Management of Shock

Wendy Amelia S

Anisa Ikawati

Shock

Definition of Shock

• Inadequate oxygen delivery to meet metabolic demands

• Results in global tissue hypoperfusion and metabolic acidosis

Oxygen Transport

• Oxygen Transport:– Hemoglobin-bound

(97%)– Dissolved in plasma

(3%)

• Monitoring:– Hemoglobin-bound

(SpO2)

– Dissolved in plasma (pO2)

Oxygen Delivery

• DO2 = Normal Oxygen Delivery

• DO2 = CO X CaO2

• DO2 = CO X (1.34 X Hb X SpO2) X 10

• Normal DO2 is 520 to 570 mL/minute/m2

Clinical Correlation

DO2 = CO X (1.34 X Hb X SpO2) X 10

What factors can affect oxygen delivery to the tissues?

Cardiac Output

Available Hemoglobin (Hb)

Oxygen Saturation (SpO2)

Oxygen Uptake

VO2 = CO X 13.4 X Hb X (SpO2-SvO2)

Oxygen Extraction Ratio

O2ER = VO2 / DO2 X 100

Normal O2ER = 0.2-0.3 (20 to 30%)

Metabolic Demand

• MRO2 :

– 1. The metabolic demand for oxygen at the tissue level.

– 2. The rate at which oxygen is utilized in the conversion of glucose to energy and water through glycolysis and Kreb’s cycle.

Shock

VO2 ≥ MRO2 = Normal Metabolism

VO2 < MRO2 =

Shock

• Causes of Shock:– Inadequate oxygen delivery

• Inadequate respiration and oxygenation– Respiratory failure (mechanical, toxins)

• Inadequate hemoglobin– Hemorrhage or anemia

• Inadequate fluid in the vascular system– Hemorrhage or fluid loss (burns, vomiting, diarrhea, sepsis)

• Inadequate blood movement– Cardiac pump failure

– Impaired oxygen uptake• Biochemical poisoning (hydrogen cyanide)

Shock

• Impaired oxygen uptake

• Cyanide:– Inhibits metal-

containing enzymes (i.e., cytochrome oxidase)

– Halts cellular respiration

Shock

• Causes of Shock:– Inadequate nutrient delivery

• Inadequate nutrient intake– Malnutrition, GI absorption disorder

• Inadequate nutrient delivery– Malnutrition, hypoproteinemia

• Inadequate fluid in the vascular system– Hemorrhage, fluid loss (burns, vomiting, diarrhea)

• Inadequate blood movement– Cardiac pump failure

– Impaired nutrient (glucose) uptake• Lack of insulin (Diabetes Mellitus)

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1. Normal cell• Hypoxia: intracellular ischemia occurs; anaerobic metabolism

begins; lactic acid builds up in cell; leading to metabolic acidosis; causes the sodium potassium pump to fail.

• Ion shift occurs Sodium rushes into the cell bringing water with it.

• Cell swelling occurs.• Mitochondrial swelling occurs; production of ATP ceases.• Intracellular disruption releases lysosomes, cell membrane

begins to break.• Cell destruction begins leading to tissue death.

Pathophysiology of Shock:Seven Stages of Cell Death

Approach to the Patient in Shock

• History• Recent illness• Fever• Chest pain, SOB• Abdominal pain• Comorbidities• Medications• Toxins/Ingestions• Recent hospitalization or

surgery• Baseline mental status

• Physical examination• Vital Signs• CNS – mental status• Skin – color, temp,

rashes, sores• CV – JVD, heart sounds• Resp – lung sounds, RR,

oxygen sat, ABG• GI – abd pain, rigidity,

guarding, rebound• Renal – urine output

Symptoms and Signs of Shock• Level of consciousness• Initially may show few symptoms

– Continuum starts with• Anxiety• Agitation• Confusion and Delirium• Obtundation and Coma

• In infants– Poor tone– Unfocused gaze– Weak cry– Lethargy/Coma– (Sunken or bulging fontanelle)

Symptoms and Signs of Shock

• Pulse – Tachycardia HR > 100 – Rapid, weak, thready distal pulses

• Respirations– Tachypnea– Shallow, irregular, labored

• Blood Pressure– May be normal!– Definition of hypotension

• Systolic < 90 mmHg • MAP < 65 mmHg• 40 mmHg drop systolic BP from from baseline

• Children– Systolic BP < 1 month = < 60 mmHg– Systolic BP 1 month - 10 years = < 70 mmHg + (2 x age in years)

• In children hypotension develops late, late, late– A pre-terminal event

Symptoms and Signs of Shock

Symptoms and Signs of Shock

• Skin– Cold, clammy (Cardiogenic,

Obstructive,Hemorrhagic)– Warm (Distributive shock)– Mottled appearance in children– Look for petechia

• Dry Mucous membranes• Low urine output <0.5 ml/kg/hr

Empiric Criteria for Shock4 out of 6 criteria have to be met

• Ill appearance or altered mental status• Heart rate >100• Respiratory rate > 22 (or PaCO2 < 32 mmHg)• Urine output < 0.5 ml/kg/hr• Arterial hypotension > 20 minutes duration• Lactate > 4

- Lactate is increased due to:Decreased O2 --> aerobic metabolism switches over to anaerobic --> byproduct = lactateDecreased hepatic clearance

Goals of Treatment

• ABCDE• Airway• control work of Breathing• optimize Circulation• assure adequate oxygen Delivery• achieve End points of resuscitation

Airway & Breathing• Decision to intubate and initiate ventilatory

support should be made on clinical basis• Determine need for intubation but remember:

intubation can worsen hypotension• Sedatives can lower blood pressure• Positive pressure ventilation decreases preload

• Consider Intubation– Is the cause quickly reversible?

• Generally no need for intubation

– 3 reasons to intubate in the setting of shock

• Inability to oxygenate• Inability to maintain airway• Work of breathing

Treatment: Airway and Breathing

Inability to oxygenate (Pulmonary edema,

SaO2 88%)

Accessory Muscle Use

Recognize signs of early respiratory failure: • Inability to speak• Labored breathing • Cyanosis• Tachypnea • Mental obtundation• Paradoxical breathing • Diaphoresis • Accessory muscle use

Optimizing Circulation

• Isotonic crystalloids

• Titrated to:• CVP 8-12 mm Hg • Urine output 0.5 ml/kg/hr (30 ml/hr) • Improving heart rate

• May require 4-6 L of fluids

Maintaining Oxygen Delivery

• Decrease oxygen demands• Provide analgesia and anxiolytics to relax muscles

and avoid shivering

• Maintain arterial oxygen saturation/content• Give supplemental oxygen• Maintain Hemoglobin > 10 g/dL

• Serial lactate levels or central venous oxygen saturations to assess tissue oxygen extraction

End Points of Resuscitation

• Goal of resuscitation is to maximize survival and minimize morbidity

• Use objective hemodynamic and physiologic values to guide therapy

• Goal directed approach• Urine output > 0.5 mL/kg/hr• CVP 8-12 mmHg• MAP 65 to 90 mmHg• Central venous oxygen concentration > 70%

Practically Speaking….

• Keep one eye on these patients

• Frequent vitals signs:• Monitor success of therapies• Watch for decompensated shock

• Let your nurses know that these patients are sick!

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Stages of Shock: Classic Shock Syndrome

1. Compensated - body is able to compensate and maintain tissue perfusion.

2. Progressive - body begins to loss its ability to compensate - inadequate perfusion begins.

3. Irreversible - Cell and tissue damage result in multi-system organ failure leading to death.

Shock (Classifications)

– Cardiogenic Shock– Hypovolemic Shock– Distributive Shock

• Spinal Shock• Septic Shock• Anaphylactic

Case 1

• 24 year old male

• Previously healthy

• Brought in by friends after a fight - he was kicked in the abdomen

• He is agitated, and won’t lie flat on the stretcher

• HR 92, BP 126/72, SaO2 95%, RR 26

Answer:

• It Was Hemorrhagic Shock

• The patient is in shock because:

-his respiratory rate is increased (tachypnea is a compensatory mechanism for early metabolic acidosis)

-he is also agitated which means he has altered mental status due to end organ lack of perfusion and dysfuction

Hypovolemic Shock

• Non-hemorrhagic • Vomiting• Diarrhea• Bowel obstruction, pancreatitis• Burns • Neglect, environmental (dehydration)

• Hemorrhagic • GI bleed• Trauma• Massive hemoptysis• AAA rupture• Ectopic pregnancy, post-partum bleeding

Hypovolemic Shock

Hypovolemic Shock:Pathophysiology

Normal

MAP = CO x SVR

Hypovolemic

MAP = ↓CO x SVR

MAP = ↓CO x ↑ SVR

↓MAP = ↓↓CO x ↑ SVR

Heart pumps well, but not enough blood volume to pump

the BaroRc sense the decreased cardiac output and lead to increased SVR in an effort to compensate for the diminished CO

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Hemorrhagic Shock

Compensated Stage• Mechanism: Volume depletion due to bleeding.

• Body detects decrease in cardiac output.

• Sympathetic nervous system is stimulated releasing epinephrine and norepinehrine to stimulate alpha and beta receptors.

• Alpha = Vasoconstriction Beta = bronchodilation and cardiac

stimulation.

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Hemorrhagic (Classic) Shock: CompensatedSigns and Symptoms

MentalStatus

Alert orslightanxiety

Skin

Becomescool, pale.Sweatingbegins atupper lipandspreads tootherareas

BloodPressure

Normal

Pulse

Normal torapid

Respiration

Normal torapid

Other

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Hemorrhagic (Classic) Shock: Progressive

Progressive Stage:

• Mechanism: Kidneys release anti-diuretic hormone which increases vasoconstriction by closing the capillary sphincters, greatly reducing peripheral circulation.

• Increased hypo-perfusion causes increase in metabolic acid build up

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Hemorrhagic (Classic) Shock: ProgressiveSigns and Symptoms

MentalStatus

Lethargic,sleepy,combative

Skin

Cool ,clammy,Pale.Mottling:Cyanosisaroundnose andmouth atfirst,spreads toextremities.

BloodPressure

Begins tofall.

Capillaryrefilldelayed

Pulse

Rapid andweak

Respiration

Rapid andshallow

Other

Decreasedurination.

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Hemorrhagic (Classic) Shock: Irreversible

• Mechanism: • Compensatory mechanisms fail.

• Pre-capillary sphincters open releasing metabolic acids, micro-emboli and other wastes into circulation.

• Cell damage, organ failure and death occur.

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Hemorrhagic (Classic) Shock: IrreversibleSigns and Symptoms

Mentalstatus

Skin Bloodpressure

Pulse Respiration Other

DecreasedLOC, tounrespon-siveness.

Grey,mottled,cyanotic,waxen.

Sweatingstops.

DecreasesBecomesundetect-able

Slows thendisappears.

AgonalRespiration

IrritableHeart,Brady-Cardia,Leads toAsystole.

KLASIFIKASI PERDARAHAN

• KLAS I – IV

• TIDAK ABSOLUT

• HANYA SEBAGAI PANDUAN KLINIS

• PENGOBATAN SELANJUTNYA TERGANTUNG RESPON PENDERITA

Class IV Hemorrhage ≥ 2000 mL BVL

Assessment of Stages of Shock% Blood % Blood Volume Volume lossloss

< 15%< 15% 15 – 30%15 – 30% 30 – 40%30 – 40% >40%>40%

HRHR <100<100 >100>100 >120>120 >140>140

SBPSBP NN N, DBP, N, DBP, postural droppostural drop

Pulse Pulse PressurePressure

N or N or

Cap RefillCap Refill < 3 sec< 3 sec > 3 sec> 3 sec >3 sec or >3 sec or absentabsent

absentabsent

RespResp 14 - 2014 - 20 20 - 3020 - 30 30 - 4030 - 40 >35>35

CNSCNS anxiousanxious v. anxiousv. anxious confusedconfused lethargiclethargic

TreatmentTreatment 1 – 2 L 1 – 2 L crystalloid, crystalloid, + + maintenancmaintenancee

2 L 2 L crystalloid, crystalloid, re-evaluatere-evaluate

2 L crystalloid, re-2 L crystalloid, re-evaluate, replace blood evaluate, replace blood loss 1:3 crystalloid, 1:1 loss 1:3 crystalloid, 1:1 colloid or blood products. colloid or blood products. Urine output >0.5 Urine output >0.5 mL/kg/hrmL/kg/hr

Management

• Hemorrhagic (Hypovolemic Shock)– ABC’s

• Monitors• O2• Intubate? • IV lines x 2, Fluid boluses, Call for Blood• Blood work including cross match

– Treat Underlying Cause

Management

• Hemorrhagic (Hypovolemic Shock)– ABC’s

• Monitors• O2• Intubate? • IV lines x 2, Fluid boluses, Call for Blood - O type• Blood work including cross match

– Treat Underlying Cause• Give Blood• Call the surgeon stat• If the patient does not respond to initial boluses and blood

products - take to the Operating Room

Blood Products

• Use blood products if no improvement to fluids– PRBC 5-10 ml/kg – +/- Platelets

Monitor terhadap pemberian cairan, meliputi :

Perbaikan perfusi (akral hangat, nadi lebih besar, kesadaran membaik dsb) Pantau produksi urin, produksi urin normal :

Dewasa : 30-50 cc/jam atau 0.5 cc/KgBB Anak : 1 cc /KgBB Bayi : 2 cc /KgBB

Monitoring syok

Monitor Respon terhadap pemberian cairan :

Bila respon terhadap cairan tidak baik, selalu pertimbangkan kemungkinan syok non- hemoragik

Bila respon buruk kemungkinan perdarahan berlanjut, cari sumber perdarahan

Cari sumber perdarahan lain :

Jika ada therapi stop perdarahan Jika tidak ada berarti non hemoragik,

therapi sesuai penyebab

Case 2

• HR 110, BP 100/72, SaO2 96%, T 39.2, RR 26• Drowsy• Warm skin• Heart - S1, S2, no Murmers• Chest - good A/E x 2• Abdomen - decreased bowel sound, tender RUQ

Septic Shock

Definitions of Sepsis

• Systemic Inflammatory Response Syndrome (SIRS) – 2 or > of:

-Temp > 38 or < 36

-RR > 20

-HR > 90/min

-WBC >12,000 or <6,000 or more than 10% immature bands

Definitions of Sepsis• Sepsis – SIRS with proven or suspected microbial

source• Severe Sepsis – sepsis with one or more signs of

organ dysfunction or hypoperfusion.• Septic shock = Sepsis + Refractory hypotension–

Vasopressor dependant- Unresponsive to initial fluids 20-40cc/kg patient still has one of the following:

• SBP < 90 mm Hg • MAP < 65 mm Hg • Decrease of 40 mm Hg from baseline

• MODS – multiple organ dysfunction syndrome -2 or more organs

Stages of Sepsis

Mortality

7%

16%

20%

70%

SIRS

SEPSIS

SEVERESEPSIS

SEPTICSHOCK

MODS/DEATH

Septic Shock

• Clinical signs:• Hyperthermia or hypothermia• Tachycardia• Wide pulse pressure• Low blood pressure (SBP<90)• Mental status changes

• Beware of compensated shock!• Blood pressure may be “normal”

Treatment of Septic Shock

• 2 large bore IVs• NS IVF bolus- 1-2 L wide open (if no

contraindications)

• Supplemental oxygen

• Empiric antibiotics, based on suspected source, as soon as possible

Treatment of Sepsis• Antibiotics- Survival correlates with how quickly the correct

drug was given• Cover gram positive and gram negative bacteria

• Zosyn 3.375 grams IV and ceftriaxone 1 gram IV or• Imipenem 1 gram IV

• Add additional coverage as indicated• Pseudomonas- Gentamicin or Cefepime• MRSA- Vancomycin • Intra-abdominal or head/neck anaerobic infections- Clindamycin or

Metronidazole • Asplenic- Ceftriaxone for N. meningitidis, H. infuenzae• Neutropenic – Cefepime or Imipenem

Persistent Hypotension

• If no response after 2-3 L IVF, start a vasopressor (norepinephrine, dopamine, etc) and titrate to effect

• Goal: MAP > 60• Consider adrenal insufficiency: hydrocortisone

100 mg IV

Treatment Algorithm

Rivers E et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock N Engl J Med. 2001:345:1368-1377.

EGDT Group

• First 6 hours in ED• More fluid (5 L vs 3.5 L)• More transfusion (64.1% vs 18.5%)• More dobutamine (13.7% vs 0.8%)

• Outcome• 3.8 days less in hospital• 2 fold less cardiopulmonary complications• Better: SvO2, lactate, base deficit, PH• Relative reduction in mortality of 34.4%

• 46.5% control vs 30.5% EGDT

Case 3

• 23 year old woman• Has been fatigued and short of breath for a few days• She fainted and family brought her in• They tell you she has a heart problem• HR 132, BP 76/36, SaO2 88%, RR 30, Temp 36.3• Appearance - obtunded• Cardiovascular exam - S1, S2, irregular, holosytolic

murmer, JVP is 5 cm ASA, no edema• Chest - bilateral crackles, accessory muscle use• Abdomen - unremarkable• Rest of exam is normal

Cardiogenic Shock

Cardiogenic Shock

• Signs:• Cool, mottled skin• Tachypnea • Hypotension• Altered mental status• Narrowed pulse

pressure• Rales, murmur

• Defined as:• SBP < 90 mmHg• CI < 2.2 L/m/m2

• PCWP > 18 mmHg

Cardiogenic Shock: Pathophysiology

Normal

MAP = CO x SVR

Cardiogenic

MAP = ↓CO x SVR

MAP = ↓CO x ↑ SVR

↓MAP = ↓↓CO x ↑ SVR

Cardiogenic Shock: Causes

↓MAP = ↓ CO (HR x Stroke Volume) x ↑SVR

• Decreased Contractility (Myocardial Infarction, myocarditis, cardiomypothy, Post resuscitation syndrome following cardiac arrest)

• Mechanical Dysfunction – (Papillary muscle rupture post-MI, Severe Aortic Stenosis, rupture of ventricular aneurysms etc)

• Arrhythmia – (Heart block, ventricular tachycardia, SVT, atrial fibrillation etc.)

• Cardiotoxicity (B blocker and Calcium Channel Blocker Overdose)

Pathophysiology of Cardiogenic Shock

• Often after ischemia, loss of LV function• Lose 40% of LV clinical shock ensues

• CO reduction = lactic acidosis, hypoxia

• Stroke volume is reduced • Tachycardia develops as compensation • Ischemia and infarction worsens

Ancillary Tests

• EKG

• CXR

• CBC, Chem 10, cardiac enzymes, coagulation studies

• Echocardiogram

Treatment of Cardiogenic Shock

• Goals- Airway stability and improving myocardial pump function

• Cardiac monitor, pulse oximetry

• Supplemental oxygen, IV access

• Intubation will decrease preload and result in hypotension • Be prepared to give fluid bolus

Treatment of Cardiogenic Shock

• AMI• Aspirin, beta blocker, morphine, heparin• If no pulmonary edema, IV fluid challenge• If pulmonary edema

• Dopamine – will ↑ HR and thus cardiac work• Dobutamine – May drop blood pressure• Combination therapy may be more effective

• PCI or thrombolytics

• RV infarct• Fluids and Dobutamine (no NTG)

• Acute mitral regurgitation or VSD • Pressors (Dobutamine and Nitroprusside)

Case 4• 36 year old woman• Pedestrian hit by a car• She is brought into the hospital 2 hrs after accident• Short of breath• Has been complaining of chest pain• HR 126, SBP 82, SaO2 70%, RR 36, Temp 35• Obtunded, Accessory muscle use• Trachea is deviated to Left• Heart - distant heart sounds• Chest - decreased air entry on the right, broken ribs, subcutaneous

emphysema• Abdominal exam - normal• Apart from bruises and scrapes no other signs of trauma

Obstructive Shock

Obstructive Shock

• Tension pneumothorax• Air trapped in pleural space with 1 way valve,

air/pressure builds up• Mediastinum shifted impeding venous return• Chest pain, SOB, decreased breath sounds• No tests needed!• Rx: Needle decompression, chest tube

Case 3: Management

• Obstructive Shock– ABC’s

• Monitors• O2• IV• Intubate?• BW

– Treat Underlying Cause• Needle thoracentesis• Chest tube• CXR

Case 3: Management

• Obstructive Shock– ABC’s

• Monitors• O2• IV• Intubate?• BW

– Treat Underlying Cause• Needle thoracentesis• Chest tube• CXR• Intubate if no response

Obstructive Shock

• 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

Obstructive Shock

• Pulmonary embolism• Virscow triad: hypercoaguable, venous injury,

venostasis• Signs: Tachypnea, tachycardia, hypoxia• Low risk: D-dimer• Higher risk: CT chest or VQ scan• Rx: Heparin, consider thrombolytics

Obstructive Shock

• 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

Anaphilactic Shock

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

• What are some symptoms of anaphylaxis?

Anaphylactic Shock

• 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

• Risk factors for fatal anaphylaxis • Poorly controlled asthma • Previous anaphylaxis

• Reoccurrence rates• 40-60% for insect stings• 20-40% for radiocontrast agents• 10-20% for penicillin

• Most common causes• Antibiotics• Insects• Food

Anaphylactic Shock

• 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

Anaphylactic Shock

Anaphylactic Shock- Diagnosis

• 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

• ABC’s• Angioedema and respiratory compromise require

immediate intubation

• IV, cardiac monitor, pulse oximetry• IVFs, oxygen• Epinephrine• Second line

• Corticosteriods• H1 and H2 blockers

Anaphylactic Shock- Treatment

• Epinephrine• 0.3 mg IM of 1:1000 (epi-pen) • Repeat every 5-10 min as needed• Caution with patients taking beta blockers- can cause

severe hypertension due to unopposed alpha stimulation• For CV collapse, 1 mg IV of 1:10,000• If refractory, start IV drip

Anaphylactic Shock- Treatment

• Corticosteroids• Methylprednisolone 125 mg IV • Prednisone 60 mg PO

• Antihistamines• H1 blocker- Diphenhydramine 25-50 mg IV• H2 blocker- Ranitidine 50 mg IV

• Bronchodilators• Albuterol nebulizer• Atrovent nebulizer• Magnesium sulfate 2 g IV over 20 minutes

• Glucagon• For patients taking beta blockers and with refractory hypotension• 1 mg IV q5 minutes until hypotension resolves

Anaphylactic Shock - Treatment

• All patients who receive epinephrine should be observed for 4-6 hours

• If symptom free, discharge home

• If on beta blockers or h/o severe reaction in past, consider admission

Anaphylactic Shock - Disposition

Neurogenic Shock

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)

• 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

Neurogenic Shock

• A,B,Cs• Remember c-spine precautions

• Fluid resuscitation• Keep MAP at 85-90 mm Hg for first 7 days• Thought to minimize secondary cord injury• If crystalloid is insufficient use vasopressors

• Search for other causes of hypotension• For bradycardia

• Atropine• Pacemaker

Neurogenic Shock- Treatment

Neurogenic Shock- Treatment

• Methylprednisolone• Used only for blunt spinal cord injury• High dose therapy for 23 hours• Must be started within 8 hours• Controversial- Risk for infection, GI bleed

Type of Shock

Insult Physiologic Effect

Compensation

CompensationHeart Rate

CompensationContractility

Cardiogenic Heart fails to pump blood out

↓CO BaroRc↑SVR

↑ ↑

Obstructive Heart pumps well, but the outflow is obstructed

↓CO BaroRc↑SVR

↑ ↑

Hemorrhagic Heart pumps well, but not enough blood volume to pump

↓CO BaroRc↑SVR

↑ ↑

Distributive Heart pumps well, but there is peripheral vasodilation

↓SVR ↑CO ↑

No Change - in neurogenic shock

↑

No Change - in neurogenic shock

The End