1. SHOCK
Sevgi Bilgen

2. Students should learn;
The definition of shock
Types of shock
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
Results in multiple organ failure and death

5. Inadequate oxygen delivery leading to shock can occur despite the patient being hypertensive or normotensive
Clinicians should not wait for the presence of hypotension before aggressively attempting to reverse shock and restore adequate tissue perfusion.

6. 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.

7. Basic Physiology Oxygen Delivery = CO x arterial content of O2
Cardiac Output = HR x Stroke Volume
CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x )
Stroke Volume is a function
Preload
Afterload
Myocardial Contractility

8. Basic Physiology

9. 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
Goal is to maintain cerebral and cardiac perfusion

10. Understanding Shock
Prolonged oxygen deprivation leads to cellular hypoxia,
derangement of critical biochemical processes at the cellular level,
which can progress to the systemic level

11. Understanding Shock
Cellular effects include cell membrane ion pump dysfunction,
intracellular edema,
leakage of intracellular contents into the extracellular space,
inadequate regulation of intracellular pH

12. Understanding Shock
Systemic effects include alterations in the serum pH,
endothelial dysfunction,
redox state,
further stimulation of inflammatory and
anti-inflammatory cascades.

13. Understanding Shock
The effects of oxygen deprivation are initially reversible, but rapidly become irreversible.
The result is sequential cell death,
end-organ dysfunction.
Progressive end-organ dysfunction leads to irreversible organ damage and patient death.

14. Clinical Endpoints of Shock
DECREASED BLOOD FLOW TO BRAIN AND HEART
Restless, agitated, confused, lethargy
Hypotension
Tachycardia
Tachypnea
END-STAGE SHOCK
Bradycardia
Arrhythmia
Death
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.

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

16. Cardinal features Cardinal features of shock include; hypotension,
oliguria,
abnormal mental status,
metabolic acidosis, and,
in some patients, cool and clammy skin.

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

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

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

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

21. Loss of plasma
Burns
Exfoliative dermatitis

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

23. Hypovolemic shock
Depending upon the cause of the hypovolemic shock, patients may report;
hematemesis, hematochezia, melena,
vomiting, diarrhea,
abdominal pain.
There may be evidence of blunt or penetrating trauma, or the patient may be postoperative.

24. Hypovolemic shock Physical manifestations may include;
decreased skin turgor (in younger patients),
dry skin,
dry axillae,
dry tongue,
dry oral mucosa.

25. Hypovolemic shock Patients may have postural hypotension,
decreased jugular venous pressure,
diminished central venous pressure.
There may be anemia, or the amylase and lipase may be elevated

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

27. Cardiogenic shock
Pump failure (secondary to myocardial infarction or other cardiomyopathy) Acute myocardial ischemia is most common cause
Arrhythmia
Tachyarrhythmia
Bradyarrhythmia
Acute valvular dysfunction
Rupture of ventricular septum or free ventricular wall

28. Cardiogenic shock
Depending upon the cause of the cardiogenic shock, patients may report;
dyspnea,
chest pain,
palpitations.
Many patients have a history of cardiovascular disease.

29. Cardiogenic shock Lung examination may reveal diffuse crackles
cardiac examination may reveal a new murmur, gallops, or soft heart sounds.
The jugular venous pressure and central venous pressure may be increased,
the distal arterial pulses may be diminished.

30. Cardiogenic shock
There may be evidence of pulmonary congestion or pulmonary edema on a chest radiograph,
recent or current ischemia on an electrocardiogram.
Cardiac enzymes may be elevated.
An echocardiogram may demonstrate the etiology.

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

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

33. Tension pneumothorax/exam
absent unilateral breath sounds on the affected side;
trachea deviated to the opposite side;
hyper-resonance to percussion on affected side

34. Cardiac tamponade/exam
muffled hearts sounds
low BP
jugular venous distention
pulsus paradoxus

35. Pulmonary emboli/exam
possible cyanosis
respiratory distress with use of accessory muscles
lung auscultation normal
jugular venous distention if large embolism
calf tenderness
tachycardia
low oxygen saturations

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

37. Distributive shock Septic shock Anaphylactic shock Neurogenic shock
Vasodilator drugs
Acute adrenal insufficiency

38. Depending upon the cause of the distributive shock; patients may report
dyspnea
productive cough
dysuria, hematuria
chills
myalgias
rashes
fatigue
malaise
headache
photophobia
pain
recent ingestion

39. Distributive shock There may be fever tachypnea tachycardia
leukocytosis
abnormal mental status
flushing

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

41. 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.

42. 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.

43. 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.

44. DIAGNOSTIC APPROACH
When a patient is suspected of having shock, diagnostic evaluation should occur at the same time as resuscitation.
Resuscitative efforts should NOT be delayed for history, physical examination, laboratory testing, or imaging.

45. 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

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

47. 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

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

49. Goals of Shock Resuscitation
Restore blood pressure
Normalize systemic perfusion
Preserve organ function

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

51. 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

52. 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

53. 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

54. 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

55. 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%

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

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

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

59. Which Pressor should I choose?
Septic shock
Norepinephrine – (alpha+beta agonists) Epinephrine+ vasopressin
Increases SVR by arteriolar constriction
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

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