@dryadav this sclassification of hemorrhagic shock should be known to u and all In Class I hemorrhagic shock, blood loss is relatively minimal, usually representing a loss of up to 15% of total blood volume. Compensatory mechanisms, such as increased heart rate and vasoconstriction, are activated to maintain perfusion to vital organs. Clinical signs may include mild tachycardia, slight anxiety, and minimal changes in blood pressure. Class II Hemorrhagic Shock: Class II hemorrhagic shock represents moderate blood loss, typically involving a loss of 15% to 30% of total blood volume. Compensatory mechanisms become more pronounced, including increased heart rate, vasoconstriction, and redistribution of blood flow to essential organs. Clinical signs may include increased tachycardia, worsening anxiety, cool and clammy skin, decreased urine output, and a slight decrease in blood pressure. Class III Hemorrhagic Shock: Class III hemorrhagic shock is characterized by severe blood loss, usually involving a loss of 30% to 40% of total blood volume. Compensatory mechanisms become overwhelmed, leading to significant tissue hypoperfusion and metabolic acidosis. Clinical signs may include profound tachycardia, marked hypotension, altered mental status (e.g., confusion, agitation), cold and pale extremities, oliguria, and worsening metabolic acidosis. Class IV Hemorrhagic Shock: Class IV hemorrhagic shock represents profound blood loss, typically exceeding 40% of total blood volume. Compensatory mechanisms fail, resulting in severe tissue hypoperfusion, multi-organ dysfunction, and a high risk of mortality. Clinical signs may include profound hypotension, tachycardia, altered mental status (e.g., lethargy, coma), cold and mottled skin, anuria, and profound metabolic acidosis. if in shock then it means > 30% blood volume is lost and needs starting prbc fast along with NS fast , other cases dont need bt urgently . the transfusion trigger is 7 gm in ugib and for cad/ post op / critically ill patients 8 is the trigger. in such patients who are not in shock the true hb value is known only after 48 hours as equilibrium is reached between intravasc and extravasc fluids. 1 prbc raises hb by 1 gm. in variceal bleed which is mostly due to cld pt/inr and platelets are abnormal however they dont reflect the true coagulation status due to dysregulation of anticoag and procoag factors . If Teg is available it is recommended to use it to guide the use of ffp and platelets ,else platelets less than 30-5000 and fibrinogen < 100 need correction with ffp / cryo . the main therapeutics is interventions - banding to stop bleeding . in pud there is no coagulation issue unless pt is on antiplatelet /anticoag . if on antiplatelet cardiology consult needs to be taken . for anticoag appropriate antidote needs to be given and ffp maybe given if required . if in shock then same principles apply as above for transfusion ras and prescription prbc has to be given max over 4 hours if not in shock. in shock u run it fast . sdp and ffp are given fast 1 sdp = 6rdp = rise of 30000 platelet count target > 50000 4 ffp are given over 24 hours in average adult target inr >1.5 / bleeding stops rate of transfusion 1 ml/min=15 drops/min so if u hv to give 1 prbc over 2 hrs then assuming 1 rbc has 350 ml , 175 ml/hr = 175 ml/60 min =3ml/min = 45 drops /min approx. similarly u can calculate the drip rate for others so prescription and drip rate will be based on these principles . there is no one prescription. if u still hv q pl post them * if giving ivf for resuscitation then 3times the estimated blood loss has to be given ref Hemorrhagic Shock N Engl J Med 2018; 378:370-379 VOL. 378 NO. 4 DOI: 10.1056/NEJMra1705649
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Excellent
Excellent Sir!
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Thanks for this amazing lecture sir. Thanks a lot 🙏🏻
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@dryadav this sclassification of hemorrhagic shock should be known to u and all
In Class I hemorrhagic shock, blood loss is relatively minimal, usually representing a loss of up to 15% of total blood volume.
Compensatory mechanisms, such as increased heart rate and vasoconstriction, are activated to maintain perfusion to vital organs.
Clinical signs may include mild tachycardia, slight anxiety, and minimal changes in blood pressure.
Class II Hemorrhagic Shock:
Class II hemorrhagic shock represents moderate blood loss, typically involving a loss of 15% to 30% of total blood volume.
Compensatory mechanisms become more pronounced, including increased heart rate, vasoconstriction, and redistribution of blood flow to essential organs.
Clinical signs may include increased tachycardia, worsening anxiety, cool and clammy skin, decreased urine output, and a slight decrease in blood pressure.
Class III Hemorrhagic Shock:
Class III hemorrhagic shock is characterized by severe blood loss, usually involving a loss of 30% to 40% of total blood volume.
Compensatory mechanisms become overwhelmed, leading to significant tissue hypoperfusion and metabolic acidosis.
Clinical signs may include profound tachycardia, marked hypotension, altered mental status (e.g., confusion, agitation), cold and pale extremities, oliguria, and worsening metabolic acidosis.
Class IV Hemorrhagic Shock:
Class IV hemorrhagic shock represents profound blood loss, typically exceeding 40% of total blood volume.
Compensatory mechanisms fail, resulting in severe tissue hypoperfusion, multi-organ dysfunction, and a high risk of mortality.
Clinical signs may include profound hypotension, tachycardia, altered mental status (e.g., lethargy, coma), cold and mottled skin, anuria, and profound metabolic acidosis.
if in shock then it means > 30% blood volume is lost and needs starting prbc fast along with NS fast , other cases dont need bt urgently . the transfusion trigger is 7 gm in ugib and for cad/ post op / critically ill patients 8 is the trigger. in such patients who are not in shock the true hb value is known only after 48 hours as equilibrium is reached between intravasc and extravasc fluids. 1 prbc raises hb by 1 gm. in variceal bleed which is mostly due to cld pt/inr and platelets are abnormal however they dont reflect the true coagulation status due to dysregulation of anticoag and procoag factors . If Teg is available it is recommended to use it to guide the use of ffp and platelets ,else platelets less than 30-5000 and fibrinogen < 100 need correction with ffp / cryo . the main therapeutics is interventions - banding to stop bleeding . in pud there is no coagulation issue unless pt is on antiplatelet /anticoag . if on antiplatelet cardiology consult needs to be taken . for anticoag appropriate antidote needs to be given and ffp maybe given if required . if in shock then same principles apply as above
for transfusion ras and prescription
prbc has to be given max over 4 hours if not in shock. in shock u run it fast . sdp and ffp are given fast
1 sdp = 6rdp = rise of 30000 platelet count target > 50000
4 ffp are given over 24 hours in average adult target inr >1.5 / bleeding stops
rate of transfusion
1 ml/min=15 drops/min
so if u hv to give 1 prbc over 2 hrs then assuming 1 rbc has 350 ml , 175 ml/hr = 175 ml/60 min =3ml/min = 45 drops /min approx.
similarly u can calculate the drip rate for others
so prescription and drip rate will be based on these principles . there is no one prescription. if u still hv q pl post them
* if giving ivf for resuscitation then 3times the estimated blood loss has to be given
ref
Hemorrhagic Shock
N Engl J Med 2018; 378:370-379
VOL. 378 NO. 4
DOI: 10.1056/NEJMra1705649
Thank you sir
Welcome
Nice sir
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Great presentation
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