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Foundations > EXAM Prep > Flashcards

EXAM Prep Flashcards

Revision

1
Q

4 Valves Where?

A

Tricuspid (R) AV)

Bicuspid/ mitral (L) AV)

Pulmonary

Aortic

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2
Q

3 vessels supplying the RA

A

Inferior vena cava

Superior vena cava

Coronary sinus

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3
Q

70% of blood supplied to the ventricles is via:

A

Passive movement

Atrial contraction is for the last 30%

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4
Q

3 layers of the heart wall

A

Epicardium

Myocardium ( Fibrous skeleton, connective tissue which supports great vessels and valves)

Endocardium (is continuous with endothelial lining of the blood vessels)

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5
Q

Which vessels are very proximal to the aortic valve

A

Coronary arteries

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6
Q

Coronary arteries perfuse on:

A

Diastole

(heart is only organ perfused on diastole)

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7
Q

What to give to decrease HR

A

Beta blockers

Digoxin

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8
Q

What to give/do to increase HR

A

Atropine

Adrenaline

Pace

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9
Q

What to give to increase preload

A

Vasopressors
- Noradrenaline
- Vasopressin
- Metaraminol

Fluids

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10
Q

What to give to decrease preload

A

Diuretics

GTN (vasodilate)

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11
Q

What to give to increase contractility

A

Adrenaline

Dobutamine

Digoxin

Milrinone

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12
Q

What to give to decrease contractility

A

Beta blockers

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13
Q

What to give to increase afterload

A

Vasopressors
- Noradrenaline
- Metaraminol
- Vasopressin

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14
Q

What to give to decrease afterload

A

Angiotensin-converting enzyme inhibitors (ACE)

Angiotensin 2 receptors (ARBS)

Calcium channel blockers

Opposite of RAAS

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15
Q

BP =

A

Cardiac output x Systemic vascular resistance

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16
Q

What to give to inhibit sympathetic nervous system

A

Beta blockers

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17
Q

What to give to inhibit the RAAS system

A

Angiotensin-converting enzyme (ACE) inhibitors

Angiotensin 2 receptor blockers (ARBs)

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18
Q

4 main coronary arteries

A

Left Circumflex (LCx)

Left anterior descending artery (LAD)

R) coronary artery (RCA)

Posterior descending (PDA) (either stems off the RCA or LCx)

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19
Q

3 layers of veins/arteries

A

Tunica intima (endothelium, mediates vasoconstriction/vasodilation)

Tunica Media (smooth muscle)

Tunica adventitia/ Externa (connective tissue)

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20
Q

Which enzyme works as a lever to expose myosin binding sites for Ca2+

A

Troponin

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21
Q

When Ca2+ attaches to myosin binding sites, what happens

A

Myocardial contraction

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22
Q

Which cells have automaticity

A

Pacemaker cells

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23
Q

Action Potential Phase 0

Depolarisation

A

Na+ (Fast) Rushes into the cell

Slow Na+ leak form neighbouring cell reaches threshold potential –> stimulates sodium channels to open

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24
Q

Action Potential Phase 1

Initial early / repolarisation

A

Na+ (fast) channel closes K+ channels open K+ out of cell

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25
Q

Action Potential Phase 2

Plateau

A

Calcium (slow) channels open

Calcium into cell

K+ continues to leave cell

= balance plateau

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26
Q

Action Potential Phase 3

Repolarisation

A

Calcium Channels close

Potassium Continues to leave the cell quickly

Causes the cell to become more negative leading to repolarisation

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27
Q

Action Potential Phase 4

Resting Potential

A

Resting membrane potential

ATPase pumps swap electrolytes

Na+/K+ ATPASe
Ca2+ ATPASe

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28
Q

Which electrolyte regulates the pumps

A

Magnesium

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29
Q

What cells have fast influx of Ca2+ instead of Na+, with no resting period

A

Nodal or ‘pacemaker cells’

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30
Q

4 classes of antiarrhythmics

A

Sodium channel blockers

Beta blockers

Potassium channel blockers

Calcium channel blockers

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31
Q

What phase does sodium channel blockers (class I) work on

A

Phase 0

Lignocaine + flecainide

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32
Q

What would a B1 agonist do?

A

(Heart)

Tachycardia

Increase contractility

Release renin (trigger RAAS)

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33
Q

What would a B2 agonist do?

A

(lungs)

Bronchodilate

Vasodilate

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34
Q

B blockers block which nodes

A

SA + AV

Decreases automaticity of pacemaker cells

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34
Q

Why would you want a selective B blocker if asthmatic

A

Blocking B2 would cause bronchoconstriciton

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35
Q

Class III

What do they do

Give examples

Indications

A

Block K+ outward flow
- Prolong QT
- May precipitate torsades

Sotalol (mixed class II + III) and amiodarone

SVT, VF, VT, AF, A Flutter

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36
Q

Why is sotalol so special

A

Class II = non selective beta blockers (decrease SA + AV function)

Also class III (prolong QT, slow down action potential duration)

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37
Q

Class IV

A

Calcium channel blockers

Vasodilation

‘dipines’
- nifedipine
- amlodipine
- Felodipine

Diltiazem + verapamil

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38
Q

Widowmaker artery

A

left anterior descending artery (LAD)

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39
Q

Function of the AV node

A

Slows conduction to allow filling (PR interval)

Backup pacemaker (40-60bpm)

Blocks atrial impulses if > 200

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40
Q

Small square =

Big square =

A

Small = 0.04

Large = 0.2

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41
Q

PR should be

QRS should be

QT should be

A

PR = 0.12 - 0.2 sec (3-5 small squares)

QRS = < 3 small squares (0.12)

QT = < 1/2 RR

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42
Q

10 second method

A

Good for irregular rhythms

Most ECG’s record for 10 seconds (4 x 2.5 seconds)

Count the number of QRS complexes in the entire rhythm strip and multiply by 6

HR = number of QRS complexes x 6

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43
Q

Large square method

A

The amount of large squares between the R waves divided by 300

1= 300
2 = 150
3 = 100
4 = 75
5 = 60
6 = 50
7 = 43
8 = 38

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44
Q
A

Sinus Exit Block

Regular rhythm

Dropped beat

Next beat is where it would be

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45
Q
A

Sinus pause / arrest

Pause = 1 dropped beat but does not resume at intended point

Arrest = > 1 impulse fails, does not return at intended point

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46
Q

Sick sinus

A

Irregular tachy-brady combination

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47
Q

Bigeminy and trigeminy

A

2/3 premature beats together

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48
Q

Proximal atrial tachycardia

A

Sometimes tachy can self revert starts & stops abruptly

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49
Q

Zones of pulmonary flow: relevant pressures of zone 1

A

No blood flow

Alveolar (PA) is greater than arterial (Pa) & venous (PV)

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50
Q

Zones of pulmonary flow

Relevant pressures of zone 2

A

Moderate blood flow

Relevant pressure gradient is between the Pa (Arterial pressure) PA (alveolar pressure)

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51
Q

Zones of pulmonary flow

Relevant pressures of zone 3

A

Greatest blood flood occurs

The relevant pressure gradient
Is between the Pa (Arterial pressure) and PV (venous pressure)

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52
Q

Oxyhaemoglobin dissociation curve

Shift to the right

A

Increased pCO2

Decreased pH

Hb decreased affinity for CO2

Increased 2,3 diphosphoglycerate (DPG) binds to Hb, increased O2 unloading

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53
Q

Oxyhaemoglobin dissociation curve

Shift to the left

A

Decreased CO2

Increased pH

Decreased temperature (decreased tissue metabolism)

Decreased 2,3 diphosphoglycerate (DPG)

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54
Q

Causes of rightward shift

A

Increased levels CO2

Increased temp, sepsis (decreased O2 available to distal tissues)

Inflammation

Burns

Severe trauma –> increased inflammation

Exercise

Panic attack

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54
Q

Oxygen delivery variables

A

Cardiac output, SaO2, Hb, PaO2

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55
Q

Causes of leftward shift

A

In lungs

Alkalosis

Hypothermia

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56
Q

Aerobic respiration

A

In mitochondria

38 ATP + CO2 + H20

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57
Q

Anaerobic Respiration

A

In cytoplasm

2 lactic acid + 2 ATP

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58
Q

V vs Q

Shunting is an issue with

A

Ventilation

Q > V

Alveolar dysfunction

Preserved perfusion

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59
Q

Why does lactate suck

A

Produced as a by-product of anaerobic respiration

Indication of cell stress or tissue hypoxia

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60
Q

V vs Q

Dead space is an issue with:

A

Perfusion

V > Q

Gas exchange not possible due to compromised perfusion

O2 in structures unable to be used

E.g. PE

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61
Q

SPO2 drops after GTN why?

A

Vasodilation to zone 3 = shunt

Increased blood flow to area with already increased blood flow but little ventilation

Normal process is to decrease blood flow or vasoconstrict to areas of poor ventilation

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62
Q

Composition of nitrogen in the alveoli

A

78%

The big nitrogen molecules hold the alveoli open. So you don’t want to wash out with oxygen otherwise they will collapse

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63
Q

Normal PaO2

A

4-5x FIO2

E.g. RA 21% = 80-100%

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64
Q

PH:

PaO2

PCO2

HCO3

A

7.35 - 7.45

80-100 (RA)

35-45

22-28

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65
Q

Contraindications NIV

A

Respiratory arrest

Untreated pneumothorax

Inability to maintain own airway

Haemodynamic instability

Facial trauma

Vomiting

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66
Q

3 Variables of diffusion

A

Surface area

Concentration difference

Thickness of barrier

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67
Q

3 PEEP benefits

A

Increased gas exchange

Increased alveolar recruitment

Decreased V/Q mismatch

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68
Q

CO =

A

SV x HR

SV = Preload, Contractility, Afterload

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69
Q

Cardiovascular Effects of NIV

A

Decrease preload + afterload

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70
Q

Tidal volume

A

What we normally breath in + out at rest

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71
Q

Inspiratory reserve volume

A

What we breath in when we force inspiration

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72
Q

Residual volume

A

Air remaining in the alveoli after forced expiration

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73
Q

Vital capacity

A

From forced inspiration to forced expiration

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74
Q

Functional Residual Capacity

A

Air remaining in alveolar after forced expiration

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75
Q

Pulmonary function tests

A

Tests of ventilation (peak flow)

Tests of diffusion

Tests of perfusion

Tests for V/Q mismatch

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76
Q

If V/Q ratio is low

A

V < Q

Ventilation less than perfusion = pneumonia etc

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77
Q

Type 1 vs Type 2 respiratory failure

A

Type 1 = Decreased O2 normal CO2 (failure to oxygenate)

Type 2 = Decreased O2 and increased CO2 (copd) (failure to ventilate)

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78
Q

Systemic inflammation is associated with hypotension because of:

A

Venous vasodilation

Third spacing due to increased vascular permeability

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79
Q

In shock pulse pressure will:

A

Narrow

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80
Q

Deadly triad of coagulopathy

A
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81
Q

PE treatment

A

O2

Fluid loading

Anticoagulation

Thrombolytics

?ETT

Surgery

Inotropes

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82
Q

Minute volume set by

A

Respiratory Rate and Tidal Volume

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83
Q

MV complications

A

Barotrauma

Volutrauma

Atelectasis

Increased intrathoracic pressure

Decreased venous return

Decreased afterload

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84
Q

Dobutamine

A

B1, B2 agonist
- Tachycardia
- Increased contractility
- Vasodilation
- B2 outweighs RAAS

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85
Q

Rate control drugs for tachyarrhythmia

A

Digoxin

Beta blockers

Calcium channel blockers

Amiodarone

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86
Q

Why might AF show ST depression

A

Rate-related ischemia

87
Q

P waves in AF

A

No, there is no P waves in AF

88
Q

If rhythm strip shows ? ST depression

A

Check 12 lead, see if depression is in >2 contiguous leads

89
Q

Classification of 1st degree AV block

A

Every P wave is conducted (but slower than usual)

90
Q

Classification of 2nd degree AV block

A

Some P waves are conducted
- Mobitz type 1 (Wenckebach)
- Mobitz type 2

91
Q

Classification of 3rd degree AV block

A

No P waves are conducted

92
Q
A

1st degree AV block

Lengthening/prolonged PR interval

93
Q
A

2nd degree AV block (Mobitz type 1 Wenckebach)

PR interval progressively lengthens until no QRS is conducted and a dropped beat occurs

94
Q
A

2nd degree AV block (Mobitz type 2)

PR interval remains the same but can be prolonged

Occasional non conducted P wave = Dropped QRS

95
Q
A

3rd degree (complete) AV block

Complete block of conduction system

Desynchrony of atrial/ ventricular conduction

Widened QRS due to conduction coming from ventricles

Increased atrial rate, decreased ventricular rate

95
Q
A

2:1 AV block

Two P waves for every conducted QRS

May be 2nd degree type 1 or 2

Type I favoured by:
- Long PR, narrow QRS - block in the AV node/ His bundle
- Inferior MI

Type II favoured by:
- Normal PR & wide QRS - block in the bundle branches
Anterior MI

95
Q
A

High grade/ Advanced AV block

> 2 consecutive QRS are blocked

95
Q

Junctional vs ventricular escape rhythms

A

Conduction comes from:

AV junction: Narrow QRS

Ventricles: Wide QRS

96
Q

Premature Junction Contraction vs Premature Atrial Contraction

A

Premature junctional beats originate in the AV junction: no p wave

Premature Atrial beats originate from the SA node: P wave

97
Q

Treatment of fine VF

A

CPR to obtain enough perfusion and then shock

98
Q

Premature Ventricular Complexes

A

Originates in ventricles

Premature to expected beat

No p wave

Compensatory pause = next complex comes later

99
Q

Unifocal vs multifocal morphology in PVCs

A

Unifocal: arise from the same ectopic focus in the ventricles and therefore have the same morphology

Multifocal: arise from two different ectopic foci within the ventricles - there will be two different morphology present.

100
Q

Treatment of PVCs

A

Only if symptomatic

Correct reversible causes e.g. hypoxia, electrolyte abnormalities, acidosis

Beta blockers

Amiodarone

101
Q

R on T phenomenon with PVCs

A

PVC ‘lands on’ second half of T wave during relative refractory period

Can go into Torsades De Pointes

102
Q

Ventricular Escape Beat

A

SA node + AV junction fails

Comes after intended beat (PVC but after intended)

No p wave

103
Q

Components of VT

A

HR > 110

Regular

Wide, bizarre complexes

P waves if seen not associated with QRS

104
Q

How to treat Torsades De Pointes

A

IV K+

IV Mg

Have defib ready

105
Q
A

Right Bundle Branch Block

If QRS in V1 is predominantly positive with an rSR pattern (M) you have a RBBB

V6 will often have a W pattern

106
Q
A

Left Bundle Branch Block

If QRS in V1 is predominantly negative with a W shape and V6 is positive with an M, you have a LBBB

107
Q

x2 diagnostic features of Bundle Branch Blocks

A

Wide QRS

R-R progression

108
Q

Left anterior fascicular block

Morphology and axis

A

Narrow QRS

Left Axis

109
Q

Left posterior fascicular block

A

Narrow QRS

R) axis

110
Q

How to work out if there is ventricular hypertrophy

A

Count deepest V1 or V2 wave + count tallest V5 and V6

If = >35mm = Ventricular hypertrophy still needs echo

111
Q

What is a strain pattern

A

Discordant ST elevation/depression to the QRS

Present in Left ventricular hypertrophy of Bundle branch block

112
Q

Left main artery corresponds to which leads

A

Left heart

Anterior: V1- V4

Lateral: I, aVL, V5 + V6

113
Q

LAD corresponds to which leads

A

Anterior: V1-V4

114
Q

L) Circumflex corresponds to which leads

A

Lateral: V5-V6, I and aVL

115
Q

RCA corresponds to which leads

A

Inferior: II, III, aVF

right heart + SA + AV

116
Q

ECG changes in Ischemia

A

T wave inversion

117
Q

ECG changes in injury

A

ST elevation

118
Q

ECG changes in infarction

A

Q wave

119
Q

If V1-V3 have ST depression

A

Do posterior ECG

120
Q

What does this indicate? (saddleback)

A

Pericarditis

121
Q

Main cause of heart failure with preserved ejection fraction (HFpEF)

A

Thick ventricles caused by chronic hypertension = cannot relax enough to fill

122
Q

Main cause of heart failure with reduced ejection fraction (HFrEF)

A

Ischemic Heart Disease

Myocardial Infarction

123
Q

R) Heart failure symptoms

A

Increased jugular venous pressure

Chest pain/ angina

Ascites

Peripheral oedema

124
Q

L) Heart failure symptoms

A

APO

Cough, crackles, wheeze, tachypnoea

Tachycardia

Fatigue

Cyanosis

125
Q

Heart failure with preserved ejection fraction (HFpEF) treatment

A

Diuresis

Beta blockers

126
Q

For the tachy algorithm

Name the 4 adverse feature which would lead to a cardioversion

A

Shock

Syncope

Myocardial Ischemia (ECG changes, chest pain)

Heart failure - acute = APO

127
Q

Define SVT

A

Any tachyarrhythmia that comes from above the AV node e.g. AF, Flutter

128
Q

If ECG appears as VT but is irregular

A

AF

Rate related BBB resulting in wide QRS

AF with aberrancy

129
Q

Diagnostic Features of VT

A

Precordial leads all negative (V1-V6)

AV dissociation (if you can find p wave)

Capture beats

Fusion beats (native beat)

130
Q

Bifasicular blocks

R-R progression and axis in RBBB + LAFB

A

QRS wide

V1 positive

V6 negative

Left axis

131
Q

Right Bundle Branch Block + Left posterior fascicular block

A

V1 positive

V6 negative

Right axis

132
Q

What is a Trifasicular block

A

Refers to the presence of conduction delay in three different parts of the heart: Bundle Branch Block, AV Block and Fascicular block

133
Q

What is shock?

A

It is a life threatening circulatory failure that results in cellular and tissue hypoxia

134
Q

Difference between PaO2 and SaO2?

A

PaO2 is the partial pressure of oxygen in arterial blood (Oxygen not bound by haemoglobin)

SaO2 is the percentage of oxygen bound to haemoglobin in arterial blood.

135
Q

(Oxygen-Hemoglobin Dissociation Curve)
What is the difference between Left-shift and Right-shift?

A

Left-shift =
Decreased P50 (increased affinity)
⬇️ Temp
⬇️ Pco2
⬇️ 2,3 - DPG
⬆️ pH

Right-shift =
Increased P50 (decreased affinity)
⬆️ Temp
⬆️ Pco2
⬆️ 2,3 - DPG
⬇️ pH

136
Q

What is a Capnometer

A

A device that measures and displays a numerical value of carbon dioxide.

137
Q

A 70 year old man with a past medical history of severe COPD on oxygen therapy at 2 L/min via nasal cannula, presents to the emergency department (ED) in respiratory distress, diaphoretic and agitated. He gives a history of progressive dyspnoea associated with a worsening productive cough, fevers and chills. On arrival to the ED his vital signs were BP 150/90mmHg, pulse rate 130bpm, temperature 38.5°C and RR 33bpm and his SpO2 was 80%. He was placed on O2 supplementation at a FiO2 30% delivered with a simple face mask. He was treated with repeated doses of nebulised bronchodilators. Whilst waiting for further workup his SpO2 increased to 90% but his breathing has become laboured and he is responding to painful stimuli only. What is the most appropriate step in the management of this patient?

A

Start bag-mask ventilation and prepare to intubate the patient

138
Q

The essential factors determining the cardiac output are:

A

Preload, contractility, afterload and heart rate

139
Q

Interpret the following arterial blood gas results:

pH 7.2

PaO2 100 mmHg

PaCO2 42 mmHg

HCO3 19 mEq/L

(FiO2 40%)

A

Metabolic acidosis with Type 1 respiratory failure

140
Q

For type II respiratory failure, the best mode of non-invasive ventilation is:

A

BiPAP

141
Q

A patient who is experiencing increased fluid loss due to vomiting and diarrhoea, and is at risk of developing hypovolaemia, is more likely to decompensate if they are on a beta-blocking drug because they:

A

Cannot increase heart rate to increase cardiac output.

142
Q

What is the primary difference between distributive shock and hypovolaemic shock?

A

Blood volume remains constant in distributive shock

143
Q

What is the correct interpretation for the Arterial Blood Gas below (FiO2 50%)?

pH 7.1

PaO2 160 mmHg

PaCO2 56 mmHg

HCO3 12 mEq/

A

Mixed acidosis and Type 2 respiratory failure

144
Q

The most accurate indication for signs of life-threatening asthma is:

A

Inability to speak, Silent chest, Sweating & vomiting, Panic and an SaO2 < 90% with O2

145
Q

Charlie fell over at a party and hit his head. He is now unconscious with slow, shallow breathing. If you were able to obtain an ABG, what would the findings indicate considering the clinical picture?

A

Respiratory Acidosis

146
Q

Interstitial Lung Disease and Sarcoidosis are two respiratory conditions that are restrictive Lung disorders.

True or False

A

True

147
Q

The pathophysiology of Asthma has three processes that interact and lead to an inflamed bronchial system. What are the three processes.

A

Bronchospasm, increased mucous production and bronchial oedema

148
Q

Arya is a 19 year old female brought in to the Emergency department with suspected MDMA (ecstasy) ingestion. She is tachycardic, tachpnoeic with an increased work of breathing, and a GCS of 12/15

If you were to take an ABG what would you expect to find?

A

Respiratory Alkalosis

149
Q

A patient with COPD on home oxygen set at 2 L/min delivered via nasal cannula, was admitted to the High Dependency Unit for the monitoring of upper gastrointestinal bleeding. The patient is comfortable with an oxygen saturation level of 92% while on oxygen 2 L/min via nasal cannula. While the patient is monitored with continuous pulse oximetry, it is recommended to do the following:

A

Continue on the current oxygen setting

150
Q

Mary is ventilated after suffering a cardiac arrest. The mechanical ventilator is set at: SIMV, 12(RR) x 550(Vt), PEEP 5, FiO2 70%

An ABG is performed.

pH 7.3

PaO2 85 mmHg

PaCO2 41 mmHg

HCO3 23 mEq/L

What would be the appropriate adjustment in parameters?

A

Increase the PEEP

151
Q

Poor circulation causes which form of hypoxia?

A

Stagnant hypoxia

152
Q

In what ways does PEEP affect haemodynamics?

A

Decreases pre load and afterload

153
Q

On examining the 12 lead ECG you identify the presence of Q waves deeper than 3mm in leads V1 to V4 accompanied by 4mm ST segment elevation. What do these changes correspond to and which artery is likely to be involved

A

A pattern of acute myocardial infarction in the anteroseptal wall - LAD

154
Q

On examining the 12 lead ECG you identify the presence of 3mm ST segment depression in leads I, aVL, v1-v6. What do these changes correspond to and which artery is likely to be involved?

A

A pattern of acute myocardial ischaemia in the anterolateral walls - LMCA

155
Q

If the PR interval was prolonged:

A

Conduction through the atrioventricular node would be delayed

156
Q

A patient presents with what looks like ventricular tachycardia. He is talking to you, complaining of chest discomfort. His HR is 178bpm, and his BP is 86/45mmHg. What the best course of action now?

A

To call for help and start preparing for cardioversion

157
Q

An arrhythmia originating in an escape pacemaker in the AV junction with a rate of 60 to 100 beats per minute is called is classified as:

A

Accelerated junctional rhythm

158
Q

A major concern with the use of class III antiarrhythmics is their association with:

A

Prolonged QT interval

159
Q

Identify the electrical axis in the presence of a predominantly negative aVF and a predominantly positive lead I:

A

Left Axis Deviation

160
Q

Some of the symptoms of right heart failure are:

A

Raised jugular venous pressure, hepatomegaly, dependent oedema and anorexia

161
Q

The Following Rhythm is diagnosed as:

A

Atrial Fibrillation

162
Q

Identify the electrical axis in the presence of a predominantly positive aVF and a predominantly positive lead I:

A

Normal Axis

163
Q

On examining the 12 lead ECG you identify the presence of 3mm ST segment depression in leads v1 and v2. What do these changes correspond to and which artery is likely to be involved?

A

A pattern of acute myocardial injury in the posterior wall - PDA

164
Q

Features of heart failure with reduced ejection fraction (HFrEF) are:

A

Dilated ventricle, congestion, EF less than 50%

165
Q

An insufficiency of the mitral valve will cause left ventricular hypertrophy.

True or False

A

True

166
Q

Identify the electrical axis in the presence of a predominantly positive aVF and a predominantly negative lead I:

A

Right Axis Deviation

167
Q

The following rhythm is diagnosed as:

A

Sinus Arrhythmia

168
Q

In Heart Failure with preserved ejection fraction the left ventricle cannot:

A

Relax appropriately during diastole

169
Q

The main cause of heart failure with preserved ejection fraction is a chronically elevated after load.

True or False

A

True

170
Q

The relative refractory period refers to the time during which:

A

Cells are ready to respond to an increased/stronger stimulus

171
Q

The following rhythm is diagnosed as:

A

2nd degree AV block Type II

172
Q

Systole

A

Contraction and Depolarisation

173
Q

Diastole

A

Relaxation and Repolarisation

174
Q

SAO2

A

Arterial saturation of oxygen

175
Q

SPO2

A

Peripheral Saturation of oxygen

176
Q

PAO2

A

Partial Pressure of O2 in artery

177
Q

P Wave

A

Depolarisation of atria

Upright, rounded, precedes QRS complex

178
Q

PR interval

A

Time from onset of atrial depolarisation to onset of ventricular depolarisation

Beginning of P wave to onset of QRS duration 0.12-0.20 seconds

179
Q

QRS complex

A

Depolarisation of the ventricles

Upright, narrow/ wide

Duration: <0.12 seconds, follows P wave

180
Q

ST segment

A

Early part of ventricular repol

Normally isoelectric (flat)

ST depression = myocardial ischaemia
ST elevation = myocardial infarction

181
Q

T wave

A

Ventricular repolarisation

Upright, rounded, 2/3 of QRS complex follows QRS complex

182
Q

Ejection fraction

A

> 50% normal person amount of blood from

183
Q

aVR

A

Must be negative for ECG to be correct - if positive check limb lead placement

184
Q

Hypoxaemic Hypoxia

A

Nil oxygenation of arterial blood

185
Q

Anaemic hypoxia

A

Not enough Iron, decreased hb

186
Q

Guess The Rhythm

Regular, narrow QRS, p wave for every QRS, 65bpm

A

Sinus Rhythm

187
Q

Guess the Rhythm

Irregular, narrow QRS, no p wave, 110bpm

A

AF

188
Q

Define Sepsis

A

A life threatening organ dysfunction caused by a dysregulated host response to infection’

189
Q

Define Septic Shock

A

A subset of sepsis which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality

190
Q

What is the management of sepsis

A

Early recognition and immediate commencement of a Sepsis 6/ Sepsis Bundle is imperative to stop Sepsis

Commence within 1st hour of recognition

Oxygen - titrate SPO2 to 94% and above
Blood cultures
IV antibiotics
Lactate
Intravenous crystalloid fluid - dependent on clinical status and Lactate
Urine Output

191
Q

Describe Aerobic Metabolism

A

Aerobic metabolism is when the body produces energy (in the form of ATP) using oxygen.

Glucose + Pyruvic Acid + O2 = 38 ATP + CO2 + H20

192
Q

Describe Anaerobic Metabolism

A

Anaerobic metabolism is when the body produces energy without oxygen

Glucose + Pyruvic acid = 2 lactic acid + 2 ATP

193
Q

What is Chronotrope? Provide examples

A

Chronotropes - Affect HR

Positive Chronotrope = increased HR
Negative chronotrope = Decreased HR

Positive Chronotrope = Adrenaline Negative chronotrope = Beta blockers

194
Q

What is an Inotrope? Provide examples

A

Inotropes Affect Cardiac Contractility

Positive Inotrope = increased cardiac contractility
Negative Inotrope = Decreased cardiac contractility

Positive inotrope = Dobutamine
Negative inotrope = beta blockers

195
Q

Main purpose of a vasopressor? Provide examples of vasopressors

A

Main purpose is to vasoconstrict

Examples: Noradrenaline + Metaraminol

196
Q

Complications for Massive Transfusion

A

Complications for massive transfusion include:

Hypothermia
Dilutional coagulopathy
Metabolic acidosis
Hypocalcaemia

197
Q

Cardiac Output in Hypovolemic Shock

A

Cardiac Output is increased

Increased HR, Contractility and Afterload

Decreased Preload

198
Q

Cardiac Output in Cardiogenic Shock

A

Cardiac output is decreased in Cardiogenic Shock

Increased Heart Rate, Preload and Afterload

Decreased Contractility

199
Q

Cardiac Output in Distributive Shock

A

Cardiac Output is Increased

Increased Heart Rate and Contractility

Decreased Afterload + Preload

200
Q

Cardiac Output in Obstructive Shock

A

Cardiac Output decreases in obstructive shock

Increased Heart rate, Contractility and Afterload

Decreased Preload

201
Q

How does PEEP effect preload

A

Increase in intrathoracic pressure –> decreased venous return —> decreased preload

202
Q

PEEP effect on Right Ventricular Afterload

A

Right ventricle needs to generate enough pressure to overcome the sum of PA pressure and PEEP. The higher the PEEP the more compensation the higher the afterload

203
Q

PEEP effect on Left Ventricular Afterload

A

Decreases Left ventricular Afterload. Increased positive pressure increases the pressure gradient making it easier for the left ventricles to pump out blood

204
Q

Opioid dosing is dependent on the following variables. What are they

A

Adults (age based), Paediatrics (weight based), route of administration, and the lipid solubility of the drug.

205
Q

Hypertensive Urgency is defined as:

A

BP greater than 180/120mmHg without signs of Target Organ Damage. Presenting symptoms may include headache, shortness of breath, anxiety, and epistaxis.

206
Q

What is the recommended approach to fluid resuscitation in massive haemorrhage?

A

Guide resuscitation and product choice with real-time clotting results - e.g. TEG/ROTEM

207
Q

In Acute Coronary syndrome, fibrinolytic therapy is given to:

A

Activate plasminogen, which activates plasmin to degrade fibrin

208
Q

In severe liver failure there is often associated coagulopathy because:

A

The liver produces and stores most coagulation factors

209
Q

The activation of the RAAS System results in:

A

Vasoconstriction, increased HR and contractility, sodium and water retention.

210
Q

Tranexamic acid is given in massive haemorrhage because it:

A

Inhibits the breakdown of fibrin by inactivating plasminogen

211
Q

The three categories of risk factors for developing a venous thrombo-embolism include:

A

stasis, endothelial injury, and hypercoagulability

212
Q

The RAAS system promotes:

A

Vasoconstriction, sympathetic stimulation, sodium and H2O retention

213
Q

Absolute Refractory Period

A

No stimulus can evoke a response

Cardiac cells have depolarised

After depolarisation cardiac cells cannot be re-exited until the cell has repolarised to its threshold potential

Phases 0,1,2 and early phase 3

214
Q

Relative Refractory Period

A

Cardiac cells have repolarised to their threshold potential (not the resting potential)

A stronger than normal stimulus can cause a response

Late phase 3 & early phase 4

Foundations (1 decks)

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