1
Q
What is the normal cardiac conduction?
A
2
Q
Label the image.
A
3
Q
What are the different phases of cardiac myocyte action potential?
A
phase 0 - rapid depolarisation
- Na+ influx = cell becomes rapidly more positive
phase 1 - initial repolarisation
- brief K+ efflux
phase 2 - plateau
- Ca+ influx via L-type calcium channels (type of VGCCs) balanced by some K+ efflux = “plateau”
- CICR from SR
phase 3 - repolarisation
- K+ efflux dominates = T wave
phase 4 - resting potential
- Na+/K+ ATPase and background currents keep membrane stable at around 90mV
4
Q
On the ECG, what is responsible for the QRS complex?
What contributes to the ST segment?
What gives the T wave?
A
Na+ influx (phase 0)
calcium influx (phase 2) - not visible as separate spike on ECG but contributes to ST segment (plateau)
K+ efflux (phase 3)
5
Q
Na+ influx is responsible for what part of the ECG?
K+ efflux gives what wave/segment?
A
QRS complex
T wave
6
Q
- Which ion is responsible for the rapid depolarisation (Phase 0) in ventricular myocytes?
- Which ECG feature corresponds to Phase 0 (Na⁺ influx)?
- What causes the small notch in Phase 1 of the cardiac action potential?
- During which phase does Ca²⁺ influx occur?
A
7
Q
- What ion movement dominates Phase 3 (repolarisation)?
- Which ECG feature corresponds to Phase 3 repolarisation?
- What maintains the resting potential in Phase 4?
A
8
Q
What is the refractory period?
What is the conduction velocity?
What do these control?
A
refractory period: time when a cell cant be re-excited
conduction velocity: how fast the impulse travels
whether circuits are normal or abnormal
9
Q
What controls whether circuits are normal or abnormal?
A
refractory period
conduction velocity
10
Q
Arrhythmias due to enhanced automaticity occur when what?
(2 reasons)
A
NORMAL PACEMAKERS ACCELERATE
- other latent pacemakers e.g AV node or purkinje fibres fire at a faster rate e.g due to increased sympathetic tone or electrolyte imbalances
ABNORMAL PACEMAKERS DEVELOP
- non-pacemaker cells in the atrial or ventricular myocardium acquire automaticity e.g in ischaemic tissue
11
Q
What is an example of why latent pacemakers e.g AV node or Purkinje fibres would fire at a faster rate?
A
- increased sympathetic tone
- electrolyte imbalance
12
Q
How would cardiac myocytes acquire automacity? (start behaving like an SA or AV node cell)
A
in situations like ischaemia, hypoxia, electrolyte disturbance
- RMP = becomes less negative (partially depolarises)
- some Na+ or Ca2+ channels can reopen spontaneously = cells start to slowly depolarise on their own
- they acquire automaticity = tachycardia, fibrillation, atrial ectopics, ventricular ectopics
13
Q
When do abnormal pacemaker cells form?
A
14
Q
What is a Triggered Activity?
What is it caused by?
What is an example of this?
A
new action potential which is “triggered” before the cell has properly reset = happens because of AFTERDEPOLARISATIONS
(abnormal bumps in the membrane potential that ride on top of or just after the previous AP)
15
Q
What are the types of afterdepolarisations?
A
these extra depolarisations can fire off abnormal beats - if enough cells do it in sync they can sustain dangerous rhythms = VT, VF, Torsades
16
Q
What is an example of afterdepolarizations?
A
torsades de pointes - a form of VT
17
Q
What are symptoms of arrhythmias?
A
- palpitations
- syncope
- dyspnoea
- chest pain
18
Q
What are risks of arrhythmias?
A
- stroke (AF)
- haemodynamic collapse
- sudden cardiac death
19
Q
What are the top 4 most common arrhythmias?
A
- AF
- SVT
- VT
- heart block
20
Q
What is THE most common arrhythmias?
A
AF
21
Q
What are some risk factors for AF?
A
- HTN
- IHD
- HF
- VHD
- acute intercurrent illness such as pneumonia
- thyrotoxicosis
- age
- alcohol excess
22
Q
AF is usually asymptomatic but what can it usually present with?
A
- palpitations
- SOB, fatigue, dizziness
- stroke
- HF
23
Q
A patient will feel very unwell when experiencing what kind of AF?
A
acute onset AF with rapid ventricular rate
24
Q
What investigations would you do for suspected AF?
A
- ECG
- bloods: FBC, U&Es, TFT
- echo
25
What is the difference between rate control vs rhythm control in AF?
rate control: managing symptoms by slowing HR
rhythm control: restoring heart back to sinus rhythm
26
Rate control in AF is usually more suitable for patients who are what?
- older
- asymptomatic or minimal symptoms
- failure of rhythm control
27
In AF, is rate control or rhythm control the more common treatment strategy?
What is the aim of this strategy?
rate control - usually aim to get heart rate under 80 bpm albeit still in AF
28
What are some common anti-arrhythmic drugs?
- beta-blockers e.g bisoprolol
- digoxin
- non-dihidropyridine calcium channel blockers ('rate limiting CCBs') such as diltiazem or verapamil
29
Name a beta-blocker and its mechanism of action.
When should this be avoided.
bisoprolol
block b1 receptors in the heart -> slow AV node conduction and reduces ventricular response rate in AF
avoid in severe asthma/COPD due to bronchospasm risk
30
What is bisoprolol and what is its mechanism of action?
beta-blocker
blocks b1 receptors in the heart - slows AV node conduction and reduces ventricular rate in AF (slows HR)
31
What is the mechanism of action of digoxin?
increases vagal (parasympathetic) tone -> slows conduction through the AV node and controls ventricular rate especially at rest
32
What is the function of 'non-dihydropyridine calcium channel blockers' and give an example of one.
block L-type calcium channels in the AV node and slows conduction through the AV node reducing ventricular response
- verapamil
- diltiazem
33
What are veramapil and diltiazem and what do they do?
non-dihydropyridine calcium channel blockers
block L-type calcium channels in the AV node and slows conduction through the AV node reducing ventricular response
34
Rhythm control is a strategy which is good for patients with what? List 4 things.
- a potentially reversible cause e.g infection, post-surgery AF
- HF due to AF
- new onset AF in last 48 hours (safe to cardiovert because clot risk is lower)
- younger patients with recent onset AF (dont want them stuck with long-term AF)
35
What are the methods of rhythm control in AF?
persistent AF -> DC cardioversion (electrical shock to reset rhythm)
paroxysmal AF -> "pill in pocket approach" - pt takes single dose of drug (bisoprolol or flexainide) at onset of AF to restore sinus rhythm
if these fail -> catheter ablation of the source of the abnormal electrical signals in the atria
36
In simple terms, explain the definition of rate control vs rhythm control?
37
AF patients are how many times more likely to have a stroke?
five times more likely
38
How do strokes form in AF?
blood pools in the atria and thromboses - breaking off as a thromboembolism
39
Most patients with AF are offered what?
However this carries what?
anticoagulation therapy
bleeding risk - so can be a challenging decision
40
List types of anticoagulants used in AF.
- warfarin
- DOACS (apixaban, edoxaban, rivaroxaban, dabigatran)
- heparin
41
What anticoagulant is no longer routinely used in AF?
aspirin
42
A patient's stroke risk is calculated using what scoring system?
CHA2DS2-VASc
43
The risk of bleeding on anticoagulation can be calculated using what?
ORBIT score
44
The CHA2DS2-VASc score is used to calculate what?
patient's risk of stroke
45
The ORBIT score is used to calculate what?
patient's bleeding risk on anticoagulation
46
SVTs can include what?
47
What occurs if there is a second electrical connection between the atria and the ventricles?
paroxysmal SVT - 'short circuit' of depolarisation travels down one path and back up in the other
48
When does a paroxysmal SVT occur?
if there is a second electrical connection between the atria and the ventricles
'short-circuit' of depolarisation travels down one path and back up the other
49
What is the difference between ANVRT and AVRT?
50
What would a patient experience in paroxysmal SVT?
palpitations - fast and regular
presyncope or syncope
chest pain/tightness
51
What is the duration of a paroxysmal SVT?
episodic - can last minutes to days
52
In what 3 ways can a paroxysmal SVT be managed?
53
If there is no pulse during VT, what should be done?
If there is a pulse during VT what should be done?
54
What is shown?
VT
55
What is shown?
VF
56
What is happening in AV heart block?
What are the degrees?
failure of conduction of electrical impulses from atria to the ventricles via the AV node or bundle of His
57
Which degree AV block is usually benign?
first degree AV block
58
Which heart block has two types and what are they?
59
What occurs in third degree AV block?
60
Which heart block requires an urgent pacemaker and why?
third degree AV block
- HR tends to be slow, too slow to maintain adequate cardiac output = dizziness, syncope, hypotension
- can result in sudden cardiac death
implanted pacemaker takes over as a reliable rhythm generator and ensures safe ventricular rate
61
Which medication acts on the following:
- supraventricular arrhythmias
- ventricular arrhythmias
- both
62
What are some adverse effects of anti-arrhythmic drugs?
63
How does electrical cardioversion work?
64
What is cardiac ablation?
minimally invasive procedure to treat recurrent or refractory arrhythmias
65
What is pacemaker therapy?
66
Answer the following in regards to vessel pathology:
1. which vessels have high pressure and can experience structural damage?
2. which vessels have low pressure and can experience stasis and reflux?
3. which vessels have thin walls and are fragile and vulnerable to damage?
1. arteries
2. veins
3. capillaries
67
1. Which blood vessel type has the thickest walls and why?
2. Which vessels have walls only one cell thick?
3. Which vessels have thin walls dominated by tunica adventitia?
68
Do arteries or veins have a wider lumen?
How narrow are capillaries compared to RBCs?
69
Which vessels carry blood under the highest pressure?
In which vessels is pressure the lowest and why?
70
Which vessels have valves to prevent backflow?
veins
71
List the main function of arteries, veins and capillaries.
72
1. List which diseases affect arteries.
2. List which diseases affect veins.
3. List which diseases affect capillaries.
73
Which vessel has a tunica intima but no tunica media or adventitia? What is it specialised for?
capillary - gas exchange
74
1. How does HTN damage capillaries?
2. How does diabetes damage capillaries?
3. How does vasculitis damage capillaries?
1. high pressure = basement membrane disruption
2. hyperglycaemia -> endothelial damage and basement membrane thickening
3. immune complexes and cytokines
75
What leaks into tissue in HTN capillary damage?
fibrin and RBCs
76
What clinical problems result from HTN capillary damage?
retinal haemorrhages
papilloedema
nephrosclerosis
77
What structural change forms in diabetic capillaries?
What conditions result from diabetic capillary pathology?
microaneurysms due to protein leakage into vessel walls
diabetic nephropathy and diabetic retinopathy
78
What leaks from vessels in vasculitis?
What are the clinical consequences of vasculitis capillary damage?
plasma proteins, RBCs and fibrin
purpura, haemorrhage, necrosis
79
Which arteries are commonly affected by atherosclerosis? What would this lead to?
coronary arteries -> CAD
peripheral arteries -> PAD
80
What are the main complications of atherosclerosis?
MI
stroke
limb ischaemia
81
What is an aneurysm and where are they commonly found?
localised dilation of an artery due to weakening of the vessel wall
abdominal aorta and cerebral arteries
82
What is the major risk of an aneurysm?
rupture -> catastrophic haemorrhage
83
What is arteritis? Give examples.
What are possible consequences of this?
inflammation of an artery, often immune-mediated - giant cell arteritis, takaysu arteritis
vessel narrowing, thrombosis, ischaemia
84
List modifiable and non-modifiable risk factors for atherosclerosis.
85
Explain the pathophysiology of atherosclerosis.
86
What are the complications of the following:
1. plaque rupture
2. chronic stenosis
3. aneurysm
4. embolisation
87
What arterial issues could occur on the various locations?
88
What's the pathophysiology of PAD?
What are clinical features of this? (signs and symptoms)
chronic atherosclerotic narrowing of arteries supplying the limbs
symptoms
- intermittent claudication
- leg pain at rest
signs
- diminished or absent peripheral pulses
- cool, pale skin
- ulceration
89
These are clinical features of what?
PAD
90
What are the 6 Ps of critical limb ischaemia?
91
What are managements for PAD?
92
In AAAs, the dilation of the AA is usually how big in diameter?
AAAS are usually what (location wise)?
>3cm in diameter
usually infrarenal - below renal arteries, above iliac bifurcation
93
List modifiable and non-modifiable risks for AAAs.
94
Explain the pathophysiology of AAAs.
95
What are symptoms of AAAs?
96
What is the screening process of AAAs? What does early detection allow?
What is the management for AAAs?
97
What makes cerebral arteries structurally weaker compared to other arteries?
cerebral arteries at branch points lack a tunica media and elastic lamina
weak walls = bulging under pressure
98
Cerebral arteries branch point lack what?
a tunica media and elastic lamina
99
What type of blood flow at branch points contributes to cerebral aneurysm formation?
pulsatile and turbulent flow
100
How does haemodynamic stress cause aneurysms?
constant pulsation adds mechanical stress -> outpouching develops
101
How does hypertension promote aneurysm formation?
How does smoking affect cerebral aneurysms?
Name two genetic syndromes associated with cerebral aneurysms.
102
What happens as the sac wall of a cerebral aneurysm thins?
What is a classic symptom of this?
103
How do cerebral aneurysms progress to rupture?
104
List 3 venous diseases.
venous insufficiency
varicose veins
DVT
105
Explain the pathophysiology of chronic venous insufficiency.
What are symptoms and signs of chronic venous insufficiency?
symptoms
- leg pain
- night cramps
- leg swellings
- pruritus
signs
- oedema
- varicose veins
- hyperpigmentation
- venous eczema
- lipodermatosclerosis
106
What is lipodermatosclerosis?
107
What is the term for 'fibrosing inflammationg of subcut tissue in the lower leg, secondary to chronic venous hypertension'?
lipodermatosclerosis
108
What are risk factors for varicose veins?
109
In regards to the management of varicose veins, what are the following:
1. conservative management
2. interventional management
3. surgical management
110
What is a DVT?
What is Virchow's Triad? What can cause each aspect of this triad?
stasis
- prolonged immobility
- HF
- pregnancy
- obesity
endothelial injury
- trauma
- surgery
-CVCs
- previous DVT
- smoking
hypercoagulability
- inherited e.g factor V leiden, protein C/S deficiency
- acquired e.g malignancy, pregnancy
- dehydration
111
List the signs and symptoms for DVTs.
112
How do you manage DVTs?
(diagnosis, lifestyle, treatment)
Med Term 3
flashcards
Decks in class (44)
# Cards
-
HPD 154
-
HPD 272
-
HPD 343
-
HDP 4 and 5101
-
HPD 6 and 7100
-
HDP 8 and 970
-
HSD 10 and 1184
-
HSD 11.265
-
Urinary System 1140
-
Urinary 2112
-
Urinary 368
-
Urinary 463
-
Urinary 551
-
Urinary 697
-
Urinary 789
-
Urinary 8137
-
Urinary 963
-
Urinary 1066
-
CVS 1129
-
CVS 294
-
CVS 390
-
CVS 465
-
CVS 589
-
CVS 6141
-
CVS 7112
-
CVS 8106
-
CVS 986
-
CVS 1063
-
CVS 1181
-
Respiratory 1132
-
Respiratory 2135
-
Respiratory 3115
-
Respiratory 480
-
Respiratory 5156
-
Respiratory 672
-
Respiratory 771
-
Respiratory 876
-
Respiratory 9112
-
Respiratory 10103
-
Respiratory 11117
-
OSCE practise15
-
ECGs117
-
PASSMED10
-
TERM 3 REVISION737
