Shock is a life-threatening condition where the cardiovascular system fails to adequately perfuse tissues with blood and oxygen. There are several types of shock that can occur depending on where the failure lies, such as hypovolemic shock which is caused by low blood volume, cardiogenic shock due to heart failure, and distributive shock where blood vessels are dilated. The lecture covers the causes, pathophysiology, clinical presentation and management of the different shock states.

1. LECTURE 13
HEMODYNAMIC DISORDERS III
LECTURE 13: . SHOCK
Dr. Sergio Muwowo

2. SHOCK
• Shock is a condition in which the cardiovascular system fails
to perfuse tissues adequately
• An impaired cardiac pump, circulatory system, and/or volume
can lead to compromised blood flow to tissues

3. SHOCK
Inadequate tissue perfusion can result in:
1. Generalized cellular hypoxia (starvation)
2. Widespread impairment of cellular metabolism
3. Tissue damage
4. organ failure
5. Death

4. 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
PATHOPHYSIOLOGY

5. COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)-Adrenal Response
SNS - Neurohormonal response Stimulated by baroreceptors
1. Increased heart rate
2. Increased contractility
3. Vasoconstriction (Afterload)
4. Increased Preload

6. COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)-Adrenal Response
SNS - Hormonal: Renin-angiotension system
1. Decrease renal perfusion
2. Releases renin
3. angiotension I
4. angiotension II
5. potent vasoconstriction & releases aldosterone adrenal cortex
6. sodium & water retention ( intravascular volume )

7. COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)-Adrenal Response
SNS - Hormonal: Antidiuretic Hormone
1. Osmoreceptors in hypothalamus stimulated
2. ADH released by Posterior pituitary gland
3. Vasopressor effect to increase BP
4. Acts on renal tubules to retain water

8. COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)-Adrenal Response
SNS - Hormonal: Adrenal Cortex
1. Anterior pituitary releases adrenocorticotropic hormone (ACTH)
2. Stimulates adrenal Cx to release glucorticoids
3. Blood sugar increases to meet increased metabolic needs

9. FAILURE OF COMPENSATORY RESPONSE
1. Decreased blood flow to the tissues causes cellular hypoxia
2. Anaerobic metabolism begins
3. Cell swelling, mitochondrial disruption, and eventual cell death
4. If Low Perfusion States persists:
IRREVERSIBLE DEATH IMMINENT!!

10. STAGES OF SHOCK
1. Initial stage
- tissues are under perfused, decreased CO, increased
Anaerobic metabolism, lactic acid is building
2. Compensatory stage
- Reversible. SNS activated by low CO, attempting to compensate for
the decrease tissue perfusion.
3. Progressive stage
- Failing compensatory mechanisms:
- profound vasoconstriction from the SNS
- ISCHEMIA Lactic acid production is high
- metabolic acidosis
4. Irreversible or refractory stage
- Cellular necrosis and Multiple Organ Dysfunction Syndrome may
occur
DEATH IS IMMINENT!!!!

11. PATHOPHYSIOLOGY SYSTEMIC LEVEL
Net results of cellular shock:
1. Decreased myocardial contractility
2. Systemic lactic acidosis
3. Decreased vascular tone
4. Decrease blood pressure, preload, and cardiac output

12. CLINICAL PRESENTATION: GENERALIZED SHOCK
Vital signs
1. Hypotensive; < 90 mmHg
2. MAP < 60 mmHg
3. Tachycardia: Weak and Thready pulse
4. Tachypneic : blow off CO2 Respiratory alkalosis
5. Mental status: restless, irritable, apprehensive unresponsive
6. Decreased Urine output

13. SHOCK SYNDROMES
1. Hypovolemic Shock
– blood VOLUME problem
2. Cardiogenic Shock
– blood PUMP problem
3. Distributive Shock [septic; anaphylactic; neurogenic]
– blood VESSEL problem

14. HYPOVOLEMIC SHOCK
 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:
1. Hemorrhage
2. Dehydration

15. HYPOVOLEMIC SHOCK
A. External loss of fluid
1. Fluid loss:
Dehydration, vomiting, diarrhea, diuresis, extensive burns
2. Blood loss:
Trauma: blunt and penetrating
B. Internal fluid loss
1. Loss of intravascular integrity
2. Increased capillary membrane permeability
3. Decreased colloidal osmotic pressure

16. PATHOPHYSIOLOGY OF HYPOVOLEMIC SHOCK
1. Decreased intravascular volume leads to….
2. Decreased venous return (Preload, RAP) leads to...
3. Decreased ventricular filling (Preload, PAWP) leads to….
4. Decreased stroke volume (HR, Preload, & Afterload) leads to …..
5. Decreased CO leads to...(Compensatory mechanisms)
6. Inadequate tissue perfusion!!!!

17. CLINICAL PRESENTATION
HYPOVOLEMIC SHOCK
1. Tachycardia and tachypnea
2. Weak, thready pulses
3. Hypotension
4. Skin cool & clammy
5. Mental status changes
6. Decreased urine output: dark & concentrated

18. INITIAL MANAGEMENT HYPOVOLEMIC SHOCK
Management goal: Restore circulating volume, tissue perfusion, &
correct cause:
1. Early Recognition- Do not relay on BP! (30% fld loss)
2. Control hemorrhage
3. Restore circulating volume
4. Optimize oxygen delivery
5. Vasoconstrictor if BP still low after volume loading

19. CARDIOGENIC SHOCK
• The impaired ability of the heart to pump blood
• Pump failure of the right or left ventricle
• Most common cause is LV MI (Anterior)
• Occurs when > 40% of ventricular mass damage
• Mortality rate of 80 % or MORE

20. CARDIOGENIC SHOCK : ETIOLOGIES
• Mechanical: complications of
MI:
– Papillary Muscle Rupture
– Ventricular aneurysm
– Ventricular septal rupture
• Other causes:
– Cardiomyopathies
– tamponade
– tension pneumothorax
– arrhythmias
– valve disease

21. CARDIOGENIC SHOCK: PATHOPHYSIOLOGY
Impaired pumping ability of LV leads to…
1. Decreased stroke volume leads to…..
2. Decreased CO leads to …..
3. Decreased BP leads to…..
4. Compensatory mechanism which may lead to
5. Decreased tissue perfusion !!!!

22. CARDIOGENIC SHOCK: PATHOPHYSIOLOGY
Impaired pumping ability of LV leads to…
 Inadequate systolic emptying leads to ...
 Left ventricular filling pressures (preload) leads to...
 Left atrial pressures leads to ….
 Pulmonary capillary pressure leads to …
 Pulmonary interstitial & intraalveolar edema !!!!

23. CLINICAL PRESENTATION
CARDIOGENIC SHOCK
• Similar catecholamine compensation changes in generalized
shock & hypovolemic shock
• May not show typical tachycardic response :
if pt on Beta blockers, in heart block, or if bradycardic in response
to nodal tissue ischemia
• Mean arterial pressure below 70 mmHg compromises coronary
perfusion
(MAP = SBP + (2) DBP/3)

24. CLINICAL PRESENTATION
CARDIOGENIC SHOCK
• Pericardial tamponade
– muffled heart tones, elevated neck veins
• Tension pneumothorax
– JVD, tracheal deviation, decreased or absent unilateral
breath sounds, and chest hyperresonance on affected
side

25. CLINICAL ASSESSMENT
1. Pulmonary &
Peripheral Edema
2. JVD
3. CO
4. Hypotension
5. Tachypnea,
6. Crackles
• PaO2
• UOP
• LOC

26. MANAGEMENT
Goal of management :
• Treat Reversible Causes
• Protect ischemic myocardium
• Improve tissue perfusion
• Early assessment & treatment!!!
• Optimizing pump by:
– Increasing myocardial O2
delivery
– Maximizing CO
– Decreasing LV workload
(Afterload)

27. MANAGEMENT
Limiting/reducing myocardial damage during Myocardial Infarction:
• Increased pumping action & decrease workload of the heart
– Inotropic agents
– Vasoactive drugs
– Intra-aortic balloon pump
– Cautious administration of fluids
– Transplantation
• Consider thrombolytics, angioplasty in specific cases

28. MANAGEMENT CARDIOGENIC SHOCK
OPTIMIZING PUMP FUNCTION:
– Pulmonary artery monitoring is a necessity !!
– Aggressive airway management: Mechanical Ventilation
– Judicious fluid management
– Vasoactive agents
• Dobutamine
• Dopamine

29. MANAGEMENT CARDIOGENIC SHOCK
OPTIMIZING PUMP FUNCTION (CONT.):
– Morphine as needed (Decreases preload, anxiety)
– Cautious use of diuretics in CHF
– Vasodilators as needed for afterload reduction
– Short acting beta blocker, for refractory tachycardia

30. VASOGENIC/DISTRIBUTIVE SHOCK
• Etiologies
– Septic Shock (Most Common)
– Anaphylactic Shock
– Neurogenic Shock

31. ANAPHYLACTIC SHOCK
• A type of distributive shock that results from
widespread systemic allergic reaction to an
antigen
• This hypersensitive reaction is LIFE THREATENING

32. PATHOPHYSIOLOGY ANAPHYLACTIC SHOCK
1. Antigen exposure
2. Body stimulated to produce ige antibodies specific to
antigen
– Drugs, bites, contrast, blood, foods, vaccines
3. Reexposure to antigen
– Ige binds to mast cells and basophils
4. Anaphylactic response

33. ANAPHYLACTIC RESPONSE
1. Vasodilatation
2. Increased vascular permeability
3. Bronchoconstriction
4. Increased mucus production
5. Increased inflammatory mediators recruitment to sites of
antigen interaction

34. CLINICAL PRESENTATION ANAPHYLACTIC SHOCK
1. Almost immediate response to inciting antigen
2. Cutaneous manifestations
– urticaria, erythema, pruritis, angioedema
3. Respiratory compromise
– stridor, wheezing, bronchorrhea, resp. distress
4. Circulatory collapse
– tachycardia, vasodilation, hypotension

35. MANAGEMENT ANAPHYLACTIC SHOCK
• Early recognition, treat aggressively
• Airway support
• Iv epinephrine (open airways)
• Antihistamines
• Corticosteroids
• Immediate withdrawal of antigen if possible
• Prevention
• Judicious crystalloid administration
• Vasopressors to maintain organ perfusion
• Positive inotropes
• Patient education

36. NEUROGENIC SHOCK
• A type of distributive shock that results from the loss or
suppression of sympathetic tone
• Causes massive vasodilatation in the venous vasculature, 
venous return to heart,  cardiac output.
• Most common etiology: Spinal cord injury above T6
• Neurogenic is the rarest form of shock!

37. PATHOPHYSIOLOGY OF NEUROGENIC SHOCK
1. Disruption of sympathetic nervous system
2. Loss of sympathetic tone
3. Venous and arterial vasodilation
4. Decreased venous return
5. Decreased stroke volume
6. Decreased cardiac output
7. Decreased cellular oxygen supply
8. Impaired tissue perfusion
9. Impaired cellular metabolism

38. ASSESSMENT, DIAGNOSIS AND MANAGEMENT OF NEUROGENIC SHOCK
PATIENT ASSESSMENT
1. Hypotension
2. Bradycardia
3. Hypothermia
4. Warm, dry skin
5. CO
6. Flaccid paralysis below level
of the spinal lesion
MEDICAL MANAGEMENT
1. Goals of Therapy are to treat
or remove the cause &
2. Prevent cardiovascular
instability, & promote
optimal tissue perfusion

39. MANAGEMENT OF NEUROGENIC SHOCK
1. Hypovolemia- RX with careful fluid replacement for
2. Observe closely for fluid overload
3. Vasopressors may be needed
4. Hypothermia- warming avoid large swings in pts body
temperature
5. Treat Hypoxia
6. Maintain ventilatory support

40. MANAGEMENT OF NEUROGENIC SHOCK
1. Observe for bradycardia-major dysrhythmia
2. Observe for DVT- venous pooling in extremities make patients
high-risk>>P.E.
3. Use prevention modalities [teds,anticoagulation]
4. Alpha agonist to augment tone if perfusion still inadequate
• Dopamine (> 10 mcg/kg per min)
• Ephedrine (12.5-25 mg IV every 3-4 hours
5. Treat bradycardia with atropine 0.5-1 mg doses to max 3 mg
• may need transcutaneous or transvenous pacing
temporarily

41. SEPSIS
Systemic Inflammatory Response (SIRS) to INFECTION
manifested by : two or more of following:
1. Temp > 38 or < 36 centigrade
2. HR > 90
3. RR > 20 or PaCO2 < 32
4. WBC > 12,000/cu mm or < 4,000 > 10% Bands
(immature wbc)
Sepsis syndrome: SIRS with confirmed infectious
process associate with organ failure or hypotention

42. RISK FACTORS ASSOCIATED WITH SEPTIC SHOCK
1. Age
2. Malnutrition
3. General debilitation
4. Use of invasive catheters
5. Traumatic wounds
6. Drug Therapy

43. PATHOPHYSIOLOGY OF SEPTIC SHOCK
1. Initiated by gram-negative (most common) or gram positive
bacteria, fungi, or viruses
2. Cell walls of organisms contain Endotoxins
3. Endotoxins release inflammatory mediators (systemic
inflammatory response) causes…...
4. Vasodilation & increase capillary permeability leads to
5. Shock due to alteration in peripheral circulation & massive
dilation

46. CLINICAL PRESENTATION SEPTIC SHOCK
• Two phases:
1. “Warm” shock - early phase
a. Hyperdynamic response
b. Vasodilation
2. “Cold” shock - late phase
a. Hypodynamic response
b. Decompensated state

47. CLINICAL MANIFESTATIONS
EARLY HYPERDYNAMIC STATE
COMPENSATION
1. Pink, warm, flushed skin
2. Increased Heart Rate
3. Tachypnea
4. Massive vasodilation
5. Increased CO
6. Crackles
LATE HYPODYNAMIC STATE
DECOMPANSATION:
1. Vasoconistriction
2. Skin is pale & cold
3. Tachycardia
4. Decrease BP
5. Change LOC
6. Decrease UOP
7. Decrease CO
8. Metabolic & respiratory acidosis
with hypoxemia

48. MANAGEMENT
1. Prevention !!!
2. Find and kill the source of
the infection
3. Fluid Resuscitation
4. Vasoconstrictors
5. Inotropic drugs
6. Maximize O2 delivery
Support
7. Nutritional Support
8. Comfort & Emotional
support
SEQUELAE OF SEPTIC SHOCK
• The effects of the bacteria’s
endotoxins can continue even
after the bacteria is dead,

49. END