identified the etiology of shock, then the treatment should be specific for it • Development of shock is a medical emergency. • Most patients with shock should be cared for in an ICU setting.
- 45. 1. Adequate intravenousaccess - 16G or 18 G 2. For patients with ongoing hypotension despite adequate volume resuscitation, • placement of a central venous catheter (CVC) is indicated to provide therapy with vasopressors and inotropes. • CVC will provide a way to monitor hemodynamic monitoring (CVP) as well as a means to obtain central venous oxygen saturations (ScvO2) • ScvO2 is a surrogate of mixed venous oxygen saturation, and thus can provide insight into the adequacy of oxygen delivery. 3. If the patient presents critically ill or in the midst of cardiopulmonary arrest, the quickest method of obtaining central access will be through the use of an intraosseous device. 4. Placement of an arterial line • allows for intravascular measurement of blood pressure and continuous determination of MAP. • facilitates repeated measures of acid base status or lactate 5. Urinary catheter rplaced to permit hourly assessment of renal function
- 46. VOLUME RESUSCITATION • Thephysiologic goal of volume resuscitation is to move the patient to the nonpreload- dependent portion of the Starling curve. • Any of the four shock types will benefit from an increase in intravascular volume. • In the past, the use of early goal-directed therapy (EGDT) in septic shock targeted specific measures of CVP, MAP, and SvO2 to guide volume resuscitation. • recent studies have demonstrated that targeted resuscitation using invasive monitoring is not required • Suspected septic shock, a minimum of 30 mL/kg is recommended by the Surviving Sepsis Campaign
- 47. • Even patientswith cardiogenic shock may benefit from cautious volume replacement. • In these patients, there should be a careful assessment of volume status prior to volume administration • Volume resuscitation will begin with crystalloid. • ongoing hemorrhage -volume replacement with packed red blood cells is warranted. • In cases of massive transfusion, platelets and fresh frozen plasma should be provided • Red cell administration may be a part of volume replacement even without hemorrhage in order to optimize oxygen delivery if hemoglobin content is <7 g/dL.
- 48. PASSIVE LEG RAISINGTEST • Predict responsiveness to additional intravenous fluid (IVF) by providing the patient with an endogenous volume bolus. • A >12% SV variation suggests a volume-responsive state
- 49. if the shockpatient is mechanically ventilated there is the option of looking at changes in SV variation (or pulse pressure variation) during the respiratory cycle to assess volume responsiveness. A >12% SV variation suggests a volume-responsive state
- 50. • The mostcommonly used parameters to assess adequacy of volume resuscitation are inferior vena cava (IVC) diameter and IVC collapse. • Pulmonary artery catheter (PAC) • another tool for assessment of volume status • Ports in the PAC (Swan-Ganz catheter) allow for direct measurement of CVP, pulmonary artery (PA), and PCWP • PCWP is used as a surrogate for LA pressure. • While studies have not identified a mortality or length-of-stay benefit with routine use of PA catheterization, there are cases where it may be beneficial • Patients with mixed shock (distributive and cardiogenic) or those with ongoing shock of unclear etiology • For patients who initially present with shock but then develop respiratory failure related to acute respiratory distress syndrome (ARDS) or renal failure, it may be reasonable to begin volume removal.
- 51. VASOPRESSOR AND INOTROPICSUPPORT • intravascular volume status has been optimized with volume resuscitation but hypotension and inadequate tissue perfusion persist. • Distributive shock • The aim is to increase the SVR. • Norepinephrine is the first-choice vasopressor. • α1 causes vasoconstriction while β1 has positive inotropic and chronotropic effects • At high doses, epinephrine has a similar profile (at lower doses the effects β predominate) but has serious side effects
- 52. • Vasopressin • Indistributive shock, vasopressin deficiency may be present. • Vasopressin acts on the vasopressin receptor to reverse vasodilation and redistribute flow to the splanchnic circulation. • Vasopressin is safe and has a role as a second agent for hypotension in septic shock • addition of low-dose vasopressin did not reduce all-cause 28-day mortality compared to norepinephrine • Dopamine • does not have a role as a first-line agent in distributive shock • study in patients with all-cause circulatory shock did not show a survival benefit but did reveal an increase in adverse events
- 53. Cardiogenic shock • Dobutamine •1st line of agent • synthetic catecholamine with primarily -mediated effects and minimal β α adrenergic effects. • β1 effect is manifest in increased inotropy and the β2 effect leads to vasodilation with decreased afterload • can be used with norepinephrine in patients with mixed distributive and cardiogenic shock
- 54. OXYGENATION ANDVENTILATION SUPPORT •Cellular hypoxemia • For patients with distributive shock, this may be related to a primary pulmonary process. • For patients with cardiogenic or obstructive shock, the hypoxemia may be related to LV dysfunction and elevations of PCWP • For patients with all types of shock, there can be development of ARDS and subsequentV/Q mismatch and shunt • Supplemental oxygen should be initiated and titrated to maintain SpO2 of 92–95%. • May require intubation and initiation of mechanical ventilation. • Patients with shock may have high minute ventilatory needs to compensate for metabolic acidosis
- 55. • As shockprogresses, they may not be able to maintain adequate respiratory compensation, which may be a second indication to initiate mechanical ventilator support • it is important to provide ventilation with lung-protective strategies focused on low tidal volume ventilation and optimization of positive end-expiratory pressure to minimize ventilator-induced lung injury. • There should be daily sedation cessation to assess underlying neurologic function and minimize time on mechanical ventilation. • Antibiotic Administration • For patients presenting with undifferentiated shock, if the diagnosis of septic shock is being entertained, then broad-spectrum antibiotics should be administered after obtaining appropriate cultures. • inability to obtain cultures should not delay the start of treatment.
- 56. SPECIFIC CAUSES OFSHOCK REQUIRING TAILORED INTERVENTION • The initial evaluation may have identified an etiology of shock that requires urgent lifesaving intervention • distributive shock secondary to anaphylaxis • removal of the inciting allergen, administration of epinephrine, and vascular support . • Adrenal insufficiency requires replacement with intravenous stress dose steroids. • Cardiogenic shock patients with arrhythmia – Anti-arrhythmic • acute ischemic events- to revascularization and temporary mechanical supportive measures. • Surgery /endoscopy – in trauma / GI loss of blood • Tension pneumothorax – Emergency decompression • Proximal pulmonary embolism requires evaluation for thrombolytic therapy or surgical removal of the clot • Dissection of the ascending -surgical intervention.
- 57. THANKYOU HARRISON'S PRINCIPLES OFINTERNAL MEDICINE , 21ST EDITION
Editor's Notes
- #3 example of impaired oxygen utilization is cyanide poisoning, which causes uncoupling of oxidative phosphorylation
- #4 With adequate oxygen, the cell metabolizes glucose to pyruvate, which then enters the mitochondria where ATP is generated via oxidative phosphorylation. Without sufficient oxygen supply, the cell is forced into anaerobic metabolism, in which pyruvate is metabolized to lactate with much less ATP generation
- #5 In addition to direct cell death, cellular hypoxia can cause damage at the organ system level via leakage of the intracellular contents
- #6 preload refers to the myocardial fiber length before contraction (the ventricular end-diastolic volume) . Contractility refers to the ability of the ventricle to contract independent of preload and afterload
- #9 It is unique among the types of shock in that there is a compensatory increase in CO .
- #10 Anaphylaxis - there is evidence of both venous and arterial vasodilation .
- #20 Compensatory -and attempts to reestablish the adequate perfusion and oxygen delivery
- #21 In early sepsis with reduction in SVR, there is a compensatory rise in HR (and CO) early hemorrhagic volume loss, there will be a compensatory increase in SVR and HR.
- #28 isolated blood pressure measurements below these values do not define shock. Many patients may have underlying conditions such as peripheral vascular disease or autonomic dysfunction or are on medications that cause longstanding low blood pressure without any evidence of organ dysfunction . observing hemodynamic trends over short time intervals are more useful than an absolute SBP or MAP value
- #48 his measurement requires that the patient be in a volume cycle mode of ventilation, without breath-to-breath variations in intrathoracic pressure and without arrhythmias.
- #51 The clinician must understand the receptor selectivity of various agents and that for some agents the selectivity may be dose-dependent . but is associated with tachyarrhythmia, myocardial ischemia, decreased splanchnic blood flow, pulmonary hypertension, and acidosis
- #54 If the patient requires intubation and initiation of mechanical ventilation, this should be provided promptly so as to minimize the duration of tissue hypoxia
- #55 When sepsis is excluded as a cause of shock, an important aspect of antibiotic stewardship is to stop all antibiotics.