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Pathophysiology > Lecture 2: Hemmorhage > Flashcards

Lecture 2: Hemmorhage Flashcards

1
Q

Define hemorrhagic shock

A

Hemorrhagic shock:
Reduction in tissue perfusion below that necessary to meet metabolic needs due to loss of blood volume

origin of the shock in hemorrhagic shock: loss of blood volume

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2
Q

Describe the initial compensatory mechanisms that develop during hemmorhagic shock:

Initially with a hemorrhage:

Decrease SV… leads to Decreased CO…… Decreased MAP

What does the sympathetic nervous system do to compensate for that?

A

The intial problem with hemorrhage is that stroke volume is decreasing

The sympathetic nervous system will kick in to INCREASE HR…. and INCREASE TPR which will in turn INCREASE MAP

This is why a patient can have a relatively normal systolic blood pressure for a long time during shock…there will be other signs of shock such as tachycardia, cool, clammy skin (due to increased peripheral resistance)

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3
Q

Where does blood get shunted to in a patient with shock?

What does that end up causing elsewhere in the body?

A

In a pt with hemorrhagic shock:

Increased shunting of blood to the Heart and the Brain

There will be a decrease in blood flow to the rest of the body, and those other areas will become hypoxic

This iw why the symptoms of shock arrise ina hemorrhage: rest of body becomes hypoxic

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4
Q

Explain what happens in terms of baroreceptors during a hemorrhage:

what happens to the heart?

The blood vessels?

The kidneys?

A

There are baroreceptors in the carotid sinus and aortic arch. They are mechanoreceptors and respond to stress

During a hemorrhage they will decrease in stretch, decreasing their firing to the brain. The brain will sense this and compensate by increasing sympathetic drive to the heart (Increasing HR and increasing contractility). The brain will also increase vasoconstriction in peripheral vessels

In terms of the kidneys: the brain will compensate by increasing sodium reabsorption (which will in turn decrease water excretion…decrease urine output)… NOTE: you will not see the effects on the kidneys until much later in the shock process

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5
Q

Explain what cardiopulmonary receptors are and how they play into compensatory mechanisms during a hemorrhage

A

hearts have cardiopulmonary receptors in the chambers of the ventricles

This usually does not happen until LATE stages of hemorrhage, but the mechanism is thought to be the heart will sense that it is contracting really hard against an essentially empty chamber, this will reduce sympathetic drive… thereby reducing HR… and can eventually cause fainting

This mechanism is one of the proposed mechanisms for paradoxycal bradycardia in hemorrhagic shock patients.

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6
Q

What are the important hormones released in shock, and explain their effects:

Catecholamines:

Renin-Angiotensin Axis

A

Important Hormones in shock:

Catecholamines: Epi and NE

  • Increased HR and contractility
  • Vasoconstriction of peripheral vessels and narrowing of pulse pressure

Renin-Angiotensin Axis: Aldosterone and ADH

  • Water and sodium conservation and vasoconstriciton
  • Increase in blood volume and blood pressure
  • Decreased urine output

Note: decreased urine output is a significant sign of shock… takes time to see the effects of the Renin axis

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7
Q

Draw the graph explaining the following relationships

Oxygen Delivery and Oxygen consumption

SvO2

O2Er (oxygen extration ratio)

Lactate levels

A
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8
Q

Explain what will start to change first in the first few stages of shock

What distinguishes stages 3 and 4 from the earlier stages?

A

First start to see changes in HR and respiratory rate

systolic bp can stay stable for a long time

The pulse pressure will start to narrow by stage 2

The blood pressure will drop by stage 3. and by stage 3 you are seeing negligible urine output

Stage 3 and 4 is where anaerobic metabolism will kick in because you aren’t supplying enough O2 (bp drops, increased lactate levels)

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9
Q

Which stages are considered compensated shock vs decompensated shock

How much blood loss do you have to endure to get to stage 4 hemorrhagic shock?

A

Compensated shock is stages 1-3

Stage 4 shock…. blood loss of over 40%, you’ll die within 6 hours

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10
Q

If oxygen extraction increases, which of the following variables is reduced?

DO2

VO2

O2ER

SvO2

A

SvO2

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11
Q

Explain the progression of blood loss to acidosis aka the steps

A

Blood Loss –> Inadequate Perfusion—> Cellular Hypoxia–> Aerobic Metabolism–> Anaerobic Metabolism—> Lactic Acid Buildup–> Cellular Edema–> Acidosis

Also, acidosis intereferes with coagulation and can lead to further blood loss

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12
Q

Explain the pathway of anaerobic metabolism that results in hemorrhage

A

Because of the hypoxia that develops in hemmorhagic shock, cells will switch to anerobic metabolism, where pyruvate will get “fermented” into lactic acid. This lactic acid can then leave the cell and contribute to acidosis

(this is becaue lactic acid is ionizable in blood, and the H+ ion will dissociate, while lactate will bind to sodium, sodium lactate is an indirect measure of acidosis in blood)

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13
Q

Explain how the different stages of hemmorhage relate to ATP supply and ATP demand

At what stage does anaerobic metabolism set in and what is the ultimate concenquence of that

A

Look at the picture attached

Essentially, ATP supply does not meet demand by stage 3 of hemorrhage

That is when anaerobic metabolism kicks in

The ATP won’t be available to supply the ATPases

Membranes will leak: Na will enter cell, K will leave, Ca will build up inside

Membranes will depolarize

Water will follow the salt inside the cell causing cellular edema

Cell death due to increasing Ca inside cell and apoptosis

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14
Q

Explain the effects of acidosis

On blood pH

and on cardiac myocyte cells

A

Increase in Lactate will cause acidosis

(increase in H+ aka lower pH)

This will cause a decrease in pH inside the cell as well

That increase in H+ ions inside the cell activates K channels, stimulates adrenoreceptor internalization

MOST IMPORTANTLY it desensitizes microfilaments, even with the increasing Ca inside the cell

That is why cardiac contractility decreases in heart muscle

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15
Q

Which one of the following is the most important contributer to loss of K+ gradient during ischemia?

Reduced production of pyruvate

Increased production of glycogen

Increased production of Acetyl-CoA

Increased production of lactic acid

Reduced glycolysis

A

Increased production of lactic acid

Another contributing factor is ATP defecits

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16
Q

List the injuries that are most prone to hemorrhage and methods used to identify sources of blood loss

A

Injuries most prone to hemorrhage:

  • Aorta
  • Spleen (receives 10-15% of total Cardiac Output)
  • Pelvis

Quickly rule out blood loss: “FAST Method”

Chest X Ray, Abdomen Ultrasound, Pelvis X Ray, Femur exam

17
Q

Explain the fractures associated with the most blood loss

Associated Soft Tissue Trauma:

Causes the release of _____

A

Fracture Associated Blood Loss:

  • Humerus (750mL)
  • Tibia (750 mL)
  • Femur (1500 mL)

Pelvis: greater than 3 L

Associated Soft Tissue Trauma: Release of cytokines

  • increased permeability of vasculature
  • Magnify fluid loss
18
Q

Describe assessments used to determine the degree of shock

A

Assessments used to determine degree of shock:

Pulse

  • Blood Pressue
  • Pulse Pressure
  • pH
  • Serum Lactate
  • Base Defecit
  • Shock index
19
Q

What is “shock index”

A

Shock index is simply the HR/systolic bp

0.5 is normal range

If it starts getting to 0.9 or higher, it suggests circulatory shock

20
Q

Pulse:

  • Lacks specificity alone
  • Dependent on ___

Affected by?

When to be concerned?

A

Pulse:

  • Lacks specificity alone
  • Age dependent
  • Affected By: emotion, fever, pain, drugs
  • Pulse rate and character together are more reliable
  • When to be concerned: greater than 100 (aka in the 110-120 and higher range)
21
Q

Any patient who is ____ and ____ is in shock until proven otherwise

A

Any patient who is cool (to the touch) and tachycardic is in shock until proven otherwise

22
Q

Parodoxical Bradycardia:

  • Define as Pulse < ____ with SBP < ___
  • Occurs in up to ___ of all hypotensive trauma
  • Cause remains ____
A

Parodoxical Bradycardia:

  • Define as pulse < 90 with systolic bp < 90
  • Occurs in up to 45% of hypotensive trauma
  • Cause remains unclear:
  • protective reflex to increase diastolic filling?
23
Q

Blood Pressure:

  • Systolic BP drop is a ____ sign
  • Systolic BP does not fall until stage ___
  • Adults: ___% blood loss
  • Children: ____% blood loss

SBP < 90 mmHg means what?

A

Blood Pressure:

  • Systolic BP drop is a late sign of shock
  • systolic BP does not fall until stage 3
  • Adults: 30% of blood loss
  • Children: 40-45% blood loss

SBP< 90 mmHG: mortality approaches 65%

24
Q

Pulse Pressure:

  • Narrowed pulse pressure suggests _____
  • Result of increasing _____ from compensatory ____ release
A

Pulse Pressure: (better indicator of shock than SBP)

  • narrowed pulse pressure suggests significant blood loss
  • Result of increasing diastolic pressure from compensatory catecholamine release

Aka diastolic pressure increases because of sympathetic nervous system compensatory mechanisms and cathecholamine release

25
Q

Hematocrit:

  • Reliable or not?
  • How long until it is reliable?
A

Hematocrit:

  • Unreliable estimation of acute blood loss
  • Lag time of several hours (initially you are losing whole blood, so no affect on RBC %… it isn’t until later stages when the kidneys start preserving water that the hematocrit level will decrease)
  • Baseline value for comparison only
26
Q

Lactate:

  • ______ measure of oxygen debt
  • Normal Value =
  • Values of ____ correlate to magnitude of shock
  • Lactate levels above ___ = increased mortality
  • Ability to clear lactate within 24 hours : predictive of _____
  • Inability to clear lactate within 12 hours indicates______
A

LACTATE: much better measure of shock

  • Indirect measure of oxygen debt
  • Normal Value = 1.0 mEq/L
  • Values > 1.0 correlate to magnitude of shock
  • Lactate levels above 5 mean increased mortality
  • Ability to clear lactate within 24 hours : predictive of survival
  • Inability to clear lactate within 12 hours is predictive of multisystem organ failure
27
Q

Base Defecit:

What is it?

Normal range is:

Worsening BD means:

A

Base Defecit:

Essentially measures how acidotic a pt is

It measures how much base you would need to add to blood to get it back to its normal pH

Normal Range is -3 to +3, +10 indicates severe acidosis

Worsening BD: ongoing bleeding, inadequate volume replacement

28
Q

How are acidosis measured in patients?

What does acidosis correlate with?

Acidosis is defined as a pt with a pH less than ___

A

Acidosis is assessed via blood pH, “Base Defecit” and lactate levels

Acidosis correlates with depth of shock and degree of tissue injury

Acidosis means pH < 7.2

If your BD > 7.5, than your mortality rate goes up

29
Q

Descibe the Trauma Triad of Death and how acidosis contributes to further pathology

A

Trauma Triad of Death:

  1. Acidic Blood (acidosis)

causes decreased cardiac output and leads to

  1. Low body temperature

which messes up enzymes and leads to

  1. Blood clotting problems/coagulopathy
30
Q

Hypothermia:

Defined as a core temp of less than ____

What does this do?

A

Hypothermia:

Core temp < 35C (95F)

Action: Decrease coagulation factors and increase platelet dysfunction

causing more blood loss

31
Q

Explain the “trauma coagulopathy therory”

A

Trauma Coagulopathy theory:
When a pt has a traumatic event and loses blood… they may develop shock… leading to acidosis

If that acidosis leads to hypothermia, they may get trauma induced coagulopathies

There is only a finite amount of coagulation factors, and they get used up, you want to give a pt resusicative fluids that are warmed

32
Q

Recognize a Pt at risk in the ED:

Pt’s at high risk are pt’s with the following:

Shock Index > ____

SBP

Base Defecit > ___

Hypothermia (temp of ___)

______ Lactate Levels

A

A pt at risk would have the following:
Shock Index > 0.9 (HR/SBP)

SBP < 90 mmHg

Base Defecit > 6

Hypothermic (Temp < 35C or 95F)

Elevated Lactate Levels

Pathophysiology (17 decks)

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