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Hypovolaemia Flashcards

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1
Q

What are the biproducts of anaerobic respiration?

A

Lactic acid
Carbon dioxide
Water

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2
Q

What are the signs of increased oxygen demand?

A

Tachypnoea
Tachycardia
Cyanosis

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3
Q

What primary factors influence how oxygen is transported?

A

Reduced haemoglobin count
Oxygen percentage of the blood
Concentration of carbon dioxide

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4
Q

What occurs in metabolic acidosis? With values for pH and bicarbonate

A

Decrease in pH <7.35 with decreased bicarbonate <22mEq/L

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5
Q

What occurs in metabolic alkalosis? With values for pH and bicarbonate

A

Increased pH >7.45 with increased bicarbonate >26mEq/L

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6
Q

What may occur to compensate for metabolic alk/acidosis?

A

Acidosis: increase in RR
Alkalosis: decrease in RR

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7
Q

What 6 aspects does adequate perfusion of body tissues depend upon?

A

Efficient respiration- inspiration of O2, expiration of CO2
Efficient contraction of the heart to maintain cardiac output
Adequate BP
Ability of the vascular system to transport blood from the left ventricle via the arteries to the cells, allowing the release of O2 and return of deoxygenated blood back to the heart via the veins to the right atrium then lungs.
Sufficient blood volume within the vascular system
Tissues ability to use and extract oxygen and nutrients from the blood

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8
Q

What is the definition of shock

A

Pathophysiological condition characterised by inadequate tissue and organ perfusion. Seriously reduces the delivery of oxygen and nutrients to the cells causing a reduction in normal cellular activity.

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9
Q

Shock alters what and what?

A

Circulation and metabolism.

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10
Q

What occurs at the capillary cellular junction?

A

Oxygen and nutrients are delivered to the body tissues and metabolic waste is removed.

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11
Q

What does shock mainly result in?

A

Reduced capillary blood flow potentially resulting in diffuse ischaemic hypoxia.

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12
Q

What two factors are involved in diffuse ischaemic hypoxia? And what do they prevent?

A

Biochemical and neurological factors which interfere with cellular uptake and use of oxygen.

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13
Q

What is the function of ATP in driving sodium-potassium pumps?

A

To maintain a constant ionic gradient across the cell wall.

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14
Q

What are the values of sodium and potassium inside of the cell?

A

Sodium: 10mmol/L
Potassium: 140mmol/L

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15
Q

What are the values of sodium and potassium outside the cell?

A

Sodium: 140mmol/L
Potassium: 10mmol/L

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16
Q

What does the maintenance of the sodium-potassium gradient determine in relation to the cell?

A

Determines the cell size, shape and function.

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17
Q

During hypoxaemia how does the cell respire?

A

Anaerobically

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18
Q

What affect does anaerobic respiration have on ATP production?

A

Decrease in ATP production up to 20 times less resulting in a cellular energy crisis.

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19
Q

What occurs during a cellular energy crisis as a result of shock ?

A

Sodium potassium pump fails.
Intracellular potassium leaks out of the cell and sodium followed by water leaks in.
This results in cells swelling and becoming irregular in shape.
This change in shape causes specialised cells to lose their specialist function.

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20
Q

What ultimately occurs as a result of a cellular energy crisis during shock?

A

The influx of sodium and resulting water into the cell causes intracellular lysosomes to rupture.
The release of hydrolytic enzymes result in the cell being autolysed.
The release of vasoactive metabolites and lysozymes from the dying cell stimulate an inflammatory reaction resulting in an accumulation of activated phagocytes.
Phagocytosis causes more cell injury, creating the lytic cycle.
The lytic cycle can result in organ damage and thus decrease in function.

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21
Q

What occurs in the lytic cycle?

A

Influx of sodium into the cell causes it to swell and lysozymes to rupture.
The release of hydrolytic enzymes autolyse the cell.
Vasoactive metabolites and lysozymes from the dying cell stimulate an inflammatory response activating phagocytes.
Increase in phagocytosis in turn causes more cellular injury increasing the number of activated phagocytes.
Ultimately leading to cell, then tissue and thus organ damage.

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22
Q

What is compensation in relation to shock? And how long does it last for?

A

Mechanisms that aim to reverse the shock process, only work short term.

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23
Q

What compensatory mechanisms occur in response to decreased arterial blood pressure? And what do they each result in?

A

Baroreceptors stimulation - increased HR and blood flow directed centrally= increased blood volume.
Volume and osmoreceptor stimulation- increased blood volume.
Juxtaglomerular apparatus stimulation- blood flow directed centrally = increased blood volume.
Cortisol production increased- increased blood volume.
Disengorgement of spleen- increased blood volume.

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24
Q

During decreased arterial BP, what stimulates baroreceptors and how do they work to increase BP?

A

Baroreceptors are stimulated by the sympathetic autonomic nervous system.
Causing adrenaline to be released which: Increases HR
Heart contractility
Peripheral vasoconstriction
ALL of which increase cardiac output which increases BP.

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25
During decreased arterial BP volume and osmoreceptors are stimulated, how do they work to increase BP?
Anti-diuretic hormone is released from the posterior pituitary gland. Causing an increase in the renal retention of water which increases blood volume, increasing cardiac output which increases BP.
26
During decreased arterial BP the juxtaglomerular apparatus is stimulated, how does this work to increase BP?
Renin release from the kidneys, hydrolyse angiotensinogen synthesised by the liver creating angiotensin I which is weakly bioactive. Angiotensin I travels in the blood to the lungs where the angioconverting enzyme (ACE) converts angiotensin I to angiotensin II which is a strong vasopressor hormone. Angiotensin II stimulates the secretion of aldosterone by the adrenal cortex which increases the renal retention of water. This causes blood flow to be directed centrally, increasing central blood volume and thus increasing cardiac output which in turn increases BP.
27
What are the clinical signs of compensation deteriorating to decompensation? (In terms of: BP, HR, pulse, RR, skin, urine, bowel, GCS, pupils)
``` BP: systolic <80-90mmHg HR: rapid, >150bpm Pulse: weak, rapid and thready RR: rapid, shallow, crackly Skin: cold and cyanotic Urine: <20ml/hr Bowel: no sounds present GCS: not responding to verbal stimuli Pupils: dilated, reacting slowly to light ```
28
What are the 9 stages of decompensation?
1. diffuse cellular hypoxia 2. Widespread anaerobic metabolism 3. Release of cellular potassium, cell death, lactic acidosis. 4. Decreased cardiac contractility, arterial vasodilation, increased capillary permeability, capillary pooling 5. Cardiac dysrthymias, decreased blood volume 6. decreased cardiac output 7. Heart failure and brain stem ischaemia 8. Vasomotor collapse 9. death
29
What causes cardiogenic shock? Examples
Results from impaired pumping ability of the heart such as post MI, post cardiac trauma
30
What causes neurogenic shock?
Results from loss of vasomotor tone caused by post brain stem injury or spinal injury above the midthoracic region.
31
What is an anaphylaxis?
An exaggerated, violent, systemic allergic response to a drug or substance.
32
What causes obstructive shock? Examples
Conditions that affect the ability of the heart to contract or empty such as pulmonary embolism or cardiac tamponade
33
What causes hypovalemic shock?
Haemorrhage or redistribution of blood, plasma or other bodily fluid which causes a decrease in the volume of circulating intravascular blood.
34
What are the 7 causes of hypovolaemic shock?
Haemorrhage Severe diarrhoea Vomiting Abnormal internal fluid distribution as in sepsis Burns- resulting in plasma loss Diuresis- increased or excessive urine production Dehydration
35
What is the most common cause of hypovolaemic shock?
Haemorrhage
36
In terms of fluid loss during hypovolamic shock, what two factors determine the degree of shock experienced?
Volume and rate of fluid loss
37
If the rate is controlled, what percentage of fluid loss can occur without significant effect?
10%
38
After blunt trauma what 5 parts of the body are likely to haemorrhage the most blood? In order of most to least. (mL for bonus points)
Pelvis 3000ml Abdominal cavity and thoracic cavity 2000ml Femur 1000mL Tibia 650ml
39
During shock what are the 3 primary goals of resuscitation?
Restore adequate tissue oxygen delivery. Treat underlying pathology. Prevent further deterioration.
40
What would be seen upon assessment of a pt in the compensated stage of hypovolaemic shock? (In terms of GCS, skin and mucous membranes, cardiovascular, respiratory, renal and gastrointestinal system and temperature)
GCS: confused about time and place. May appear restless and anxious. Skin and mucous membranes: pale, moist and clammy. Cardio: high HR. Potentially thready pulse. NORMAL BP Resp: Increased RR and depth Renal: reduced UO GI: dry mouth, reduced bowel sounds. Temperature: reduced
41
What would be seen upon assessment of a pt in the progressive stage of hypovolaemic shock? (In terms of GCS, skin and mucous membranes, cardiovascular, respiratory, renal and gastrointestinal system and temperature)
GCS: disengaged, increasingly disorientated, limited verbal response. Skin and mucous membranes: developing cyanosis, moist and clammy. Cardio: high HR. Weak thready pulse. Decreasing BP. Potentially cardiac arrhythmias. Renal: UO declining GI: dry mouth. Reduced bowel sounds. Temp: reduced
42
What would be seen upon assessment of a pt in the decompensated stage of hypovolaemic shock? (In terms of GCS, skin and mucous membranes, cardiovascular, respiratory, renal and gastrointestinal system and temperature)
GCS: unconscious. No response to stimuli. Skin and mucous membranes: cyanosed, cold and clammy. May be jaundiced, bleeding appearing under skin. Cardio: slow, weak, irregular pulse. Very low BP. Cardiac arrhythmias. Resp: slow, shallow, irregular RR. Crackles and wheezes. Renal: <0.5ml/kg/hr. Or anuria. GI: absent bowel sounds. Distended abdomen. Haematemesis or malaena- dark sticky faeces. Temp: reduced
43
During shock what are the 3 primary goals of resuscitation?
Restore adequate tissue oxygen delivery. Treat underlying pathology. Prevent further deterioration.
44
What are the three types of fluid that can be used to replace lost volume?
Crystalloid. Colloid. Blood products.
45
What makes up crystalloid fluids?
Water and electrolytes.
46
What are the 4 benefits of crystalloid fluids?
Cost effective. Nonallergenic. Reduced viscosity. Allows for microcirculation.
47
What about crystalloid fluids dictates it’s distribution between the ECF and ICF?
Concentration of sodium. High sodium concentration = more fluid will flow out into the ECF. Low sodium concentration = more fluid into the intracellular space.
48
What would be the distribution in mls of 1L of 0.9NaCl divided between the ECF and ICF?
750mls ECF | 250mls ICF
49
What is the overall effect of 0.9NaCl on ECF and ICF?
Generally expands the ECF volume with little effect on ICF volume.
50
What would be the distribution in mls of 1L of 5% dextrose solution between the ECF and ICF?
880mls ECF | 120mls ICF
51
What type of fluid is dextrose and why does more of it go to ECF than ICF when given in fluid resuscitation?
It’s an isotonic fluid which contains no sodium therefore isn’t able to change the distribution of fluid.
52
What is the main use of 5% dextrose in fluid resuscitation? In what clinical presentation would it be used?
Used mainly to replace water loss when it exceeds input such as in coma or dysphagia.
53
What happens to fluid distribution between ICF and ECF when hypertonic solutions of NaCl are used in fluid resuscitation? And what about hypertonic NaCl solutions causes this distribution? What effect does this redistribution have on intracellular and intravascular volumes?
Fluid leaves the cells and enters the plasma by osmosis down a concentration gradient. This is because hypertonic NaCl solutions contain a higher amount of sodium than that within intracellular fluid. This causes intravascular volumes to increase and intracellular volumes to decrease.
54
What effect do hypotonic NaCl solutions have on the distribution of fluid between the ECF and ICF?
Hypotonic solutions cause water to move from the ECF to the ICF.
55
What are hypotonic solutions of NaCl used for to manage?
Management of cellular dehydration.
56
What effect do colloids have on intravascular volume?
Colloids have a high osmolality as they contain molecules with high molecular weight which cannot cross through the capillaries. Therefore they stay in the intravascular circulation and increase the movement of water into circulation via osmosis thus increasing plasma volume.
57
What process occurs to the distribution of fluid that you need to be aware of when doing fluid resuscitation?
As fluid is lost from the intravascular space, fluid is drawn from the cells to compensate. Thus leading to increased concentration of ECF. When fluid resuscitation occurs initially fluid moves out of vasculature and cells to ECF where solute conc is highest. Fluid resuscitation needs to replace fluid within cells as well as within the vasculature.
58
Which compartment (vascular, ICF, ECF) do colloids effect?
Vascular
59
Which compartment (vascular, ICF, ECF) do crystalloids effect?
Intravascular and extracellular spaces.
60
When will blood products be used in fluid resuscitation?
When blood loss occurs.
61
What is the main purpose of blood transfusion in blood loss?
To restore oxygen carrying capacity of the blood.
62
Which blood product produces the best results for blood loss? And why?
Packed RBCs as they provide the best volume expansion and oxygen carrying capacity.
63
How much does 1 unit of erythrocytes increase haemoglobin concentration by?
1g/dL
64
What is the best resuscitation fluid?
Blood to replace blood. | Otherwise 0.9NaCl solution with small volumes of colloid.
65
What are the 4 consistent clinical features of shock?
Reduced BP. Hypoperfusion (diminished capillary blood flow). Widespread tissue hypoxia. Abnormal metabolism.
66
What are the 6 different classifications of shock?
``` Cardiogenic Neurogenic Anaphylactic Septic Obstructive Hypovolaemic ```
67
What occurs in cardiogenic shock?
Hearts ability to pump becomes impaired causing CO and therefore BP to drop.
68
Cardiogenic shock is most commonly seen after what 3 events?
Following open heart surgery. Trauma to the heart. After large MI.
69
What treatment methods are used in the treatment of cardiogenic shock?
Restoration of blood supply to the myocardium and use of drugs to support heart function.
70
What role does the autonomic nervous system play in maintaining BP?
The ANS controls involuntary muscles in the blood vessel walls that maintain vasotone so that the pressure stays constant even if the body moves position against gravity.
71
What occurs during neurogenic shock and what effect does this have?
Neurogenic shock happens as a result of impulses from the sympathetic autonomic nervous system are lost. Allowing the parasympathetic nervous system to take over, resulting in mass vasodilation aka loss of vasotone. Resulting in a fall in BP.
72
What can cause neurogenic shock?
Following anaesthesia. At times of severe emotional distress. In those experiencing extreme pain.
73
What can neurogenic shock appear to be and what clinical sign is there that decrease in BP is a result of loss of vasotone?
Neurogenic shock can appear to be hypovolaemia. | Differentiated from the other classifications of shock by the HR being slow rather than increasing.
74
What occurs in anaphylactic shock?
Sudden, mass vasodilation resulting in pooling of blood in the peripheries and increased capillary permeability. Can result in real blood loss.
75
What occurs in septic shock?
Mass vasodilation and increased capillary permeability. Depression of the myocardium. Disseminated intravascular coagulation (DIC). Multiple organ dysfunction. Can result in real blood loss.
76
Which three classifications result in abnormal fluid distribution? And what is the collective name for these types of shock?
Neurogenic, septic and anaphylactic shock. | Collectively known as distributive shock.
77
List the pathological causes of hypovolaemic shock?
``` Haemorrhage Dehydration Severe vomiting/diarrhoea Excessive urine output Burns injury Sepsis ```
78
What are the defining characteristics of hypovolaemic shock?
Decreased circulating volume leading to inadequate filling of blood vessels resulting in the body’s metabolic requirements not being met.
79
What percentage/ volume of circulating blood is lost before compensatory mechanisms start?
10-15% which is equal to around 750ml of blood
80
In terms of the CO=HRxSV why does heart rate increase during hypovolaemic shock?
Because SV is decreased therefore HR increases to maintain CO
81
What does a difference of 20mmHg between lying and standing BP indicate as a percentage blood loss?
20% loss of circulating blood volume
82
What % of blood loss is likely in a pt who is hypotensive when in a supine position?
40% loss of circulating blood volume
83
Why is a sudden increase in BP contraindicated in haemorrhage? And what should the value of the aimed BP be?
Sudden BP increase may dislodge a clot worsening the volume of blood loss. BP of 90mmHg should be sought.
84
Which three aspects of shock pathophysiology and management result in altered serum electrolyte levels?
Renal impairment, fluid replacement and altered physiology.
85
True or false: all causes of shock lead to metabolic acidosis?
True
86
What are the resulting events from metabolic acidosis?
Cardiac dysrhythmias. Impaired cardiac conduction. Decline in BP and CO. Depression of CNS.
87
What does a pH of <7.0 lead to?
Disorientation, coma.
88
Which pH is incompatible with life?
<6.8
89
What is a fluid loss of 50% associated with?
Death.
90
What is a sign of brain ischaemia?
Dilated pupils that are slow to react to light.
91
MODS stands for
Multiple organ dysfunction syndrome
92
Why does hyperglycaemia occur in the compensatory stage of shock?
Sympathetic nervous system stimulation releases catecholamines such as adrenaline, stimulating the liver to convert glycogen into glucose to provide an energy supply for cellular metabolism.

Nursing Acutely Ill (11 decks)

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