DR BIKU 2ND YEAR PG,MEDICINE

Objectives
Definition
Approach to the hypotensive patient Types Specific treatments

Epidemiology
Mortality Septic shock 35-40% (1 month mortality) Cardiogenic shock 60-90% Hypovolemic shock variable/mechanism

Definition of Shock
Inadequate oxygen delivery to meet metabolic demands Results in global tissue hypoperfusion and metabolic acidosis Shock can occur with a normal blood pressure and hypotension can occur without shock

PATHOGENESIS OF SHOCK
Inadequate systemic oxygen delivery activates autonomic responses to maintain systemic oxygen delivery
Sympathetic nervous system
NE, epinephrine, dopamine, and cortisol release
Causes vasoconstriction, increase in HR, and increase of cardiac contractility (cardiac output)

Renin-angiotensin axis
Water and sodium conservation and vasoconstriction Increase in blood volume and blood pressure

CONDT..
Cellular responses to decreased systemic oxygen delivery ATP depletion ion pump dysfunction Cellular edema Hydrolysis of cellular membranes and cellular death Goal is to maintain cerebral and cardiac perfusion Vasoconstriction of splanchnic, musculoskeletal, and renal blood flow Leads to systemic metabolic lactic acidosis that overcomes the bodys compensatory mechanisms

Global Tissue Hypoxia

Endothelial inflammation and disruption Inability of O2 delivery to meet demand Result:
Lactic acidosis Cardiovascular insufficiency Increased metabolic demands

Multiorgan Dysfunction Syndrome (MODS)

Progression of physiologic effects as shock ensues
Cardiac depression Respiratory distress Renal failure DIC

Result is end organ failure

Cellular Response to Shock Cellular Response to Shock

O2 O2 use use Anaerobic Anaerobic metabolism metabolism ATP ATP synthesis synthesis Na++Pump Na Pump Function Function Tissue Tissue perfusion perfusion Stimulation of Stimulation of clotting cascade & clotting cascade & inflammatory inflammatory response response Intracellular Na++ Intracellular Na & water & water Impaired cellular Impaired cellular metabolism metabolism Impaired Impaired glucose glucose usage usage

Cellular edema Cellular edema Vascular volume Vascular volume

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Stages of Shock Stages of Shock

Compensated Compensated Uncompensated Uncompensated Irreversible Irreversible

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Compensated Shock Compensated Shock

Defense mechanisms are successful in Defense mechanisms are successful in maintaining perfusion maintaining perfusion Presentation Presentation
Tachycardia Tachycardia Decreased skin perfusion Decreased skin perfusion Altered mental status Altered mental status

Uncompenstated Shock Uncompenstated Shock

Defense mechanisms begin to fail Defense mechanisms begin to fail Presentation Presentation
Hypotension Hypotension Prolonged Cap refill Prolonged Cap refill Marked increase in heart rate Marked increase in heart rate Rapid, thready pulse Rapid, thready pulse Agitation, restlessness, confusion Agitation, restlessness, confusion

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Irreversible Shock Irreversible Shock

Complete failure of compensatory Complete failure of compensatory mechanisms mechanisms Death even in presence of resuscitation Death even in presence of resuscitation

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PHYSIOLOGIC CHARACTERISTICS OF THE VARIOUS FORMS OF SHOCK

Type of shock

Cvp&pcwp
Decrease Increase Both Both Decrease

Cardiac output
Decrease Decrease Decrease Increase Decrease

SVR
Increase Increase Increase Decrease Decrease

Venous o2 sat%
Decrease Decrease Both Decrease

hypovolemic cardiogenic septic hypodynamic hyperdynamic Neurogenic

Hypoadrenal

Both

Decrease

Equal/Decrease Decrease

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

Approach to the Patient in Shock

ABCs
Cardiorespiratory monitor Pulse oximetry Supplemental oxygen IV access ABG, labs Foley catheter Vital signs including rectal temperature

Diagnosis
Physical exam (VS, mental status, skin color,
temperature, pulses, etc)

Infectious source Labs:

CBC Chemistries Lactate Coagulation studies Cultures ABG

Further Evaluation
CT of head/sinuses Lumbar puncture Wound cultures Acute abdominal series Abdominal/pelvic CT or US Cortisol level Fibrinogen, FDPs, D-dimer

Is This Patient in Shock?

Patient looks ill Altered mental status Skin cool and mottled or hot and flushed Weak or absent Yes! peripheral pulses These are all signs and SBP <110 symptoms of shock Tachycardia

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

Airway
Determine need for intubation but remember: intubation can worsen hypotension
Sedatives can lower blood pressure Positive pressure ventilation decreases preload

May need volume resuscitation prior to intubation to avoid hemodynamic collapse

Control Work of Breathing

Respiratory muscles consume a significant amount of oxygen Tachypnea can contribute to lactic acidosis Mechanical ventilation and sedation decrease WOB and improves survival

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 No outcome benefit from colloids

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%

Persistent Hypotension
Inadequate volume resuscitation Pneumothorax Cardiac tamponade Hidden bleeding Adrenal insufficiency Medication allergy

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!

Types of Shock
Hypovolemic Septic Cardiogenic Anaphylactic Neurogenic Obstructive

What Type of Shock is This?

68 yo M with hx of HTN and DM presents to the ER with abrupt onset of diffuse abdominal pain with radiation to his low back. The pt is hypotensive, tachycardic, afebrile, with cool but dry skin

Types of Shock Hypovolemic Septic Cardiogenic Anaphylactic Neurogenic Obstructive

Hypovolemic Shock

Hypovolemic Shock
Non-hemorrhagic
Vomiting Diarrhea Bowel obstruction, pancreatitis Burns Neglect, environmental (dehydration) GI bleed Trauma Massive hemoptysis AAA rupture Ectopic pregnancy, post-partum bleeding

Hemorrhagic

Hypovolemic Shock
ABCs Establish 2 large bore IVs or a central line Crystalloids
Normal Saline or Lactate Ringers Up to 3 liters

PRBCs
O negative or cross matched

Control any bleeding Arrange definitive treatment

Evaluation of Hypovolemic Shock

CBC ABG/lactate Electrolytes BUN, Creatinine Coagulation studies Type and cross-match
As indicated
CXR Pelvic x-ray Abd/pelvis CT Chest CT GI endoscopy Bronchoscopy Vascular radiology

SEVERITY OF HYPOVOLEMIC
MLID

(<20% BLOOD LOSS)

Cool Extremities
Increased capillary refill time Diaphoresis Collapsed veins Anxiety

MODERATE (20-40% BLOOD LOSS)

Same,plus
tachycardia oliguria postural changes

SEVERE (>40% BLOOD LOSS)

Same ,plus
hemod..instability hypotension mental status deterioration (coma)

Hypovolemic Shock
Hemorrhagic Shock
Parameter Blood loss (ml) Blood loss (%) Pulse rate (beats/min) Blood pressure Respiratory rate (bpm) Urine output (ml/hour) CNS symptoms I <750 <15% <100 Normal 1420 >30 Normal II 7501500 1530% >100 Decreased 2030 2030 Anxious III 15002000 3040% >120 Decreased 3040 515 Confused IV >2000 >40% >140 Decreased >35 Negligible Lethargic

Crit Care. 2004; 8(5): 373381.

RESUSCITATION OF PATIENT IN HYPOVOLEMIA

PULMONARY ARTERY CATHETER

CARDIAC INDEX<3.5 administer crystalloid+/- blood pcwp>15,hct>30

CI<3.5,PCWP<2o 500ml crystalloid boluses until preload-maximal CI monitor CI deterioration

CI<3.5,PCWP>20 inotrope as indicated consider ECHO

maintain optimal PCWP Crystalloid Blood(hct>30)

Infusion Rates
Access
18 g peripheral IV 16 g peripheral IV 14 g peripheral IV 8.5 Fr CV cordis

Gravity
50 mL/min 100 mL/min 150 mL/min 200 mL/min

Pressure
150 mL/min 225 mL/min 275 mL/min 450 mL/min

What Type of Shock is This?

An 81 yo F resident of a nursing home presents to the ED with altered mental status. She is febrile to 39.4, hypotensive with a widened pulse pressure, tachycardic, with warm extremities

Types of Shock Hypovolemic Septic Cardiogenic Anaphylactic Neurogenic Obstructive

Septic Shock

Sepsis
Two or more of SIRS criteria
Temp > 38 or < 36 C HR > 90 RR > 20 WBC > 12,000 or < 4,000

Plus the presumed existence of infection Blood pressure can be normal!

Septic Shock
Sepsis Plus refractory hypotension
After bolus of 20-40 mL/Kg patient still has one of the following:

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

Sepsis

Pathogenesis of Sepsis

Nguyen H et al. Severe Sepsis and Septic-Shock: Review of the Literature and Emergency Department Management Guidelines. Ann Emerg Med. 2006;42:28-54.

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

MONITORING
Cardiac monitor Pulse oximetry CBC, coags, LFTs, lipase,KFT ABG Blood culture x 2, urine culture CXR Foley catheter (why do you need this?)

Treatment of Septic Shock

2 large bore IVs
NS IVF bolus- 1-2 L

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
TAZECT 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 infectionsClindamycin 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

What Type of Shock is This?

A 55 yo M with hx of HTN, DM presents with crushing substernal CP, diaphoresis, hypotension, tachycardia and cool, clammy extremities

Types of Shock Hypovolemic Septic Cardiogenic Anaphylactic Neurogenic Obstructive

Cardiogenic Shock

Physiology

Basic unit of life = cell Cells get energy needed to stay alive by reacting oxygen with fuel (usually glucose) No oxygen, no energy No energy, no life

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Frank-Starling Law Of The Heart

The heart normally pumps the blood returned to it

Therefore, the more blood that is returned to the heart (venous return) the higher the EDV and therefore the higher the stroke volume.

The extent of cardiac filling is referred to as the preload It is called the preload, because it is the work load imposed on the heart before contraction even begins

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Factors Affecting The Pump Factors Affecting The Pump

Preload Preload Contractile force Contractile force
Frank-starling mechanism Frank-starling mechanism

Afterload Afterload

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What Affects Blood Pressure? What Affects Blood Pressure?

ANS balance ANS balance Contractility Contractility
Preload Preload
Starlings law Starlings law

Afterload Afterload

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Changes in Afterload and Preload Changes in Afterload and Preload

Peripheral Peripheral vasoconstriction vasoconstriction peripheral vascular peripheral vascular resistance resistance afterload afterload blood pressure. blood pressure.
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Changes in Afterload and Preload Changes in Afterload and Preload

Peripheral Peripheral vasodilation vasodilation

peripheral vascular peripheral vascular

resistance resistance

afterload afterload blood pressure. blood pressure.

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Changes in Afterload and Preload Changes in Afterload and Preload

fluid volume fluid volume
preload preload contractility contractility (Starlings Law) (Starlings Law) blood pressure. blood pressure. cardiac output. cardiac output.
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Changes in Afterload and Preload Changes in Afterload and Preload

fluid volume fluid volume preload preload contractility contractility blood pressure. blood pressure.

(Starlings Law) (Starlings Law)

cardiac output. cardiac output.

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Cardiogenic Shock Cardiogenic Shock

R.A.S. R.A.S. Activation Activation CO CO Catecholamine Catecholamine Release Release SVR SVR O22 O supply supply Peripheral Peripheral & pulmonary & pulmonary edema edema
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Volume/ Volume/ Preload Preload

Myocardial Myocardial O2 demand O2 demand

Impaired Impaired myocardial function myocardial function

Dyspnea Dyspnea

Cardiogenic Shock
Defined as:
SBP < 90 mmHg CI < 2.2 L/m/m2 PCWP > 18 mmHg

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

Etiologies
What are some causes of cardiogenic shock?
AMI Sepsis Myocarditis Myocardial contusion Aortic or mitral stenosis, HCM Acute aortic insufficiency

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

EARLY TESTS
ECG CXR CBC, cardiac enzymes, coagulation studies Echocardiogram

Swan-Ganz Catheter

Swan-Ganz Interpretation
Etiology
cardiogenic
hypovolemic

CO
decreased decreased increased decreased

PCWP
increased decreased decreased Increased

SVR
increased increased decreased increased

distributive obstructive

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)

Autonomic Drugs in Shock

DRUGS
DOPAMINE

INDICATIONS
RENAL PERFUSION HYPOTENSION HYPOTENSION

DOSES
2-5mcg/kg/min 5-10mcg/kg/min >10mcg/kg/min 2.5-25mcg/kg/min 0.5-30mcg/min 40-180mcg/kg/min

MOA
dopaminergic BETA 1& Dopaminergic Alpha 1 Selective Beta 1 Alpha 1 &Beta 1 Selective alpha 1

PRINCIPAL OF ACTION
RENAL DILATION +INOTROPE

VASOCONSTRICTIO N +INOTROPE

DOBUTAMINE NOREPINEPHRINE PHENYLEPHRINE

CARDIOGENIC SHOCK HYPOTENSION HYPOTENSION

VASOCONSTRICTIO N

VASOCONSTRICTIO N

Management of Cardiogenic Shock

Attempt to correct problem and increase cardiac

output by diuresing and providing inotropic support. IABP is utilized if medical therapy is ineffective. Catheterization if ongoing ischemia Cardiogenic shock is the exception to the rule that NS is always given for hypotension NS will exacerbate cardiac shock.

LOW OUTPUT CARDIOGENIC SHOCK check BP Systolic BP >100mmhg Systolic BP 70-100mmhg No signs/symptoms of shock dobutamine 2-20mcg/kg/min Systolic BP <100mmhg signs/symptoms of shock

Norepinephrine o.5-30mcg/min or dopamine 5-15mcg/kg /min

What Type of Shock is This?

A 34 yo F presents to the ER after dining at a restaurant where shortly after eating the first few bites of her meal, became anxious, diaphoretic, began wheezing, noted diffuse pruritic rash, nausea, and a sensation of her throat closing off. She is currently hypotensive, tachycardic and ill appearing.

Types of Shock Hypovolemic Septic Cardiogenic Anaphylactic Neurogenic Obstructive

Anaphalactic 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

Anaphylactic Shock
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

Anaphylactic Shock
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 lifethreatening laryngeal edema

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

Anaphylactic Shock- Treatment

ABCs
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 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 - Disposition

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

What Type of Shock is This?

A 41 yo M presents to the ER with an RTA complaining of decreased sensation below his waist and is now hypotensive, bradycardic, with warm extremities

Types of Shock Hypovolemic Septic Cardiogenic Anaphylactic Neurogenic Obstructive

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)

Neurogenic Shock
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- Treatment

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

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

What Type of Shock is This?

A 24 yo M presents to the ED aft c/o chest pain and difficulty breathing. On PE, you note the pt to be tachycardic, hypotensive, hypoxic, and with decreased breath sounds on left

Types of Shock Hypovolemic Septic Cardiogenic Anaphylactic Neurogenic Obstructive

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

Obstructive Shock
Cardiac tamponade
Blood in pericardial sac prevents venous return to and contraction of heart Related to trauma, pericarditis, MI Becks triad: hypotension, muffled heart sounds, JVD Diagnosis: large heart CXR, echo Rx: Pericardiocentisis

Obstructive Shock
Pulmonary embolism
Virchow 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 Rx: Valve surgery

Addisons Disease
Deficiency of cortisol and aldosterone production in

the adrenal glands This is suspected when patient is non-responsive to fluids and antibiotics. Electrolytes may reveal hyponatremia and hyperkalemia Hydrocortisone 100 mg IV immediately

Psychogenic Shock
Brought on by strong emotion,

fear or unpleasant sights Commonly referred to as fainting or syncope Produces a temporary, generalized vascular dilation and bradycardia

Any Questions?

References
Tintinalli. Emergency Medicine. 6th edition
Rivers et al. Early Goal-Directed Therapy in the

Treatment of Severe Sepsis and Septic Shock. NEJM 2001; 345(19):1368.