EXAM Prep Flashcards
Revision (219 cards)
1
Q
4 Valves Where?
A
Tricuspid (R) AV)
Bicuspid/ mitral (L) AV)
Pulmonary
Aortic
2
Q
3 vessels supplying the RA
A
Inferior vena cava
Superior vena cava
Coronary sinus
3
Q
70% of blood supplied to the ventricles is via:
A
Passive movement
Atrial contraction is for the last 30%
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)
5
Q
Which vessels are very proximal to the aortic valve
A
Coronary arteries
6
Q
Coronary arteries perfuse on:
A
Diastole
(heart is only organ perfused on diastole)
7
Q
What to give to decrease HR
A
Beta blockers
Digoxin
8
Q
What to give/do to increase HR
A
Atropine
Adrenaline
Pace
9
Q
What to give to increase preload
A
Vasopressors
- Noradrenaline
- Vasopressin
- Metaraminol
Fluids
10
Q
What to give to decrease preload
A
Diuretics
GTN (vasodilate)
11
Q
What to give to increase contractility
A
Adrenaline
Dobutamine
Digoxin
Milrinone
12
Q
What to give to decrease contractility
A
Beta blockers
13
Q
What to give to increase afterload
A
Vasopressors
- Noradrenaline
- Metaraminol
- Vasopressin
14
Q
What to give to decrease afterload
A
Angiotensin-converting enzyme inhibitors (ACE)
Angiotensin 2 receptors (ARBS)
Calcium channel blockers
Opposite of RAAS
15
Q
BP =
A
Cardiac output x Systemic vascular resistance
16
Q
What to give to inhibit sympathetic nervous system
A
Beta blockers
17
Q
What to give to inhibit the RAAS system
A
Angiotensin-converting enzyme (ACE) inhibitors
Angiotensin 2 receptor blockers (ARBs)
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)
19
Q
3 layers of veins/arteries
A
Tunica intima (endothelium, mediates vasoconstriction/vasodilation)
Tunica Media (smooth muscle)
Tunica adventitia/ Externa (connective tissue)
20
Q
Which enzyme works as a lever to expose myosin binding sites for Ca2+
A
Troponin
21
Q
When Ca2+ attaches to myosin binding sites, what happens
A
Myocardial contraction
22
Q
Which cells have automaticity
A
Pacemaker cells
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
24
Q
Action Potential Phase 1
Initial early / repolarisation
A
Na+ (fast) channel closes K+ channels open K+ out of cell
25
Action Potential Phase 2
Plateau
Calcium (slow) channels open
Calcium into cell
K+ continues to leave cell
= balance plateau
26
Action Potential Phase 3
Repolarisation
Calcium Channels close
Potassium Continues to leave the cell quickly
Causes the cell to become more negative leading to repolarisation
27
Action Potential Phase 4
Resting Potential
Resting membrane potential
ATPase pumps swap electrolytes
Na+/K+ ATPASe
Ca2+ ATPASe
28
Which electrolyte regulates the pumps
Magnesium
29
What cells have fast influx of Ca2+ instead of Na+, with no resting period
Nodal or 'pacemaker cells'
30
4 classes of antiarrhythmics
Sodium channel blockers
Beta blockers
Potassium channel blockers
Calcium channel blockers
31
What phase does sodium channel blockers (class I) work on
Phase 0
Lignocaine + flecainide
32
What would a B1 agonist do?
(Heart)
Tachycardia
Increase contractility
Release renin (trigger RAAS)
33
What would a B2 agonist do?
(lungs)
Bronchodilate
Vasodilate
34
B blockers block which nodes
SA + AV
Decreases automaticity of pacemaker cells
34
Why would you want a selective B blocker if asthmatic
Blocking B2 would cause bronchoconstriciton
35
Class III
What do they do
Give examples
Indications
Block K+ outward flow
- Prolong QT
- May precipitate torsades
Sotalol (mixed class II + III) and amiodarone
SVT, VF, VT, AF, A Flutter
36
Why is sotalol so special
Class II = non selective beta blockers (decrease SA + AV function)
Also class III (prolong QT, slow down action potential duration)
37
Class IV
Calcium channel blockers
Vasodilation
'dipines'
- nifedipine
- amlodipine
- Felodipine
Diltiazem + verapamil
38
Widowmaker artery
left anterior descending artery (LAD)
39
Function of the AV node
Slows conduction to allow filling (PR interval)
Backup pacemaker (40-60bpm)
Blocks atrial impulses if > 200
40
Small square =
Big square =
Small = 0.04
Large = 0.2
41
PR should be
QRS should be
QT should be
PR = 0.12 - 0.2 sec (3-5 small squares)
QRS = < 3 small squares (0.12)
QT = < 1/2 RR
42
10 second method
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
43
Large square method
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
44
Sinus Exit Block
Regular rhythm
Dropped beat
Next beat is where it would be
45
Sinus pause / arrest
Pause = 1 dropped beat but does not resume at intended point
Arrest = > 1 impulse fails, does not return at intended point
46
Sick sinus
Irregular tachy-brady combination
47
Bigeminy and trigeminy
2/3 premature beats together
48
Proximal atrial tachycardia
Sometimes tachy can self revert starts & stops abruptly
49
Zones of pulmonary flow: relevant pressures of zone 1
No blood flow
Alveolar (PA) is greater than arterial (Pa) & venous (PV)
50
Zones of pulmonary flow
Relevant pressures of zone 2
Moderate blood flow
Relevant pressure gradient is between the Pa (Arterial pressure) PA (alveolar pressure)
51
Zones of pulmonary flow
Relevant pressures of zone 3
Greatest blood flood occurs
The relevant pressure gradient
Is between the Pa (Arterial pressure) and PV (venous pressure)
52
Oxyhaemoglobin dissociation curve
Shift to the right
Increased pCO2
Decreased pH
Hb decreased affinity for CO2
Increased 2,3 diphosphoglycerate (DPG) binds to Hb, increased O2 unloading
53
Oxyhaemoglobin dissociation curve
Shift to the left
Decreased CO2
Increased pH
Decreased temperature (decreased tissue metabolism)
Decreased 2,3 diphosphoglycerate (DPG)
54
Causes of rightward shift
Increased levels CO2
Increased temp, sepsis (decreased O2 available to distal tissues)
Inflammation
Burns
Severe trauma --> increased inflammation
Exercise
Panic attack
54
Oxygen delivery variables
Cardiac output, SaO2, Hb, PaO2
55
Causes of leftward shift
In lungs
Alkalosis
Hypothermia
56
Aerobic respiration
In mitochondria
38 ATP + CO2 + H20
57
Anaerobic Respiration
In cytoplasm
2 lactic acid + 2 ATP
58
V vs Q
Shunting is an issue with
Ventilation
Q > V
Alveolar dysfunction
Preserved perfusion
59
Why does lactate suck
Produced as a by-product of anaerobic respiration
Indication of cell stress or tissue hypoxia
60
V vs Q
Dead space is an issue with:
Perfusion
V > Q
Gas exchange not possible due to compromised perfusion
O2 in structures unable to be used
E.g. PE
61
SPO2 drops after GTN why?
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
62
Composition of nitrogen in the alveoli
78%
The big nitrogen molecules hold the alveoli open. So you don't want to wash out with oxygen otherwise they will collapse
63
Normal PaO2
4-5x FIO2
E.g. RA 21% = 80-100%
64
PH:
PaO2
PCO2
HCO3
7.35 - 7.45
80-100 (RA)
35-45
22-28
65
Contraindications NIV
Respiratory arrest
Untreated pneumothorax
Inability to maintain own airway
Haemodynamic instability
Facial trauma
Vomiting
66
3 Variables of diffusion
Surface area
Concentration difference
Thickness of barrier
67
3 PEEP benefits
Increased gas exchange
Increased alveolar recruitment
Decreased V/Q mismatch
68
CO =
SV x HR
SV = Preload, Contractility, Afterload
69
Cardiovascular Effects of NIV
Decrease preload + afterload
70
Tidal volume
What we normally breath in + out at rest
71
Inspiratory reserve volume
What we breath in when we force inspiration
72
Residual volume
Air remaining in the alveoli after forced expiration
73
Vital capacity
From forced inspiration to forced expiration
74
Functional Residual Capacity
Air remaining in alveolar after forced expiration
75
Pulmonary function tests
Tests of ventilation (peak flow)
Tests of diffusion
Tests of perfusion
Tests for V/Q mismatch
76
If V/Q ratio is low
V < Q
Ventilation less than perfusion = pneumonia etc
77
Type 1 vs Type 2 respiratory failure
Type 1 = Decreased O2 normal CO2 (failure to oxygenate)
Type 2 = Decreased O2 and increased CO2 (copd) (failure to ventilate)
78
Systemic inflammation is associated with hypotension because of:
Venous vasodilation
Third spacing due to increased vascular permeability
79
In shock pulse pressure will:
Narrow
80
Deadly triad of coagulopathy
81
PE treatment
O2
Fluid loading
Anticoagulation
Thrombolytics
?ETT
Surgery
Inotropes
82
Minute volume set by
Respiratory Rate and Tidal Volume
83
MV complications
Barotrauma
Volutrauma
Atelectasis
Increased intrathoracic pressure
Decreased venous return
Decreased afterload
84
Dobutamine
B1, B2 agonist
- Tachycardia
- Increased contractility
- Vasodilation
- B2 outweighs RAAS
85
Rate control drugs for tachyarrhythmia
Digoxin
Beta blockers
Calcium channel blockers
Amiodarone
86
Why might AF show ST depression
Rate-related ischemia
87
P waves in AF
No, there is no P waves in AF
88
If rhythm strip shows ? ST depression
Check 12 lead, see if depression is in >2 contiguous leads
89
Classification of 1st degree AV block
Every P wave is conducted (but slower than usual)
90
Classification of 2nd degree AV block
Some P waves are conducted
- Mobitz type 1 (Wenckebach)
- Mobitz type 2
91
Classification of 3rd degree AV block
No P waves are conducted
92
1st degree AV block
Lengthening/prolonged PR interval
93
2nd degree AV block (Mobitz type 1 Wenckebach)
PR interval progressively lengthens until no QRS is conducted and a dropped beat occurs
94
2nd degree AV block (Mobitz type 2)
PR interval remains the same but can be prolonged
Occasional non conducted P wave = Dropped QRS
95
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
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
High grade/ Advanced AV block
>2 consecutive QRS are blocked
95
Junctional vs ventricular escape rhythms
Conduction comes from:
AV junction: Narrow QRS
Ventricles: Wide QRS
96
Premature Junction Contraction vs Premature Atrial Contraction
Premature junctional beats originate in the AV junction: no p wave
Premature Atrial beats originate from the SA node: P wave
97
Treatment of fine VF
CPR to obtain enough perfusion and then shock
98
Premature Ventricular Complexes
Originates in ventricles
Premature to expected beat
No p wave
Compensatory pause = next complex comes later
99
Unifocal vs multifocal morphology in PVCs
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
Treatment of PVCs
Only if symptomatic
Correct reversible causes e.g. hypoxia, electrolyte abnormalities, acidosis
Beta blockers
Amiodarone
101
R on T phenomenon with PVCs
PVC 'lands on' second half of T wave during relative refractory period
Can go into Torsades De Pointes
102
Ventricular Escape Beat
SA node + AV junction fails
Comes after intended beat (PVC but after intended)
No p wave
103
Components of VT
HR > 110
Regular
Wide, bizarre complexes
P waves if seen not associated with QRS
104
How to treat Torsades De Pointes
IV K+
IV Mg
Have defib ready
105
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
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
x2 diagnostic features of Bundle Branch Blocks
Wide QRS
R-R progression
108
Left anterior fascicular block
Morphology and axis
Narrow QRS
Left Axis
109
Left posterior fascicular block
Narrow QRS
R) axis
110
How to work out if there is ventricular hypertrophy
Count deepest V1 or V2 wave + count tallest V5 and V6
If = >35mm = Ventricular hypertrophy still needs echo
111
What is a strain pattern
Discordant ST elevation/depression to the QRS
Present in Left ventricular hypertrophy of Bundle branch block
112
Left main artery corresponds to which leads
Left heart
Anterior: V1- V4
Lateral: I, aVL, V5 + V6
113
LAD corresponds to which leads
Anterior: V1-V4
114
L) Circumflex corresponds to which leads
Lateral: V5-V6, I and aVL
115
RCA corresponds to which leads
Inferior: II, III, aVF
right heart + SA + AV
116
ECG changes in Ischemia
T wave inversion
117
ECG changes in injury
ST elevation
118
ECG changes in infarction
Q wave
119
If V1-V3 have ST depression
Do posterior ECG
120
What does this indicate? (saddleback)
Pericarditis
121
Main cause of heart failure with preserved ejection fraction (HFpEF)
Thick ventricles caused by chronic hypertension = cannot relax enough to fill
122
Main cause of heart failure with reduced ejection fraction (HFrEF)
Ischemic Heart Disease
Myocardial Infarction
123
R) Heart failure symptoms
Increased jugular venous pressure
Chest pain/ angina
Ascites
Peripheral oedema
124
L) Heart failure symptoms
APO
Cough, crackles, wheeze, tachypnoea
Tachycardia
Fatigue
Cyanosis
125
Heart failure with preserved ejection fraction (HFpEF) treatment
Diuresis
Beta blockers
126
For the tachy algorithm
Name the 4 adverse feature which would lead to a cardioversion
Shock
Syncope
Myocardial Ischemia (ECG changes, chest pain)
Heart failure - acute = APO
127
Define SVT
Any tachyarrhythmia that comes from above the AV node e.g. AF, Flutter
128
If ECG appears as VT but is irregular
AF
Rate related BBB resulting in wide QRS
AF with aberrancy
129
Diagnostic Features of VT
Precordial leads all negative (V1-V6)
AV dissociation (if you can find p wave)
Capture beats
Fusion beats (native beat)
130
Bifasicular blocks
R-R progression and axis in RBBB + LAFB
QRS wide
V1 positive
V6 negative
Left axis
131
Right Bundle Branch Block + Left posterior fascicular block
V1 positive
V6 negative
Right axis
132
What is a Trifasicular block
Refers to the presence of conduction delay in three different parts of the heart: Bundle Branch Block, AV Block and Fascicular block
133
What is shock?
It is a life threatening circulatory failure that results in cellular and tissue hypoxia
134
Difference between PaO2 and SaO2?
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
(Oxygen-Hemoglobin Dissociation Curve)
What is the difference between Left-shift and Right-shift?
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
What is a Capnometer
A device that measures and displays a numerical value of carbon dioxide.
137
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?
Start bag-mask ventilation and prepare to intubate the patient
138
The essential factors determining the cardiac output are:
Preload, contractility, afterload and heart rate
139
Interpret the following arterial blood gas results:
pH 7.2
PaO2 100 mmHg
PaCO2 42 mmHg
HCO3 19 mEq/L
(FiO2 40%)
Metabolic acidosis with Type 1 respiratory failure
140
For type II respiratory failure, the best mode of non-invasive ventilation is:
BiPAP
141
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:
Cannot increase heart rate to increase cardiac output.
142
What is the primary difference between distributive shock and hypovolaemic shock?
Blood volume remains constant in distributive shock
143
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/
Mixed acidosis and Type 2 respiratory failure
144
The most accurate indication for signs of life-threatening asthma is:
Inability to speak, Silent chest, Sweating & vomiting, Panic and an SaO2 < 90% with O2
145
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?
Respiratory Acidosis
146
Interstitial Lung Disease and Sarcoidosis are two respiratory conditions that are restrictive Lung disorders.
True or False
True
147
The pathophysiology of Asthma has three processes that interact and lead to an inflamed bronchial system. What are the three processes.
Bronchospasm, increased mucous production and bronchial oedema
148
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?
Respiratory Alkalosis
149
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:
Continue on the current oxygen setting
150
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?
Increase the PEEP
151
Poor circulation causes which form of hypoxia?
Stagnant hypoxia
152
In what ways does PEEP affect haemodynamics?
Decreases pre load and afterload
153
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 pattern of acute myocardial infarction in the anteroseptal wall - LAD
154
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 pattern of acute myocardial ischaemia in the anterolateral walls - LMCA
155
If the PR interval was prolonged:
Conduction through the atrioventricular node would be delayed
156
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?
To call for help and start preparing for cardioversion
157
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:
Accelerated junctional rhythm
158
A major concern with the use of class III antiarrhythmics is their association with:
Prolonged QT interval
159
Identify the electrical axis in the presence of a predominantly negative aVF and a predominantly positive lead I:
Left Axis Deviation
160
Some of the symptoms of right heart failure are:
Raised jugular venous pressure, hepatomegaly, dependent oedema and anorexia
161
The Following Rhythm is diagnosed as:
Atrial Fibrillation
162
Identify the electrical axis in the presence of a predominantly positive aVF and a predominantly positive lead I:
Normal Axis
163
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 pattern of acute myocardial injury in the posterior wall - PDA
164
Features of heart failure with reduced ejection fraction (HFrEF) are:
Dilated ventricle, congestion, EF less than 50%
165
An insufficiency of the mitral valve will cause left ventricular hypertrophy.
True or False
True
166
Identify the electrical axis in the presence of a predominantly positive aVF and a predominantly negative lead I:
Right Axis Deviation
167
The following rhythm is diagnosed as:
Sinus Arrhythmia
168
In Heart Failure with preserved ejection fraction the left ventricle cannot:
Relax appropriately during diastole
169
The main cause of heart failure with preserved ejection fraction is a chronically elevated after load.
True or False
True
170
The relative refractory period refers to the time during which:
Cells are ready to respond to an increased/stronger stimulus
171
The following rhythm is diagnosed as:
2nd degree AV block Type II
172
Systole
Contraction and Depolarisation
173
Diastole
Relaxation and Repolarisation
174
SAO2
Arterial saturation of oxygen
175
SPO2
Peripheral Saturation of oxygen
176
PAO2
Partial Pressure of O2 in artery
177
P Wave
Depolarisation of atria
Upright, rounded, precedes QRS complex
178
PR interval
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
QRS complex
Depolarisation of the ventricles
Upright, narrow/ wide
Duration: <0.12 seconds, follows P wave
180
ST segment
Early part of ventricular repol
Normally isoelectric (flat)
ST depression = myocardial ischaemia
ST elevation = myocardial infarction
181
T wave
Ventricular repolarisation
Upright, rounded, 2/3 of QRS complex follows QRS complex
182
Ejection fraction
>50% normal person amount of blood from
183
aVR
Must be negative for ECG to be correct - if positive check limb lead placement
184
Hypoxaemic Hypoxia
Nil oxygenation of arterial blood
185
Anaemic hypoxia
Not enough Iron, decreased hb
186
Guess The Rhythm
Regular, narrow QRS, p wave for every QRS, 65bpm
Sinus Rhythm
187
Guess the Rhythm
Irregular, narrow QRS, no p wave, 110bpm
AF
188
Define Sepsis
A life threatening organ dysfunction caused by a dysregulated host response to infection'
189
Define Septic Shock
A subset of sepsis which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality
190
What is the management of sepsis
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
Describe Aerobic Metabolism
Aerobic metabolism is when the body produces energy (in the form of ATP) using oxygen.
Glucose + Pyruvic Acid + O2 = 38 ATP + CO2 + H20
192
Describe Anaerobic Metabolism
Anaerobic metabolism is when the body produces energy without oxygen
Glucose + Pyruvic acid = 2 lactic acid + 2 ATP
193
What is Chronotrope? Provide examples
Chronotropes - Affect HR
Positive Chronotrope = increased HR
Negative chronotrope = Decreased HR
Positive Chronotrope = Adrenaline Negative chronotrope = Beta blockers
194
What is an Inotrope? Provide examples
Inotropes Affect Cardiac Contractility
Positive Inotrope = increased cardiac contractility
Negative Inotrope = Decreased cardiac contractility
Positive inotrope = Dobutamine
Negative inotrope = beta blockers
195
Main purpose of a vasopressor? Provide examples of vasopressors
Main purpose is to vasoconstrict
Examples: Noradrenaline + Metaraminol
196
Complications for Massive Transfusion
Complications for massive transfusion include:
Hypothermia
Dilutional coagulopathy
Metabolic acidosis
Hypocalcaemia
197
Cardiac Output in Hypovolemic Shock
Cardiac Output is increased
Increased HR, Contractility and Afterload
Decreased Preload
198
Cardiac Output in Cardiogenic Shock
Cardiac output is decreased in Cardiogenic Shock
Increased Heart Rate, Preload and Afterload
Decreased Contractility
199
Cardiac Output in Distributive Shock
Cardiac Output is Increased
Increased Heart Rate and Contractility
Decreased Afterload + Preload
200
Cardiac Output in Obstructive Shock
Cardiac Output decreases in obstructive shock
Increased Heart rate, Contractility and Afterload
Decreased Preload
201
How does PEEP effect preload
Increase in intrathoracic pressure --> decreased venous return —> decreased preload
202
PEEP effect on Right Ventricular Afterload
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
PEEP effect on Left Ventricular Afterload
Decreases Left ventricular Afterload. Increased positive pressure increases the pressure gradient making it easier for the left ventricles to pump out blood
204
Opioid dosing is dependent on the following variables. What are they
Adults (age based), Paediatrics (weight based), route of administration, and the lipid solubility of the drug.
205
Hypertensive Urgency is defined as:
BP greater than 180/120mmHg without signs of Target Organ Damage. Presenting symptoms may include headache, shortness of breath, anxiety, and epistaxis.
206
What is the recommended approach to fluid resuscitation in massive haemorrhage?
Guide resuscitation and product choice with real-time clotting results - e.g. TEG/ROTEM
207
In Acute Coronary syndrome, fibrinolytic therapy is given to:
Activate plasminogen, which activates plasmin to degrade fibrin
208
In severe liver failure there is often associated coagulopathy because:
The liver produces and stores most coagulation factors
209
The activation of the RAAS System results in:
Vasoconstriction, increased HR and contractility, sodium and water retention.
210
Tranexamic acid is given in massive haemorrhage because it:
Inhibits the breakdown of fibrin by inactivating plasminogen
211
The three categories of risk factors for developing a venous thrombo-embolism include:
stasis, endothelial injury, and hypercoagulability
212
The RAAS system promotes:
Vasoconstriction, sympathetic stimulation, sodium and H2O retention
213
Absolute Refractory Period
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
Relative Refractory Period
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
