Circulatory Shock

1. Circulatory Shock Kaukab Azim, MBBS, PhD, M.Sc

2. DEFINITION Shock refers to conditions manifested by hemodynamic alterationsi.e. Causes • Intravascular volume deficit • Myocardial pump failure • Peripheral vasodilation (hypovolemic shock) (cardiogenic shock) (septic, anaphylactic, or neurogenic shock) The underlying problem in these situations is inadequate tissue perfusion resulting from circulatory failure.

3. PATHOPHYSIOLOGY

4. Mechanisms of Failure • Shock results in failure of the circulatory system to deliver sufficient oxygen (O2) to body tissues despite normal or reduced O2 consumption. • General pathophysiologic mechanisms of different forms of shock are similar except for initiating events.

5. A 33-year-old man admitted to the hospital because of a car accident, started a blood transfusion. Few minutes later he complained of nausea and pruritus and developed dyspnea with audibly wheezing. His skin was mottled and cold, heart rate was 120 bpm and blood pressure fell to 80/ 40 mm Hg. An IV injection of epinephrine was given. Which of the following actions of the drug most likely contributed to its therapeutic efficacy in this patient? • Increased glycogenolysis • Beta-2 receptor mediated vasodilation • Stimulation of platelet aggregation • Inhibition of insulin secretion • Inhibition of mast cell degranulation • Stimulation of eicosanoid biosynthesis

6. A 33-year-old man admitted to the hospital because of a car accident, started a blood transfusion. Few minutes later he complained of nausea and pruritus and developed dyspnea with audibly wheezing. His skin was mottled and cold, heart rate was 120 bpm and blood pressure fell to 80/ 40 mm Hg. An IV injection of epinephrine was given. Which of the following actions of the drug most likely contributed to its therapeutic efficacy in this patient? • Increased glycogenolysis • Beta-2 receptor mediated vasodilation • Stimulation of platelet aggregation • Inhibition of insulin secretion • Inhibition of mast cell degranulation • Stimulation of eicosanoid biosynthesis

7. Hypovolemic shock Hypovolemic shock is characterized by acute intravascular volume deficiency due to external losses or internal redistribution of extracellular water.This type of shock can be precipitated by

8. Can Over-aggressive loop diuretic administration lead to hypovolemic shock? • Yes • No • Yes

9. Process Relative hypovolemialeading to hypovolemic shock occurs during significant vasodilation, which accompanies anaphylaxis, sepsis, and neurogenic shock. Fall in blood pressure (BP) is compensated by Increase in sympathetic outflow Activation of the renin-angiotensin system Humoralfactors that stimulate peripheral vasoconstriction.

10. Process • Compensatory vasoconstrictionredistributes blood away from the skin, skeletal muscles, kidneys, and GI tract toward vital organs (e.g., heart, brain) in an attempt to maintain oxygenation, nutrition, and organ function. • Severe metabolic lactic acidosisoften develops secondary to tissue ischemia and causes localized vasodilation, which further exacerbates the impaired cardiovascular state. Where and how is oxygen used in the body? The metabolic acids, acetoacetic acid and hydroxybutyric acid are produced from fatty acid oxidation to ketone bodies in the liver, and lactic acid is produced by glycolysis in muscle and other tissues.

11. Peripheral pooling of blood Inadequate perfusion Recap of Pathophysiology Cell Hypoxia Failure of pre-capillary sphincters Energy Deficit Lactic acid accumulation and  pH Vasoconstriction Metabolic acidosis Anaerobic metabolism Cell membrane dysfunction and failure of Na+ pump Influx of Na+& H2O Intracellular lysosomes release digestive enzymes Efflux of K+ Toxic substances enter circulation Capillary endothelium damage Destruction, dysfunction, and cell death

12. CLINICAL PRESENTATION

13. A 45-year-old man is involved in a high-speed automobile collision. He arrives at the ER in coma, with bilateral fixed dilated pupils. He has multiple other injuries (extremities, etc). His blood pressure is 70 over 50, with a feeble pulse at a rate of 130. What is the reason for the low BP and high pulse rate? Can traumatic brain injury cause low BP? What is Glasgow Coma Scale (GCS) Fixed and dilated pupils in comatose patients are well known to be related to a poor prognosis, especially when present bilaterally. If not caused by local trauma or drug action, this symptom indicates injury or compression of the third cranial nerve and the upper brain stem, mainly caused by an extending intracranial mass lesion or by diffuse brain injury. Point of the question: It is not from neurological injury. (Not enough room in the head for enough blood loss to cause shock). Look for answer of significant blood loss to the outside (could be scalp laceration), or inside (abdomen, pelvic fractures).

14. Signs & Symptoms • Shock presents with a diversity of signs and symptoms. Patients with hypovolemic shock may present with thirst, anxiousness, weakness, lightheadedness, and dizziness. Patients may also report scanty urine output and dark-yellow-colored urine. • Hypotension, tachycardia, tachypnea, confusion, and oliguria are common symptoms. • Myocardial and cerebral ischemia, pulmonary edema (cardiogenic shock), and multisystem organ failure often follow.

15. Signs & Symptoms: • Significant hypotension (systolic blood pressure [SBP] less than 90 mm Hg) with • Reflex sinus tachycardia (greater than 120 beats/min) and • Increased respiratory rate(more than 30 breaths/min) are often observed in hypovolemic patients. Clinically, the patient presents with • Extremities cool to the touch and • A “thready” pulse. • The patient may be cyanotic due to hypoxemia. • Sweating results in a moist, clammy feel. • Digits will have severely slowed capillary refill.

16. Cyanosis

17. Signs & Symptoms • Mental status changesassociated with volume depletion may range from subtle fluctuations in mood to agitation to unconsciousness. • Respiratory alkalosissecondary to hyperventilation is usually observed secondary to CNS stimulation of ventilatory centers as a result of trauma, sepsis, or shock. • Lung auscultation may reveal crackles (pulmonary edema in cardiogenic shock) or absence of breath sounds (pneumothorax, hemothorax in chest trauma). Continued insult to the lungs may result in adult respiratory distress syndrome.

18. Signs & Symptoms • Kidneysare exquisitely sensitive to changes in perfusion pressures. Moderate alterations can lead to significant changes in glomerular filtration rate. • Oliguria, progressing to anuria, occurs because of vasoconstrictionof afferentarterioles. • Redistribution of blood flow away from the GI tract may cause stress gastritis, gut ischemia, and, in some cases, infarction, resulting in GI bleeding.

19. Signs & Symptoms Blood Clotting Video Tissue Injury Surface Contact Collagen, platelets prekallikrein Progressive liverdamage (shock liver) manifests as elevated serum hepatic transaminases and unconjugated bilirubin. Impaired synthesis ofclotting factorsmay increase PT, INR, and aPTT. Partial Thromboplastin time (30-50 secs) Prothrombin Time (12-13 secs) HMWK: High Molecular Weight Kininogen

20. International Normalized Ratio(Video)

21. DIAGNOSIS AND MONITORING

22. DIAGNOSIS AND MONITORING Information from • Noninvasive and invasive monitoring • Evaluation of past medical history • Clinical presentation • Laboratory findings are key components in establishing the diagnosis as well as in assessing general mechanisms responsible for shock. Regardless of the etiology, consistent findings include • Hypotension(SBP less than 90 mm Hg) • Depressed cardiac index(CI less than 2.2 L/min/m2) • Tachycardia(heart rate greater than 100 beats/min), and • Low urine output (less than 20 mL/hour).

23. Assessments Noninvasive assessment of BP using the sphygmomanometer and stethoscope may be inaccurate in the shock state. A pulmonary artery catheter can be used to determine • Central venous pressure (CVP) • Pulmonary artery pressure • Cardiac output and • Pulmonary artery occlusive pressure (PAOP) • An approximate measure of the left ventricular end-diastolic volume and • A major determinant of left ventricular preload.

26. Swan Ganz Physiology (Video)

27. SvO2 = Mixed venous oxygen saturation CCO = Continuous cardiac output EDVI = End diastolic volume index RVEF = Right ventricular ejection fraction BT = Body temp. SVRI = Systemic vascular resistance index

28. An 84 year old female is admitted with an episode of loss of consciousness. Her blood pressure is 76/44 on cuff measurement. Her heart rate is 40. No collateral history is available. Physical exam shows slight dehydration. Which of the following is the correct diagnosis in this case? • Septic shock • Hypovolemic shock • Cardiogenic shock • Neurogenic shock

29. An 84 year old female is admitted with an episode of loss of consciousness. Her blood pressure is 76/44 on cuff measurement. Her heart rate is 40. No collateral history is available. Physical exam shows slight dehydration. Which of the following is the correct diagnosis in this case? • Septic shock • Hypovolemic shock • Cardiogenic shock • Neurogenic shock

30. Assessments • CO(2.5 to 3 L/min) and mixed venous oxygen saturation (60% to 80% normal) may be very low in a patient with extensive myocardial damage. • Respiratory alkalosis is associated with low partial pressure of PaCO2(25 to 35 mm Hg) and alkaline pH, but normal bicarbonate. The first two values are measured by arterial blood gas, which also yields partial pressure of carbon dioxide and arterial oxygen saturation. Circulating arterial oxygen saturation can also be measured by an oximeter, which is a noninvasive method that is fairly accurate and useful at the patient’s bedside.

31. Oximeter & ABG kit

32. Oximeter Video (Time. 3:20 – 5:10 mins)

33. Assessments • Renal function can be grossly assessed by hourlymeasurements of urine output • Estimation of creatinine clearance based on isolated serum creatininevalues in critically ill patients may yield erroneous results. • Decreased renal perfusion and aldosterone release result in sodium retentionand, thus, low urinary sodium (<30 mEq/L).

34. Measuring Urine Output

35. Oxygen Consumption vs Oxygen Delivery • In normal individuals, oxygen consumption (VO2) is dependent on oxygen delivery (DO2) up to a certain critical level (VO2flow dependency). • At this point, tissue O2requirements have apparently been satisfied and further increases in DO2will not alter VO2(flow independency). • However, studies in critically ill patients show a continuous, pathologic dependence relationship of VO2on DO2. These indexed parameters are calculated as: • DO2 = CI x (CaO2) • VO2 = CI x (CaO2 – CVO2) where CI = Cardiac index, CaO2= arterial oxygen content, and CVO2= mixed venous oxygen content. Currently available data do not support the concept that patient outcome or survival is altered by treatment measures directed to achieve supranormallevels of DO2and VO2

36. Cardiac Index (CI)

37. DESIRED OUTCOME Initial Goal Ultimate Goal The ultimate goals are to Prevent further progression of the disease Prevent organ damage If possible, to reverse organ dysfunction that has already occurred. The initial goal is to • Support O2 delivery through the circulatory system by assuring • Effective intravascular plasma volume • Optimal O2-carrying capacity • Adequate BP

38. TREATMENT

39. GENERAL PRINCIPLES • Supplemental O2 should be initiated at the earliest signs of shock, beginning with • 4 to 6 L/min via nasal cannula or • 6 to 10 L/min by face mask. • Adequate fluid resuscitation to maintain circulating blood volume is essential in managing all forms of shock. • If fluid challenge does not achieve desired end points, pharmacologic support is necessary with inotropic and vasoactive drugs.

40. Oxygen Therapy Video (Time: 20.50 – End)

41. A 74 year old female was admitted to intensive care on Thursday evening, following a laporotomy for bowel obstruction. There was a small amount of fecal soiling intra operatively, but the patient remained reasonably stable. The patient has a 40 pack year history of smoking, type II diabetes, two previous myocardial infarctions, a permanent pacemaker, and had a right carotid endarterectomy four years ago. During the night following the operation, she became hypotensive, blood pressure 80/56, heart rate 70. The resident on call commenced treatment with dobutamine, titrated against blood pressure response to a mean arterial pressure of 70. 
When you come into work on Sunday morning, the patient is still in the intensive care, extubated, apparently well, and still on dobutamine at 5 mic/kg/min, blood pressure 110/70, heart rate 70. You need the bed for the day’s admissions, but the patient cannot go out to the floor on inotropes, which the weekend staff were unable to wean. Why is there no compensatory tachycardia?

42. A 74 year old female was admitted to intensive care on Thursday evening, following a laporotomy for bowel obstruction. There was a small amount of fecal soiling intra operatively, but the patient remained reasonably stable. The patient has a 40 pack year history of smoking, type II diabetes, two previous myocardial infarctions, a permanent pacemaker, and had a right carotid endarterectomy four years ago. During the night following the operation, she became hypotensive, blood pressure 80/56, heart rate 70. The resident on call commenced treatment with dobutamine, titrated against blood pressure response to a mean arterial pressure of 70. 
When you come into work on Sunday morning, the patient is still in the intensive care, extubated, apparently well, and still on dobutamine at 5 mic/kg/min, blood pressure 110/70, heart rate 70. You need the bed for the day’s admissions, but the patient cannot go out to the floor on inotropes, which the weekend staff were unable to wean. Why is there no compensatory tachycardia?

43. A 74 year old female was admitted to intensive care on Thursday evening, following a laporotomy for bowel obstruction. There was a small amount of fecal soiling intra operatively, but the patient remained reasonably stable. The patient has a 40 pack year history of smoking, type II diabetes, two previous myocardial infarctions, a permanent pacemaker, and had a right carotid endarterectomy four years ago. During the night following the operation, she became hypotensive, blood pressure 80/56, heart rate 70. The resident on call commenced treatment with dobutamine, titrated against blood pressure response to a mean arterial pressure of 70. 
When you come into work on Sunday morning, the patient is still in the intensive care, extubated, apparently well, and still on dobutamine at 5 mic/kg/min, blood pressure 110/70, heart rate 70. You need the bed for the day’s admissions, but the patient cannot go out to the floor on inotropes, which the weekend staff were unable to wean. Why is there no compensatory tachycardia? Because her heart rate is controlled by pacemaker

44. A 74 year old female was admitted to intensive care on Thursday evening, following a laporotomy for bowel obstruction. There was a small amount of fecal soiling intra operatively, but the patient remained reasonably stable. The patient has a 40 pack year history of smoking, type II diabetes, two previous myocardial infarctions, a permanent pacemaker, and had a right carotid endarterectomy four years ago. During the night following the operation, she became hypotensive, blood pressure 80/56, heart rate 70. The resident on call commenced treatment with dobutamine, titrated against blood pressure response to a mean arterial pressure of 70. 
When you come into work on Sunday morning, the patient is still in the intensive care, extubated, apparently well, and still on dobutamine at 5 mic/kg/min, blood pressure 110/70, heart rate 70. You need the bed for the day’s admissions, but the patient cannot go out to the floor on inotropes, which the weekend staff were unable to wean. Why is her blood pressure low? • Low cardiac output • Vasodilation

45. A 74 year old female was admitted to intensive care on Thursday evening, following a laporotomy for bowel obstruction. There was a small amount of fecal soiling intra operatively, but the patient remained reasonably stable. The patient has a 40 pack year history of smoking, type II diabetes, two previous myocardial infarctions, a permanent pacemaker, and had a right carotid endarterectomy four years ago. During the night following the operation, she became hypotensive, blood pressure 80/56, heart rate 70. The resident on call commenced treatment with dobutamine, titrated against blood pressure response to a mean arterial pressure of 70. 
When you come into work on Sunday morning, the patient is still in the intensive care, extubated, apparently well, and still on dobutamine at 5 mic/kg/min, blood pressure 110/70, heart rate 70. You need the bed for the day’s admissions, but the patient cannot go out to the floor on inotropes, which the weekend staff were unable to wean. Why is her blood pressure low? • Low cardiac output • Vasodilation (SIRS)

46. Fluid Resuscitation For Hypovolemic Shock Initial fluid resuscitation consists of isotonic Choice of solution is based on O2-carrying capacity (e.g., hemoglobin, hematocrit) Cause of hypovolemic shock Accompanying disease states Degree of fluid loss, and Required speed of fluid delivery.

47. Fluid Resuscitation For Hypovolemic Shock • Most clinicians agree that crystalloids should be the initial therapy of circulatory insufficiency. Crystalloids are preferred over colloids as initial therapy for burn patients(hypovolemic)because they are less likely to cause interstitial fluid accumulation. • If volume resuscitation is suboptimal following several liters of crystalloid, colloids should be considered. • Some patients may require blood products to assure maintenance of O2-carrying capacity, as well as clotting factors and platelets for blood hemostasis.

48. Crystalloids • Crystalloids consist of electrolytes (e.g., Na+, Cl–, K+) in water solutions, with or without dextrose. • Lactated Ringer’s solution may be preferred because it is unlikely to cause the hyperchloremic metabolic acidosis seen with infusion of large amounts of normal saline. • Crystalloids are administered at a rate of 500 to 2,000 mL/hour, depending on the severity of the deficit, degree of ongoing fluid loss, and toleranceto infusion volume. Usually 2 to 4 L of crystalloid normalizes intravascular volume.

49. Crystalloids Advantages Disadvantages Large volume necessary to replace or augment intravascular volume. Approximately 4 L of NS must be infused to replace 1 L of blood loss. Dilution of colloid oncotic pressure leading to pulmonaryedema is more likely to follow crystalloid than colloid resuscitation. • Rapidity and ease of administration • Compatibility with most drugs • Absence of serum sickness • Low cost.

50. Colloids • Colloids are larger molecular weight solutions that have been recommended for use in conjunction with or as replacements for crystalloid solutions. • Examples are: Albumin; hetastarch and dextran • The theoretical advantage of colloids is their prolonged intravascular retention time compared to crystalloid solutions.