Slide 4 Shock1

7/29/2019 Slide 4 Shock1

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Hemorrhage is classified according to :

Source

Time of onset

Site of bleeding


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1. Arterial hemorrhage Bright red blood Spurting as a jet which rises & falls with

the pulse.

2. Venous bleeding Darker red.

Steady & copious flow.

3. Capillary bleeding Bright red often rapid ooze.


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1. Primary hemorrhage: Occurs at the time of injury or operation.

2. Reactionary hemorrhage

3. Secondary hemorrhage


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follow primary hemorrhage within 24hours(Usually 4-6) hours.

Mainly due to slipping of a ligature,dislodgment of a clot or cessation of reflexvasospasm.

Precipitating factors are :

i. Rise in blood pressure.ii. Refilling of the venous system on recovery from shockiii. Restlessnes, coughing & vomiting which raise the

venous pressure.(bleeding after thyroidectomy)


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Occurs 7-14 days after injury

Predisposing factors are1. Pressure of a drainage tube2. Ligature in infected area.3. Cancer.


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I. External hemorrhage:- Is visible & is called revealed hemorrhage.

II. Internal hemorrhage:- Is invisible & is concealed hemorrhage as in rupturedspleen or liver, fracture femur, ruptured ectopic

gestation.

Concealed hemorrhage may become revealed

as in hematemesis & melena or hematuria in

ruptured kidney.


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Total blood volume can be derived from patientsweight : Infants 80-85ml\kg Adults 65-75ml/kg

Measuring blood loss

1. Blood clot the size of fist is roughly equal to500ml.

2. Swelling in closed fractures Moderate swelling in closed fracture of the tibia equals

500-1500ml blood loss.

Moderate swelling in closed fracture of femur 500-2000mlblood loss.


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3. On the operation table : Swab weighing , blood loss can be measured by

weighing swabs after use & subtracting the dryweight. (1gm=1ml)

Measuring the blood collected in the suction &drainage bottles.

In big extensive operations keep in mindevaporation & sweating . for e.g in radical

mastectomy or partial gastrectomy multiply theswab weighing total by 1.5 & for more prolongedoperations via large wounds such asabdominothoracic or abdomino-perinealoperations multiply by 2.


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4. Hemoglobin level.

This is estimated in g/100ml or g/dl.

normal values 12-16 g/dl

There will be no immediate change after somehours , the level falls as a result of the influx of

interstitial fluid.


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Can occur as a consequence of a wide variety of

pathological processes.

Is an acute medical emergency.

It decreases oxygen transport & increases the

risk of tissue hypoxia & multi organ failure.

The greater the degree & duration of

hypovolemia, the greater the risk.

Hypovolemia is divided into THREE categories.


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Is the commonest form but the least oftendiagnosed.

Hypovolemia is present without very obvious

physical signs. It is very difficult to diagnose

In conscious patient ,CNSsymptoms are the

best guide which range from drowsiness &nausea to hiccoughs

Any thirsty patient should be consideredhypovolemic.


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Urine analysis show increase osmolality &sodium concentration both are considered tobe the most useful laparatory investigations.

Although it is very common, most patientswithstand the insult

If untreated patient usually enters the state ofovert compensated hypovolemia


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Blood pressure is maintained still. Hypovolemia is present to an extent that reflex

mechanisms are required to maintain supply tovital organs & this is obvious clinically.

History is very important & on examinationthere is increase sympathetic drive such astachycardia; increased systolic pressure. Widearterial pulse pressure, cool skin particularly

hands and feet. CNS signsas drowsiness, confusion & an

increased respiratory rate.


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In acute phase most laparatory investigationsare of little use.

Arterial blood gasanalysis can be done rapidly

; hypovolemic patients are hypoxic & may havemetabolic acidosis.

Urine analysis may support the diagnosis butno single test is diagnostic.

Cenratl venous pressure catheter may beinserted in difficult cases


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This is what is refered to as shock.

Protective mechanisms are unable to control& maintain the blood pressure

Vital organs are no longer adequatelyperfused

Mean arterial pressure falls & may be difficult

to record Peripheral pulses are often impalpable.


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Blood supply to heart & lungs is compromisedwhich causes further reduction in cardiac output .

As myocardial oxygenation becomes criticalTachycardia changes to bradycardia & level ofconscioussnes deteriorate.

If untreated ,this condition will progress to totalcirculatory arrest.


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Shock is Described as a clinical syndromearising frominadequate tissueperfusion, oftencomplicated by cellular metabolic dysfunction.

When the mismatch between cardiac out put &the metabolic needs of the patient is greatenough the patient is said to be in shock.

Shock is not simply a low blood pressure, lowblood pressure is called hypotension whichmay accompany shock .


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Inadequate oxygen delivery to meetmetabolic demands

Results in global tissue hypoperfusionand metabolic acidosis

Shock can occur with a normal bloodpressure and hypotension can occurwithout shock


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1.

Decreased circulating volume or decreasedpreload True Hypovolemia

Blood loss Plasma loss

Dehydration

Apparent hypovolemia (vasodilatation) Adrenal insuficiency Anaphylaxis Neurogenic factors

Sepsis

2. Compromised cardiac function Cardiac compressive shock (Extrinsic) Cardiogenic shock (intrinsic)


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A critical reduction in oxygen level to the cell isthe final common pathway leading to shock ofall varities

Reduced substrate supply & accumulation ofthe products of cell metabolism e.g lactate arecontributing factors.

At cellular level decreased O2 level lead todecrease in level of ATP (Adenosinetriphosphate)


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Deficiency of ATP will lead to :

1. Depression of the pump function of the cell with anincrease in intracellular sodium, calcium and waterwith loss of potassium and magnesium (Sick cellsyndrome)

2. High intracellular calcium >> leads to myocardialcell fatigue, failure & cardiac arrest.

3. Lactic acidosis which has adverse action on enzymesystem of the cell.


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Phagocytes will stop functioning Plasma kinins ,prostaglandins,leukotrienes are

synthesized from the cell membrane & exert theirdiverse effects on circulation.

Neutrophils are stimulated to produce elastasewhich is very injurious to pneumocytes resulting inARDS

Stimulation of the coagulation pathway will lead to

consumptive coagulopathy resulting indisseminated intravascular coagulation DIC

All the systems of the body are affected leading toMODS (Multi organ dysfunction syndrome)


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Progression of physiologic effects as shockensues

Cardiac depression

Respiratory distress Renal failure

DIC

Result is end organ failure


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Inadequate systemic oxygen deliveryactivates autonomic responses to maintainsystemic 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


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ABCs Cardiorespiratory monitor

Pulse oximetry

Supplemental oxygen

IV access

ABG, labs

Foley catheter

Vital signs


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

Infectious source

Labs: CBC

Chemistries

Lactate

Coagulation studies

Cultures

ABG


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Lumbar puncture

Wound cultures

Acute abdominal series

Abdominal/pelvic CT or US

Cortisol level

Fibrinogen, FDPs, D-dimer


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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


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Do you remember howto quickly estimate blood

pressure by pulse?

60

80

70

90

If you palpate a pulse,you know SBP is at

least this number


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Mild 40%vol lossPallor Pallor PallorCool extremities Cool extremities Cool extremitiesCapillary refill Capillary refill Capillary refillCollapsed veins Collapsed veins Collapsed veinsTachycardia Tachycardia Tachycardia

Oliguria OligoureaPostural hypotension Postural hypotension

Mental status changesAgitationRestlessness

Hemorrhage of less than 20% of circulating blood volume causes little or no alteration in

blood pressure & heart rate. As more volume is lost and more rapid ;signs are moreprominent


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ABCDE

Airway

control work of Breathing

optimize Circulation assure adequate oxygen Delivery

achieve End points of resuscitation


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Determine need for intubation but remember:intubation can worsen hypotension

Sedatives can lower blood pressure Positive pressure ventilation decreases preload


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Respiratory muscles consume a significantamount of oxygen

Tachypnea can contribute to lactic acidosis

Mechanical ventilation and sedation decreaseWOB and improves survival


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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


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Decrease oxygen demands

Provide analgesia and anxiolytics to relaxmuscles and avoid shivering

Maintain arterial oxygen saturation/content

Give supplemental oxygen

Maintain Hemoglobin > 10 g/dL

Serial lactate levels or central venousoxygen saturations to assess tissue oxygenextraction


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Goal of resuscitation is to maximize survivaland minimize morbidity

Use objective hemodynamic and physiologicvalues 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%


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If restoration of blood volume, red cell mass, &adequate oxygenation fail to restore anadequate cardiac out put & oxygen delivery

then pharmacological agents may be required. Dopamine improves the cardiac output & urine

output

Dobutamine acting directly on B1-adrenergic

receptors has more inotropic action on theheart.


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Inadequate volume resuscitation

Pneumothorax

Cardiac tamponade Hidden bleeding

Adrenal insufficiency

Medication allergy


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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!


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Sepsis (remember definition?)

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


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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.


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Clinical signs: Hyperthermia or hypothermia

Tachycardia

Wide pulse pressure

Low blood pressure (SBP


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Cardiac monitor

Pulse oximetry

CBC, Biochem. labs, coags, LFTs, lipase, UA

ABG with lactate

Blood culture x 2, urine culture

CXR

Foley catheter (why do you need this?)


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2 large bore IVs

NS IVF bolus- 1-2 L wide open (if nocontraindications)

Supplemental oxygen Empiric antibiotics, based on suspected

source, as soon as possible


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Antibiotics- Survival correlates with how quicklythe 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


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

Goal: MAP > 60

Consider adrenal insufficiency:hydrocortisone 100 mg IV

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Slide 4 Shock1