1.

DEF- It is a life threatening clinical state of cardiovascular collapse

characterized by hypotension and hypoperfusion.
2. CLASSIFICATION-
a. Hypovolemic
b. Traumatic
c. Cardiogenic
i. Intrinsic
ii. Compressive
d. Distributive
i. Septic
1. Hyperdynamic
2. Hypodynamic
ii. Neurogenic
iii. Anaphylactic
e. Hypo adrenal
3. HYPOVOLEMIC SHOCK
a. MC
b. ETIOLOGY
i. Loss of RBCs and plasma from hemorrhage
ii. Loss of plasma volume alone d/t extravascular fluid sequestration.
iii. Grading
Mild Moderate Severe
<20% BV lost 20-40% >40%
Cool Same, Same
extremities Plus tachycardia, tachypnoea, plus hemodynamic
Capillary refill oliguria, postural changes. instability
Diaphoresis marked tachycardia
Collapsed hypotension
veins mental state
Anxiety deterioration- coma
4. DIAGNOSIS
a. C/F
b. Obvious source of volume loss.
5. TRAUMATIC SHOCK
a. ETIOLOGY- Mostly hypovolemia

6. CARDIOGENIC SHOCK
a. Intrinsic type
i. ETIO- sudden failure of heart as an effective pump due to -
 1. AMI (Acute MI)- MC
2. Severe brady ir tachyarrhythmias
3. Valvular heart diseases
4. Significant cardiac contusion
5. End stage CHF
ii. C/F
1. Dec CO
2. Dec peripheral perfusion
3. Pulmonary congestion
4. Inc systemic vascular resistance
5. Inc pulmonary vascular pressure
b. Compressive type
i. ETIOLOGY
1. Tension pneumothorax
2. Pericardial tamponade
3. Abdominal hernia
4. Excess +ve pressure ventilation
ii. PATHOGENESIS
1. Compression of heart and surrounding structures
2. Decreased compliance of heart to contract
3. Inadequate diastole filling despite normal filling pressure.
iii. Diagnosis - C/F, CXR, ECG
iv. C/F - triad of-
1. Hypotension
2. Neck vein distension
3. Muffled heart sounds
4. Pulsus paradoxus
7. DISTRIBUTIVE SHOCK- Dec tissue perfusion due to dec systemic
vascular resistance. (vessels highly dilated).
8. SEPTIC SHOCK
a. ETIOLOGY
i. Caused by a systemic response to a severe infection.
ii. By gram +ve, -ve, virus, fungi etc. gram -ve release endotoxins and
are most deadly.
iii. MC infections of lung, abdomen, urinary tract etc.
b. PATHOGENESIS
i. Endotoxins / other chemical toxins released by microbes
ii. Act on tissues
iii. Inflammatory mediators released by tissues
iv. These act on mast cells
v. Stimulated mast cells release histamine, leukotrienes etc.
vi. These dilate BVs and increase their vascular permeability.
 vii. Fluid accumulation in interstitium and BV decreases.
viii. Complement system activated and increased inflammation.
c. PREDISPOSING FACTORS
i. Elderly
ii. Immunocompromised
iii. Invasive procedure pts.
d. C/F
i. Fever
ii. Inc acute phase reactants
iii. Hypotension
iv. Decreased tissue perfusion>> ischemic tissues.
v. HEMODYNAMIC CHANGES
1. HYPERDYNAMIC (WARM) SHOCK (abnormally increased
muscular activity, in this case, heart and BVs)
a. This occurs first
b. Fever
c. Tachypnea
d. Tachycardia
e. CO normal or inc
f. SVR (Systemic vascular resistance) dec
g. Warm extremities
h. PVR (PERIPHERAL VASCULAR RESISTANCE) dec
i. Profound diuresis
j. However, compensatory mechanisms eventually
fail.
k. Microvascular occlusions and DIC
2. HYPODYNAMIC (COLD or "low-output" or "high
resistance") SHOCK
a. Cool mottled, cyanotic extremities
b. Low WBC count
c. Profound hypotension and hypoperfusion
d. Tachycardia, tachypnea
e. CO dec
f. Diaphoretic
g. Obtunded (reduced consciousness)
h. Later stages- oliguria,
i. Renal failure
j. S lactate inc
k. Eventual multisystem failure
9. ANAPHYLACTIC SHOCK
a. Allergic reaction
b. Etio- allergens like bee stings, penicilin, foods, IV contrast fluids.
c. Pathogenesis
 10. C/F
a. Severe respiratory distress
b. Vasodilated BVs- hypotension
c. Hypoperfusion- ischemia and necrosis of tissues >> organ failure
d. Edema
e. Laryngeal edema >> resp obstt.
f. Swelling of lips and eyes.
g. Pruritis and urticaria
h. Rashes
11. NEUROGENIC SHOCK
a. Etiology- interruption of sympathetic vasomotor output d/t-
i. High cervical spinal cord injury
ii. Severe head injury
b. C/F
i. Unopposed vagal tone >> bradycardia
ii. Warm extremities
iii. Both arteriolar and venodilatation >> dec SVR >> dec BP >>
hypotension and hypoperfusion
iv. Pooling in the venous system
v. Decreased venous return and hence CO
12. HYPOADRENAL SHOCK
a. ETIOPATHOGENESIS
i.
ii. Chronic administration of high doses of exogenous
glucocorticoids.
iii. Idiopathic atrophy
iv. TB
v. Metastatic disease
vi. Blood hemorrhage
vii. Amyloidosis
 
 
 
TREATMENT
13. HYPOVOLEMIC SHOCK
a. 2 strategies
i. Rapid re-expansion of BV
1. Rapid infusion of normal saline or Ringer's lactate- 2-3 L
over 20-30 mins
2. If Hb<10 gm- blood transfusion
 3. Sever or prolonged hypovolemia- give inotropic support-
dopamine, dobutamine or vasopressin.
ii. Control blood loss - apply pressure to wound, sutures etc.
14. TRAUMATIC SHOCK
a. Check ABC-
i. A-airway patency
ii. B-breathing
iii. C circulation
b. Control hemorrhage
c. Stabilize fractures if any
d. Debride devitalised or contaminated tissues.
e. Evaluate hematomas
15. INTRINSIC CARDIOGENIC SHOCK
a. Inotropic agents
b. IV furosemide
c. IABP- Intra-aortic balloon counter pulsations
d. Correct anatomic defects
16. COMPRESSIVE CARDIOGENIC SHOCK
a. Immediate chest/ heart decompression
17. SEPTIC SHOCK
a. Treatment of infection by:
i. Appropriate antibiotics
ii. Surgical drainage/debridement of wound
b. Treatment of shock by:
i. I/V fluid infusion.
ii. Vasopressor drugs.
iii. Steroids in high doses over a short period. Single dose of methyl
prednisolone (15-30 mg/kg) is given I/V and repeated after 4 hrs.
18. NEUROGENIC SHOCK
a. Volume correction
b. Vasopressors- dobutamine, epinephrine, atropine , Norepinephrine to
increase systemic vascular resistance.
19. HYPOADRENAL SHOCK
a. Hemodynamically unstable patients-give dexamethasone4 mg IV or
hydrocortisone 100 mg IV TID or QID with tapering doses.
20. ANAPHYLACTIC SHOCK
a. Epinephrine - constricts BVs
b. Antihistamines - ranitidine etc.
c. Monitor patient. (attacks recur after few hrs- called biphasic
phenomenon).