1. SHOCK
Sevgi Bilgen
2014

2. Students should learn;
The definition of shock
Types of shock and differential diagnosis
Shock treatment

3. Introduction
In order to treat shock appropriately, it must first be recognized, then identify the cause
In order to recognize it, it is important to understand some of the physiology of the disease process

4. The definition of shock
Shock is a physiologic state characterized by systemic reduction in tissue perfusion, resulting in decreased tissue oxygen delivery
Hypotension is not a requirement
Shock can occur with a normal blood pressure and hypotension can occur without shock
Poor tissue perfusion
Results in multiple organ failure and death

5. Basic Physiology Tissue perfusion is dependent on SVR and CO
Imbalance between oxygen delivery and oxygen consumption which leads to cell death, end organ damage, multi-system organ failure, and death.

6. Basic Physiology Oxygen Delivery = CO x arterial content of O2
Cardiac Output = HR x Stroke Volume
Stroke Volume is a function
Preload
Afterload
Myocardial Contractility

7. Basic Physiology

8. Understanding Shock
Inadequate systemic oxygen delivery activates autonomic responses to maintain systemic oxygen delivery
Sympathetic nervous system
NE, epinephrine, dopamine, and cortisol release
Causes vasoconstriction, increase in HR, and increase of cardiac contractility (cardiac output)
Renin-angiotensin axis
Water and sodium conservation and vasoconstriction
Increase in blood volume and blood pressure

9. Understanding Shock
Cellular responses to decreased systemic oxygen delivery
ATP depletion → ion pump dysfunction
Cellular edema
Hydrolysis of cellular membranes and cellular death
Goal is to maintain cerebral and cardiac perfusion
Vasoconstriction of splanchnic, musculoskeletal, and renal blood flow
Leads to systemic metabolic lactic acidosis that overcomes the body’s compensatory mechanisms

10. Global Tissue Hypoxia Endothelial inflammation and disruption
Inability of O2 delivery to meet demand
Result:
Lactic acidosis
Cardiovascular insufficiency
Increased metabolic demands

11. Multi organ Dysfunction Syndrome (MODS)
Progression of physiologic effects as shock ensues
Cardiac depression
Respiratory distress
Renal failure
DIC
Result is end organ failure

12. Initial Patient Assessment
Recognition of Shock
Clinical signs and symptoms depends on the severity of the shock
Early manifestations include tachycardia and cutaneous vasoconstriction

13. Clinical Pathophysiology of Shock
General / Vital signs
Cardiovascular- tachycardia
Skin- vasoconstriction vs. vasodilation
Respiratory- increased RR
Urinary- decrease urine output
Neurologic- confusion, agitation
Extremities- cold vs. warm

14. Clinical Endpoints of Shock
DECREASED BLOOD FLOW TO BRAIN AND HEART
Restless, agitated, confused, lethargy
Hypotension
Tachycardia
Tachypnea
The clinical manifestations of hypovolemic shock are a direct result of decreased end organ perfusion to the heart and brain. In the long run, all types of shock will result in death from myocardial dysfunction which manifests as bradycardia, and arrythmias, and then death.
END-STAGE SHOCK
Bradycardia
Arrhythmias
Death

15. Types of shock and differential diagnosis
1.Hypovolemic shock
2.Cardiogenic shock
3.Obstructive shock
4.Distributive shock

16. Common Causes 1.Hypovolemic shock
Due to decreased circulating blood volume in relation to the total vascular capacity and characterized by a reduction of diastolic filling pressures

17. 1. Hypovolemic shock Loss of blood (hemorrhagic shock) Loss of plasma
Loos of fluid and electrolytes

18. Loss of blood (hemorrhagic shock)
External hemorrhage
Trauma
Gastrointestinal tract bleeding
Internal hemorrhage
Hematoma
Hemothorax or hemoperitoneum

19. Loss of plasma
Burns
Exfoliative dermatitis

20. Loos of fluid and electrolytes
External
Vomiting
Diarrhea
Excessive sweating
Hyperosmolar states (diabetic ketoacidosis, hyperosmolar nonketotic coma)
Internal (third-spacing)
Pancreatitis
Ascites
Bowel obstruction

21. 2. Cardiogenic shock
Due to cardiac pump failure related to loss of myocardial contractility/functional myocardium or structural/mechanical failure of the cardiac anatomy and characterized by elevations of diastolic filling pressures and volumes

22. 2. Cardiogenic shock Dysrhythmia Tachyarrhythmia Bradyarrhythmia
Pump failure (secondary to myocardial infarction or other cardiomyopathy)
Acute valvular dysfunction (especially regurgitant lesions)
Rupture of ventricular septum or free ventricular wall

23. 3. Obstructive shock
Due to obstruction to flow in the cardiovascular circuit and characterized by either impairment of diastolic filling or excessive afterload

24. 3. Obstructive shock Tension pneumothorax
Pericardial disease (tamponade, construction)
Disease of pulmonary vasculature (massive pulmonary emboli, pulmonary hypertension)
Cardiac tumor (atrial myxoma)
Left atrial mural thrombus
Obstructive valvular disease (aortic or mitral stenosis)

25. 4. Distributive shock
Caused by loss of vasomotor control resulting in arteriolar/venular dilatation and characterized (after fluid resuscitation) by increased cardiac output and decreased SVR

26. 4. Distributive shock Septic shock Anaphylactic shock Neurogenic shock
Vasodilator drugs
Acute adrenal insufficiency

27. Clinical classification of shock
Mild (<20% of blood volume lost)
Moderate (20-40% of blood volume lost)
Severe (>40% of blood volume lost)

28. Mild (<20% of blood volume lost)
Pathophysiology
Decreased peripheral perfusion only of organs able to withstand prolonged ischemia (skin, fat, muscle, and bone).
Arterial pH normal
Clinical Manifestations
Patient complains of feeling cold.
Postural hypotension and tachycardia.
Cool, pale, moist skin; collapsed neck veins; concentrated urine.

29. Moderate (20-40% of blood volume lost)
Pathophysiology
Decreased central perfusion of organs able to tolerate only brief ischemia (liver, gut, kidneys).
Metabolic acidosis present
Clinical Manifestations
Thirst
Supine hypotension and tachycardia (variable)
Oliguria and anuria.

30. Severe (>40% of blood volume lost)
Pathophysiology
Decreased perfusion of heart and brain.
Severe metabolic acidosis.
Respiratory acidosis possibly present.
Clinical Manifestations
Agitation, confusion or obtundation.
Supine hypotension and tachycardia invariably present.
Rapid, deep respiration.

31. Evaluation Airway: includes brief evaluation of mental status
Breathing: If patient is conversing with you, A & B are fine.
Circulation: Vitals (HR, BP). Includes placement of adequate IV access,
Disability: identification of gross neurologic injury
Exposure: ensures complete exam

32. Evaluation Laboratory Hgb, WBC, platelets PT/PTT
Electrolytes, arterial blood gases
BUN, Cr
Ca, Mg
Serum lactate, mixed venous oxygen saturation (SVO2)
ECG

33. Evaluation Chest x-ray Pelvic x-ray Abd/pelvis CT Chest CT
Invazive monitoring
Arterial pressure catheter
CVP monitoring
Pulmonary artery catheter
Mixed or central venous oxygen saturation (SvO2/ScvO2)
Oxygen delivery(DO2) and oxygen consumption(VO2)
As indicated
Chest x-ray
Pelvic x-ray
Abd/pelvis CT
Chest CT
GI endoscopy
Bronchoscopy
Vascular radiology

34. Treatment Identify & reverse the cause Restore tissue perfusion
Restore organ function

35. Treatment of Shock General Management
ABCDE
Airway
control work of Breathing
optimize Circulation
assure adequate oxygen Delivery
achieve End points of resuscitation

36. Airway
Determine need for intubation but remember: intubation can worsen hypotension
Sedatives can lower blood pressure
Positive pressure ventilation decreases preload
May need volume resuscitation prior to intubation to avoid hemodynamic collapse

37. Control Work of Breathing
Respiratory muscles consume a significant amount of oxygen
Resting ventilatory muscles will permit diversion of cardiac output to other hypo perfused organs
Tachypnea can contribute to lactic acidosis
Mechanical ventilation and sedation decrease WOB and improves survival

38. Optimizing Circulation
Unless there are signs of intravascular volume overload initial resuscitation with IV fluids is generally indicated.
Isotonic crystalloids
Titrated to:
CVP 8-12 mm Hg
Urine output 0.5 ml/kg/hr. (30 ml/hr.)
Improving heart rate
May require 4-6 L of fluids
No outcome benefit from colloids
Vasopressor medications should be selected based on the cause of shock

39. Maintaining Oxygen Delivery
Decrease oxygen demands
Provide analgesia and anxiolytics to relax muscles and avoid shivering
Maintain arterial oxygen saturation/content
Give supplemental oxygen
Maintain Hemoglobin > 10 g/dL
Serial lactate levels or central venous oxygen saturations to assess tissue oxygen extraction
SmvO2 – mixed venous oxygen saturation from a PAC
ScvO2 – central venous oxygen saturation from central line

40. End Points of Resuscitation
Goal of resuscitation is to maximize survival and minimize morbidity
Use objective hemodynamic and physiologic values to guide therapy
Goal directed approach
Urine output > 0.5 mL/kg/hr.
CVP 8-12 mmHg
MAP 65 to 90 mmHg
Central venous oxygen concentration > 70%

41. Persistent Hypotension
Inadequate volume resuscitation
Pneumothorax
Cardiac tamponade
Hidden bleeding
Adrenal insufficiency
Medication allergy

42. Resuscitation Fluids Blood Lactated Ringers Normal Saline Colloids
Hypertonic Saline
Blood Substitutes

43. Evaluation of Treatment
Assess organ perfusion
Urinary output
Mental Status
Skin exam
Vitals

44. Which Pressor should I choose?
Septic shock
Phenylephrine- alpha agonist
Increases SVR by arteriolar constriction
Norepinephrine - alpha and beta agonists
Dopamine
Low Dose - increases renal blood supply
Medium Dose - beta effects (increases heart rate and squeeze)
High Dose - alpha effects (arteriolar constriction)
Hypovolemic shock
Fluids and Blood
Cardiogenic shock
Dobutamine - 1 agonist
Increases squeeze and heart rate
Neurogenic shock
Fluids, phenylephrine, norepinephrine, look for another type of shock if it is persistent
Anaphylactic shock
Fluids and epinephrine

45. Early versus delayed administration of norepinephrine in patients with septic shock.
The 28-day mortality was 37.6% overall.
Among the 213 patients, a strong relationship between delayed initial norepinephrine administration and 28-day mortality was noted.
The average time to initial norepinephrine administration was 3.1¿±¿2.5 hours.
Every 1-hour delay in norepinephrine initiation during the first 6 hours after septic shock onset was associated with a 5.3% increase in mortality.
Twenty-eight day mortality rates were significantly higher when norepinephrine administration was started more than or equal to 2 hours after septic shock onset (Late-NE) compared to less than 2 hours (Early-NE).
Mean arterial pressures at 1, 2, 4, and 6 hours after septic shock onset were significantly higher and serum lactate levels at 2, 4, 6, and 8 hours were significantly lower in the Early-NE than the Late-NE group.
The duration of hypotension and norepinephrine administration was significantly shorter and the quantity of norepinephrine administered in a 24-hour period was significantly less for the Early-NE group compared to the Late-NE group.
The time to initial antimicrobial treatment was not significantly different between the Early-NE and Late-NE groups.

46. Conclusion: Early administration of norepinephrine in septic shock patients is associated with an increased survival rate.
Crit Care Oct 3;18(5):532.
Bai X, Yu W, Ji W, Lin Z, Tan S, Duan K, Dong Y, Xu L, Li N.

47. Survival and outcomes improve with early perfusion, adequate oxygenation, and identification with appropriate treatment of the cause of shock.