slide 4 shock1
TRANSCRIPT
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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