Shock & Hemorrhage (Repaired)

7/29/2019 Shock & Hemorrhage (Repaired)

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Hemorrhage is classified according to:

Source

Time of onset

Site of bleeding -> either internal or external bleeding.

Hemorrhage according to the source of-1

bleeding:

1- Arterial Hemorrhage:

Ex. A patient with RTA road traffic accident, trauma (gun shotto his lower limb) so there's arterial hemorrhage. It is a brightfresh blood (Oxygenated blood) and its pulsatile (in systoleit gives ejection, and stops in diastole) so it works as on/offpulsatite. So in an operation there's a bleeding if itspulsatile bleeding we know this is an arterial hemorrhagefor an injured artery.

2- Venous Bleeding:As we know that the pressure is lower in the veincompared to the artery, so the injured vein is notpulsatile but its continuous . Always we have venousreturn to the heart so this give the venous bleeding thecontinuity with a steady and copious flow, now if you look atthe surgical field you'll find it's full of blood, but you can't find

the source; one of the veins is injured with a steady slowcontinuous flow of the blood.About the color of blood its dark red (Deoxygenated blood).

3- Capillary Bleeding:Usually it's like the arterial bleeding; bright red blood oftenrapid ooze not pulsatile.


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2- Onset of the Bleeding:

primary hemorrhage: A bleeding developed at the time ofinjury or during surgery (intra-operative), usually it's the easiest to

handle; because we know the source of it. Ex. In an operation ofGastrictomy and during this surgery the operator injured an artery.OR someone injured with a shot and he had a bleeding artery sothese are examples for primary hemorrhage.

Reactionary hemorrhage: Follow the primary hemorrhagewithin 24 hrs and most commonly in the first 4-6 hrs after theprimary hemorrhage (Mainly due to slipping of a ligature,dislodgment of a clot or cessation of reflex vasospasm.

Ex. A. splenctomy operation for hypotensive patientin shockandduring this operation and after excision for hilum of spleen forsplenic artery after the operation he received IV fluids and bloodand this led to increase the pressure and venous return so this ledto escaping the surgical sutures due to the high pressure so thiswhat we called reactionary hemorrhage (slipping of a ligature).

B. patient in ER with a shock and internal hemorrhage he had aclot at injury site and this clot closed the source of bleeding thenhe given blood and fluids so this 'll increase the pressure and bythat the clot will be dislodged and the bleeding continue again(Dislodgment) .

C. After the arterial injury will be vasospasm of the artery (it maycontinued to 4-5 hrs then the reflex mechanism removed and thereactionary hemorrhage takes place).

Secondary hemorrhage: usually occurs one week to twoweeks after primary injury.

Ex. Patient with a drain in his abdomen after the surgery and led tonecrotic pressure on one of the arteries then the artery opened.

Or infection in the operation place which made it a fragile. Orpatient with cancer and after operation the cancer eroded theartery again and causing secondary hemorrhage.


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3-Site of the hemorrhage:

visible & is called revealedisItExternal hemorrhage:hemorrhage.

, liver, kidney,Ruptured spleenEx.Internal hemorrhage:ruptured ectopic gestation or pt' with closed fracture (fractured

femur but the skin and fascia intact).

Sometimes the internal bleeding could converts to external

one Pt' with gastric cancer and erosion for one of the gastric

arteries so this is internal bleeding but after that he vomited blood

(Hematemesis) then defecated blood (Melena).

Pt' with gunshot and blood loss and the doctor should estimate

the loosed blood ,, how this occurs?

kg\85ml-80ximately hasAccording to age the infant appro

assume that you've a newborn and his weight is 4kg

(4kg*80=320ml) so Total blood volume ~300 ml, if he loses100ml so this equal 1/3 blood so this considered a big problem for

a newborn.

For Adult 65-75ml/kg ~70 ml/kg and his weight is 70 kg so

(70*70=4900) so Total blood volume ~5000ml (5 liters ) so if this

Pt' loses 100ml thats mean 100/5000 (1/50) of his blood and this

is very small ratio for an adult. And thats mean the infants can't

tolerate blood loss like adults and if we give them fluids the amount

should be small not the same as adults.

We have multiple measures to measure the amount of

bleeding:

1.Blood clot the size of fist is roughly equal to 500ml so each

clot = 0.5 liter and this is useful way in operations.


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2.Swelling in closed fracturesThe estimated blood loss in

closed fractured femur approximately equal ( 0.5-2 L) for tibia it'll

be less than that (0.5-1.5 L) .

3. On the operation room Swab weighing, blood loss can bemeasured by weighing swabs after use & subtracting the dryweight. (1gm BLOOD =1ml) in short operations

For long operations (thoracoabdominal surgeries or abdomino-

perineal operations) >4 hrs so (1gm BLOOD =2ml)

Ex. 200gm of blood in gauzes = 2*200 =400 ml blood loss.

4. Measuring the blood collected in the suction & drainage

bottles

5. Hemoglobin level normal values 12-16 g/dlEX. Hb level for patient before injury is 15 g/dl after 30 min's of

hemorrhage Hb level will still the same but after 2-3 hrs it'll

decrease 5L the amount of blood in the body after injury Pt'

loses 1ml (same amount of RBC's and Plasma lost so Hb level still

the same) but after 2-3 hrs there'll be reabsorption of fluids from

interstitial space to the intravascular volume (inside the veins) so

this'll increase the plasma more than RBC's and by that Hb level 'll

decrease.

Hematocrit = RBC's

Total Blood

So by increasing the plasma Hematocrit and Hb will decrease.

Hb level isn't a good indicator adequately after the injury but its

benefit after 4 hrs of injuries.


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Hypovolemia (Reduced Blood Volume)

*Can occur as a consequence of a wide variety of pathologicalprocesses. (Traumasevere dehydration, severe vomiting,

severe diarrhea) or Gastric Cancer led to ascites (accumulationof fluids within the peritoneal cavity in abdomen "third

spacing") so this pt' lose blood from intravascular space to

another site either inside or outside the body

*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:

1. Covert compensated hypovolemia

* Is the commonest form but the least often diagnosed

*Hypovolemia is present without very obvious physical signs

(no problems in the history and physical examinations but the

blood volume is less than normal but even that it may appear in

urine analysis a concentrated urinehigh urine osmolarity and

high sodium concentration )

*In conscious patient, CNS symptoms are the best guide

which range from drowsiness & nausea to hiccoughs, thirsty.

*If untreated, patient usually enters the state of overt

compensated hypovolemia.

compensated2. Overt

Due to decreasing in blood volume and blood pressure so there'll

in order to increase bloodactivitysympatheticincreasing inbe

pressure so this will increase heart rate "Tachycardia",

increasing in contractility of heart "pumping activity",


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vasoconstriction in peripheral arteries so they've cold

.particularly hands and feetextremities

Wide arterial pulse pressure (difference between systolic and

diastolic pressures) so hypovolemic pt's 've reflex mechanisms

lead to tachycardia and as a result systolic BP and pulse pressure

will increase.

Urine analysis show*

Increasing in osmolality &

Sodium concentration, in

ABG (Arterial Blood

Gases) they've metabolic acidosis.

* Central venous pressure catheter may be inserted in difficult

cases as normal it ranges between (8-12) but in hypovolemia

it's less than 8, and in overloaded cases (excess fluid in venoussystem) its more than 12.

3. Decompensated hypovolemia

mechanisms are unable to control & maintainProtective*the blood pressure

.shock* This is what is referred to as

in Overt there was hypotension, tachycardia, vasoconstriction,increasing in the contractility of heart to increase BP.

So if the previous mechanisms fail to return the normal BP this

will lead to hypotension and decompensated hypovolemia.

re no longer adequatelya), heart, lungsbrain(organs*Vital

perfused.

Mean arterial pressure falls & may be difficult to record.*

:CNS signs


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Mean arterial pressure = [diastolic BP+ 1/3 (systolic-diastolic)]

Pt' with BP of 120/80 so

MAP= 80 + 1/3(40) = 93.3 mm Hg

* Peripheral pulses are often impalpable (in hypovolemia and

hypotension)

* Blood supply to heart & lungs is compromised which causes

further reduction in cardiac output.

* As myocardial oxygenation becomes critical Tachycardia

changes to bradycardia (in Heart Failure) & level of

consciousness deteriorate.

* If untreated, this condition will progress to total circulatory

arrest.

:Shock

* Shock is described as a clinical syndrome arising from

inadequate tissueperfusion, often complicated by cellular

metabolic dysfunction

*Commonest cause is hypovolemia

* When the mismatch between cardiac output & the metabolic

needs of the patient is great enough, the patient is said to be in

shock.

* Shock is not simply a low blood pressure; low blood pressureis called hypotension which may accompany shock.

Normal BP determined by:

-Contractility of the Heart (Heart Rate)

-Blood volume

So the blood will reach to the cellsadequately with oxygen and eliminate waste

product especially Lactic Acid


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(due to heartInadequate oxygen delivery to meet metabolic demands*

failure, bradycardia and hypovolemia which lead to hypotension).

.metabolic acidosisandhypo perfusionResults in global tissue*

*Shock can occur with a normal blood pressure (normotensive) andhypotension can occur without shock

Ex. Hypertensive Pt' his BP (200/120) with trauma and hemorrhage sohis BP will decrease to (130/80) so this pt' is shocked although the BP is

normal.

Ex. Hypotensive Pt' his normal BP (100/60), (90/50) such as athletes who

are considered as hypotensive pt's, but the pt' has good tissue perfusion so

we can't say he's shocked.

hypotension.of the cases pt' with a shock has severeIN MOST*

Classification of Shock:

1-Decreased circulating volume or decreased preload::

hypotension and shockMI so the heart can't pump blood wellHeart

2-Compromised cardiac function:: Cardiac compressive shock (Extrinsic) pericardiatis "inflammationof pericardium that surround the heart " heart can't expand and contract

wellhypotension and shock

Tension pneumothorax (accumulation of air within pleural cavity)it'll compress over the heart and the heart can't functioning well

hypotension and shock

3-Blood volume abnormality (Hypovolemia)::

a. True hypovolemia pt' with external/internal bleeding ,severe

nausea ,severe vomiting, severe diarrhea dehydration and

hypovolemia.

b. False hypovolemia in vasodilatation case

Ex. Pt' with adrenal insufficiency (not enough amount of cortisol)vasodilatation reduction in BP.

OR : pt' with anaphylactic shock (snake sting) severe dilatation

hypotension and shock.


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hypotension andspinal cord vasodilatationNeurogenic shockshock.

severe vasodilatationsevere infectionshockSeptichypotension and decreased tissue perfusion (shock).

So 1- any disorder lead to vasodilatation will lead to shock

2- Affecting the BV will lead to shock

3-Affecting heart pumping will lead to shock

Pathophysiology of shock:

to the cell is the final commoncritical reduction in oxygen levelA*

pathway leading to shock of all varieties

* Reduced substrate supply & accumulation of the products of cell

metabolism e.g. lactate are contributing factors.

*At cellular level decreased O2 level lead to decrease in level of ATP

(Adenosine triphosphate)

Deficiency of ATP will lead to:

1. Depression of the pump function of the cell with an increase in

intracellular sodium, calcium and water with loss of potassium and

magnesium (Sick cell syndrome)

2. High intracellular calcium >> leads to myocardial cell fatigue, failure

& cardiac arrest.

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

Phagocytes will stop functioning*

*Plasma kinins, prostaglandins, leukotrienes are synthesized from the cell

membrane & exert their diverse effects on circulation.

*Neutrophils are stimulated to produce elastase which is very injurious to

pneumocytes (lung cells) resulting in ARDS (Acute Respiratory DistressSyndrome) fatal

*Stimulation of the coagulation pathway will lead to consumptive

coagulopathy resulting in disseminated intravascular coagulation DIC (Pt'

with bleeding tendency and thrombosis tendency at the same time)fatal


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*All the systems of the body are affected leading to MODS (Multi Organ

Dysfunction Syndrome)Progression of physiologic effects as shockensues:

Cardiac depression

Respiratory distress

Renal failure

DIC

Result is end organ failure

Inadequate systemic oxygen delivery activates autonomic responses

to maintain systemic oxygen delivery:

1- Sympathetic nervous system

NE, epinephrine, dopamine, and cortisol release.*

*Causes vasoconstriction, increase in HR, and increase of cardiac

contractility (cardiac output).

2- Renin-angiotensin axis

* Water and sodium conservation and vasoconstriction.

*Increase in blood volume and blood pressure.

irculation )Creathing,Birway,(AABCs

Cardio respiratory monitor (ECG, heart rate, respiratory rate to monitor

the Pt')

Pulse oximetry HR, O2 saturation > 92% normally but in hypoxia it's

less than that.

Supplemental oxygen facemask

IV access Canula

ABG, labs blood cross match (need 30-45 min's) its long time so we

give the pt' IV fluids (crystalloids = Normal Saline)


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Foley catheter to monitor urine output

Vital signs BP, HR

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

Ex. Hypovolic shock pt' tachycardia , hypotension , confusion,

seizures "in severe cases", vasoconstriction in non vital organs "skin,

GIT, muscles " so cold and blue hands and feet .

Do you remember how to quickly

estimate blood pressure by pulse?

If you palpate a pulse:

Radial artery at least 70 mm Hg

Foot at least 90 mm Hg

60

80

90

70


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Hypovolemia also classified to:

1-Mild < 20% pallor, cold extremities, delayed capillary refill,

collapsed veins, tachycardia.

2-Moderate 20-40% same signs for mild plus oliguria "decreased urineoutput", postural hypotension.

3-Severe >40% same signs plus mental status changes "confusion,

seizures, anxiety"

:Goals of Treatment

ABCDE

AirwayControl work ofBreathing

optimize Circulation

assure adequate oxygen Delivery

Achieve End points of resuscitation

1- Airway*Determine need for intubation "endotracheal tube".

* Control Work of Breathing

Respiratory muscles consume a significant amount of oxygen : if we

make Mechanical ventilation for the pt' this will supply O2 to him so

this oxygen will reach to the brain,lungs,heart so this will improve the

survival in severe shock.

2- Optimizing Circulation

* We give the pt' IV fluids (crystalloids = Normal Saline) while we're

waiting for blood group test then we watch the pt' after IV fluids

supplying.

* CVP "Central Venous Pressure" 8-12 mm Hg.

* Urine output 0.5 ml/kg/hr (30 ml/hr): in hypovolemia it'll be less thanthat.


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* Improving heart rate > 100 in hypovolemia "tachycardia".

3- Maintaining Oxygen Delivery

* We can transport blood to the pt' to increase Hb level.* Decrease oxygen demands.

* Provide analgesia and anxiolytics to relax muscles and avoid

shivering.

4- End Points of Resuscitation

Goal directed approach*

Urine output > 0.5 ml/kg/hr

CVP 8-12 mmHg

MAP 65 to 90 mmHg

Pharmacological Agents:

If restoration of blood volume, red cell mass, & adequate oxygenation fail

to restore an adequate cardiac output & oxygen delivery then

pharmacological agents may be required.

Dopamine improves the cardiac output & urine output so this will

increase BP.

Dobutamine acting directly on B1-adrenergic receptors has moreinotropic action on the heart.

Persistent Hypotension:

Inadequate volume resuscitation

Pneumothorax (accumulation of air in pleural cavity) not improved

by giving IV fluids.


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Cardiac tamponade (accumulation of blood or fluids around the heart)

Hidden bleeding (internal bleeding)

Adrenal insufficiency

Medication allergy

I tried my best in this script but the lecture too onerous.

Forgive me for any mistake


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Shock & Hemorrhage (Repaired)

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