SHOCK

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Waleed    on Nov 03, 2011 Says :

Perfect presentation for shock specially the pathophysiology
Zainab    on Apr 16, 2010 Says :

Most of the slides are empty. Perhaps try actually putting down salient points.
waheed    on Jul 26, 2009 Says :

it is no in running condition
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Slide 1 : Shock DR Fiaz Fazili Dr Badria eid Surgical department King Fahad hospital Al-madinamunawarah ,ksa Shock Dr.Badria Eid Surgical department King fahad hospital Almadena,ksa
Slide 2 : Shock-Definition ...a reduction in blood flow by diminished cardiac output or maldistributed output such that potential irreversible tissue damage occurs..
Slide 3 : Flow = Perfusion Adequate Flow = Adequate Perfusion Inadequate Flow = Indequate Perfusion (Hypoperfusion) Hypoperfusion = Shock
Slide 4 : Physiology of Perfusion Dependant on 3 components of circulatory system; *Pump *Fluid *Container
Slide 5 : Causes of Inadequate Perfusion Inadequate pump Inadequate preload Poor contractility Excessive after load Inadequate heart rate Inadequate fluid volume Hypo volemia Inadequate container Excessive dilation Inadequate systematic vascular resistance
Slide 6 : What Is Blood Pressure? BP = Cardiac Output X Systemic Vascular Resistance CO = Stroke Volume X Heart Rate
Slide 7 : Changes in Afterload and Preload ? Peripheral vasoconstriction… ?
Slide 8 : Changes in Afterload and Preload ? Peripheral vasodilation… ? ?
Slide 9 : Changes in Afterload and Preload ? fluid volume… ?
Slide 10 : Changes in Afterload and Preload ? fluid volume… ?
Slide 11 : Maintenance of Fluid Volume Renin-Angiotensin-Aldosterone system. Works through kidneys to regulate balance of Na+ and water.
Slide 12 : Renin-Angiotensin-Aldosterone Plasma volume ? [Na+] &/Or
Slide 13 : Renin-Angiotensin-Aldosterone Angiotensin II…
Slide 14 : Container Vasculature is continuous, closed and pressurized system Microcirculation responds to local tissue needs Blood flow dependent on PVR
Slide 15 : Responses to Shock Catecholamine release causes increased: heart rate heart contractility venous and arteriolar tone preload cardiac output Neuroendocrine response Hypothalamic - glucocorticoid, GH, & aldostero Renal - ADH, renin, & angiotensin
Slide 16 : Responses to Shock Normal compensation includes: Progressive vasoconstriction Increased blood flow to major organs Increased cardiac output Increased respiratory rate and volume Decreased urine output
Slide 17 : Cellular Response to Shock Tissue perfusion
Slide 18 : Aerobic Metabolism METABOLISM 6 CO2 6 H2O 36 ATP HEAT (417 kcal)
Slide 19 : Anaerobic Metabolism GLUCOSE METABOLISM 2 LACTIC ACID 2 ATP HEAT (32 kcal)
Slide 20 : Anaerobic? So What? Inadequate Cellular Oxygenation
Slide 21 : Cellular Response to Shock Net results of cellular shock: systemic lactic acidosis decreased myocardial contractility decreased vascular tone decrease blood pressure, preload and cardiac output
Slide 22 : Stages of Shock *Compensated *Uncompensated *Irreversible
Slide 23 : Compensated Shock #Defense mechanisms are successful in maintaining perfusion #Presentation Tachycardia Decreased skin perfusion Altered mental status
Slide 24 : Uncompenstated Shock #Defense mechanisms begin to fail #Presentation Hypotension Prolonged Cap refill Marked increase in heart rate Rapid, thready pulse Agitation, restlessness, confusion
Slide 25 : Irreversible Shock #Complete failure of compensatory mechanisms #Death even in presence of resuscitation
Slide 26 : Shock:Signs and Symptoms Restlessness, anxiety Decreasing level of consciousness Dull eyes Rapid, shallow respirations Nausea, vomiting Thirst Diminished urine output
Slide 27 : Shock: Signs and Symptoms Hypovolemia will cause Weak, rapid pulse Pale, cool, clammy skin Cardiogenic shock may cause: Weak, rapid pulse or weak, slow pulse Pale, cool, clammy skin Neurogenic shock will cause: Weak, slow pulse Dry, flushed skin Sepsis and anaphylaxis will cause: Weak, rapid pulse Dry, flushed skin
Slide 28 : Type of shock Hypovolemic shock blood VOLUME problem Cardiogenic shock blood PUMP problem Vasogenic shock blood VESSEL problem
Slide 29 : Hypovolemic Shock #rapid fluid loss results in multiple organ failure due to inadequate perfusion. #Most often, hypovolemic shock is secondary to rapid blood loss (hemorrhagic shock).
Slide 30 : Hypovolemic Shock Loss of volume Causes Blood loss: trauma, vascular, GIT, pregnancy related Plasma loss: burns Water loss: Vomiting, diarrhea, sweating, increased urine, increased respiratory loss
Slide 31 : Hypovolemic Shock *Traumatic causes can result from penetrating and blunt trauma. *Common traumatic injuries that can result in hemorrhagic shock include the following: myocardial laceration and rupture, major vessel laceration, solid abdominal organ injury, pelvic and femoral fractures, and scalp lacerations.
Slide 32 : Hypovolemic Shock Vascular disorders that can result in significant blood loss include; *aneurysms *dissections *arteriovenous malformations.
Slide 33 : Hypovolemic Shock GI disorders that can result in hemorrhagic shock include the following: *bleeding esophageal varices. * bleeding peptic ulcers. *Mallory-Weiss tears. *aortointestinal fistulas.
Slide 34 : Hypovolemic Shock Pregnancy-related disorders include; *ruptured ectopic pregnancy. * placenta previa. *abruption of the placenta. Hypovolemic shock secondary to an ectopic pregnancy is common. Hypovolemic shock secondary to an ectopic pregnancy in a patient with a negative urine pregnancy test is rare but has been reported.
Slide 35 : Hypovolemic Shock Lab Studies: Initial laboratory studies should include analysis of the CBC, electrolyte levels (eg, Na, K, Cl, HCO3, BUN, creatinine, glucose levels), prothrombin time, activated partial thromboplastin time, ABGs, and urinalysis (in patients with trauma). Blood should be typed and cross-matched.
Slide 36 : Hypovolemic Shock Patients with marked hypotension and/or unstable conditions must first be resuscitated adequately. This treatment takes precedence over imaging studies and may include immediate interventions and immediately taking the patient to the operating room.
Slide 37 : Hypovolemic Shock The workup for the patient with trauma and signs and symptoms of hypovolemic is directed toward finding the source of blood loss.
Slide 38 : Hypovolemic Shock *The traumatic patient with hypovolemic shock requires ultrasonographic examination in the ED if an abdominal aortic aneurysm is suspected. *If GI bleeding is suspected, a nasogastric tube should be placed, and gastric lavage should be performed.
Slide 39 : Hypovolemic Shock *An upright chest radiograph should be obtained if a perforated ulcer or Boerhaave syndrome is a possibility. *Endoscopy can be performed (usually after the patient has been admitted) to further delineate the source of bleeding.
Slide 40 : Hypovolemic Shock *A pregnancy test should be performed in all female patients of childbearing age. *If the patient is pregnant and in shock, surgical consultation and the consideration of bedside pelvic ultrasonography should be immediately performed in the ED. *Hypovolemic shock secondary to an ectopic pregnancy in a patient with a negative pregnancy test, has been reported.
Slide 41 : Hypovolemic Shock *If thoracic dissection is suspected because of the mechanism and initial chest radiographic findings, the workup may include transesophageal echocardiography, aortography, or CT scanning of the chest.
Slide 42 : Hypovolemic Shock *If a traumatic abdominal injury is suspected, a FAST (Focused Abdominal Sonography for Trauma) ultrasound exam may be performed in the stable or unstable patient. Computed Tomography (CT) scanning typically is performed in the stable patient. *If long-bone fractures are suspected, radiographs should be obtained
Slide 43 : Hypovolemic Shock Mangment; Prehospital Care: The treatment of patients with hypovolemic shock often begins at an accident scene or at home. The prehospital care team should work to prevent further injury, transport the patient to the hospital as rapidly as possible, and initiate appropriate treatment in the field.
Slide 44 : Hypovolemic Shock *Prevention of further injury applies mostly to the patient with trauma. *The cervical spine must be immobilized, and the patient must be extricated, if applicable, and moved to a stretcher. * Splinting of fractures can minimize further neurovascular injury and blood loss.
Slide 45 : Hypovolemic Shock *Although in selected cases stabilization may be beneficial, rapid transport of sick patients to the hospital remains the most important aspect of prehospital care. *Definitive care of the hypovolemic patient usually requires hospital, and sometimes surgical intervention. Any delay in definitive care, eg, such as delayed transport, is potentially harmful.
Slide 46 : Hypovolemic Shock *Most prehospital interventions involve immobilizing the patient (if trauma is involved), securing an adequate airway, ensuring ventilation, and maximizing circulation. *Some procedures, such as starting intravenous (IV) lines or splinting of extremities, can be performed while a patient is being extricated.
Slide 47 : Hypovolemic Shock In recent years, there has been considerable debate regarding the use of military antishock trousers (MAST). MAST were introduced in the 1960s and, based mostly on anecdotal reports of success, their use became standard therapy in the prehospital treatment of hypovolemic shock in the late 1970s. By the 1980s, the American College of Surgeons Committee on Trauma included their use in the standard of care for all patients with trauma and signs or symptoms of shock. Since that time, studies have failed to show improved outcome with the use of MAST. The American College of Surgeons Committee on Trauma no longer recommends the use of MAST.
Slide 48 : Hypovolemic Shock Emergency Department Care; maximize oxygen delivery (2) control further blood loss (3) fluid resuscitation.
Slide 49 : Hypovolemic Shock Maximizing oxygen delivery; The patient's airway should be assessed immediately upon arrival and stabilized if necessary. The depth and rate of respirations, as well as breath sounds, should be assessed. If pathology (eg, pneumothorax, hemothorax, flail chest) that interferes with breathing is found, it should be addressed immediately. High-flow supplemental oxygen should be administered to all patients, and ventilatory support should be given, if needed.
Slide 50 : Hypovolemic Shock Maximizing oxygen delivery; Two large bore IV lines should be started.., a short large-caliber IV catheter is ideal. IV access may be obtained by means of percutaneous access in the antecubital veins, cutdown of saphenous or arm veins, or access in the central veins . If central lines are obtained, a large-bore single-lumen catheter should be used. In children younger than 6 years, intraosseous access also may be used.
Slide 51 : Hypovolemic Shock Maximizing oxygen delivery; Once IV access is obtained, initial fluid resuscitation is performed with an isotonic crystalloid, such as lactated Ringer solution or normal saline. An initial bolus of 1-2 L is given in an adult (20 mL/kg in a pediatric patient), and the patient's response is assessed.
Slide 52 : Hypovolemic Shock Maximizing oxygen delivery; *If vital signs return to normal, the patient may be monitored to ensure stability, and blood should be sent for typed and cross-matched.
Slide 53 : Hypovolemic Shock If vital signs transiently improve, crystalloid infusion should continue and type-specific blood obtained
Slide 54 : Hypovolemic Shock * If little or no improvement is seen, crystalloid infusion should continue, and type O blood should be given (type O Rh-negative blood should be given to female patients of childbearing age to prevent sensitization and future complications).
Slide 55 : Hypovolemic Shock Maximizing oxygen delivery; If a patient is moribund and markedly hypotensive), both crystalloid and type O blood should be started initially. These guidelines for crystalloid and blood infusion are not rules; therapy should be based on the condition of the patient.
Slide 56 : Hypovolemic Shock Maximizing oxygen delivery #The position of the patient can be used to improve circulation; one example is raising the hypotensive patient's legs while fluid is being given or rolling a hypotensive gravid patient with trauma onto her left side which displaces the fetus from the inferior vena cava and increases circulation.
Slide 57 : Hypovolemic Shock Controlling further blood loss; external bleeding should be controlled with direct pressure internal bleeding requires surgical intervention. Long-bone fractures should be treated with traction to decrease blood loss.
Slide 58 : Hypovolemic Shock Controlling further blood loss; In the patient whose pulse is lost in the ED or just prior to arrival, an emergency thoracotomy with cross-clamping of the aorta may be indicated to preserve blood flow to the brain. This procedure is palliative at best and requires immediate transfer to the operating room.
Slide 59 : Hypovolemic Shock Controlling further blood loss; *In the patient with GI bleeding, intravenous vasopressin and H2 blockers have been used. Vasopressin commonly is associated with adverse reactions, such as hypertension, arrhythmias, gangrene, and myocardial or splanchnic ischemia. *Somatostatin and octreotide infusions have been shown to reduce gastrointestinal bleeding from varices and peptic ulcer disease. These agents possess the advantages of vasopression without the significant side effects.
Slide 60 : Hypovolemic Shock Controlling further blood loss; *In patients with variceal bleeding, use of a Sengstaken-Blakemore tube can be considered. *These devices have a gastric balloon and an esophageal balloon. The gastric one is inflated first, and then the esophageal one is inflated if bleeding continues. *The use of this tube has been associated with severe adverse reactions, such as esophageal rupture, asphyxiation, aspiration and mucosal ulceration. For this reason, its use should be considered only as a temporary measure in extreme circumstances.
Slide 61 : Hypovolemic Shock Controlling further blood loss; all causes of acute gynecological bleeding that cause hypovolemia (eg, ectopic pregnancy, placenta previa, abruptio placenta, ruptured cyst, miscarriage) require surgical intervention.
Slide 62 : Hypovolemic Shock fluid resuscitation; crystalloids or colloids are best for resuscitation
Slide 63 : Cardiogenic shock shock is characterized by primary myocardial dysfunction resulting in the inability of the heart to maintain adequate cardiac output
Slide 64 : Cardiogenic shock Etiologies *Inflow problems *Intrinsic pump problems *Outflow problems
Slide 65 : Cardiogenic Shock ? CO
Slide 66 : Cardiogenic shock Inflow Problems; #Pericardial tamponade #Tension pneumothorax #Mitral and tricuspid valve stenosis #Idiopathic Hypertrophic Subaortic Stenosis (IHSS) with filling defect
Slide 67 : Cardiogenic shock Pump Problems; Acute Myocardial Infarction (AMI) Myocarditis Cardiomyopathy Myocardial contusion
Slide 68 : Cardiogenic shock Outflow Problems; *Pulmonary embolism *Aortic and pulmonic stenosis *Mitral insufficiency (especially in the setting of AMI secondary to papillary muscle rupture or dysfunction) *Ventricular septal defect *Air embolism
Slide 69 : Cardiogenic shock Clinical Presentation; #Abnormal heart sounds +Murmurs mitral stenosis mitral insufficiency aortic stenosis pulmonic stenosis ventricular septal defect
Slide 70 : Cardiogenic shock Clinical Presentation(cont); Other heart sounds +Pathologic S3 (ventricular gallop) +Pathologic S4 (atrial gallop)
Slide 71 : Cardiogenic shock Clinical Presentation; #ECG abnormalities *Pericardial tamponade low voltage and/or electrical alternans *Acute Myocardial Infarction (AMI) ST segment elevation, pathologic Q waves new bundle branch blocks and other conduction abnormalities (ie. nodal blocks and dysrhythmias)
Slide 72 : Cardiogenic shock Clinical Presentation(cont) #Pericardial tamponade muffled heart tones, elevated neck veins #Tension pneumothorax JVD, tracheal deviation, decreased or absent unilateral breath sounds, and chest hyperresonance on affected side
Slide 73 : Cardiogenic shock Management; 1)Treat reversible causes 2)Optimize pump function 3)Myocardial salvage 4)Consider thrombolytics, angioplasty, aortic balloon counterpulsation in specific cases
Slide 74 : Cardiogenic shock Management; Optimizing pump function *Invasive monitoring if available *Aggressive airway management *Judicious fluid management *Pressor agents *Dobutamine if tachycardic and increased SVR *Dopamine if less tachycardic and low SVR
Slide 75 : Cardiogenic shock Management; Optimizing pump function (cont.) *Morphine as needed for anxiolysis *Cautious use of diuretics in CHF *Vasodilators as needed for afterload reduction *Short acting beta blocker, esmolol, for refractory tachycardia
Slide 76 : Vasogenic Shock Etiologies #sepsis(septic shock) #anaphylaxis(anaphylactic shock) #neurologic insult(neuroginc shock)
Slide 77 : Septic Shock Definition: perfusion embarrassment secondary to dilated vascular bed in response to bacteria and their products circulating in the blood
Slide 78 : Septic Shock Septicemia is a state of microbial invasion from a portal of entry into the blood stream which causes sign of illness. Sepsis: a systemic inflammatory response to a documented infection. The manifestations of sepsis are the same as SIRS. The clinical features include 2 or more of the following conditions as a
Slide 79 : Septic Shock Systemic inflammatory response syndrome (SIRS): The systemic inflammatory response to a wide variety of severe clinical insults manifests by 2 or more of the following conditions: Temperature greater than 38°C or less than 36°C Heart rate greater than 90 beats per minute (bpm) Respiratory rate greater than 20 breaths per minute or PaCO2 less than 32 mm Hg White blood cell count greater than 12,000/mL, less than 4000/mL, or 10% immature (band) forms
Slide 80 : Septic Shock Severe sepsis: This is sepsis and SIRS associated with organ dysfunction, hypoperfusion, or hypotension. Hypoperfusion and perfusion abnormalities may include, but are not limited to, lactic acidosis, oliguria, or an acute alteration in mental status.
Slide 81 : Septic Shock Multiple organ dysfunction syndrome (MODS): This is the presence of altered organ function in a patient who is acutely ill and in whom homeostasis cannot be maintained without intervention.
Slide 82 : Septic Shock Results from body’s response to bacteria in bloodstream Vessels dilate, become “leaky”
Slide 83 : Septic Shock Pathophysiology Mediator-induced cellular injury Circulatory and metabolic
Slide 84 : Septic Shock Pathophysiology Mediator-induced cellular injury The gram-positive and gram-negative bacteria induce a variety of proinflammatory mediators, including cytokines induced in host cells (macrophages/monocytes and neutrophils) by the bacterial cell wall component. * lipopolysaccharide (gram-negative bacteria), *lipeptidoglycan (gram-positive and gram-negative bacteria) *lipoteichoic acid (gram-positive bacteri.
Slide 85 : Septic Shock Circulatory and metabolic The predominant hemodynamic feature of septic shock is arterial vasodilation vasodilation to result in hypotension and SHOCK Factors responsible for myocardial depression of sepsis are myocardial depressant substances, coronary blood flow abnormalities, pulmonary hypertension, various cytokines, nitric oxide, and beta-receptor down-regulation.
Slide 86 : Septic Shock
Slide 87 :
Slide 88 : Septic Shock Causes 1)Infection; *Lower respiratory tract infections >Streptococcus pneumoniae >Klebsiella pneumoniae >Staphylococcus aureus >Escherichia coli >Legionella species >Haemophilus species >Anaerobes >Gram-negative bacteria >Fungi
Slide 89 : Septic Shock *Urinary tract infections >E coli >Proteus species >Klebsiella species >Pseudomonas species >Enterobacter species >Serratia species
Slide 90 : Septic Shock *Soft tissue infections S aureus Staphylococcus epidermidis Streptococci Clostridia Gram-negative bacteria Anaerobes
Slide 91 : Septic Shock *GI tract infections E coli Streptococcus faecalis Bacteroides fragilis Acinetobacter species Pseudomonas species Enterobacter species Salmonella species
Slide 92 : Septic Shock Infections of the male and female reproductive systems Neisseria gonorrhoeae Gram-negative bacteria Gram-negative bacteria Streptococci Anaerobes
Slide 93 : Septic Shock 2)Foreign bodies ; S aureus, S epidermidis, 3)fungi/yeasts (Candida species) 4)Miscellaneous ; Neisseria meningitidis
Slide 94 : Septic Shock Risk factors for severe sepsis and septic shock; 1)Extremes of age (<10 y and >70 y) 2)Primary diseases Liver cirrhosis Alcoholism Diabetes mellitus Cardiopulmonary diseases Solid malignancy Hematologic malignancy
Slide 95 : Septic Shock 3)Immunosuppression Neutropenia Immunosuppressive therapy Corticosteroid therapy Intravenous drug abuse Compliment deficiencies Asplenia 4) Major surgery, trauma, burns
Slide 96 : Septic Shock 5) Invasiv procedures Catheters Intravascular devices Prosthetic devices Hemodialysis and peritoneal dialysis catheters Endotracheal tube 6) Prior antibiotic treatment 7) Prolonged hospitalization 8) - Childbirth, abortion, and 9) Other factors Malnutrition
Slide 97 : Septic Shock Lab Studies *CBC count with differential(Hg,PLT,WBC) *serum electrolytes(Mg, Ca, phos, and glucose) *renal and hepatic function; Serum creatinine BUN Bilirubin Alkaline phosphate Alanine aminotransferase (ALT) Aspartate aminotransferase (AST) Albumin *ABG
Slide 98 : Septic Shock (CONT)Lab Studies *coagulation status with (PT) and aPTT *Blood cultures *urinalysis and urine culture *secretions or tissue for Gram stain and culture from the sites of potential infection
Slide 99 : Septic Shock Imaging Studies; CXR supine and upright or lateral decubitus abdominal films Abd US CT SCAN LP if menigitis is suspected
Slide 100 : Septic Shock If a patient is thought to have meningitis or encephalitis, perform an LP urgently. In patients with an acute fulminant presentation, a rapid onset of septic shock, and a severe impairment of mental status, use this procedure to rule out bacterial meningitis.
Slide 101 : Septic Shock MANGMENT Cardiac monitoring, noninvasive blood pressure monitoring, and pulse oximetry are necessary because these patients often require intensive care admission for invasive monitoring and support. Supplemental oxygen is provided during initial stabilization and resuscitation.
Slide 102 : Septic Shock Ensure that all patients in septic shock receive adequate venous access for volume resuscitation. A central venous line also can be used to monitor central venous pressure to assess intravascular volume status. Use an indwelling urinary catheter to monitor urinary output, which is a marker for adequate renal perfusion and cardiac output.
Slide 103 : Septic Shock Patients who develop septic shock require a right heart catheterization with a pulmonary artery (Swan Ganz) catheter. Most patients with sepsis develop respiratory distress as a manifestation of severe sepsis or septic shock. The lung injury is characterized pathologically as diffuse alveolar damage and ranges from acute lung injury to ARDS. These patients need intubation and mechanical ventilation for optimum respiratory support.
Slide 104 : Septic Shock 1)Resuscitate the patient from septic shock using supportive measures to correct hypoxia, hypotension, and impaired tissue oxygenation. (2) Identify the source of infection and treat with antimicrobial therapy, surgery, or both. (3) Maintain adequate organ system function guided by cardiovascular monitoring and interrupt the pathogenesis of multiorgan system dysfunction.
Slide 105 : Neurogenic Shock Definition: hypotension is the result of the loss of sympathetic vascular tone below the level of spinal cord injury may also lose sympathetic tone to heart usually a transient (3-7 day) phenomenon
Slide 106 : Clinical Presentation Neurogenic Shock Moderate hypotension Relative bradycardia Warm, dry skin Flaccid paralysis below level of spinal cord injury
Slide 107 : Management Neurogenic Shock #Shock in the trauma patient is ALWAYS hypovolemia/hemorrhage until proven otherwise #neurogenic shock is a diagnosis of exclusion
Slide 108 : Management Neurogenic Shock *Alpha agonist to augment tone if perfusion still inadequate dopamine at alpha doses (> 10 mcg/kg per min) ephedrine (12.5-25 mg IV every 3-4 hour) *Treat bradycardia with atropine 0.5-1 mg doses to maximum 3 mg may need transcutaneous or transvenous pacing temporarily
Slide 109 : Anaphylactic Shock Results from severe allergic reaction Body responds to allergen by releasing histamine Histamine causes vessels to dilate and become “leaky”
Slide 110 : Anaphylactic Shock
Slide 111 : Anaphylactic Shock Patients with anaphylaxis will: -Hypotention Develop hives (urticaria) Itch Develop wheezing and difficulty breathing (bronchospasm) angioedema

 


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