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  1. 1. .
  2. 2. ‫‪shock‬‬‫د / جيهان عبد الحكيم‬ ‫مدرس التمريضيونس‬‫الباطني والجراحي والحالت‬ ‫الحرجة‬
  3. 3. Introduction Shock is a condition that leads to inadequate tissue perfusion that results in impaired cellular metabolism. To maintain an adequate blood flow to the tissues, a balance exists between the blood volume, myocardial contractility and the peripheral resistance. Disturbance in any of these three
  4. 4. Classification of shock• Hypovolaemic shock is due to diminished blood volume.• Cardiogenic shock is due to inefficient myocardial function.• Neurogenic shock is due to peripheral vasodilatation, reduced peripheral resistance, and peripheral pooling of blood.
  5. 5. 4.Anaphylactic shock is due to antigen antibody reaction that leads to peripheral pooling of blood.5. Septic shock: chemical mediators are released. These mediators affect the microcirculation resulting in deficient perfusion of the tissues.
  6. 6. Hypovolaemic Shock This type is due to diminished blood volume. It is the most common types of shock. Etiologymay occur secondary to loss of: Blood as in internal or external hemorrhage. Plasma as in burns, acute pancreatitis and peritonitis. Sodium-containing fluids as in severe vomiting, diarrhea, intestinal obstruction.
  7. 7. Pathophysiology of hypovolemic shock: Blood and/or fluids loss in the body, causing a decreased amount of the blood vessels. Venous return is decreased because of the lack of fluid in the vascular space, causing decreased ventricular filling. The ventricles do not have enough blood to pump out, so the stroke volume is decreased.
  8. 8.  The heart rate will increase to compensate for the diminished stroke volume and resulting poor cardiac output and blood pressure. If the fluid or blood loss continues, the heart rate will not be able to compensate for the decreased stroke volume. The end result of hypovolemic shock is inadequate tissue perfusion.
  9. 9. Clinical picture Weakness and fainting especially when standing. The patient feels cold and thirsty. The patient look tired . Rapid, weak, thready pulse, tachypnea and air hunger. Hypothermia. Skin become pale, cold (vasodilation)
  10. 10. Treatment of hypovoiaemic shock:1) Fluid rsuscitation.  Venous access. At least two large-gauge catheters are inserted into appropriate veins.  At the same time, blood is drawn for typing and cross matching.  Lactated Ringers solution is begun immediately.
  11. 11.  The lactated Ringers solution is run at a rapid rate so that in a period of 45 minutes between 1000 and 2000 ml of lactated Ringers solution are given intravenously. Blood should be given immediately after typed and cross-matched. Colloid solutions: In the absence of whole blood, many substances have been given as human plasma, albumin solution, dextran.
  12. 12.  Hypovoiaemic shock from other causes other than bleeding, e.g., plasma loss in major bums, or crystalloid loss in intestinal obstruction does not need blood, and infusion is by plasma or crystalloids respectively. A modified Trendelenburg position is recommended in hypovolemic shock. Elevating the legs promotes the return of venous blood.
  13. 13. Dopamine and dobutamineused to improve myocardialcontractility and increases renalblood flow and urine output aswell.
  14. 14. 2) Pulmonary support: Oxygen mask for all shocked patients. Oxygen at high concentration at first through a face mask. Later adjustment of rate and concentration depends on arterial gas measurements. Endotracheal intubation and mechanical ventilation may be used.
  15. 15. 3 M o ring:) nito A fre u mnito q nt o ring o patie w hypo o m f nt ith v lae ic sho to che the ade u o v lu e re mnt. ck ck q acy f o m place e M o ring clinical paramte as the pu , blod nito e rs lse o pre re ssu . A F o y cathe r is intro ce to che u le te du d ck rine o tpu u t e e ho r, o u o tpu is 0 -1 m kg/ ho r. v ry u ptimm u t .5 l/ u
  16. 16.  Measuring central venous pressure (CVP). The normal pressure is 5-10 cm of water Assuming that cardiac function is normal, a high centeral venous pressure indicates over transfusion of blood , while a low pressure indicates hypovolaemia. Repeated hematocrit and haemoglobin assessment.
  17. 17. 4) Monitoring blood gases:  PaO2 is normally between 80-100mmhg.  PaCO2 is normally between 35-45 mm Hg. 5)Positioning:  Elevating both legs with maintaining the trunk and the remainder of the patient in the supine position is the preferred position in patients with hypovolaemic shock.
  18. 18. 6) Pain relief: If analgesics are needed, the intravenous route is used because of the poor absorption from the subcutaneous tissues or the muscles which are hypoperfused.
  19. 19. Cardiogenic Shocko In cardiogenic shock, the left ventricle has been injured leading to impaired pumping.o There is inadequate blood flow to vital organs due to inadequate cardiac output, despite a normal blood volume.
  20. 20. Etiology of cardiogenic shock: Acute myocardial infarction (commonest cause). Severe arrhythmias. Massive pulmonary embolism. Cardiac tamponade due to penetrating wounds of the chest. Myocarditis. High spinal anaesthesia, can cause paralysis of the sympathetic supply of the heart.
  21. 21. Pathophysiology of cardiogenic shock: Because the pumping is ineffective, less blood is pushed out with each heartbeat, leading to a decreased stroke volume. Theheart rate increases to compensate for a low cardiac output and blood pressure.
  22. 22.  The tissues begin to be inadequately perfused. The impaired pumping also leads to less blood being pushed from the ventricle during systole. The left ventricle gradually fills with more and more blood, causing an elevated pressure within the LV and left atrium. This pressure "backs up" into the pulmonary vasculature, causing an increased pulmonary capillary pressure
  23. 23. Clinical picture: The systolic and diastolic pressures fail, leading to compensatory peripheral vasoconstriction. A cold sweaty skin. Inadequate tissue perfusion. Cardiogenic shock is characterized by congested neck veins and a high CVP.
  24. 24. Treatment:2. Oxygen should be administered,3. Treatment of the cause:  Myocardial infarction is treated by early thrombolytic agent and potent analgesics.  Relief of cardiac tamponade by emergency insertion of a needle to drain blood in the pericardium.
  25. 25. Neurogenic Shock In neurogenic shock there is paralysis of the vasomotor fibers leading to peripheral pooling of blood and inadequate venous return..
  26. 26. Etiology:2. Vasovagal attack due to hearing bad news or watching an unpleasant event.3. In severe painful stimuli.4. Spinal cord injury5. Anxiety6. Spinal anaesthesia or deep general anaesthesia
  27. 27. Pathophysiology: Neurogenic shock is caused by the loss of sympathetic control (tone) of resistance vessels, resulting in the massive dilatation of arterioles and venules. There is an insult to the nervous system so that impulses from the sympathetic nervous system cannot maintain normal vascular tone. This causes a small degree of arterial blood pooling, which decreases the amount of blood returning to the heart.
  28. 28.  On the arterial side, there is decreased peripheral vascular resistance, which actually helps the heart to pump with less energy. Decreased peripheral pressure, there is not the driving force to get blood, oxygen, and nutrients to the cells.
  29. 29. • The lack of SNS stimulation causes a massive venous and arterial vasodilation.• On the venous side, blood pools in the distensible veins and does not return to the larger veins. Because of this pooling, there is a diminished amount of blood that returns to the heart. Stroke volume, cardiac output, and blood pressure all fall.
  30. 30. Clinical picture: In neurogenic shock there is hypotension, A normal pulse rate or bradycardia Warm dry skin.Treatment: – Positioning the patient by keeping him flat and elevate the leg to increase the venous. – I.V crystalloid solution as ringers lactate – Vassopressors may be given.
  31. 31. Anaphylactic Shock• This type of shock may follow administration of antibiotics especially penicillin, anaesthetics. The antigen unites with the antibodies leading to the release of large amounts of histamine. The patient develops bronchospasm, laryngeal edema and respiratory distress. Massive vasodilatation occurs and there is hypotension.
  32. 32. Etiology:2. Shock due to the severe allergic antigen antibody reaction to substances such as drugs, contrast media, blood products, or insect.3. Animal venom causes anaphylactic shock.4. Food products such as seafood, also causes anaphylactic shock.
  33. 33. Pathophysiology: The individual is exposed to the substance and develops antibodies against it. On subsequent exposure to the substance (the antigen), these antibodies will bind to the antigen, forming an antigen-antibody complex. This complex causes the release of chemicals that cause vasodilation.
  34. 34.  Both veins and arteries vasodilate, leading to decreased blood returning to the heart. The capillaries become permeable to nearly everything, allowing fluids, proteins, and sometimes blood to pass through into the interstitial space. This causes massive interstitial edema.
  35. 35. Treatment:2. Intravenous crystalloid infusion.3. Antihistaminic.4. Endotracheal intubation may be needed if laryngeal edema and stridor are developing.
  36. 36. Septic ShockThis is the most lethal type of shock and is recognized as one of the major killers in surgical practice. Despite the availability of more powerful antibiotics, the incidences of septicemia and septic shock are rising.
  37. 37.  Sepsis is the systemic response to infection. Many types of organisms can cause sepsis, including gram-negative bacteria, gram-positive bacteria, and fungi. The infections can occur anywhere in the body; urinary tract infections are the most common cause of sepsis.
  38. 38. Etiology: Developing reservoirs of resistant and virulent organisms. Concentration of infected patients in critical care units. More extensive operations in elderly and poor-risk patients. Patients who are immunosuppressed by organ transplantation, and by chemotherapy.
  39. 39. Common sources of bacteria: Peritonitiscaused by perforated viscus, gangrenous bowel, or leaking anastomosis. Genitourinary infections. Infected central venous catheter that may be used for monitoring or for nutrition.
  40. 40. Predisposing factors: All conditions which suppress the immune mechanism predispose to septic shock. These include: Old-age, Diabetes mellitus, Corticosteroids, Chemotherapy, malignancy, HIV / AIDS.
  41. 41. Pathophysiology:• The immune and inflammatory response begins to try to combat the organism that is causing an infection.• The body releases multiple chemicals into the blood stream, including cytokines, vasodilators.• In septic shock, this response is not adequate to eliminate the infection and actually causes increased damage.• The organism itself also releases substances called endotoxins or exotoxins, which further harm the organs and tissues.
  42. 42. • The combination of these chemicals and toxins cause: (1) peripheral vasodilation – interstitial edema and decreased blood return to the heart, and (2) decreased ability of the cells and tissues to take up oxygen and nutrients.• The heart tries harder and harder to get oxygen and nutrients to the cells by increasing the heart rate and contractility initially, sometimes driving the cardiac output twice to three times its normal amount.• However, the immune response and compensatory mechanisms may not enough to combat the infection and resulting cellular destruction. The patient may develop multiorgan dysfunction.
  43. 43. Clinical features: Restlessness and confusion. Fever above 38°C and chills. Mild reduction in blood pressure. Tachypnoea. Tachycardia. Patient is flushed with warm dry extremities. Oliguria. The cardiac output is elevated at first then it will decrease if this shock not treated immediately.
  44. 44. Treatment:1) Support of different systems:(a) Cardiovascular support: The initial priority in managing septic shock is to keep the patient alive. Fluid replacement. Prompt correction of fluid deficit is essential. Most of these deficits are replaced with a balanced salt solution such as Ringers Lactate. Any deficiency in red blood cell as evidenced by low hematocrit can be corrected by transfusion of packed red blood cells.
  45. 45. • Huge quantities of fluids are often needed to maintain an effective circulating volume. The amount often exceeds 10L within a few hours.• Give medications as vasopressors.• If the patient remains hypotensive despite adequate fluid replacement, as shown by a normal CVP dopamine (or a combination of dopamine and dobutarhine) drip is given to raise the blood pressure.
  46. 46. (b) Respiratory support: Oxygen administration is essential for all types of shock. Usually 100% oxygen is administered as a start, and is later adjusted according to the response. If the arterial oxygen is mildly reduced oxygen by mask will be sufficient. Reduction of its level below 60 mrpHg calls for endotracheal intubation and mechanical ventilation.
  47. 47. (c) Renal support:• Adequate volume replacement and dopamine administration improve renal blood flow.• Haemodialysis is required in case of acute renal failure, until the kidneys recover.
  48. 48. • 2) Fighting infection:• Eradication of sepsis, e.g., drainage of a huge abscess or peritonitis, or resection of gangrenous bowel.• Antibiotics is started immediately without waiting for the results of culture and sensitivity.