types of shock and management

1. SHOCK
“A momentary pause in the act of
death.”
-John Collins Warren, 1800s
SAI KUMAR

2.  Shock is the “physiologic state characterized by
significant reduction of systemic tissue perfusion,
resulting in decreased tissue oxygen delivery.”
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

3. Clinical features of shock
 drop of systolic blood pressure
 low cardiac output and tachycardia
 vasoconstriction: skin and splanchnic areas
 oliguria (< 20 ml/hour)
 cold wet skin
 constriction of superficial veins
 marked muscle weakness
 usualy  body temperature (except septic shock)
 disorientation
 metabolic acidosis

4. Three Types of Shock
 Hypovolemic
 Distributive
Septic
Anaphylactic
Neurogenic
 Cardiogenic

5. Hypovolemic Shock
 Shock caused by decreased preload due to intravascular
volume loss (1/5 of blood volume)
 Results in decreased CO
 SVR is typically increased in an effort to compensate
 Causes:
Hemorrhagic – trauma, GI bleed, hemorrhagic
pancreatitis, fractures
Fluid loss induced – Diarrhea, vomiting, burns

6. Stages of shock
1. Nonprogressive stage (compensated)
Compensatory mechanisms (negative feedback) of the
circulation can return CO and BP to normal levels
 baroreceptor reflexes  sympathetic stimulation 
constrict arteriols in most parts of the body and venous
reservoirs  protection of coronary and cerebral blood
flow
angiotensin-aldosteron, ADH  vasoconstriction,
 water and salt retention by the kidneys
 absorption of fluid from ISF and GIT, increased thirst

7. 2. Progressive shock
circulatory system themselves begin to deteriorate, without
therapy shock becomes steadily worse until death
positive feedback mechanisms are developed and can
cause vicious circle of progressively decreasing CO
Cardiac depression -  coronary blood flow,  contractility
Vasomotor failure -  cerebral blood flow
Release of toxins by ischemic tissues: histamine, serotonin,
tissue enzymes
Intestines hypoperfusion  mucosal barrier disturbance 
endotoxin formation and absorption  vasodilatation,
cardiac depression

8.  Vasodilation in precapillary bed
 Generalised cellular deterioration:  K+ ,  ATP, release of
hydrolases – first signs of multiorgan failure

9. 3. Irreversible shock
- despite therapy circulatory system continues to
 deteriorate and death ensues
 - marked hypoxic tissue damage
- endothelial dysfunction  adhesive molecules,
 neutrophils, macrophages  inflammation
 - progressive acidosis
- microcirculation failure  plasma proteins
leak to interstitium
- advanced disseminated intravascular
coagulation

10. Treatment of Hypovolemic Shock
Maximize oxygen delivery
Control further blood loss
Tourniquets
Surgical intervention
Fluid resuscitation
NS fluid boluses
Blood product administration

11. Distributive Shock
 Shock as a result of severely diminished SVR
 CO is typically increased in an effort to maintain
perfusion
 Subtypes:
Septic – secondary to an overwhelming infection
Anaphylactic – secondary to a life-threatening
allergic reaction
Neurogenic – secondary to a sudden loss of the
autonomic nervous system function

12. Treatment of Septic Shock
 Resuscitate
 30cc/kg of NS bolus
 Identify Source
 Pan cultures
 CT scan
 Line removal
 Foley removal
 Surgical exploration
 Antibiotics

13. Anaphylactic Shock
• Anaphylaxis – a severe systemic
hypersensitivity reaction characterized by
multisystem involvement
• IgE mediated
• Anaphylactoid reaction – clinically
indistinguishable from anaphylaxis, do not
require a sensitizing exposure
• Not IgE mediated

14. What are some symptoms of anaphylaxis?
• 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

15. CLINICAL FEATURES
• Mild, localized urticaria can progress to full anaphylaxis
• Symptoms usually begin within 60 minutes of exposure
• Faster the onset of symptoms = more severe reaction
• Biphasic phenomenon occurs in up to 20% of patients
• Symptoms return 3-4 hours after initial reaction has cleared
• A “lump in my throat” and “hoarseness” heralds life-
threatening laryngeal edema

16. Clinical diagnosis
• Defined by airway compromise, hypotension, or
involvement of cutaneous, respiratory, or GI
systems
• Look for exposure to drug, food, or insect
• Labs have no role

17. Treatment of Anaphylactic Shock
 Remove offending agent
 Establish an airway and return circulation
 Pharmacologic support:
 Epinephrine – reverses peripheral vasodilation, dilates
bronchial airways, increases myocardial contractility,
and suppresses histamine/ leukotriene release
 Antihistamine (benadryl) – may help counter histamine-
mediated vasodilation and bronchoconstriction
 Corticosteroids (hydrocortisone) – may help shorten
reaction
 Bronchodilators

18. Neurogenic Shock
• Occurs after acute spinal cord injury
• Sympathetic outflow is disrupted leaving
unopposed vagal tone
• Results in hypotension and bradycardia
• 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)

19. • Loss of sympathetic tone results in warm and dry
skin
• Shock usually lasts from 1 to 3 weeks
• Any injury above T1 can disrupt the entire
sympathetic system
• Higher injuries = worse paralysis

20. Treatment of Neurogenic Shock
 Establish an airway to maintain adequate
oxygenation and ventilation
 Fluid resuscitation for MAP>65mmHg
 Inotropic support
Dobutamine
Dopamine
 Atropine for severe bradycardia
 High dose methylprednisolone therapy

21. Cardiogenic Shock
 Shock caused as a result of cardiac pump failure
 Results in a decrease in CO
 SVR is increased in an effort to compensate to maintain organ
perfusion
 Causes:
Myocardial Infarction
Arrythmias (Atrial fibrillation, ventricular tachycardias,
bradycardias, etc)
Mechanical abnormalities (valvular defects)
Extracardiac abnormalities (PE, pulm HTN, tension
pneumothorax)

22. • Signs:
• Cool, mottled skin
• Tachypnea
• Hypotension
• Altered mental status
• Narrowed pulse pressure
• Rales, murmur

23. Treatment of Cardiogenic Shock
 Correct hypotension:
 Fluid resuscitation to correct hypovolemia
 Inotropic or Vasopressor support:
 Dobutamine
 Milrinone
 Norepinephrine
 Dopamine
 Epinephrine
 Oxygenation
 If MI – ASA, Heparin, and Revascularization
 If arrthymia – correct arrthymia
 If extracardiac abnormality – reverse or treat cause

24. Obstructive Shock
 Tension pneumothorax
 Cardiac tamponade
 Pulmonary embolism
 Aortic stenosis

25. Tension pneumothorax
• Air trapped in pleural space with 1 way valve,
air/pressure builds up
• Mediastinum shifted impeding venous return
• Chest pain, decreased breath sounds
• No tests needed!
• Rx: Needle decompression, chest tube

26. Cardiac tamponade
• Blood in pericardial sac prevents venous return
to and contraction of heart
• Related to trauma, pericarditis, MI
• Beck’s triad: hypotension, muffled heart
sounds, JVD
• Diagnosis: large heart CXR, echo
• Rx: Pericardiocentisis

27. Pulmonary embolism
• Virscow triad: hypercoaguable, venous injury,
venostasis
• Signs: Tachypnea, tachycardia, hypoxia
• Higher risk: CT chest
• Rx: Heparin, consider thrombolytics

28. Aortic stenosis
• Resistance to systolic ejection causes decreased
cardiac function
• Chest pain with syncope
• Systolic ejection murmur
• Diagnosed with echo
• Vasodilators (NTG) will drop pressure!
• Rx: Valve surgery

29. The End
Any Questions?