Approach to a patient in shock

GUIDES: DR.A.PAL

DR.S.SIDDIQUE

BY: DR.ANKUR KAUSHIK

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.

Hypovolemic

Traumatic

Cardiogenic

Intrinsic

Compressive

Septic

Hyperdynamic (early)

Hypodynamic (late)

Neurogenic

Hypoadrenal

• 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.

OTHER VASOCONSTRICTOR SUBSTANCES

Angiotensin II

Vasopressin

Endothelin I

Thromboxane A2

CIRCULATORY VASODILATORS

PGI2

NO

• 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

PULMONARY RESPONSE

• Increased Pulmonary vascular resistance

• Tachypnea

• Decreased tidal volume and increased dead space and

minute ventilation

RENAL RESPONSE

• ATN

Elevated Lactate/Pyruvate ratio

Significant rise in Triglyceride levels

Increased protein catabolism

Increased production of glucose

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

Compensated shock

Decompensated shock

Irreversible shock

Compensatory mechanisms attempts to maintain BP

NORMAL BLOOD PRESSURE

Unexplained tachycardia

Mild tachypnea

Delayed capillary refill

Orthostatic changes in pressure or pulse

irritability

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

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

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.

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

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

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, varicealbleed:

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

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

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 aortaECG: 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 infectionToxin screening won’t help unless used as confirmatory test b/c it doesn’t pick up most toxins which cause hypotensionEmergency ultrasound

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)

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

• Elderly: lack of sympathetic reserve

• Medications: Beta Blockers, Calcium Channel

Blockers, digoxin

• Intraabdominal pathology (vagal tone)

• Neurogenic shock also

• Hypothyroidism

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)

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.

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

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

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)

LPS binds to CD14 on surfaces of monocytes,

macrophages and neutrophils.

Which is then transferred to MD-2, that is bound toTLR-4

This transduce signals to interior of cell.

This activates various cytokines

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

NO

B-Endorphin

Bradykinin

Platelet activating factor

Prostacyclin

WARM SHOCK COLD SHOCK

TEMP 38 - 40 degrees with chills > 40 degrees or hypothermia

SKIN warm cool

CNS confused/obtunded stupor/coma

CVS tachycardia, hypotensionwide pulse pressurebounding pulsegood response to fluids/pressorsmyocardial depression

tachycardia, hypotensionnarrow pulse pressurethready pulsepoor response to fluids/pressorsmyocardial depression

RESP tachypnea, hypocarbia, mildhypoxemia

tachypnea, hypercarbia,hypoxemic respiratory failure

BLOOD leukocytosis w/ left shiftinc or dec plateletsnormal coagulation

leukocytosis or leukopeniathrombocytopeniaDIC

RENAL pre-renal failure renal failure

METABOLIC hyperglycemia, hypoalbuminemia,mild hepatic enzyme changes,mild respiratory alkalosis

hyper or hypoglycemia, lacticacidosis, hepatic failure

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

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

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-Ganzcatheter

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.

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).

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).

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

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 ionotropiceffect with least chronotropic effect and BP effects

Dose is 5 - 25 ug/kg/min: start 2 and increase to 20 ug/kg/min

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

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.

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 caspofungin70mg loading dose and then 50 mg daily or lipolized Amphotericin-B.

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.

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.

Recombinant activated protein C (Apc): approved by

FDA

Small molecule endotoxin antagonist: ERITORAN

Granulocyte-macrophage colony-stimulating factor

The most common type of shock

It has 4 types:

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.

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.

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

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.

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.

ColloidsAdvantages:less fluid required, more volume remains in vascular space, potential to draw fluids into vascular spaceDisadvantages: expensive, potential for allergic reactions, coagulopathies,seizuresExample: Albumin, hetastarch, pentastarch, dextran

CrystalloidsAdvantages: 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 osmolarityDisadvantages: hypernatremia, hyperosmolarity, seizures, coagulopathy, anaphylactoid reaction with dextran added.

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

Occurs in 5-10% of MI patients;

Mortality: 50 - 80%

Mean time to onset is 6hrs post admission thus EARLY

management important

LV failure 74%

acute MR 8%,

VSR 4%,

isolated RV failure 3%,

tamponade or cardiac rupture 2%,

other causes 8%

elderly

DM

antior MI

previous MI/PVD/CVA

previous poor EF

large infarctions

Female sex

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 HFAvoid BZD, morphine, barbituates, ketamine for sedationChoose fentanyl and etomidate for sedation

Fluids

Small boluses 250 ml NS over 10 min

Repeat if respiratory status not deteriorating

Should increase BP if hypotension due to hypovolemia.

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

Low doses 2-5 ug/kg/min: dopaminergic; renal/splanhnicvasodilation

Moderate 5-15 ug/kg/min: beta adreneragic; increased contractility, HR

High doses > 15 ug/kg/min: alpha adrenergic; vasoconstrictall vessels, increases BP, HR, contractility (may precipitate ishcemia, may worsen pulmonary edema

Indications

Hypotension SBP 70 - 100 with signs of hypoperfusionfailing fluid challenge:10-20 ug/kg/min

oliguria: 2-5 ug/kg/min

Mainly B1 agonist, some B2 and some alpha activityB1 is +ve ionotrope and venodilatorMay lead to hypotension by vasodilation if CO doesn’t increase muchExcellent 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 effectsDose is 5 - 25 ug/kg/min: start 2 and increase to 20 ug/kg/minIndications

Hypotension SBP 70 - 100 with no s/s of hypoperfusionafter fluid challenge

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

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

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

Assessment: stridor? can patient talk? angioedema of face?Management: chin-lift, jaw thrust, suction excess secretions,nasopharyngeal or oropharyngeal airwayRacemic epinephrine: 0.5 ml of 2.25% in 2.5 ml NS as temporizing measureEndotracheal 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

Breathing Assessment: respiratory effort, respiratory rate, wheezing, pulmonary edema

Management: ventilate as necessary, oxygen, pulsoximeter

Sedation may be necessary for ventilation after intubation

Drug of choice in anaphylaxisAlpha - agonism: peripheral vasoconstriction reduces vasodilation and vascular permeability to reduce hypotension; can precipitate hypertensive crisisBeta - agonism: bronchodilation, + ve ionotropic, +ve chronotropic; can precipitate myocardial ischemia, SVT and ventricular tachycardia's, stunned heart syndromeAbsolute contraindication: ventricular tachycardiasRelative contraindications: elderly, known CAD, hypertension

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

H1 antagonists: Should be used in all cases of anaphylaxisMany options although diphendydramine is the most commonly usedMild: adult:25 - 50 mg po q6h.Moderate:50 - 100 mg imSevere:50 - 100 mg iv over 3 minutesRepeat in 4 - 6 hrsH2 antagonists: H2 antagonism to block myocardial and peripheral vascular tissue responses to histamine Consider with persistent symptomsAdult: cimetidine 300 mg iv followe by 300 mg po q6h X 3/7

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

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

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

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

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.

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

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.

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.)