1. SHOCK Dr.Mohammed Sharique Ahmed Quadri Assistant Prof.Physiology
Almaarefa College

2. Inadequate Tissue Perfusion
WHAT IS SHOCK?
Shock is the term used to describe acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in generalized cellular hypoxia and/or an inability of the cells to utilize oxygen.
Inadequate Tissue Perfusion
SHOCK IS A SYNDROME THAT CAN OCCUR IN THE COURSE OF MANY LIFE THREATENING TRAUMATIC CONDITIONS OR DISEASE STATES

3. Or it can be define simply as
A clinical state in which tissues do not receive adequate blood flow and O2 to meet their metabolic needs.
Firstly, we are going to recap some basic physiological principles and apply them to a patient with shock.
SBP, SVR and CO are intrinsically linked to blood flow.

4. Physiological Principles
Tissue perfusion is driven by blood pressure
BP = CO X PVR
CO – Cardiac Output
PVR – Peripheral Vascular resistance

5. CO = SV X HR This means that BP= SV X HR X PVR
Cardiac Output
CO = SV X HR
This means that
BP= SV X HR X PVR
Blood Pressure = Stroke Volume X Heart Rate X Peripheral Vascular Resistance

6. What affects Stroke volume?
Volume of Blood pumped by the heart during 1 cycle
What affects Stroke volume?
Rhythm Problems
Blood Volume
Stroke Volume
Heart Muscle Damage
MechanicalObstruction
Mechanical Obstruction

7. What makes up blood volume
Plasma
RBCs
WBCs
Platelets

8. What Alters Blood Volume?
Haemorrhage
Plasma Loss
Loss /Redistribution of Extracellular Volume

9. Heart rate too fast to allow adequate refilling of heart between beats
Heart rate increases as a compensatory response to Shock
Heart rate too fast to allow adequate refilling of heart between beats

10. Peripheral Vascular Resistance
PVR regulated by ARTERIOLAR tone.
Dilatation opens Arteriovenous beds & increases volume of circulatory system

11. What Alters PVR?
Circulating cytokines & Inflammatory mediators (e.g. Histamine)
Endotoxins
Drugs (e.g. Nitrates)

12. Mechanical Obstruction
Blood Volume
Mechanical Obstruction
Heart Damage / Rhythm
Stroke Volume
Heart Rate
PVR
Blood Pressure

13. TYPES OF SHOCK
HYPOVOLEMIC
CARDIOGENIC
OBSTRUCTIVE
DISTRIBUTIVE

14. DISTRIBUTIVE SHOCK

15. Hypovolaemic Volume Loss Blood loss -Haemorrhage Plasma Loss -Burns
ECF Loss - Vomiting & Diarrhoea

16. Cardiogenic Pump Failure May be due to
Inability of heart to Contract or
Inability of heart to pump blood
Myocardial damage ( M.I)
Arrhythmias
Valvular damage

17. Distributive Decreased Peripheral Vascular Resistance
Septic Shock (inflammatory mediators)
Neurogenic Shock (loss of sympathetic control on vascular tone)
ANAPHYLACTIC shock (presence of vasodilator substances like histamine)

18. PATHOPHYSIOLOGY OF SHOCK
The manifestation of shock reflects both
The impaired perfusion of body tissue &
The body’s attempt to maintain tissue perfusion (compensatory mechanism)

19. COMPENSATORY MECHANISMS

20. Compensatory mechanism and shock
PRE-LOAD
AFTER-LOAD
Fluid
Volume
(CVP/JVP)
Cardiac
Output
(SV x HR)
Vascular
Diameter
(SVR)

21. Hypovolaemic shock PRE-LOAD AFTER-LOAD Fluid Volume (CVP/JVP) Cardiac
Output
(SV x HR)
Vascular
Diameter
(SVR) 1

22. Hypovolaemic shock PRE-LOAD AFTER-LOAD Fluid Volume (CVP/JVP) Cardiac
Output
(SV x HR)
Vascular
Diameter
(SVR) 1 2

23. Hypovolaemic shock PRE-LOAD AFTER-LOAD Fluid Volume (CVP/JVP) Cardiac
Output
(SV x HR)
Vascular
Diameter
(SVR) 1 2 3

24. Cardiogenic shock PRE-LOAD AFTER-LOAD Fluid Volume (CVP/JVP) Cardiac
Output
(SV x HR)
Vascular
Diameter
(SVR) 1

25. Cardiogenic shock PRE-LOAD AFTER-LOAD Fluid Volume (CVP/JVP) Cardiac
Output
(SV x HR)
Vascular
Diameter
(SVR) 1 2

26. Cardiogenic shock PRE-LOAD AFTER-LOAD Fluid Volume (CVP/JVP) Cardiac
Output
(SV x HR)
Vascular
Diameter
(SVR) 3 1 2

27. Distributive shock PRE-LOAD AFTER-LOAD Fluid Volume (CVP/JVP) Cardiac
Output
(SV x HR)
Vascular
Diameter
(SVR) 1

28. Distributive shock PRE-LOAD AFTER-LOAD Fluid Volume (CVP/JVP) Cardiac
Output
(SV x HR)
Vascular
Diameter
(SVR) 2 1

29. Distributive shock PRE-LOAD AFTER-LOAD Fluid Volume (CVP/JVP) Cardiac
Output
(SV x HR)
Vascular
Diameter
(SVR) 2 3 1

30. Sympatho-Adrenal Response to Shock
Most immediate of compensatory mechanisms are those of sympathetic nervous system and renin angiotensin mechanism
Sympathetic nervous system
NE, epinephrine, 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

31. Sympatho-Adrenal Response to Shock

33. Compensatory reactions activated by hemorrhage.
Vasoconstriction
Tachycardia
Venoconstriction
Tachypnea→increased thoracic pumping
Restlessness→increased skeletal muscle pumping (in some cases)
Increased movement of interstitial fluid into capillaries
Increased secretion of norepinephrine and epinephrine
Increased secretion of vasopressin
Increased secretion of renin and aldosterone
Increased secretion of erythropoietin
Increased plasma protein synthesis
Restlessness and agitation is common in early shock , it is because of increase sympathetic stimulation and epinephrine release .as shock progresses blood supply to brain is decreased and restlessness is replaced by altered mentation and uncontiousness.

34. Effect of hemorrhage on mean arterial pressure

35. Sympathetic activation
Tachycardia
Increased myocardial contractility (β1)
α-adrenergic receptor-mediated vasoconstriction (β2-receptor-mediated vasodilatation in skeletal muscle, bronchodialatation )
Overall increased COP and redistribution of flow: cardiac, cerebral, hepatic and muscle vascular beds
There are other effects mediated by the SNS, but these are the important factors when considering shock.

36. Points to Ponder Goal is to maintain cerebral and cardiac perfusion
Vasoconstriction of splanchnic, and renal blood flow
Compensatory mechanisms are not effective over the long term and fails when shock state is prolonged.

37. Neuroendocrine response
Release of pituitary hormones such as adrenocorticotrophic hormone (ACTH), vasopressin(antidiuretic hormone, ADH).
There is release of cortisol, which causes fluid retention and antagonizes insulin.
There is release of glucagon, which raises the blood sugar level.
Absolute adrenocortical insufficiency due to bilateral adrenal hemorrhage or necrosis is rare(in septic shock) and that this may be associated with an impaired pressor response to norepinephrine(noradrenaline) and a worsen the prognosis.
cause of this phenomenon remain unclear.

38. Pathophysiology of shock cellular responses
Inadequate tissue perfusion
Decreased oxygen supply
Anaerobic metabolism
Accumulation metabolic waste & lactate
Cellular failure (limited ATP produce)
Inadequate tissue perfusion due to inadequate blood supply.

39. Understanding Shock
Cellular responses to decreased systemic oxygen delivery
ATP depletion → Na+/ K+ pump dysfunction
Cellular edema – Due to accumulation of Na+ inside the cell
Hydrolysis of cellular membranes and cellular death
Mitochondrial activity severely depressed and lysosomal rupture may occur
systemic metabolic lactic acidosis that overcomes the body’s compensatory mechanisms

40. Release of Pro- and Anti Inflammatory Mediators
Trigger an exaggerated inflammatory response (systemic activation of leucocytes & release
of potentially damaging ‘mediators’)
Severe infection
(bacteraemia/endotoxaemia),
Presence of large areas of
damaged tissue
(following trauma /extensive surgery)
Prolonged episodes of hypoperfusion

41. Release of Pro- and Anti Inflammatory Mediators (continued)
Pro inflammatory Mediators:
Proteases
Toxic free radicals & other reactive oxygen species
Cytokines IL
TNF
Platelet activating factor
Hypotension, Inc. vascular permeability, platelet aggregation.
Anti inflammatory mediators:
Interleukin 10 ( IL-10)
Are involved in leukocyte adhesion ,local inflammation, neutrophil activation, fever, lactic acidosis, ventilation perfusion abnormalities

42. Release of Pro- and Anti Inflammatory Mediators (continued)
Although beneficial when targeted against local areas of infection or necrotic tissue--dissemination of this ‘innate immune’ response can produce shock and widespread tissue damage.
Characteristically the initial episode of overwhelming inflammation is followed by a period of immune suppression--- increased risk of developing secondary infections.

43. Harmful effects of inflammatory mediators
Damage to cell membranes
Impaired mitochondrial respiration
DNA strand breakage
Apoptosis, which may contribute to the organ damage
Vasodilatation
Maldistribution of regional blood flow
Abnormalities in the microcirculation:
– capillaries are obstructed
– increased capillary permeability with interstitial oedema.
and immune hypo-responsiveness associated with sepsis.
Coagulation disorders

44. VICIOUS CYCLE Hypoperfusion
Cellular injury
Inflammatory mediators
Functional & structural changes in microvascular circulation

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

46. BREAK !

47. CLINICAL FEATURES OF SHOCK

48. Symptoms of Shock Hx of Trauma / other illness Vomiting & Diarrhoea
General Symptoms
Specific Symptoms
Anxiety /Nervousness
Dizziness
Weakness
Faintness
Nausea & Vomiting
Thirst
Confusion
Decreased UO
Hx of Trauma / other illness
Vomiting & Diarrhoea
Chest Pain
Fevers / Rigors
SOB

49. Signs of Shock Pale Cold & Clammy skin Sweating Cyanosis Tachycardia
Tachypnoea
Confused / Aggiatated
Unconscious
Hypotensive
Stridor / SOB

50. Hypovolaemic Shock

51. Clinical Feature of Hypovolaemic shock
Inadequate tissue perfusion:
Skin – Cold, Pale, Slate-grey, ‘Clammy’, Slow capillary refill,
Kidneys – Oliguria, Anuria
(c) Brain – Drowsiness, Confusion and Irritability.

52. Clinical Feature of Hypovolaemic shock
Increased sympathetic tone:
Tachycardia, narrowed pulse pressure, ‘weak’ or ‘thready’ pulse
(b) Sweating
(c) Blood pressure – may be maintained initially (despite up to a 25% reduction in circulating volume if the patient is young and fit),but later hypotension supervenes.

53. Clinical Feature of Hypovolaemic shock
Metabolic acidosis – compensatory tachypnoea.
Extreme hypovolaemia may be associated with bradycardia.

54. Cardiogenic Shock

56. Clinical Feature of Cardiogenic Shock
Sign & symptoms are consistent with those of heart failure
Stagnation of blood flow & increase extraction of O2 from hemoglobin:
Lips, nail beds and skin become cyanotic
Poor stroke volume :
Decrease in MAP & SBP
Near normal diastolic B.P due to vasoconstriction
Narrow pulse pressure

57. Clinical Feature of Cardiogenic Shock
Low renal perfusion pressure & aldosterone release:
Decrease urine output
Elevated preload :
Rise in CVP and pulmonary capillary wedge pressure
Poor cerebral perfusion:
Alteration in cognition and consciousness

58. Clinical Feature of Cardiogenic Shock
Acute pulmonary oedema:
Tachypnoea, orthopnea, pulmonary crackles, oxygen saturation < 90% on air, pulmonary oedema on CXR

59. Obstructive Shock

60. Clinical Feature of Obstructive Shock
Elevated JVP and CVP
Pulsus paradoxus and muffled heart sounds in cardiac ,tamponade.
Signs of pulmonary embolism
Pulmonary oligaemia on X-ray
Dyspnoea
On ECG – P-Pulmonale, RAD
Systolic blood pressure normally falls during quiet inspiration in normal individuals. Pulsus paradoxus is defined as a fall of systolic blood pressure of >10 mmHg during the inspiratory phaseNormally during inspiration, systolic blood pressure decreases ≤10 mmHg.,[1] and pulse rate goes up slightly. This is because inspiration makes intrathoracic pressure more negative relative to atmospheric pressure. The negative pressure in the thorax increases venous return, so more blood flows into the right side of the heart. However, the decrease in intrathoracic pressure also expands the compliant pulmonary vasculature. This increase in pulmonary blood capacity pools the blood in the lungs, and decreases pulmonary venous return, so flow is reduced to the left side of the heart. Also the increased systemic venous return to the right side of the heart expands the right heart and directly compromises filling of the left side of the heart. Reduced left-heart filling leads to a reduced stroke volume which manifests as a decrease in systolic blood pressure. The decrease in systolic blood pressure leads to a faster heart rate due to the baroreceptor reflex, which stimulates sympathetic outflow to the heart.

61. Distributive Shock

62. Causes of Distributive Shock
Decreased sympathetic activity: neurogenic
Brain or spine injury; anesthetics; emotion
Vasodilator substances in blood
Type I hypersensitivity (anaphylactic shock)
Inflammatory response to infection (sepsis)
Vessel damage from severe hypervolemia

63. Neurogenic Shock Occurs after acute spinal cord injury or
defect in vasomotor center in brainstem
or sympathetic outflow to blood vessels
Brain injury
Depressant action of drugs
General anesthesia (barbiturate)
Hypoxia/hypoglycemia
Sympathetic outflow is disrupted leaving unopposed vagal tone
Results in hypotension and bradycardia
Skin is dry and warm

64. Anaphylaxis
Systemic response to the inflammatory mediators released in type I hypersensitivity
Histamine, acetylcholine, kinins, leukotrienes, and prostaglandins all cause vasodilation
What will happen when arterioles vasodilate throughout the body?
Acetylcholine, kinins, leukotrienes, and prostaglandins all can cause bronchoconstriction
What will happen when the bronchioles constrict?

65. Clinical Feature of Anaphylactic shock
Signs of profound vasodilatation:
(a) Warm peripheries
(b) Low blood pressure
(c) Tachycardia.
Erythema, urticaria, angio-oedema, pallor, cyanosis.
Bronchospasm, rhinitis.
Oedema of the face, pharynx and larynx.
Pulmonary oedema.
Hypovolaemia due to capillary leak.
Nausea, vomiting, abdominal cramps, diarrhea.

66. Angio-oedema

67. Septic Shock

68. Sepsis or Systemic Inflammatory Response Syndrome (SIRS)
Inflammatory mediators released into the circulation
Tumor necrosis factor
Interleukins
Prostaglandins
Cause systemic signs of inflammation
Fever and increased respiration, respiratory alkalosis, vasodilation, warm flushed skin
Activate inflammatory pathways
Coagulation, complement

69. Sepsis and Systemic Inflammatory Response
Infection: Invasion of normally sterile host tissue by microorganisms
Bacteremia: Viable bacteria in blood
Systemic inflammatory response syndrome (SIRS):The systemic inflammatory response to a variety of severe clinical insults. The response is manifested by two or more of the following:
■ Temperature > 38°C or < 36°C
■ Heart rate > 90 beats/min
■ Respiratory rate > 20 breaths/min or Paco2 < 4.3 kPa
■ White cell count > 12 × 109/L, < 4 × 109/L or > 10% immature forms
Sepsis: SIRS resulting from documented infection
Partial pressure of oxygen (PaO2) mmHg
Partial pressure of carbon dioxide (PaCO2) mmHg
Arterial blood pH of
Oxygen saturation (SaO2) %
Bicarbonate - (HCO3) mEq/L

70. Sepsis

71. Severe sepsis :Sepsis associated with organ dysfunction, hypoperfusion or hypotension. Hypoperfusion and perfusion abnormalities may include, but are not limited to, lactic acidosis, oliguria or an acute alteration in mental state, thrombocytopenia
Septic shock:
Severe sepsis with hypotension (systolic BP < 90 mmHg or a reduction of > 40 mmHg from baseline) in the absence of other causes for hypotension and despite adequate fluid resuscitation

72. Sepsis or Systemic Inflammatory Response Syndrome (SIRS) (cont.)
Discussion:
Why is septic shock called distributive?
In the later phases of septic shock, blood volume decreases. What part of the inflammatory process explains this?

73. Septic Shock vasodilation decreased peripheral resistance decreased
blood pressure
SEPTIC SHOCK
40% mortality

74. Septic Shock
Also called systemic inflammatory response syndrome (SIRS)
Inflammatory mediators also increase the metabolic rate of tissues, so they need more oxygen

75. Pattern of systemic inflammatory response
CARS: compensatory anti-inflammatory
response syndrome;
SIRS: systemic inflammatory response
syndrome.

76. Clinical Feature of Septic shock
■ Pyrexia and rigors, or hypothermia (unusual).
■ Nausea, vomiting.
■ Vasodilatation, warm peripheries.
■ Bounding pulse.
■ Rapid capillary refill.
■ Hypotension (septic shock).
■ Other signs:
(a) Jaundice
(b) Coma, stupor
(c) Bleeding due to coagulopathy (e.g. from vascular puncture sites, GI tract and surgical wounds)
(d) Rash and meningism

77. Shock Types & Physiology
CVP/PCWP CO
PVR
Hypovolumic
Septic
Cardiogenic
Neurogenic
Cardiac temponade
Anaphylactic

78. Shock Types & Physiology
CVP/PCWP CO
PVR
Hypovolemic ↓ ↑
Septic
Cardiogenic
Neurogenic
Cardiac temponade
Anaphylactic

79. Shock Types & Physiology
CVP/PCWP CO
PVR
Hypovolemic ↓ ↑
Septic
Cardiogenic
Neurogenic
Cardiac temponade
Anaphylactic

80. Shock Types & Physiology
CVP/PCWP CO
PVR
Hypovolemic ↓ ↑
Septic
Cardiogenic
Neurogenic
Cardiac temponade
Anaphylactic

81. Shock Types & Physiology
CVP/PCWP CO
PVR
Hypovolemic ↓ ↑
Septic
Cardiogenic
Neurogenic
Cardiac temponade
Anaphylactic

82. Shock Types & Physiology
CVP/PCWP CO
PVR
Hypovolemic ↓ ↑
Septic
Cardiogenic
Neurogenic
Cardiac temponade
Anaphylactic

83. Shock Types & Physiology
CVP/PCWP CO
PVR
Hypovolemic ↓ ↑
Septic
Cardiogenic
Neurogenic
Cardiac temponade
Anaphylactic

84. Any questions?

85. Refrences
Essentials of pathophysiology by carol Mattson Porth, 3rd edition.
Kumar & Clark's Clinical Medicine, 7th Edition