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Cardiorespiratory 2 > Haemorrhage and Shock > Flashcards

Haemorrhage and Shock Flashcards

1
Q

what is the definition of clinical shock

A

• Clinical Shock is an acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in cellular hypoxia

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2
Q

name two things that are part of the shock syndrome

A
  • hypotension and end organ injury
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3
Q

name an effect of cellular hypoxia

A
  • If you don’t have enough ATP for the sodium potassium pump this means that sodium is seaked in and sodium draws water into it by osmosis
  • There is a raise in intracranial pressure, can have a viscious circle ending in cerebral death
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4
Q

what happens during cellular hypoxia

A
  1. Cells swtich from aerobic to anaerobic metabolism
  2. This causes lactic acid production
  3. The cell function ceases and swells
  4. The membrane becomes more permable
  5. Electroclytes and fluids seep in and out of the cell
  6. Cells swell and mitochondria damage occurs in cell death
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5
Q

what needs to happen in order to maintain adequate oxygen supply to the tissues

A

CO and BP must be maintained above certain minimum values

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6
Q

what does the mean arterial pressure have to be less than in order to cause shock

A

If the mean arterial pressure is less than 60mmHg than shock is likely

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7
Q

what minimum levels do oxygen and blood pressure need to be above in order to prevent shock

A
  • CO 5l/min
  • Systolic BP – 120mmHg
  • MAP – 100mmHg
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8
Q

when is a shock diagnosis likely

A

Shock diagnosis is likely if mean arterial pressure (MAP) <60 mm Hg
and there are clinical signs of hypo-perfusion of vital organs. These include tachycardia, tachypnea, mental confusion, pallor

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9
Q

what can cause a low blood pressure

A
  1. Low cardiac output
  2. Low systemic vascular resistance
  3. Both
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10
Q

how does shock occur due to a decrease in CO

A

Normally due to

  • reduced preload
  • reduced myocardial contractility
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11
Q

what can cause a reduced preload

A
  1. Tension pneumothorax
  2. Pulmonary embolism
  3. Reduced venous return due to haemorrhage
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12
Q

what can cause a decrease myocardial contractility

A
  1. Cardiac disease
  2. Hypoxia/hypercapnia
  3. pH or electrolyte disturbance
  4. drugs (eg beta blockers, calcium channel blockers)
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13
Q

how does shock occur due to a low SVR

A
  • the SVR is normally maintained at an appropriate level by a balance between vasoconstrictor factors and vasodilators factors
  • vasoconstrictors act mainly on arterioles in end organs
  • usually caused by pathogens in the blood relating toxin which act on the vascular smooth muscle and relax it - toxins block the actions of the vasoconstrictors
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14
Q

what is the diameter of arterioles

A
  • Remember that arterioles are less than 1 mm in diameter, usually 100-300 microns
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15
Q

what systems cause vasoconstriction

A
  • angiotensin- renin system

- sympathetic nervous system

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16
Q

How does the sympathetic nervous system cause vasoconstriction

A
  • the sympathetic nervous system releasing noradrenaline locally on alpha receptors on the outside of the arterioles
  • Circulating adrenaline is a relatively ineffective vasoconstrictor as it cannot easily pass through the endothelium to access the alpha receptors
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17
Q

how does angiotensin II cause vasoconstriction

A
  • Secondly angiotensin II is carried in the plasma, and acts on angiotensin AT1 receptors on the endothelium lining arterioles.
  • This stimulates contraction of the underlying smooth muscle
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18
Q

what released from the endothelium causes vasoconstriction

A

endothelin.

- The role of endothelin in normal tissue is not clear; it may help constrict injured blood vessels

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19
Q

name the vasodilators

A

1) Prostacyclin is produced in endothelial cells from arachidonic acid. Prostacyclin is usually called PGI2 .It reduces calcium entry into smooth muscle cells surrounding the endothelium thus reducing the contractility of the smooth muscle
2) Nitric Oxide gas is produced in endothelial cells from arginine. It diffuses into the underlying smooth muscle where it stimulates cyclic AMP formation which decreases calcium entry and relaxes the muscle. It is continually produced in healthy arterioles by the action of moving blood on glycyoproteins on the endothelial membrane
3) Adenosine is released from endothelial cells and smooth muscle during activity.

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20
Q

what produced by immune cells can lead to a low SVR

A

Excess nitric oxide produced by immune cells fighting the infection may contribute to the loss of vasoconstrictor tone

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21
Q

what are the phases of shock

A
  • compensatory phase

- decompensation phase

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22
Q

what happens during compensation phases of shock

A

Either the systemic vascular resistance is not maintained (arterioles no longer constrict effectively ), or the cardiac output decreases (loss of blood volume or obstruction to flow). In both cases there is an initial stage where homeostatic mechanisms are activated.

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23
Q

what happens during the decompensation phase of shock

A
  • There is a later stage where the arterioles cannot maintain constriction or the blood preload reduction is too great. End organs are not perfused with oxygenated blood and start to fail.
  • This is DECOMPENSATION, or decompensated shock.
  • Decompensated shock if allowed to continue is fatal.
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24
Q

describe an example of the compensation stage and decompensation stages in shock

A

Sepsis or anaphylaxis produces a pathological vasodilation in one or more end organs and prevents the normal arteriolar constriction. SVR cannot be maintained. Blood pressure falls.
Baroreceptors detect the fall in BP and increase heart rate to compensate. Increased heart rate causes increased cardiac output which acts to restore blood pressure. There is COMPENSATION for the pathological vasodilation. If compensation is successful perfusion of end organs is maintained and the individual will survive.
If the vasodilation is excessive and despite a maximal increase in heart rate the blood pressure fails to recover, a state of DECOMPENSATION will occur. The low blood pressure is inadequate to perfuse end organs (other than those with pathological vasodilation). End organ failure will progressively occur, and the individual will die unless brought back to a state of compensation

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25
Q

what are the 4 main classes of shock

A
  1. Obstructive shock
  2. Distributive shock
  3. Hypovolaemic shock
  4. Cardiogenic shock
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26
Q

describe obstructive shock

A

is where there is a physical obstruction to the vessels entering or leaving the heart. For example, shock due to a pulmonary embolism would be counted as obstructive shock.

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27
Q

describe distributive shock

A

(example is sepsis) is due to loss of vasoconstriction in one or more end organs, producing excess blood flow in this system and poor perfusion of other organs.

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28
Q

describe hypovolaemic shock

A

(low blood volume) is normally due to haemorrhage, so it is often called haemorrhagic shock

29
Q

describe cariogenic shock

A

is due to failure of the heart to pump efficiently and supply blood to the body.

30
Q

what two classes of shock are sometimes grouped together

A

Sometimes cardiogenic and obstructive shock are often grouped together as cardiopulmonary obstructive shock

31
Q

what are the classes of shock in the US

A

1) Hypovolemic (as before)
2) Septic: distributive shock due to sepsis
3) Cardiogenic (as before)
4) Neurogenic:

32
Q

what is neurogenic shock

A
  • This is a type of distributive shock resulting in low blood pressure, occasionally with a slowed heart rate, that is attributed to the disruption of the autonomic pathways within the spinal cord.
  • It can occur after damage to the central nervous system such as spinal cord injury.
33
Q

name examples of

  • obstructive shock
  • distributive shock
  • hypovolaemic shock
  • cardiogenic shock
A
  1. Obstructive shock
    pulmonary embolism
    pneumothorax
    cardiac tamponade
  2. Distributive shock
    sepsis
    anaphylaxis
    neurogenic
3. Hypovolaemic shock
haemorrhage
burns
surgery or trauma
loss of fluid and electrolytes from the gut
4. Cardiogenic shock
myocardial infarction
heart failure
arrhythmias such as ventricular fibrillation 
ventricular septal rupture
Ischaemic Cardiomyopathy
Valvular Disease etc
34
Q

what are the signs of hypovalemic shock

A
  • confusion / anxiety,
  • cold
  • clammy skin (sympathetic nervous system turns of taps to the skin),
  • low BP,
  • high heart rate,
  • slow capillary refill,
  • greyish pallor,
  • oliguria,
  • absent bowel sounds.
  • Reduction in blood flow to the kidney – not the first line of defence
35
Q

what do the signs of hypovalemic shock indicate

A

*These indicate that the sympathetic nervous system is attempting to maintain oxygen supply to heart and brain despite reduced preload: if it is succeeding the body is in compensation mode; if it is failing, the body is in decompensation

36
Q

most patients with cardiogenic shock have an….

A

AMI

37
Q

what are the symptoms of patients with cardiogenic shock

A

present with the constellation of symptoms of acute cardiac ischemia
- chest pain
- shortness of breath
- diaphoresis
- nausea
- vomiting
Patients experiencing cardiogenic shock also may present with pulmonary edema, acute circulatory collapse, and presyncopal or syncopal symptoms.

38
Q

what are the signs of cardiogenic shock

A

ECG shows the pattern of AMI or acute coronary insufficiency
Systolic BP < 80 mm Hg *
Pulse rate is 100 per min or faster
The urinary output is low, 30 ml or less per hour
There are clinical signs of peripheral circulatory collapse

39
Q

what is the treatment of cardiogenic shock

A

The first priority is to expand the circulating blood volume with IV fluids, using the CVP (Central Venous Pressure) as a basic guide

40
Q

when does cardiogenic shock usually develop and what mortality does that leave patients with

A

Cardiogenic shock develops in 10-20% of patients hospitalized after AMI
Mortality of such patients approximately 80% or higher

41
Q

what are the symptoms of septic (distributive shock)

A
  • low BP
  • tachycardia
  • fever - this could be absent in elderly or immunosuppressed patients
  • chills
  • rigors
  • fatigue
  • malaise
  • nausea
  • vomiting
  • difficulty breathing
  • anxiety
  • confusion
42
Q

what happens if you don’t treat septic shock

A

Untreated septic shock is rapidly fatal. It is estimated that up to 50% of patients with fully developed septic shock will die or have permanent organ damage despite treatment.

43
Q

what often produces obstructive shock

A

tension pneumothorax

44
Q

what are the signs of obstructive shock

A
  • tachycardia and anxiety of hypovolemic shock are present.
  • chest pain
  • breath sounds are absent on the affected hemiothorax - the trachea deviates away from the affected side.
  • A pulmonary embolism* (PE) can cause obstructive shock.
45
Q

what is a classical presentation of PE

A
  • pleuritic chest pain
  • shortness of breath
  • hypoxia
46
Q

what are systems respond to hypovolemic shock

A
  • hematologic system
  • cardiovascular system
  • renal system
  • neuroendocrine system
47
Q

how does the hematologic system respond to shock

A

The hematologic system responds by activating the coagulation cascade and contracting the bleeding vessels (by means of local thromboxane A2 release).

In addition, platelets are activated (also by means of local thromboxane A2 release) and form an immature clot on the bleeding source.

48
Q

how does the cardiovascular system respond to shock

A

The cardiovascular system responds by activating the sympathetic nervous system.

This causes an increased heart rate, increased myocardial contractility, and constriction of peripheral blood vessels in skin, muscle, and GI tract..

This helps redistribute blood to the brain, heart, and kidneys

49
Q

how does the renal system respond to shock

A

The renal system increases renin secretion and hence angiotensin II.

Angiotensin II has 2 main effects, both of which help to reverse hemorrhagic shock, vasoconstriction of arteriolar smooth muscle in skin, muscle and GI tract and stimulation of aldosterone secretion by the adrenal cortex.

Aldosterone increases sodium reabsorption and subsequent water reabsorption. (hence oliguria is a sign of shock.)

50
Q

how does the neuroendocrine system respond to shock

A

The neuroendocrine system responds by releasing ADH from the posterior pituitary gland in response to a decrease in BP (as detected by baroreceptors) and a decrease in the plasma sodium concentration (as detected by osmoreceptors).

ADH indirectly leads to an increased reabsorption of water and salt (NaCl) by the distal tubule, the collecting ducts, and the loop of Henle.

51
Q

how much blood loss is life threatening

A

Acute loss of >40% of blood volume (>2 litres) is immediately life threatening.
40% takes you into decompensation

52
Q

what is the fluid levels in each of these

  • total body wate r
  • intracellular
  • extracellular
  • blood volume
A

Total body water – 45L
Intracellular 27L
Extracellular 18L
Blood volume 4.5-5L

53
Q

what is the comepensatory response with a venous bleed

A
  • With a venous bleed, the drop in venous return (preload) reduces stroke volume and thus cardiac output.
  • Blood pressure therefore falls.
  • Baroreceptors detect the fall and compensate by increasing sympathetic outflow.
  • This increases heart rate and contractility.
  • The sympathetic nervous system constricts the large veins to move blood out from the venous reservoir and restore preload.
54
Q

what is the compensatory response of an arterial bleed

A

With an arterial bleed, blood pressure drops immediately and is detected by the baroreceptors, triggering a similar response.

The vasomotor centre in the medulla signals to the hypothalamus to release vasopressin (ADH).

The reduced preload reduces release of atrial natriuretic peptide.

Urine flow and sodium excretion decrease

55
Q

what are the long term (hours to days) response to haemorrhage

A
  • angiotensin II has a long lasting effect in increasing sodium retention.
  • Thirst is also stimulated by angiotensin II receptors in the brain (in the subfornical organ above the hypothalamus).
  • This increases water intake. Thus both sodium and water retention are increased to restore the circulating blood volume.
  • There is stimulation of albumin and other plasma protein synthesis in the liver.
  • Fibroblasts in the extracellular space surrounding the kidney tubules (peritubular cells) are sensitive to hypoxia and release increased amounts of erythropoetin to stimulate red cell production so that the haematocrit is restored to normal
56
Q

what are the clinical symptoms of hypovolaemic shock

A
  • Tachycardia,
  • Pale, Shut down
  • Sweaty, Clammy
  • Oliguria
  • Confusion
57
Q

how many stages is hypovolaemic shock divided into

A

4 stages

58
Q

describe class I hypovalemic shock

  • blood loss amount
  • pulse
  • BP
  • pulse pressure
  • respiratory rate
  • urine output
  • CNS
A
  • is loss of less than 15% - it occurs after a blood donation or a minor injury, it is normally fully compensated, the patient feels normal or may be slightly fatigues
  • Pulse is not over 100
  • BP is normal
  • Pulse pressure is normal
  • Respriation Rate is 14-20 (normal is 12-15) so slightly raised
  • Urine output is greater than 30
  • CNS slightly anxious psychological effect of seeing the blood
59
Q

describe class II hypovalemic shock

  • blood loss amount
  • pulse
  • BP
  • pulse pressure
  • respiratory rate
  • urine output
  • CNS
  • symptoms
  • treatment
A
  • 15-30% of blood loss
  • Clear signs reaching edge of compensation
  • There is greater than 100 pulse
  • Normal blood pressure
  • Pulse pressure decreased
  • RR 20-30
  • Urine output 20-30ml/hr
  • CNS mildly anxious
  • Clinical symptoms include tachycardia (rate >100 beats per minute), tachypnea, decrease in pulse pressure, cool clammy skin, delayed capillary refill, and slight anxiety.
  • Allowed rest and normal access to water and food, these patients will compensate for the blood loss and eventually fully recover without intervention
  • Don’t normally need a blood transfusion
60
Q

describe class III hypovalemic shock

  • blood loss amount
  • pulse
  • BP
  • pulse pressure
  • respiratory rate
  • urine output
  • CNS
  • treatment
A
  • Shcok involves a loss of greater than 30% of blood, 30-40%
  • Pulse of greater than 120
  • Decreased BP
  • Pulse pressure decreased
  • RR 30-40
  • Urine output is 5-15 ml/hr
  • CNS is anxious/confused
  • Shock involves a loss of 30% of blood
  • This will normally produce a persistent drop in blood pressure
  • The patient will be anxious and or confused
  • Most of these patients will require plasma volume expanders or blood transfusion
  • May have end organ damage especially to the kidneys
61
Q

describe Class IV hypovalemic shock

  • blood loss amount
  • pulse
  • BP
  • pulse pressure
  • respiratory rate
  • urine output
  • CNS
  • treatment
A
  • Occurs when there is greater than 40% of blood volume loss
  • Pulse greater thant 140
  • BP decreased
  • Pulse pressure decreased
  • RR greater than 35
  • Negligible urine output
  • CNS – confused and lethargic
  • The patient will be very confused or unconscious with marked tachycardia, no urine output and severely decreased systolic pressure.
  • This degree of hemorrhage is immediately life threatening and a blood transfusion should be initiated immediately.
62
Q

what kind of shock is septic shock

A

distributive shock

63
Q

what is sepsis

A 
-	Sepsis; a systemic response to the presence of pathogens in blood or other organs 
manifested by ≥ 2 of:
-	Temp > 38oC or < 36oC
-	HR > 90 bpm
-	RR > 20 bpm or PaCO2 < 32 mmHg
-	WBC > 12 x 109/L, or >10% band form
64
Q

what are the symptoms of sepsis

A
  • Temp > 38oC or < 36oC
  • HR > 90 bpm
  • RR > 20 bpm or PaCO2 < 32 mmHg
  • WBC > 12 x 109/L, or >10% band form
65
Q

what is septic shock

A
  • Septic shock = sepsis with hypotension
66
Q

how does sepsis cause distributive shock

A
  • Bacterial toxins and or host response leads to microvascular damage in one or more end organs
  • *Lipopolysaccharide (LPS) in gram-negative bacterial cell walls stimulates neutrophils and monocytes to release cytokines.
  • These may damage endothelium and prevent normal vasoconstriction thus reducing vascular resistance in the affected organs.
  • This may be severe enough to lower blood pressure to shock levels.
  • Alternatively there may be microvascular occlusion due to thrombus formation in capillaries
67
Q

what is the management of shock

A
  • Keep patient lying down with head at heart level to maintain cerebral perfusion
  • If cause of shock is hypovolemia restore circulating blood volume with i.v. colloids (gelatins, dextrans, hydroxyethyl starches, or 4% or 20% albumin) or crystalloids (isotonic or hypertonic saline, or Ringer lactate solution)
  • This will restore preload and hopefully cardiac output
  • Use standard vasopressor drugs (dopamine, noradrenaline, phenylephrine, ADH) to restore blood pressure
  • If cause of shock is sepsis use appropriate antimicrobials
68
Q

what are the therapeutic goals of shock

A

Central venous pressure: 8 – 12 mmHg
Mean arterial pressure: ≥ 65 mmHg
Urine output: 0.5 mL/kg/h
Central venous (SVC) or mixed venous oxygen saturation: ≥ 70%

Cardiorespiratory 2 (43 decks)

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