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Source Time of onset Site of bleeding -> either internal or external bleeding. 1-Hemorrhage according to the source of bleeding: 1- Arterial Hemorrhage: Ex. A patient with RTA road traffic accident, trauma (gun shot
to his lower limb) so there's arterial hemorrhage. It is a bright fresh blood (Oxygenated blood) and its pulsatile ( in systole it gives ejection, and stops in diastole) so it works as on/off pulsatite. So in an operation there's a bleeding if its pulsatile bleeding we know this is an arterial hemorrhage for an injured artery. 2- Venous Bleeding: As we know that the pressure is lower in the vein compared to the artery, so the injured vein is not pulsatile but its continuous . Always we have venous return to the heart so this give the venous bleeding the continuity with a steady and copious flow, now if you look at the 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 slow continuous 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 often rapid ooze not pulsatile.
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.
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 be measured by weighing swabs after use & subtracting the dry weight. (1gm BLOOD =1ml) in short operations For long operations (thoracoabdominal surgeries or abdominoperineal 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/dl EX. 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.
2. Overt compensated
Due to decreasing in blood volume and blood pressure so there'll be increasing in sympathetic activity in order to increase blood pressure so this will increase heart rate "Tachycardia", increasing in contractility of heart "pumping activity",
vasoconstriction in peripheral arteries so they've cold extremities particularly hands and feet . 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.
CNS signs:
*Urine analysis show
-Drowsiness
Increasing in osmolality & -Confusion Sodium concentration, in -Increased respiratory rate (tachypnea) 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 venous system) its more than 12.
3. Decompensated hypovolemia
* Protective mechanisms are unable to control & maintain
the blood pressure
* This is what is referred to as shock.
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. *Vital organs (brain, heart, lungs) are no longer adequately perfused. *Mean arterial pressure falls & may be difficult to record.
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 tissue perfusion, 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 pressure is 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 cells adequately with oxygen and eliminate waste product especially Lactic Acid
* Inadequate oxygen delivery to meet metabolic demands (due to heart failure, bradycardia and hypovolemia which lead to hypotension). *Results in global tissue hypo perfusion and metabolic acidosis. *Shock can occur with a normal blood pressure (normotensive) and hypotension can occur without shock Ex. Hypertensive Pt' his BP (200/120) with trauma and hemorrhage so his 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. *IN MOST of the cases pt' with a shock has severe hypotension.
Classification of Shock:
1-Decreased circulating volume or decreased preload:: Heart MI so the heart can't pump blood wellhypotension and shock 2-Compromised cardiac function:: Cardiac compressive shock (Extrinsic) pericardiatis "inflammation of pericardium that surround the heart " heart can't expand and contract well hypotension 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 hypovolemiapt' 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.
Neurogenic shock spinal cord vasodilatation hypotension and shock. Septic shock severe infection severe vasodilatation hypotension 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:
* A critical reduction in oxygen level to the cell is the final common 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)
*All the systems of the body are affected leading to MODS (Multi Organ Dysfunction Syndrome) Progression of physiologic effects as shock ensues: 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.
ABCs (Airway, Breathing, Circulation ) 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)
Physical exam (VS, mental status, skin color, temperature, pulses, etc) 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
60
70
Foot at least 90 mm Hg
80
90
Goals of Treatment : ABCDE Airway Control work of Breathing 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 than that.
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 more inotropic action on the heart.
Persistent Hypotension:
Inadequate volume resuscitation Pneumothorax (accumulation of air in pleural cavity) not improved by giving IV fluids.
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