management of shock

1. GUIDES: DR.A.PAL
DR.S.SIDDIQUE
BY: DR.ANKUR KAUSHIK

2. Shock is the physiologic state characterized by
significant reduction of systemic tissue perfusion,
resulting in decreased tissue oxygen delivery. This
creates an imbalance between oxygen delivery and
oxygen consumption. Prolonged oxygen deprivation
leads to cellular hypoxia and derangement of critical
biochemical processes at the cellular level, which can
progress to the systemic level.

3.  Hypovolemic
 Traumatic
 Cardiogenic
 Intrinsic
 Compressive
 Septic
 Hyperdynamic (early)
 Hypodynamic (late)
 Neurogenic
 Hypoadrenal

5. • Mean Arterial Pressure (MAP) is dependent on two
variables
Cardiac Output (CO)
Systemic Vascular Resistance (SVR)
• MAP in shock drops to less than <70 mmHg
• Α1 receptor mediate vasoconstriction, B2 receptors
mediate vasodilation.
• Norepinepherine acts on A1 receptor, is one of the most
fundamental pathway in reduced perfusion pressure.

6. OTHER VASOCONSTRICTOR SUBSTANCES
Angiotensin II
Vasopressin
Endothelin I
Thromboxane A2
CIRCULATORY VASODILATORS
PGI2
NO

7. • Parameters controlling stroke volume
Ventricular filling (Preload)
Resistance to Ventricular ejection (Afterload)
Myocardial contractility
• CO=SV x HR
• Myocardial compliance is impaired in shock.
 Decreased preload
 Increased filling pressure – lead to secretion of BNP

9. PULMONARY RESPONSE
• Increased Pulmonary vascular resistance
• Tachypnea
• Decreased tidal volume and increased dead space and
minute ventilation
RENAL RESPONSE
• ATN

10. Elevated Lactate/Pyruvate ratio
Significant rise in Triglyceride levels
Increased protein catabolism
Increased production of glucose

11. Activation of compliment cascade (Both classical and
alternate pathways)
Activation of coagulation pathways
Activation of Eicosanoids- Cyclooxygenase derived
PGs, Thromboxane A2 and cysteinyl leukotrienes
TNF-A - causes hypotension, lactic acidosis and
respiratory failure
Interleukin 1b

12. Compensated shock
Decompensated shock
Irreversible shock

13. Compensatory mechanisms attempts to maintain BP
NORMAL BLOOD PRESSURE
Unexplained tachycardia
Mild tachypnea
Delayed capillary refill
Orthostatic changes in pressure or pulse
irritability

14. Baroreceptors and Chemoreceptors- Disinhibits
vasomotor centers which increases adrenergic output
Renin-Angiotension system- Angiotensin I and
Angiotensin II
Antidiuretic Hormone
Adrenal Cortex- Aldosterone
Posterior Pituitary- Vasopressin
ACTH from pituitary- Cortisol

15. It is a state of inadequate end-organ perfusion
Compensatory mechanisms fails and HYPOTENSION
occurs.
Increased tachycardia, increased tachypnea
Altered mental state, low urine output,
Poor peripheral pulses.
Capillary refill markedly delayed
Cool extremities

16. It occurs as a consequence of decompensated shock not
managed properly and at right time.
Permanent cellular damage & MODS.
Recovery does not occur even with adequate
restoration of circulatory volume
Death occurs due to refractory acidosis, myocardial and
brain ischemia.

17. LOOK FOR SIGNS OF SHOCK
Heart Rate: Tachycardia is defined as:
• Adult: >100
• School age: > 120
• Preschool: >140
• Infant: >160
(Tachycardia in the elderly may be limited by reduced cardiac reserve, Beta
Blockers, pacemakers, so we use narrow pulse pressure to suggest shock)
Blood Pressure: Sole reliance on BP may miss early diagnosis of shock
because of compensatory mechanisms
Respiratory rate: There is tachypnea
Altered mental status/Loss of consciousness
Pulse pressure: Pulse pressure is narrow (<30 mmHg)
Skin: Cold and clumsy or warm
urine output: decreased

18. Decreased consciousness or looks ill
HR > 100/min
RR > 24/min or PCO2 < 32 mmHg
Base Deficit < -5 mEq/L or lactate > 4 mmol/L
Urine output < 0.5 ml/kg/hr
Hypotension (SBP <90 mmHg) > 20 min duration

19. Targeted History
 Chest pain: MI, Pulmonary Embolism, aortic dissection
 Trauma: hemorrhage, tamponade, pneumothorax, spinal
 Immunocompromised/fever: septic
 Medications: pharmacologic, cardiodepression; CHRONIC
STEROIDS is a clue to adrenal crisis
 Hemorrhagic:Melena, hematemasis, hemoptysis, hematuria, variceal
bleed:
 GI loss:Vomiting, diarrhea
 Abdominal pain: pancreatitis, bowel perforation, intestinal ischemia,
ectopic rupture,inflammation, sepsis, third spacing, AAA rupture
 Back pain: AAA rupture
 Exposures: inhalation, drugs, hypo/hyperthermia,
dyshemoglobinopathy

20. General Examination: Level of consciousness,
responsiveness, toxic looking, cyanosis. Patient should be
fully exposed. Look for evidence of trauma, smell of alcohol
etc, raised JVP.
Chest: Auscultate for pulmonary edema (rales), wheezing
with anaphylaxis, Air entry for evidence of pneumothorax or
hydrothorax
CVS: muffled HS, new murmur.
PA: solid organ tenderness, evidence of trauma, peritonitis,
AAA
CNS: GCS, pupils, movement, reflexes
Rectal: ? blood

21. Look for hypoglycemia, electrolyte abnormalities,
leukocytosis or leukopenia with sepsis, increased BUN with
UGI bleed or dehydration, HB for hemorrhage, blood cultures
if febrile.
CXR: pulmonary edema, pneumothorax, cardiomegaly,
infiltrates, wide aorta
ECG: mandatory in adults, look for MI.
ABG: Discrepancy between Sa02 on pulse oximeter and Pa02
on think hemoglobinopathy (CO, HS, Methemoglobinemia)
Urinalysis : for focus of infection
Toxin screening won’t help unless used as confirmatory test
b/c it doesn’t pick up most toxins which cause hypotension
Emergency ultrasound

22. Routine: BP, cardiac, pulsoximeter, input/output.
Invasive: arterial pressure (art line), CVP (central line),
pulmonary artery pressure (Swan-Ganz), PCWP
Shock index = HR/SBP : > 0.9 as an indicator of incipient
shock
Arterial - venous blood gas to determine oxygen
extraction
Lactate: predict poor outcomes,
End - tidal CO2: estimation of cardiac output and response
to resuscitation (initially low because poor flow and
hyperventilation but increases with resuscitation)

23. Consciousness can be maintained until MAP 40 thus
LOC a late sign.
Shock index : HR/SBP: suggests shock if > 0.9
Lactate clearance index :More resuscitation required
if lactate has not decreased by > 50%. Goal lactate < 2
mmol/l

24. • Elderly: lack of sympathetic reserve
• Medications: Beta Blockers, Calcium Channel
Blockers, digoxin
• Intraabdominal pathology (vagal tone)
• Neurogenic shock also
• Hypothyroidism

25. Unresponsive to fluids or pressors for more than 1hr.
MUST think of adrenal crisis
Labs of decreased Na, increased K+ only with primary
adrenal crisis
Dexamethasone 4 mg iv
Hydrocortisone 50mg q6h (maximum dose of 200
mg/day)

27. Bacteremia = blood culture positive for bacteria
SIRS
• Temp > 38.0 Cor < 36.0 C
• HR > 90 bpm
• RR > 24/m
• Wbc > 12,000/uL or < 4,000/uL or > 10% bands
Sepsis = SIRS + documented infection
Severe Sepsis = Sepsis + MODS: decreased
consciousness , ARF, DIC, ARDS, Hepatic dysfunction
Septic shock = Sepsis + Hypotension (<90 mmHg or 40
mmHg less than patients normal BP) refractory to
volume resuscitation (requiring pressors) for more than
1hr.

28. It’s a grading system for sepsis
Predisposition: age, chronic obstructive pulmonary
disease, liver disease, nursing home residency, and
malignancy with and without metastasis.
Infection: pneumonia and cellulitis
Response: tachypnea, bandemia, and tachycardia
Organ dysfunction: renal, respiratory, cardiac,
metabolic, and hematologic

29. Inadequate corticosteroid activity for the patient’s
severity of illness
Should be suspected when hypotension is not relieved
by fluid administration
Due to adrenal gland failure

30. Mostly due to bacteria and fungal infections.
Blood culture +ve in 20-40% patients of severe sepsis,
40-70% cases of septic shock
Any bacterium can cause sepsis but most due to gram
negative bacteria. (Both of them causes 70% cases of
sepsis)
Gram positives do not have LPS
LPS (lipopolysaccharide) part of gram –ve’s outer
membrane (endotoxin) which is a potent activator of
mediators of septic shock (lipid A moiety is specific
part, hexaacyl moiety)

31. LPS binds to CD14 on surfaces of monocytes,
macrophages and neutrophils.
Which is then transferred to MD-2, that is bound to
TLR-4
This transduce signals to interior of cell.
This activates various cytokines

32. THREE MAIN COMPONENTS
(i) hypovolemia (ii) Cardiovascular depression (iii) systemic
inflammation
Relative hypovolemia due to vasodilation and decreased SVR
Absolute hypovolemia due to increased insensible losses and
capillary leaking/ third spacing
Note there is EARLY cardiac depression (was previously
thought to be late)
ARDS: capillary leaking into lungs

33. NO
B-Endorphin
Bradykinin
Platelet activating factor
Prostacyclin

34. WARM SHOCK COLD SHOCK
TEMP 38 - 40 degrees with chills > 40 degrees or hypothermia
SKIN warm cool
CNS confused/obtunded stupor/coma
CVS tachycardia, hypotension
wide pulse pressure
bounding pulse
good response to
fluids/pressors
myocardial depression
tachycardia, hypotension
narrow pulse pressure
thready pulse
poor response to
fluids/pressors
myocardial depression
RESP tachypnea, hypocarbia, mild
hypoxemia
tachypnea, hypercarbia,
hypoxemic respiratory failure
BLOOD leukocytosis w/ left shift
inc or dec platelets
normal coagulation
leukocytosis or leukopenia
thrombocytopenia
DIC
RENAL pre-renal failure renal failure
METABOLIC hyperglycemia,
hypoalbuminemia,
mild hepatic enzyme changes,
mild respiratory alkalosis
hyper or hypoglycemia, lactic
acidosis, hepatic failure

35. Acute Renal Failure
Adult Respiratory Distress Syndrome (ARDS)
Acute Hepatic Dysfunction
Disseminated Intravascular Coagulation
LOC
Adrenal insufficiency
Death : occurs in 20%-80% of the patients
Multi-Organ Dysfunction = abnormal function of >2
vital organs in association with SIRS

36. ABC with establishment of 2 large bore ivs, starting oxygen
putting on cardiac, BP, and pulsox monitors (may require
intubation/ventilation if very sick)
Draw blood for CBC, Ur, Cr, electrolytes, blood cultures,
PT, PTT, d-dimer,
Type and cross, ABG, order CXR and ECG, put in foley to
monitor fluid status, you may want central line and Swan-
Ganz, urinalysis and culture,
Procalcitonin is very specific marker for sepsis
May need LP
Brief History and systemic examination
Initial treatment: fluids, pressors, empiric antibiotics

37. Fluids
To achieve adequate fluid resuscitation, the Surviving
Sepsis Guidelines advise at least 30 ml/kg of
crystalloids (1.5-3 liters) be infused for most patients
(Grade 1C) in septic shock.
• 500 ml NS boluses q10 min until perfusion restored
• Commonly require 4 - 6 L
• Consider pressors for requiring > 3 L or signs of fluid
overload.
• Monitor status with foley, central line, Swan-Ganz
catheter

38. Norepinephrine should be provided as the first-line vasopressor
(Grade 1B).
Epinephrine is considered the next-line agent for septic shock after
norepinephrine in the Surviving Sepsis Guidelines. When
norepinephrine is insufficient to maintain MAP 65 mm Hg, epinephrine
should be added to or substituted for norepinephrine (Grade 2B).
Vasopressin at 0.03 units/minute is appropriate to use with
norephinephrine, either to improve perfusion (increase MAP) or to
reduce the required dose of norepinephrine (ungraded
recommendation).
Vasopressin is not recommended for use as a single vasopressor for
septic shock .
Vasopressin doses higher than 0.03 – 0.04 units/min are recommended
to be reserved only for dire situations of septic shock refractory to
standard doses of multiple vasopressors.

39. Dopamine is suggested to not be used as an alternative to
norepinephrine in septic shock, except in highly selected
patients such as those with inappropriately low heart rates
(absolute or relative bradycardia) who are at low risk for
tachyarrhythmias (Grade 2C). Dopamine is recommended
to not be used in low doses in a so-called renal-protective
strategy (Grade 1A).
Phenylephrine is recommended to not be used for septic
shock, except when 1) septic shock persists despite the use
of 2 or more inotrope/vasopressor agents along with low-
dose vasopressin; 2) cardiac output is known to be high, or
3) norepinephrine is considered to have already caused
serious arrhythmias (Grade 1C).

40. Dobutamine should be tried for patients in septic shock
who have low cardiac output with high filling pressures
while on vasopressors, or who have persistent evidence of
hypoperfusion after attaining an adequate mean arterial
pressure and intravascular volume (with or without
vasopressors) (Grade 1C).
A dobutamine infusion up to 20 mcg/kg/min can be added
to any vasopressor(s) in use. Dobutamine is also an
appropriate first-line agent in patients with severe sepsis
and low cardiac output, with a preserved mean arterial
pressure (i.e., who are not in septic shock) (Grade 1C).
Dobutamine is recommended not to be used to deliberately
raise cardiac output to higher than normal levels in an
attempt to improve perfusion (Grade 1B).

41. Norepinephrine
0.5- 30 ug/min iv
Start with or add to dopamine
B1 agonist and potent alpha1 agonism with minimal B2 effect thus very
effective to increase systemic vascular resistance
Dopamine
5- 20 ug/kg/min iv infusion
Add norepinephrine if unable to keep SBP > 60 with 20 ug/kg/min of
dopamine
1- 2 ug/kg/min (LOW): DOPAMINERGIC; increases renal and mesenteric
flow
2- 10ug/kg/min (MOD): Beta ADRENERGIC; increases contractility by B1
> 20ug/kg/min (HIGH): Alpha ADRENERGIC; increases BP due to alpha1

42. Mainly B1 agonist, some B2 and some alpha activity
B1 is +ve ionotrope and venodilator
May lead to hypotension by vasodilation if CO doesn’t
increase much
Excellent for normotensive, caution with borderline
hypotension, don’t use alone in hypotensive
Advantage:
Less tachycardia for given increase in CO than others
(no NE release form nerve endings), greatest ionotropic
effect with least chronotropic effect and BP effects
Dose is 5 - 25 ug/kg/min: start 2 and increase to 20
ug/kg/min

43. EARLY ANTIBIOTICS have been shown to decrease
mortality.
Should be started ASAP after cultures drawn
Broad-spectrum and maximum doses
Broad-spectrum = gram +ve’s, gram –ve’s, anaerobes

44. Immunocompetent adult: 1. Piperacillin-
tazobactam(3.375g q4-6h), 2. Imipenem-cilastine(0.5g
q6h). If allergic to B-lactam agents; ciprofloxacin(
400mg q12h) or levofloxacin(500-750 mg q12h) plus
clindamycin(600mg q8h). Vancomycin (15mg/kg 12h)
should be added to each of the above regimens.

45. 1. Imipenem-cilastine(0.5g q6h) or
meropenem(1gm/q12h) or cefepime(2g q8h).
2. Piperacillin-tazobactam(3.375g q4-6h)
plus tobramycin(5-7mg/kg q24h)
Vancomycin (15mg/kg 12h) should be added
to above regimens. Emperical antifungal
therapy should be started with caspofungin
70mg loading dose and then 50 mg daily or
lipolized Amphotericin-B.

46. Splenectomy: Cefotaxime(2g q6-8h) or
ceftriaxone(2g q12h), if local cephalosporin-
resistant pneumococci is high add vancomycin.
IV Drug users: Vancomycin (15mg/kg q12h)
AIDS: cefepime(2g q8h), Piperacillin-
tazobactam(3.375g q4-6h) plus tobramycin(5-
7mg/kg q24h), If allergic to B-lactam agents;
ciprofloxacin( 400mg q12h) or levofloxacin(500-
750 mg q12h) plus clindamycin(600mg q8h).
Vancomycin (15mg/kg 12h) should be added to
each of the above regimens.

47. Glucocorticoids — Evidence from randomized trials suggest that
corticosteroid therapy is most likely to be beneficial in patients
who have severe septic shock (defined as a systolic blood
pressure <90 mmHg) that is unresponsive to adequate fluid
resuscitation and vasopressor administration. Data from ongoing
clinical trials are needed to confirm that benefit.
Nutrition — There is consensus that nutritional support improves
nutritional outcomes in critically ill patients, such as body weight
and mid-arm muscle mass.
Intensive insulin therapy — Hyperglycemia and insulin resistance
are common in critically ill patients, Most clinicians target blood
glucose levels between 140 and 180 mg/dL (7.7 to
19 mmol/L). This topic is discussed separately.
External cooling — External cooling is preferable to no cooling,
but they do not provide guidance about whether external cooling
is preferable to antipyretic medications.

48. Recombinant activated protein C (Apc): approved by
FDA
Small molecule endotoxin antagonist: ERITORAN
Granulocyte-macrophage colony-stimulating factor

49. The most common type of shock

50. It has 4 types:

51. Physical Exam
ABCs are priority
Neurologic exam reflects cerebral perfusion
Vascular Access
• At least 2 16 (or larger) gauge needles in upper
extremities
• should not be placed in an injured extremity
• if peripheral lines cannot be established, femoral or
saphenous vein may be used for rapid infusion
• subclavian and internal jugular veins are useful for
CVP monitoring.

52. Rapid infusion of either isotonic saline or ringer lactate
should be started.
Care must be taken to avoid hyperchloremic acidosis
from loss of bicarbonate buffering capacity and
replacement with excess chloride.
Ringer lactate should be avoided in hyperkalemia and
renal dysfunction.
Infusion of 2-3 lit fluid over 20-30 mins should restore
normal hemodynamic parameters.

53. Monitoring Response
 BP, pulse pressure, HR, skin, level of consciousness
 Urinary output is the best parameter
 0.5cc/Kg/hr is normal in adults (35cc/hr in 75kg man)
Acid/Base Balance
• Early shock: respiratory alkalosis due to hyperventilation
• Middle: mild metabolic acidosis
• Late: severe metabolic acidosis due to inadequate tissue
perfusion
• Lactate levels and base deficits have been suggested as
best laboratory parameters to monitor hypovolemic shock
resuscitation
• Base deficit = amount of base required to be added to
neutralize the pH; normal is > -2 mmol/l; BD decreases
before pH drop or BP drop

54. Packed RBC is preffered over whole blood.
Crossmatched blood: preferable but takes 1hr
Type-Specific blood: type and screen takes 10min
Unmatched blood: type O- is indicated for all pts with
exsanguinating hemorrhage, type O+ can be given to
males and all women above child bearing age
Warming Fluids is Essential: heat fluid to 39 degrees;
cool blood leads to hypothermia and DIC
Coagulopathy: rare in first hour but DIC may develop
later; more of a concern with massive transfusion.

55. Equating BP with CO: an increase in BP does not
necessarily mean an increase in CO because
increased SVR can increase BP without increase in
CO
Elderly: reduced catacholamine response,
medications, pre-existing hypovolemia, reduced
cardiac function, other physiological reserve
(lungs, kidneys) is reduced
Athletes may not have tachycardia
Pregnancy is a hypervolemic state
Medications preventing response: BB, CCBs,
diuretics.

56. Colloids
Advantages:
less fluid required, more volume remains in vascular space,
potential to draw fluids into vascular space
Disadvantages: expensive, potential for allergic reactions,
coagulopathies,
seizures
Example: Albumin, hetastarch, pentastarch, dextran
Crystalloids
Advantages: less volume needed, stays in intravascular
space better, draws in interstitial fluid, increases cardiac
output and MAP, inotrope, decreases SVR due to vasodilation
of precapillary vessels as a result of osmolarity
Disadvantages: hypernatremia, hyperosmolarity, seizures,
coagulopathy, anaphylactoid reaction with dextran added.

58. Decreased cardiac output and evidence of tissue
hypoxia in presence of adequate intravascular volume
Cardiac Failure = clinical CHF
Cardiogenic Shock = clinical CHF + 4/6 empiric
criteria for shock (see above)
Cardiogenic shock generally occurs when > 40% of
myocardium not working
Hemodynamic criteria: hypotension (SBP < 90) for >
30 min), cardiac index <2.2L/min/m2, PCWP > 18
mmHg

59. Occurs in 5-10% of MI patients;
Mortality: 50 - 80%
Mean time to onset is 6hrs post admission thus EARLY
management important

60. LV failure 74%
acute MR 8%,
VSR 4%,
isolated RV failure 3%,
tamponade or cardiac rupture 2%,
other causes 8%

61. elderly
DM
antior MI
previous MI/PVD/CVA
previous poor EF
large infarctions
Female sex

62. Intraarterial BP monitoring essential because of huge
differences that can be found between cuff BP and true
pressures. Allows agressive use of venodilators and possible
avoidance of vasopressors; allow accurate titration of
ionotropes, venodilators, vasopressors.
Hypotensive: cardiogenic shock versus true volume
depletion cannot be determined clinically; needs invasive
monitoring of CVP, PAP, PCWP (low PAP/CVP is
hypovolemia)
Vasopressors are good to increase coronary perfusion but
bad because increased afterload worsens HF
Avoid BZD, morphine, barbituates, ketamine for sedation
Choose fentanyl and etomidate for sedation

63. Fluids
Small boluses 250 ml NS over 10 min
Repeat if respiratory status not deteriorating
Should increase BP if hypotension due to hypovolemia.

64. Other
 ETT and ventilation
 Left Ventriclar Assist Device (LVAD)
 PCI/CABG: in cases of acute MI
 Intra-Aortic Balloon pump (IABP)
 Indication:
cardiogenic shock not stabilized by ionotropes
Increases coronary perfusion by 30%
Contraindication: aortic insufficiency, severe PVD

65. Low doses 2-5 ug/kg/min: dopaminergic; renal/splanhnic
vasodilation
Moderate 5-15 ug/kg/min: beta adreneragic; increased
contractility, HR
High doses > 15 ug/kg/min: alpha adrenergic; vasoconstrict
all vessels, increases BP, HR, contractility (may precipitate
ishcemia, may worsen pulmonary edema
Indications
Hypotension SBP 70 - 100 with signs of hypoperfusion
failing fluid challenge:10-20 ug/kg/min
oliguria: 2-5 ug/kg/min

66. Mainly B1 agonist, some B2 and some alpha activity
B1 is +ve ionotrope and venodilator
May lead to hypotension by vasodilation if CO doesn’t
increase much
Excellent for normotensive, caution with borderline
hypotension, don’t use alone in hypotensive
Advantage:
Less tachycardia for given increase in CO than others (no NE
release form nerve endings), greatest ionotropic effect with
least chronotropic effect and BP effects
Dose is 5 - 25 ug/kg/min: start 2 and increase to 20
ug/kg/min
Indications
Hypotension SBP 70 - 100 with no s/s of hypoperfusion
after fluid challenge

67. Mostly alpha agonist (some beta)
Drug of choice for volume repleated profound
hypotensive (SBP < 70)
May add dopaminergic doses (2-5 ug/kg/min) to
preserve renal perfusion
Goal: temporary management until IABP, PTCA,
surgery
Dose is 0.5 ug/kg/min
Indication hypotension SBP < 70 failing fluid challenge

68. Isoproteronol: potent beta agonist, profound
tachycardia, it should be avoided
Digitalis: little role in acute HF, some role in rate
control with Afib/flutter
Amrinone/Milrinone: phosphodiesterase III inhibitior
thus increases cAMP and acts as vasodilator, ionotrope
with minimal HR/BP changes

69. 5-10% of Mi
Mortality 70%
Thrombolysis unlikely to be effective b/c of low
coronary perfusion pressure thus drug isn’t delivered to
site of thrombosis
Options for management
Thrombolysis
PTCA
Emergent CABG

71. Assessment: stridor? can patient talk? angioedema of face?
Management: chin-lift, jaw thrust, suction excess
secretions,
nasopharyngeal or oropharyngeal airway
Racemic epinephrine: 0.5 ml of 2.25% in 2.5 ml NS as
temporizing measure
Endotracheal intubation is preferred route of intubation,
should be done early before complete obstruction,
fiberoptic bronchoscopy may help,nasotracheal intubation
is an option in awake, uncooperative patient.
Sedation and paralysis is relatively contraindicated
because of a distorted airway may preclude intubation
after paralysis.
Surgical airway may be needed: should be prepared

72. Breathing Assessment: respiratory effort,
respiratory rate, wheezing, pulmonary edema
Management: ventilate as necessary, oxygen,
pulsoximeter
Sedation may be necessary for ventilation
after intubation

73. Drug of choice in anaphylaxis
Alpha - agonism: peripheral vasoconstriction
reduces vasodilation and vascular permeability to
reduce hypotension; can precipitate hypertensive
crisis
Beta - agonism: bronchodilation, + ve ionotropic,
+ve chronotropic; can precipitate myocardial
ischemia, SVT and ventricular tachycardia's,
stunned heart syndrome
Absolute contraindication: ventricular
tachycardias
Relative contraindications: elderly, known CAD,
hypertension

74. Mild adult: 0.3 - 0.5 ml of 1:1000
subcutaneous
Moderate adult: 0.3 - 0.5 ml of 1:1000
intramuscular
Severe adult: 10 ml of 1:100,000 intravenous
over10 min then infusion of 1 - 4 ug/min if
necessary or 1ml of 1:10,000 q 30 sec to
effect

75. H1 antagonists: Should be used in all cases of
anaphylaxis
Many options although diphendydramine is the most
commonly used
Mild: adult:25 - 50 mg po q6h.
Moderate:50 - 100 mg im
Severe:50 - 100 mg iv over 3 minutes
Repeat in 4 - 6 hrs
H2 antagonists: H2 antagonism to block myocardial
and peripheral vascular tissue responses to histamine
Consider with persistent symptoms
Adult: cimetidine 300 mg iv followe by 300 mg po
q6h X 3/7

76. Should be added if bronchospasm does not respond to
epinephrine
Albuterol nebulizer 2.5 - 5.0 mg neb and repeat (may
need continous)
Ipratropium: 250 - 500 ug neb may help
Aminophylline: another option, 5.6 mg/kg load over 20
min then 0.1mg/kg/hr

77. Limited benefit acutely as onset of action is 4 - 6hrs
blunting the late phase
Loading: Hydrocortisone 250 mg iv or
Methylprednisone 125 mg.
A convenient oral corticosteroid is prednisone at dose
of 1mg/kg/day.
Have role in biphasic anaphylaxis

78. Fluids: 1st thing to do in anaphylactic shock is giving
fluids in form of crystalloids.
Consider vasopressors for refractory hypotension
Dopamine:5 ug/kg/min
Intravenous epinephrine (1:10,000 v/v preparation) can
be administered as a continuous infusion

79. Positive ionotropic and chronotropic cardiac effects
(independent of alpha and beta adrenergic receptors)
Enhances CAMP synthesis
Consider in patients refractory to treatment and
epinephrine – resistant patients who are on beta
blockers
Adults: 1 mg sc, im, iv then infusion 1 - 5 mg/hr
Watch for hypokalemia and hyperglycemia

80. Anti-IgE (omalizumab) complexes circulating (but not
receptor-bound) IgE and keeps it from binding to its
receptors. It does not remove IgE bound to receptors
and can take several weeks to months to have a
substantial effect. It should not be used in an acute
setting and would not be expected to influence IgE-
independent or nonimmunologic events.

82. Initial loss of somatic motor, sensory, and sympathetic,
autonomic function due to spinal cord injury.
Sympathetic component: this is neurogenic shock
(one manifestation of spinal shock which is systemic
hypotension due to loss of sympathetic function but
preservation of parasympathetic function)
Motor component: flaccid paralysis, areflexia
Sensory component: anesthesia to all modalities

83. Hypotension + Paradoxical Bradycardia + warm/dry skin
and adequate urine output
May not have actual bradycardia; may simply have failure
to respond to become tachycardia with hypotension
BRADYCARDIA: loss of sympathetic innervation to the
heart (unopposed vagal stimulation); occurs with injuries at
or above T4
HYPOTENSION: due to vasodilation due to loss of
sympathetic tone; usually occurs with injuries at or above
T6 because if it is below T6 there is enough sympathetic
tone left to the torso and upper body that the BP doesn’t
drop.

84. Fluid is always the initial treatment of shock, especially
since concomitant hemorrhagic shock must be excluded
following trauma. Most institutions will additionally
utilize pressor agents to achieve hemodynamic stability.
Dopamine is often used either alone or in combination with
other inotropic agents.
Vasopressin (antidiuretic hormone [ADH])
Certain vasopressors (ephedrine, norepinephrine). Phenylep
hrine may be used as a first line treatment, or secondarily in
patients who do not respond adequately to dopamine.
Atropine (administer if bradycardia is severe.)