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Semester 2: Cardiorespiratory Fitness > PBL Topic 2 Case 9 > Flashcards

PBL Topic 2 Case 9 Flashcards

1
Q

What is an acid?

A
  • A molecule containing hydrogen atoms that can release protons
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2
Q

What is a strong acid? Give an example of a strong acid

A
  • One that rapidly dissociates and releases large amounts of protons
  • Hydrochloric acid
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3
Q

What is a weak acid? Give an example of a weak acid

A
  • One that has a lower tendency to dissociate protons

- Carbonic acid

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4
Q

What is a base?

A
  • A molecule that can accept a proton
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5
Q

What is a strong base? Give an example of a strong base

A
  • One that reacts rapidly and strongly with protons

- Hydroxide ion

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6
Q

What is a weak base? Give an example of a weak base?

A
  • One that reacts much more weakly with protons

- Bicarbonate ion

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7
Q

How does one calculate pH from [H+]?

A

pH = -log [H+]

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8
Q

What is the normal pH of blood?

A

7.4

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9
Q

Why is the pH of venous blood lower than that of arterial blood?

A
  • Carbon dioxide is released from tissues to form carbonic acid
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10
Q

Why is intracellular pH lower than plasma pH?

A
  • Metabolism of cells produced carbonic acid
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11
Q

Identify three systems that help regulate [H+]

A
  • Buffer systems
  • Respiratory centre
  • Kidneys
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12
Q

What is a buffer?

A
  • Any substance that can reversible bind H+
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13
Q

What is Ka and how is it calculated?

A
  • The concentration of the acid relative to its dissociated ions
  • Ka = [H+][A-] / [HA]
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14
Q

What is pKa and how is it calculated?

A
  • Negative log of the Ka value

- pKa = -log [Ka]

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15
Q

What is the pKa in the bicarbonate buffer system?

A
  • 6.1
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16
Q

Give the Henderson-Hasselbalch Equation

A

pH = 6.1 + log [HCO3-] / (0.03 x [PCO2])

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17
Q

In the Henderson-Hasselbalch Equation:

Why is [CO2] calculated rather than H2CO3?

A
  • H2CO3 rapidly dissociated into CO2

- Which is proportional to the amount of undissociated H2CO3

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18
Q

Using the Henderson-Hasselbalch Equation:

What is the result of an increase in [HCO3-]

A
  • pH increases

- Shift towards alkalosis

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19
Q

Using the Henderson-Hasselbalch Equation:

What is the result of an increase in pCO2

A
  • pH decreases

- Shift towards acidosis

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20
Q

Why is a change in the [HCO3-] referred to as a metabolic disturbance?

A
  • [HCO3-] is regulated by the kidneys
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21
Q

Why is a change in the pCO2 referred to as a respiratory disturbance?

A
  • PCO2 is controlled by the rate of respiration
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22
Q

An increase in [HCO3-] is termed a [A]

A decrease in pCO2 is termed a [B]

An increase in pCO2 is termed a [C]

A decrease in [HCO3-] is termed a [D}

A
  • [A] Metabolic alkalosis
  • [B} Respiratory alkalosis
  • [C] Respiratory acidosis
  • [D] Metabolic acidosis
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23
Q

What is the effect of increased ventilation on [H+]

A
  • Reduced CO2 from extracellular fluid

- Reduced [H+]

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24
Q

What is the effect of decreased [H+] on ventilation

A
  • Alveolar ventilation decreases

- Reduced [H+]

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25
Q

Explain why respiratory acidosis occurs in emphysema

A
  • Loss of elastic recoil
  • Airflow limitation
  • Build up of CO2
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26
Q

Outline the mechanism by which the kidneys excrete acidic or basic urine

A
  • HCO3- is filtered into the tubules, thus removing base from the blood
  • H+ is filtered into the tubules, thus removing acid from the blood
  • Net effect is based on relative concentrations in tubular lumen
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27
Q

How does the removal of HCO3- raise the extracellular [H+] in alkalosis

A
  • Kidneys fail to reabsorb HCO3-
  • Increased excretion of bicarbonate
  • Decrease in HCO3- shifts acid base balance towards acidosis (Henderson-Hasselbalch equation)
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28
Q

How does the reabsorption of HCO3- reduce the extracellular [H+] in acidosis

A
  • Increase in HCO3 shifts acid base balance towards alkalosis (Henderson-Hasselbalch equation)
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29
Q

In which region of the kidneys does HCO3- reabsorption and H+ secretion not occur?

A
  • Loop of Henle
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30
Q

Outline the features of metabolic acidosis

A
  • pH < 7.4

- PO2 > 40 mm Hg

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31
Q

What is the compensatory mechanism for metabolic acidosis?

A
  • Increased ventilation
  • Reduced pCO2
  • Reduced H+
  • Increased pH
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32
Q

Outline the features of a respiratory acidosis

A
  • pH < 7.4

- HCO3- <24 mEq/L

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33
Q

What is the compensatory mechanism for respiratory acidosis?

A
  • Increased H+ secretion
  • Increased reabsorption of bicarbonate
  • Increased pH
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34
Q

Outline the features of a metabolic alkalosis

A
  • pH > 7.4

- PO2 < 40 mm Hg

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35
Q

What is the compensatory mechanism for metabolic alkalosis?

A
  • Decreased ventilation
  • Increased CO2
  • Increased H+
  • Reduced pH
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36
Q

Outline the features of a respiratory alkalosis

A
  • pH > 7.4

- HCO3- > 24 mEq/L

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37
Q

What is the compensatory mechanism for respiratory alkalosis?

A
  • Reduced H+ secretion
  • Reduced reabsorption of HCO3-
  • Reduced pH
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38
Q

Define circulatory shock

A
  • Generalised inadequate blood flow

- Damage to body tissues due to lack of oxygen and other nutrients

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39
Q

Outline the three stages of shock

A
  • Non progressive / compensatory stage
  • Progressive stage
  • Irreversible stage
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40
Q

What is meant by the term hypovolaemia?

A
  • Reduced blood volume
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41
Q

What is the most common cause of hypovolaemia?

A
  • Haemorrhage
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42
Q

How does haemorrhage result in shock?

A
  • Reduced filling pressure
  • Reduced venous return
  • Reduced cardiac output
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43
Q

Identify the sympathetic reflexes that occur as a result of decreased arterial pressure after haemorrhage

A
  • Arterioles constrict, increasing total peripheral resistance
  • Veins and venous reservoirs constrict, increasing venous return
  • Increased heart rate
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44
Q

Identify the role of baroreceptors in non-progressive shock

A
  • Elicit powerful sympathetic stimulation of the circulation
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45
Q

Identify the role of the CNS ischaemic response in non-progressive shock

When is this response activated?

A
  • Elicits even more powerful sympathetic stimulation of the circulation
  • When the arterial pressure falls below 50 mm Hg
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46
Q

What is the role of reverse stress-relaxation in non-progressive shock ?

A
  • Contraction of blood vessels around the diminished blood volume
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47
Q

What is the role of angiotensin in non-progressive shock ?

A
  • Constriction of peripheral arteries

- Decreased output of water and salt by the kidneys

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48
Q

What is the role of ADH in non-progressive shock ?

A
  • Constricts arteries and veins

- Greatly increases water retention by the kidneys

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49
Q

What causes cardiac depression?

A
  • Fall in arterial pressure
  • Reduced coronary blood flow
  • For adequate nutrition of the myocardium
  • Weakness of the heart muscle
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50
Q

What causes vasomotor failure?

A
  • Reduced cardiac output

- Reduced blood flow to the vasomotor centre

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51
Q

How does failure of the vasomotor centre cause a decreased cardiac output?

A
  • Vascular dilation
  • Venous pooling of blood
  • Decreased venous return
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52
Q

Identify three effects of sluggish blood flow

A
  • Tissue metabolism continues despite low flow
  • Large amounts of acid continue to empty into the local vessels and increase the acidity of the blood
  • Resulting in agglutination and blood clots
  • Leading to plugging of small vessels
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53
Q

Why is there increased capillary permeability and what is the effect of this?

A
  • Due to hypoxia

- Decreased cardiac output

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54
Q

Explain what occurs to the phosphate reserves in irreversible shock

A
  • Creatine phosphate is degraded
  • ATP is degraded to ADP
  • ADP is degraded to AMP
  • AMP is degraded to adenosine
  • Which diffuses out of cells and is converted to uric acid
  • Uric acid cannot re=enter the cells
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55
Q

Explain how intestinal obstruction can result in hypovolaemic shock

A
  • Distension of intestine block venous return
  • Increase in capillary pressure
  • Fluid leakage from capillaries into intestinal wall and lumen
  • Reduced plasma volume
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56
Q

Explain how severe burns can result in hypovolaemic shock

A
  • Loss of plasma through the denuding skin
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57
Q

Why does blood viscosity increase in hypovolaemic shock? What is the effect of this?

A
  • Increased red cell concentration

- Increased sluggishness of blood

58
Q

Identify four causes of hypovolaemic shock caused by dehydration

A
  • Excessive sweating
  • Fluid loss in diarrhoea or vomiting
  • Fluid loss by nephrotic kidney
  • Inadequate intake of fluid and electrolytes
59
Q

Outline the pathophysiology of neurogenic shock

A
  • Loss of vasomotor tone
  • Massive dilation of veins
  • Reduced mean systemic filling pressure
  • Reduced venous return
  • Increased venous pooling
60
Q

Explain how anaesthesia causes neurogenic shock

A
  • Blockage of sympathetic nervous outflow from nervous system
61
Q

Explain how brain damage causes neurogenic shock

A
  • Brain ischaemia is prolonged

- Inactivation of vasomotor centre

62
Q

Identify a cause of compartment syndrome

A
  • Bone fracture
63
Q

Outline the pathophysiology of compartment syndrome

A
  • Tissue hypoxia
  • Release of histamine like substances
  • Causing vasodilation
  • Increased endothelial permeability
  • Transudation of plasma into the intramuscular compartment
  • Swelling and oedema
64
Q

What causes the collapse of a vessel in compartment syndrome?

A
  • Increased critical closing pressure
65
Q

Outline the treatment of compartment syndrome

A
  • Incision through the deep fascia
  • To open up the compression
  • To cause decompression
66
Q

Outline the pathophysiology of anaphylactic shock

A
  • Antigen-antibody reaction
  • Release of basophils and mast cells
  • Release of histamine
  • Increased venous dilation and decreased venous return
  • Dilation of arterioles and reduced arterial pressure
  • Increased capillary permeability
  • Loss of fluid into the tissue spaces
67
Q

What is the main cause of sepsis?

A
  • ‘Blood poisoning’

- Caused by bacterial infection

68
Q

Outline the clinical features of hypovolaemic shock stemming from inadequate perfusion

A
  • Cold, pale and clammy skin with slow capillary refill
  • Anuria and oliguria
  • Drowsiness, confusion and irritability
69
Q

Outline the clinical features of hypovolaemic shock stemming from increased sympathetic tone

A
  • Tachycardia
  • Hypotension
  • Sweating
70
Q

Outline the clinical features of cardiogenic shock

A
  • Raised jugular venous pressure
  • Pulmonary oedema
  • Gallop rhythm
  • Basal crackles
  • Pulmonary oedema
71
Q

Outline the clinical features of anaphylactic shock

A
  • Low blood pressure and tachycardia (vasodilation)
  • Bronchospasm
  • Oedema of the face, pharynx and larynx
  • Nausea, vomiting, abdominal cramps and diarrhoea
72
Q

Outline the clinical features sepsis

A
  • Pyrexia and rigors
  • Nausea and vomiting
  • Hypotension
  • Bounding pulse
73
Q

Outline the management of shock

A
  • Oxygen (via endotracheal tube where necessary)
  • Antibiotics for sepsis
  • Fluid Replacement by wide-bore intravenous cannula
74
Q

What is packed cell volume?

A
  • Proportion of blood made up of red blood cells

- Essentially the same thing as hematocrit

75
Q

When giving fluid replacement what is the optimal packed cell volume and why is this the case?

A
  • 30-35%
  • Balance oxygen carrying capacity
  • And tissue flow
76
Q

A massive transfusion involves the transfer of how many units of blood?

A
  • 80 > 100 units of red cells
77
Q

Why can blood transfusion cause hypothermia?

A
  • Bank blood is stored at four degrees celsius
78
Q

Why can blood transfusion cause coagulopathy

A
  • Bank blood contains few platelets or clotting factors
79
Q

Why can blood transfusion cause hypocalcaemia?

A
  • Citrate stored in blood binds to calcium ions reducing ionised calcium levels
80
Q

Why can blood transfusion cause increased oxygen affinity

A
  • 2,3-BPG in stored blood is reduced
  • Oxygen dissociation curve shifts to the left
  • Increased affinity and reduced unloading
81
Q

What do crystalloid fluids involve? Identify an example of a crystalloid

A
  • Addition of volume to blood
  • Addition of electrolytes
  • Saline
82
Q

What do colloid fluids involve? Identify an example of a colloid

A
  • Volume expanders resulting in an increase in blood volume, blood flow, cardiac output and oxygen transportation
  • Gelofusine
83
Q

Which are preferred colloids or crystalloids?

A
  • Colloids

- Since the volume of crystalloid needed to produce the same effect as colloid is far greater

84
Q

Identify two potential sites of heart block

A
  • AV Block in AV node or Bundle of His

- Bundle Branch Block in lower conductive system

85
Q

What is a Stokes-Adams attack?

A
  • Associated with heart block

- Causes syncope

86
Q

What is seen on an ECG with first degree heart block?

A
  • Prolongation of PR interval greater than 0.22
87
Q

Identify three types of second degree AV block

A
  • Mobitz 1 Block (Wenckeback block)
  • Mobitz II Block
  • 2:1 or 3:1 Block
88
Q

What is seen on an ECG with Mobitz 1 block

A
  • Progressive PR prolongation

- Until P wave fails to conduct

89
Q

Where is Mobitz I block most likely to occur?

A
  • AV Node
90
Q

What is seen on an ECG with Mobitz II block?

A
  • A dropped QRS complex

- Not preceded by PR interval prolongation

91
Q

Where is Mobitz II block most likely to occur?

A
  • Bundle of His
92
Q

What is seen on an ECG with a 2:1 or 3:1 advanced block?

A
  • Every second or third P wave conducts to the ventricles
93
Q

Identify two types of third degree AV block

A
  • Congenital complete heart block

- Acquired complete heart block

94
Q

What is seen on an ECG with a congenital complete AV block?

A
  • QRS complex is narrow

- QRS rate is rapid

95
Q

What is seen on an ECG with an acquired complete AV block?

A
  • QRS complex is broad

- QRS complex is slow

96
Q

What is seen in right bundle branch block on an ECG?

A
  • Deep S waves in leads I and V6

- Tall R wave in lead V1

97
Q

What are the clinical features of right bundle branch block?

A
  • Splitting of the second heart sound
98
Q

What is seen in left bundle branch block on an ECG?

A
  • Deep S wave in lead V1

- Tall R wave in leads 1 and V6

99
Q

What are the clinical features of right bundle branch block?

A
  • Reverse splitting of the second heart sound
100
Q

Identify the two functioning systems that determine consciousness

A
  • Ascending Reticular Activating System (ARAS)

- Cerebral Cortex

101
Q

Identify the three principal causes of coma

A
  • Diffuse brain dysfunction e.g. traumatic brain injury or drug overdose
  • Direct effect within brainstem e.g. haemorrhage or infarction
  • Pressure effect on brainstem e.g. tumour, oedema, abscess
102
Q

What does Glasgow Coma Scale record?

A
  • Best Eye, Verbal and Motor Responses
103
Q

A Glasgow Come Scale score of less than which value denotes a coma?

A
  • 8
104
Q

What is meant by the term delirium?

A
  • Confusion state
  • Reduced attention
  • Altered behaviour
105
Q

What is a Swan-Ganz catheter?

A
  • Balloon Flotation Catheter

- Used to determine pulmonary artery pressure

106
Q

Identify two locations where the Swan-Ganz catheter may be inserted?

A
  • Femoral Vein

- Antecubital Fossa

107
Q

Identify three conditions that can be diagnosed using a Swan-Ganz catheter

A
  • Cardiac tamponade
  • Pulmonary hypertension
  • Cardiomyopathy
108
Q

Identify three conditions that are often monitored using a Swan Ganz catheter

A
  • Heart failure
  • Cardiogenic Shock
  • Doubtful fluid status
109
Q

Why is the pulmonary artery pressure recorded a reasonable reflection of left atrial pressure?

A
  • Catheter becomes so wedged

- Due to fluid between the catheter lumen and left atrium

110
Q

Identify two invasive means of ventilating a patietn

A
  • Endotracheal tube

- Tracheostomy

111
Q

Explain how sedation, muscle anaesthesia and muscle relaxation can cause hypotension

A
  • Loss of sympathetic drive

- Vasodilation

112
Q

Explain how positive pressure ventilation can cause hypotension

A
  • Increased intrathroacic pressure
  • Reduced venous return
  • Reduced cardiac output
113
Q

When is a tracheostomy performed?

A
  • When endotracheal intubation is likely to be required for a prolonged period
  • Typically over 14 days
114
Q

What is IPPV and how is it achieved?

A
  • Intermittent Positive Pressure Ventilation
  • Intermittent inflation of lungs with positive pressure
  • Air is forced into lungs
  • Elastic recoil carries out expiration
115
Q

When is CMV used and outline two ways in which it is achieved

A
  • Controlled Mechanical Ventilation
  • With patients in whom respiratory efforts are absent
  • Volume controlled ventilation
  • Pressure controlled ventilation
116
Q

Outline the process of volume controlled ventilation

A
  • Tidal volume and respiratory rate are preset

- Airway pressure varies according to the ventilator setting and the lung mechanics (e.g. resistance and compliance)

117
Q

Outline the process of pressure controlled ventilation

A
  • Inspiratory pressure and respiratory rate are preset

- Tidal volume varies according to patient’s lung mechanics

118
Q

What is IMV ?

A
  • Intermittent mandatory ventilation
  • Allows patient to breathe spontaneously between the mandatory tidal volumes delivered by ventilator
  • Timed to coincide with patients own respiratory efforts
119
Q

What is weaning?

A
  • Process of progressively reducing and eventually removing external ventilatory support
120
Q

How is the decision made to wean a patient from artificial ventilation?

A
  • Subjective criteria including responses to short periods of spontaneous breathing
  • Objective criteria based on blood gas analysis, lung mechanics and muscular strength
  • Patient’s mood, and consciousness level, as well as any drugs
121
Q

Identify two causes of a fall in cardiac output associated with artificial ventilation

A
  • Positive pressure to the lungs impeded venous return

- Stretching of pulmonary capillaries causing a rise in pulmonary vascular resistance

122
Q

What is barotrauma and how is it associated with artificial ventilation

A
  • Damage to body tissues caused by a difference in pressure
  • Caused by high tidal volumes and PEEP
  • Which may rupture alveoli and cause air to dissect along the perivascular sheath
123
Q

Identify three sets of signs of a tension pneumothorax associated with artificial ventilation

A
  • Hypoxia and hypercapnia
  • Hypotension and tachycardia
  • Mediastinal shift and tracheal displacement
124
Q

How may ventilator associated pneumonia occur?

A
  • Leakage of infected oropharyngeal secretions

- Promoted by regurgitation of colonised gastric fluid

125
Q

Identify three organisms associated with ventilator associated pneumonia

A
  • Pseudomonas aeruginosa
  • Klebsiella pneumoniae
  • Staphylococcus aureus
126
Q

Identify a specific marker that be may helpful when there is suspected ventilator associated pneumonia

A
  • Serum procalcitonin
127
Q

Outline the pathophysiology of disseminated intravascular coagulation

A
  • Endothelial damage results in platelet aggregation
  • Tissue injury results in thrombin
  • Vascular occlusion and consumption of platelets
128
Q

Outline how tranexamic acid is used in disseminated intravascular coagulation

A
  • Inhibits plasminogen activation
  • Prevents fibrinolysis
  • Given orally or by IV injection
129
Q

What is an opioid?

A
  • Any substance that produces morphine like effects
130
Q

Identify a drug that blocks opioids

A
  • Naloxone
131
Q

What is the function of u receptors?

A
  • Analgesic effects of opioids
132
Q

Outline the mechanism of action of opioids

A
  • Opening of inward K+ channels causing hyperpolarisation

- Closure of Na+ channels resulting in reduced Ca2+ entry

133
Q

Outline how opioids can result in physical dependence

A
  • Inhibition of adenylyl cyclase and MAP activation
134
Q

Identify three regions of the brain where analgesics have an effect

A
  • Insular cortex
  • Amygdala
  • Hypothalamus
135
Q

What is diamorphine?

A
  • Prodrug that has a high analgesic potency

-

136
Q

Why does diamorphine give a greater ‘buzz’ than morphine

A
  • Greater lipid solubility

- More easily crosses the blood brain barrier

137
Q

How is diamorphine metabolised?

A
  • By glucuronide in the liver

- Metabolised to 6-monoacetylmorphine

138
Q

Why does morphine cause respiratory depression?

A
  • Decrease in sensitivity of receptors to arterial PCO2
139
Q

Why does morphine cause constipation?

A
  • Increased tone

- Reduced motility in GI system

140
Q

Why does morphine cause urticaria and itching?

A
  • Release of histamine from mast cells
141
Q

Why are opioids unsuitable for asthmatic patients?

A
  • Release of histamine from mast cells

- Causing bronchoconstriction and hypotension

Semester 2: Cardiorespiratory Fitness (18 decks)

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