1. Omar alnoubani MD,MRCS Balqa Applied University
Shock
Omar alnoubani MD,MRCS
Balqa Applied University

2. Shock is the manifestation of the rude unhinging of the machinery of life.”
_Samuel V. Gross, 1872
What is shock ??

3. Learning Objectives Define and classify shock
Describe the pathophysiology of shock
Describe the clinical approach to a shocked patient using the ABCDE approach
Describe investigation and management of shock

4. Definition
failure to meet the metabolic demands of cells and tissues and the consequences that ensue.
Results in global tissue hypoperfusion and metabolic acidosis.
decreased tissue perfusion,This may be a direct consequence of the etiology of shock, such as in hypovolemic/hemorrhagic, cardiogenic, or neurogenic etiologies, or may be secondary to elaborated or released molecules or cellular products that result in endothelial/cellular activation, such as in septic shock or traumatic shock.

5. 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.

6. Cells switch from aerobic to anaerobic metabolism
lactic acid production
Cell function ceases & swells
membrane becomes more permeable
electrolytes & fluids seep in & out of cell
Na+/K+ pump impaired
mitochondria damage
cell death

8. COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)-Adrenal Response
SNS - Neurohormonal response Stimulated by baroreceptors
Increased heart rate
Increased contractility
Vasoconstriction (SVR-Afterload)
Increased Preload

9. SNS - Hormonal: Renin-angiotension system
Decrease renal perfusion
Releases renin angiotension I
angiotension II potent vasoconstriction & releases aldosterone adrenal cortex
sodium & water retention

10. SNS - Hormonal: Antidiuretic Hormone
Osmoreceptors in hypothalamus stimulated
ADH released by Posterior pituitary gland
Vasopressor effect to increase BP
Acts on renal tubules to retain water

11. SNS - Hormonal: Adrenal Cortex
Anterior pituitary releases
adrenocorticotropic hormone (ACTH)Stimulates adrenal Cx to release
glucorticoids
Blood sugar increases to meet increased metabolic needs

12. Failure of Compensatory Response
Decreased blood flow to the tissues causes cellular hypoxia
Anaerobic metabolism begins
Cell swelling, mitochondrial disruption, and eventual cell death
If Low Perfusion States persists:
IRREVERSIBLE CELLULAR DEATH

13. Neuroendocrine and Organ-Specific Responses to Hemorrhage.
Circulatory Homeostasis
METABOLIC EFFECTS
IMMUNE AND INFLAMMATORY RESPONSES
Read from Schwartzs-Principles-of-Surgery-Tenth-Edition.

15. Hypovolemic Shock
blood VOLUME problem
Cardiogenic Shock
blood PUMP problem
Distributive Shock
septic;anaphylactic;neurogenic
blood VESSEL problem

16. Mixed venous oxygen saturation (SvO2) can help to determine whether the cardiac output and oxygen delivery is high enough to meet a patient's needs
SvO2) is the percentage of oxygen bound to hemoglobin in blood returning to the right side of the heart.

17. Clinical approach At the bedside three questions need to be addressed:
Is the patient critically ill?
Does the patient have shock?
If so, what type of shock is it?

18. always history and physical exam
Conduct clinical examination using the Airway, Breathing, Circulation, Disability and Exposure (ABCDE) algorithm.

19. Does the patient have shock?
Clinical findings which might suggest this include:
Relevant history
Tachycardia (heart rate > 120 beats/minute)
Hypotension (SBP < 90 mmHg)
Tachypnoea (Respiratory rate > 25 breaths per minute)
Altered mental status
Delayed capillary refill time/cold extremities
Oliguria (<0.5 ml/kg/hr)

20. What Type of Shock is This?
68 yo M with hx of HTN and DM presents to the ER with abrupt onset of diffuse abdominal pain with radiation to his low back.
The pt is hypotensive, tachycardic, afebrile, with cool but dry skin
Hypovolemic Shock

21. The most common cause of shock in the surgical or trauma patient is loss of circulating volume from haemorrhage.
A Shock in a trauma patient or postoperative patient should be presumed to be due to hemorrhage until proven otherwise.

22. Loss of circulating volume “Empty tank ” decrease tissue perfusion general shock response.
ETIOLOGY:
–Internal or External fluid loss
– Intracellular and extracellular compartments
Most common causes:
Hemmorhage
Dehydration

23. Causes of hypovolemic Shock
Non-hemorrhagic
Vomiting
Diarrhea
Bowel obstruction, pancreatitis
Burns
Hemorrhagic BLOOD YOU SEE OR BLOOD YOU DON’T SEE
GI bleed
Trauma
Massive hemoptysis
AAA rupture
Ectopic pregnancy, post-partum bleeding.

24. Pathophysiology of Hypovolemic Shock
Decreased intravascular volume leads to….
Decreased venous return (Preload, RAP) leads to...
Decreased ventricular filling (Preload, PAWP) leads to….
Decreased stroke volume (HR, Preload, & Afterload) leads to …..
Decreased CO leads to...(Compensatory mechanisms)
Inadequate tissue perfusion!!!!

25. Classification

26. Do you remember how to quickly estimate blood pressure by pulse?60
If you palpate a pulse,
you know SBP is at
least this number 70 80 90

27. Initial management of hypovolemic Shock
Always ABCs
Establish 2 large bore Ivs.
Crystalloids
PRBCs
Control any bleeding
hypotensive resuscitation strategies
Avoid hypothermia in trauma patients .
Arrange definitive treatment

28. Trauma triad of death

29. Evaluation of Hypovolemic Shock
CBC
ABG/lactate
Electrolytes
BUN, Creatinine
Coagulation studies
Type and cross-match
As indicated
CXR
Pelvic x-ray
Abd/pelvis CT
Chest CT
GI endoscopy
Bronchoscopy
Vascular radiology

30. What Type of Shock is This?
An 81 yo F resident of a nursing home presents to the ED with altered mental status. She is febrile to 39.4, hypotensive with a widened pulse pressure, tachycardic, with warm extremities
Septic

31. Septic Shock (Vasodilatory Shock)
Vasodilatory shock is the result of dysfunction of the endothelium and vasculature secondary to circulating inflammatory mediators and cells or as a response to prolonged and severe hypoperfusion.
Syndrome of profound hypotension due to release of endotoxins / TNF / vasoactive peptides following bacterial destruction.

32. Pathophysiology of Septic shock
Initiated by gram-negative (most common) or gram positive bacteria, fungi, or viruses
Cell walls of organisms contain Endotoxins
Endotoxins release inflammatory mediators
(systemic inflammatory response) causes…...
Vasodilation & increase capillary permeability leads to Shock due to alteration in peripheral circulation & massive dilation

33. Pathogenesis of Sepsis
Nguyen H et al. Severe Sepsis and Septic-Shock: Review of the Literature and Emergency Department Management Guidelines. Ann Emerg Med. 2006;42:28-54.

34. Two phases:
Warm shock - early phase
hyperdynamic response,
VASODILATION
Cold shock - late phase
hypodynamic response
DECOMPENSATED STATE

36. Septic Shock Clinical signs: Beware of compensated shock!
Hyperthermia or hypothermia
Tachycardia
Wide pulse pressure
Low blood pressure (SBP<90)
Mental status changes
Beware of compensated shock!
Blood pressure may be “normal”

37. Treatment of septic shock
Always ABCs in any type of shock
2 large bore IVs
Supplemental oxygen
Empiric antibiotics, based on suspected source, as soon as possible.
Vasopressors as needed.

39. What Type of Shock is This?
A 55 yo M with hx of HTN, DM presents with “crushing” substernal CP, diaphoresis, hypotension, tachycardia and cool, clammy extremities.
Cardiogenic

40. circulatory pump failure leading to diminished forward flow and subsequent tissue hypoxia.
Acute, extensive MI is the most common cause of cardiogenic shock.
The pathophysiology of cardiogenic shock involves a vicious cycle of myocardial ischemia that causes myocardial dysfunction, which results in more myocardial ischemia.

41. Stroke volume is reduced
Tachycardia develops as compensation
Ischemia and infarction worsens

42. Symptoms: dyspnoea, poor exercise tolerance, confusion, sweating, PND
Signs: tachycardia, cold skin, high JVP, added heart sounds, engorged liver, peripheral oedema

44. Diagnosis Rapid identification is important !!! EKG CXR
CBC, KFT, cardiac enzymes, coagulation studies.
Echocardiogram

45. Mangment Cardiac monitor, pulse oximetry
Goals- Airway stability and improving myocardial pump function.
Cardiac monitor, pulse oximetry
Supplemental oxygen, IV access
Intubation will decrease preload and result in hypotension
Be prepared to give fluid bolus

46. What Type of Shock is This?
A 24 yo M presents to the ED after an MVC c/o chest pain and difficulty breathing.
On PE, you note the pt to be tachycardic, hypotensive, hypoxic, and with decreased breath sounds on left
Obstructive

47. most commonly due to the presence of tension pneumothorax.

48. Diagnosis
The diagnosis of tension pneumothorax should be made on clinical examination.
Air trapped in pleural space with 1 way valve, air/pressure builds up
The classic findings include respiratory distress (in an awake patient), hypotension, diminished breath sounds over one hemithorax, hyperresonance to percussion, jugular venous distention, and shift of mediastinal structures to the unaffected side with tracheal deviation.
Rx: Needle decompression, chest tube

49. Cardiac tamponade
results from the accumulation of blood within the pericardial sac, usually from penetrating trauma or chronic medical conditions such as heart failure or uremia.
A high index of suspicion is warranted to make a rapid diagnosis.
Beck’s triad :

50. Elevated central venous pressure, pulsus paradoxus (i. e
Elevated central venous pressure, pulsus paradoxus (i.e., decreased systemic arterial pressure with inspiration), or elevated right atrial and right ventricular pressure by pulmonary artery catheter is present.
Diagnosis: CXR, echo.
Pericardiocentesis to diagnose pericardial blood and potentially relieve tamponade may be used.
Diagnostic pericardial window represents the most direct method to determine the presence of blood within the pericardium.

51. Pulmonary embolism
Virchow’s triad: hypercoaguable, endothelial injury, venostasis
Signs: Tachypnea, tachycardia, hypoxia
Low risk: D-dimer
Higher risk: CT chest or VQ scan
Rx: Heparin, consider thrombolytics

52. What Type of Shock is This?
A 41 yo M presents to the ER after an MVC complaining of decreased sensation below his waist and is now hypotensive, bradycardic, with warm extremities.
Neurogenic

53. diminished tissue perfusion as a result of loss of vasomotor tone to peripheral arterial beds.
Results in hypotension, bradycardia and decreased peripheral vascular resistance.

54. Spinal shock- temporary loss of spinal reflex activity below a total or near total spinal cord injury (not the same as neurogenic shock, the terms are not interchangeable)

55. Management A,B,Cs Fluid resuscitation
Remember c-spine precautions.
Fluid resuscitation
Keep MAP at mm Hg for first 7 days
Thought to minimize secondary cord injury
If crystalloid is insufficient use vasopressors
phenylephrine
Search for other causes of hypotension
For bradycardia
Atropine

56. What Type of Shock is This?
A 34 yo F presents to the ER after dining at a restaurant where shortly after eating the first few bites of her meal, became anxious, diaphoretic, began wheezing, noted diffuse pruritic rash, nausea, and a sensation of her “throat closing off”. She is currently hypotensive, tachycardic and ill appearing.
Anaphylactic

57. Anaphylaxis – a severe systemic hypersensitivity reaction characterized by multisystem involvement
IgE mediated

58. First- Pruritus, flushing, urticaria appear
Next- Throat fullness, anxiety, chest tightness, shortness of breath and lightheadedness
Finally- Altered mental status, respiratory distress and circulatory collapse

59. Look for exposure to drug, food, or insect.
Clinical diagnosis
Defined by airway compromise, hypotension, or involvement of cutaneous, respiratory, or GI systems
Look for exposure to drug, food, or insect.

60. Management ABC’s IV, cardiac monitor, pulse oximetry IVFs, oxygen
Angioedema and respiratory compromise require immediate intubation
IV, cardiac monitor, pulse oximetry
IVFs, oxygen
Epinephrine
Second line
Corticosteriods
H1 and H2 blockers

61. End Points of Resuscitation:
Restoration of normal vital signs
Adequate Urine output
cc/kg/hr
Tissue Oxygenation measurement
Adequate Cardiac Index
Normalization of Oxygen delivery DO2I
Normal Serum Lactate levels