Cardiology Flashcards
1
Q
betaRisk factors for Atherosclerosis
A
Tobacco Smoking (nicotine damages endothelial cells)
High Serum Cholesterol (LDL)
Obesity
Diabetes
Hypertension
Male - no oestrogen which is cardioprotective.
2
Q
Where are atherosclerotic plaques more likely to occur?
A
Areas of high turbulence
Bifurcations, aortic arch.
3
Q
Components of atherosclerotic plaque
A
Lipid, necrotic core, connective tissue, fibrous cap.
4
Q
What arterial layer can can thin during atherosclerosis?
A
Tunica media
5
Q
Pathogenesis of atherosclerosis
A
Endothelial cell damage causes increased expression of cell adhesion molecules and increased lipid permeability to lipids such as LDL.
This results in the deposition of inflammatory cells and lipids in the tunica intima.
Inflammatory cytokine release causes more cells to migrate and deposit.
Foam cells that take up these lipids apoptose and spill lipid contents to further enlarge plaque.
Growth factor release such as platelet derived growth factor stimulate proliferation of smooth muscle cells, collagen etc to form the fibrous cap.
The initial enlargement causes microthrombotic events to occur resulting in more and more plaque buildup and arterial stenosis.
6
Q
What are the stages of atherosclerotic plaque formation?
A
Fatty Streaks
Intermediate Lesions
Advanced Lesions/Fibrous Plaques
Plaque Rupture/Plaque Erosion
7
Q
What are some cytokines found in atherosclerotic plaques?
A
IL-1,6,8
IFN-gamma
8
Q
Features of fatty streaks
A
Composed of lipid-laden macrophages & T-cells.
Can occur in people less than 10 years old.
9
Q
Features of intermediate lesions
A
Presence of smooth muscle cells and platelet aggregation.
10
Q
Features of advanced lesions
A
Covered by dense fibrous cap
Prone to rupture and calcification
11
Q
What happens during plaque ruptures?
A
Weakening of fibrous cap can cause plaque ruptures and cause collagen exposure and tissue factor release.
12
Q
Consequence of plaque rupture?
A
Can result in thrombosis causing stenosis and coronary syndromes.
13
Q
How is plaque erosion different to plaque rupture?
A
Occurs in earlier stage plaques having a smaller lipid core.
Larger lumen remaining.
14
Q
What thrombus is formed in plaque erosion?
A
White thrombus
15
Q
What thrombus is formed in plaque rupture?
A
Red thrombus
16
Q
Management of coronary atherosclerosis
A
Percutaneous coronary intervention (PCI)
17
Q
Limitation of PCI
A
Risk of re-stenosis
18
Q
How can re-stenosis be prevented?
A
Usage of drug eluting stents.
19
Q
What are coronary artery stents normally made of?
A
Stainless steel.
20
Q
What is angina?
A
Mismatch of oxygen demand and blood supply causing ischaemia and pain.
21
Q
What are some ‘low supply’ exacerbating factors of angina?
A
Anaemia
Hypothermia
Hypoxia
Polycythaemia
22
Q
What are some ‘high demand’ exacerbating factors of angina?
A
Hyperthyroidism
Hypertrophic cardiomyopathy
23
Q
Causes of myocardial ischaemia?
A
Impairment of blood flow e.g proximal arterial stenosis
Increased distal resistance e.gg left ventricular hypertrophy
Reduced oxygen-carrying capacity of blood e.g anaemia
24
Q
How much stenosis can occur before presenting symptoms?
A
70% stenosis.
25
What are the different types of angina?
Stable angina
Crescendo angina
Unstable angina
Prinzmental's angina
Microvascular angina
26
What is stable angina?
Pain upon exertion, not at rest.
27
What is crescendo angina?
Increasing angina over time.
28
What is unstable angina?
Acute onset of pain upon exertion and at rest.
29
What is prinzmental's angina?
Angina due to coronary artery spasm.
30
What is microvascular angina?
Angina with normal coronary arteries.
31
Non-modifiable risk factors for atherosclerosis
Increasing age
Male gender
Family history
32
What is the gold standard investigation for angina?
CT coronary angiogram
33
What are other investigations for stable angina?
ECG
CT coronary angiography
Stress echo
Exercise testing
Myoview scan
34
Lifestyle management of stable angina
Smoking cessation
Exercise
Low cholesterol diet
35
First-line pharmacological treatment for stable angina
Short-acting nitrates e.g GTN spray.
Beta blockers or CCB if contraindicatred.
36
Pharmacodynamics of nitrates
Cause venodilation to reduce preload.
37
Pharmacodynacmics of beta blockers
Prevent activation of B1 adrenergic receptors causing a negative chronotropic and ionotropic effect.
38
What other drugs are used to treat stable angina?
Calcium channel blockers e.g amlodipine
ACE inhibitors e.g ramipril
Statins e.g atorvastatin
NSAIDs e.g aspirin
39
Side effects of nitrates
Headaches due to sudden hypotension.
40
Side effects of beta blockers
Erectile dysfunction, bradycardia, cold extremities, nightmares, headache, fatigue.
41
Pharmacodynamics of calcium channel blockers
Block L-type calcium channels in cardiac and vascular smooth muscle, lowering BP and causing a negative chronotropic + ionotropic effect.
42
Side effects of calcium channel blockers
Postural hypotension, ankle swelling, flushing
43
Contraindications of beta blockers
Asthmatics, heart block, heart failure, bradycardia, PVD
44
Pharmacodynamics of aspirin
Inhibits cyclo-oxygenase 1
This inhibits prostaglandin and thromboxane A2 production.
Prevents platelet aggregation, is anti inflammatory, antipyretic, analgesic.
45
Side effects of aspirin
Gastric ulcers
46
Pharmacodynamics of statins
Inhibits HMG- CoA reductase, the rate limiting enzyme in cholesterol synthesis pathway.
47
Pharmacodynamics of ACE inhibitors
Inhibits angiotensin converting enzyme which converts angiotensin I to II.
Prevents rise in blood pressure.
48
Interventional management of stable angina.
Percutaenous coronary intervention or coronary artery bypass graft.
49
What are potential graft sources for CABG?
Left internal mammary artery for LAD graft.
Long saphenous vein can be used for RCA graft.
50
Side effects of statins
Headache, dizziness, myalgia.
51
Side effects of ACE inhibitors
Hypotension - over
Acute renal failure due to lack of efferent arteriole constriction to reduce glomerular filtration.
Hyperkalaemia - effect of too little aldosterone due to RAAS.
Teratogenic effects in pregnancy - can cause foetal abnormalities.
ACEi can cause increased bradykinin levels.
Dry cough, rash, anaphylactoid reactions.
52
What is an acute coronary syndrome?
A spectrum of acute cardiac conditions from unstable angina to varying degrees of myocardial infarctions.
53
Investigation for unstable angina
ECG
Serum troponin
54
What can the ECG show in unstable angina?
ST depression
T-wave inversion
55
What will the serum troponin I levels look like in unstable angina?
Non-elevated.
56
What are the 5 types of myocardial infarction?
Type 1: MI with ischaemia (due to primary coronary event e.g atherosclerotic rupture)
Type 2: MI secondary to ischaemia (due to increased oxygen demand e.g anaemia, coronary spasm)
Type 3: Diagnosis of MI in sudden cardiac death.
Type 4a: MI related to PCI
Type 4b: MI related to stent thrombosing
Type 5: MI related to CABG
57
What are the ECG related classifcations of a myocardial infarction?
NSTEMI (non-ST elevated myocardial infarction)
STEMI (ST-elevated myocardial infarction)
58
Clinical presentation of myocardial infarction
Unremitting central chest pain
Usually severe but may be mild/absent.
Can radiate to jaw/shoulder.
Occurs at rest.
Associated with sweating, dyspnoea, nausea, vomiting.
One third occur in bed at night.
59
Pathophysiology of STEMI
Full occlusion causes transmural (full thickness) infarction.
60
Investigation of STEMI
ECG - elevated S-T segment and subsequent pathologic Q-wave formation.
Raised serum troponin and creatinine kinase MB
(CK-MB)
61
Pathophysiology of NSTEMI
Can be caused by partial stenosis of major artery/complete occlusion of minor artery.
Causes partial thickness damage - subendocardial infarct
62
Pathophysiology of NSTEMI
Can be caused by partial stenosis of major artery/complete occlusion of minor artery.
Causes partial thickness damage - subendocardial infarct
63
Investigation of NSTEMI
ECG - ST-segment depression, T-wave inversion.
Raised troponin and CK-MB.
64
First line management of ACS
Loading dose of Aspirin 300mg + P2Y12 inhibitor e.g clopidogrel.
Morphine if in severe pain
Oxygen if hypoxic (<94%)
Nitrates for angina pain relief
If ST elevation/raised troponin, refer for PCI.
65
What is the clinical significance of troponin?
Troponins are involved in cardiac excitation contraction coupling.
They are released into the circualtion during mycardial injury and so are a good blood marker.
66
What are some non-ACS causes for raised troponin?
Gram negative sepsis.
Pulmonary embolism.
Myocarditis.
Heart failure
Arrhythmias.
67
What is the secondary treatment of ACS?
Dual antiplatelet therapy
Glycoprotein II/bIIIa antagonists
Antithrombins
68
Pharmacodynamics of P2Y12 antagonists.
Prevents ADP binding to P2Y12 receptors on platelets, inhibiting further platelet activation and aggregation.
69
Examples of P2Y12 antagonists
Clopidogrel, ticagrelor, prasugrel
70
Side effects of P2Y12 antagonists.
Bleeding.
Rash
Diarrhoea
71
Pharmacodynamics of glycoprotein IIb/IIIa antagonists
Inhibits the action of glycoprotein IIb/IIIa which binds fibrinogen and vWF to facilitate platelet aggregation.
72
Examples of glycoprotein IIb/IIIa antagonists
Abciximab, tirofiban
73
Side effects of glycoprotein IIb/IIIa antagonists
Increased bleeding
74
What situations are glycoprotein IIb/IIIa antagonists mainly used for?
In patients with heavey thrombotic burden undergoing PCI.
75
What does dual antiplatelet therapy consist of?
Aspirin + P2Y12 inhibitor.
76
Examples of antithrombins
Unfractionated heparin, enoxaparin (low molecular weight heparin), bivalirudin, fondaparinux.
77
Pharmacodynamics of heparin
Binds to antithrombin III protein which degrades thrombin in the clotting cascade.
78
Pharmacodynamics of bivalirudin
Direct thrombin inhibitor, binds reversibly to thrombin.
79
Pharmacodynamics of fondaparinux
Selectively binds to antithrombin, increasing its activity in inactivating factor Xa to prevent clotting.
80
When is fondaparinux usually used?
Before coronary angiography in unstable angina/NSTEMI.
81
Positives of PCI
Less invasive
More convenient
Repeatable
82
Negatives of PCI
Re-stenosis risk
Stent thrombosis risk
Not applicable for more complex disease
83
Positives of CABG
Good prognosis after surgery
Can resolve complex pathology.
84
Negatives of CABG
Very invasive.
Longer recovery time
Increased risk of stroke
85
What is the rate of the SA node?
60-100 bpm.
86
What is the rate of the AV node?
40-60 bpm
87
What is the rate of ventricular cells?
20-25 bpm
88
At what speed are EKGs calibrated?
Recorded at speed of 25mm/sec
89
How are EKGs vertically calibrated?
1 mm = 0.1mV
90
What does a positive deflection mean?
Impulse is traveling towards the electrode.
91
What does 1 small square horizontally mean on an ECG?
0.04 sec
92
What does 1 large square horizontally mean on an ECG?
0.20 sec
93
What does 1 large square vertically mean on an ECG?
0.5 mV
94
What voltage do bipolar leads measure?
Voltage between 2 different points on the body
95
What voltage do unipolar leads measure?
Voltage between 1 point on the body and a virtual point with 0 electrical potential located in the center of the heart.
96
What are the leads in an 12 Lead ECG
3 limb leads
6 chest leads
3 augmented leads
97
Where does lead I of an ECG go?
Right arm (-) to left arm (+)
98
Where does lead 2 of an ECG go?
Right arm (-) to left leg (+)
99
Where does lead 3 of an ECG go?
Left arm (-) to left leg (+)
100
What angle is lead 1 in?
0 degrees (right horizontal line)
101
What angle is lead II in?
60 degrees (below 0 degrees)
102
What angle is lead 3 in?
120 degrees (below and left from 0 degrees)
103
Where is lead aVR placed?
Right shoulder
104
Where is lead aVF placed?
Left leg
105
Where is lead aVL placed?
Left arm
106
Which intercostal space are the V1-V3 chest leads placed in?
4th intercostal space.
107
Which lead is to the right of the sternum?
V1
108
What angle is lead avR
-150 degrees (up and left from 0 degrees)
109
What angle is lead avF
90 degrees (perpendicular and below 0 degrees)
110
What angle is lead avL
-30 (up from 0 degrees)
111
Which ECG leads are unipolar?
Augmented and chest leads.
112
Which ECG leads are bipolar?
Limb leads.
113
What is Einthoven's triangle?
An imaginary triangle formed by all 3 limb leads.
114
Which intercostal space are the V4-V6 leads placed in?
5th intercostal space.
115
Which leads measure activity of the septum?
V1-V2
116
Which leads measure activity of the anterior portion of the heart?
V1-V4
117
Which leads measure activity of the lateral portion of the heart?
V5-V6, I, aVL
118
Which leads measure activity of the inferior portion of the heart?
II, III, avF
119
What does the P-wave symbolise?
Atrial depolarization
120
In which leads is the P-wave always positive?
Leads I, II, V2-V6
121
What is the expected duration of P-waves?
<3 small squares (<0.12 sec)
122
What is the expected amplitude of P-waves?
<3 small squares
123
Which lead are P-waves best seen in?
Lead II
124
What are tall, pointed P-waves (P-pulmonale) an indication of?
Right atrial enlargement.
125
What are M-shaped, biphasic P-waves (P-mitrale) an indication of?
Left atrial enlargement.
126
In which lead are P-waves commonly biphasic NORMALLY?
V1
127
What is a potential cause for right atrial enlargement?
Pulmonary hypertension causing right sided hypertrophy resulting in taller P-waves.
128
What is indicated by the P-R interval?
Time taken between atrial depolarization and ventricular depolarization, time taken for electrical activation to get through AV node.
129
What is the normal P-R interval duration?
0.12-0.20 sec (3-5 little squares)
130
Cause for short P-R interval
Wolff-Parkinson-White syndrome
131
Cause for long P-R interval
First degree heart block.
132
What does the QRS complex indicate?
Ventricular depolarization.
133
What is the normal duration for a QRS complex?
<0.12 sec
134
How does a pathological Q-wave look?
Greater than 1 smal square wide, or greater than 25% amplitude of subsequent R-wave.
135
In which leads should the QRS complex be dominantly upright?
I and II.
136
In which leads must the R-wave grow?
V1-V4.
137
In which leads must the S-wave grow?
V1-V3
138
In which leads will the S-waves become smaller and finally disappear?
V4-V6.
139
Why do the R-waves grow from V1-V4?
Left ventricle depolarization is detected more as you progress from V1-V4.
140
How would left ventricular hypertrophy look on lead V1?
Large S-waves, small R-waves.
141
How would left ventricular hypertrophy look on lead V6?
Large R-waves, small/non-existent S-wave.
142
How would right ventricular hypertrophy look on lead V1?
Dominant R wave
143
How would right ventricular hypertrophy look on lead V6?
Large S-wave.
144
What does the ST segment indicate?
Time between ventricular depolarization and repolarization.
145
What is the appearance of a normal ST-segment?
Flat (isoelectric)
146
In which leads is there NORMAL ST elevation/depression?
V1 & V2.
147
What is the J-point?
The junction point between the QRS complex and ST segment.
148
What can ST elevation indicate?
STEMI
Pericarditis - saddle shaped
149
What could ST depression indicate?
NSTEMI, possible unstable angina.
150
How does the septum depolarize normally?
Left side first then goes to right side of septum.
151
What causes the R-wave in V1?
Septal depolarization. Depolarization from left to right causes the current to approach the lead.
152
What causes the Q-wave in V6?
Left to right septal depolarization causes current to go away from the lead.
153
Why does V1 have a deep S wave and V6 have a high R-wave?
Effect of left ventrcle depolarization is greater so current goes away from V1 and towards V6.
154
What happens during right bundle branch block?
Delayed right ventricular depolarization.
155
What does delayed right ventricular depolarization cause
A second R-wave in V1.
156
What does right bundle branch block look like on an ECG?
M-like QRS in V1 and W-like QRS in V6.
157
What happens in left bundle branch block?
Delayed left ventricular depolarization
Right to left septal depolarization.
158
What is the appearance of left bundle branch block on an ECG?
W-like V1 and M-like V6.
159
What causes the Q-wave in V1 and the initial R-wave in V6 in left bundle branch block?
Right to left septal depolarization.
160
What causes the R-wave in V1 and the S-wave in V6 during left bundle branch block?
Right ventricular depolarization.
161
What causes the S-wave in V1 and second R-wave in V6 during left bundle branch block?
Left ventricular depolarization.
162
What does the T-wave indicate?
Ventricular repolarization.
163
How are T-waves normally oriented?
Same orientation as the QRS complex.
164
In which leads should T waves be upright?
I, II, V2-V6
165
How should the T wave amplitude be?
Less than 2/3 of the R wave.
166
What are some characeristics of abnormal T-waves?
Symmetrical, tall, peaked, inverted.
167
When can T-wave inversion occur?
NSTEMI.
168
What does the QT interval indicate?
Duration of ventricular repolarization and depolarization.
169
What is the normal duration of the QT interval.
0.35-0.45 sec (9-11 small squares)
Should not be more than half of R-R interval.
170
What happens to the QT interval when heart rate increases?
It decreases.
171
What lead is the QT interval normally measured in?
aVL.
172
What do U waves represent?
Afterdepolarizations which occur after repolarization.
173
What leads are U waves seen in?
Lead II.
174
What is the orientation of U waves?
Same as T waves.
175
When are U waves more prominent?
During slower heart rates.
176
In what lead is all the waves inverted?
Lead aVR.
177
What are the 2 methods used to determine heart rate on an ECG?
Rule of 300
10 second rule
178
What is the rule of 300?
Dividing 300 by the number of big squares between 2 QRS complexes.
179
What is the 10 second rule?
Since ECGs are printed for 10 second durations, counting the number of QRS complexes (beats) and multiplying by 6 gives HR.
180
What is the normal QRS axis range?
-30 to 90 degrees.
181
What is meant by left axis deviation?
If the axis is deviated to -30 to -90 degrees.
182
What is meant by right axis deviation?
If the axis is deviated to +90 to +180 degrees.
183
What are 2 methods of determining the QRS axis?
Equiphasic approach
4 quadrant approach
184
What is the quadrant approach?
Look at leads I and avF
Determine if the QRS complex is predominantly positive or negative
185
What happens if both leads are positive?
The QRS axis is normal
186
What happens if lead I is positive and aVF is negative?
There is left axis deviation.
187
What happens if lead I is negative and aVF is positive?
There is right axis deviation.
188
What happens if both are negative?
The axis is indeterminate.
189
What is the equiphasic approach?
Determine limb lead with most equiphasic QRS complex.
Find lead 90 degrees to it.
190
What is pericarditis?
inflammatory pericardial syndrome with or without effusion.
191
Epidemiology of pericarditis
80-90% is idiopathic.
Seasonal with viral trends.
192
General aetiology of pericarditis
Viral infection
Bacterial infection
Malignancy
Autoimmune
Metabolic
Trauma
Iatrogenic
Post-MI
193
What viruses can cause pericarditis?
Coxsackieviruses, enteroviruses, adenoviruses, herpesvirues (EBV, CMV, HHV-6), parvovirus-B09
194
What bacteria can cause pericarditis?
Haemophilus influenzae
Mycobacterium tuberculosis
195
Metastasis from what cancers commonly causes pericarditis?
Lung + breast carcinomas, lymphomas.
196
What are some autoimmune causes of pericarditis?
Rheumatoid arthritis, lupus, sjogren syndrome.
197
What are some metabolic causes of pericarditis
Uraemia, myxoedema
198
What are some traumatic causes of pericarditis?
Penetrating thoracic injury, oesophageal perforation, radiation.
199
What are some iatrogenic causes of pericarditis?
PCI, pacemaker insertion.
200
Clinical presentation of pericarditis
Chest pain
Hiccups - phrenic nerve irritation
Dyspnoea
201
What is the nature of chest pain for pericarditis?
Pleuritic chest pain
Exacerbated when lying down and upon inspiration
Releived when sitting forwards
Radiates to trapezius ridge
202
What is expected upon examination of a patient with pericarditis?
Pericardial rub - crunching sound near 2nd heart sound
Pericardial effusion
203
What can pericardial effusion result in?
Cardiac tamponade.
204
What is the clinical presentation of cardiac tamponade?
Beck's triad
Pulsus paradoxus
205
What are the components of Beck's triad?
Hypotension, distended neck veins (elevated JVP), muffled heart sounds.
206
What is pulsus paradoxus?
Normally, fall of systolic BP by <10mmHg during inspiration.
In pulsus paradoxus, this fall is >10mmHg during inspiration.
207
Investigation of pericarditis
ECG,
FBC, ESR, troponin
CXR
208
What does pericarditis show on an ECG?
Widespread addle shaped ST-elevation, PR depression
209
What will be expected in the FBC & ESR with pericarditis?
Raised leukocytes & ESR.
210
What would a raised troponin in pericarditis suggest?
Myopericarditis.
211
What could be seen in a CXR with pericarditis?
Cardiac silhouette enlargement could be a sign of pericardial effusion. Needs to be ruled out.
212
Management of pericarditis
Sedentary activity until resolution of symptoms and normal ECG/labs.
750-1000mg aspirin/600-800mg ibuprofen TDS 1-2 weeks
Along with Colchine 0.5 mg BD for 3 months.
213
What is colchine?
Anti-gout agent which is anti-inflammatory.
214
What are the 4 types of cardiomyopathy?
Dilated cardiomyopathy, hypertrophic cardiomyopathy, arrythmogenic cardiomyopathy, restrictive cardiomyopathy.
215
Aetiology of Hypertrophic Cardiomyopathy
Mutations in genes encoding for sarcomere proteins.
Myosin binding protein C, B-myosin heavy chain.
216
Pathophysiology of Hypertrophic Cardiomyopathy
Primary hypertrophy of the heart.
Causes high ejection fraction
Diastolic dysfunction due to low ventricular compliance.
Mycoyte and myofibril disarray
217
What can be obstruced in hypertrophic cardiomyopathy?
Left ventricle outflow tract
218
What causes LVOO in hypertrophic caridomyopathy?
Systolic anterior motion of mitral valve
Assymetric septal hypertrophy.
219
Clinical Presentation of Hypertrophic Cardiomyopathy
Syncope upon exertion
Angina
Dyspnoea
Palpitations
220
Investigation of Hypertrophic Cardiomyopathy
ECG
Echocardiography diagnostic
221
What can an ECG show with HC?
T-wave inversion
Ventricular tachycardia
Deep S-waves in V1 and large R-waves in V6 due to LVH.
222
What can an echocardiogram show with hypertrophic cardiomyopathy?
Assymetric LV hypertrophy.
Mitral valve anterior systolic motion, vigorously contracting LV.
223
Management of hypertrophic cardiomyopathy
Cessation of high-intensity athletics
Use of β-blocker or non-dihydropyridine CCBs (eg, verapamil).
ICD (implantable cardioverter defibrillator) insertion
224
What type of drugs should be avoided with HC?
Avoid drugs that decrease preload (eg, diuretics, vasodilators).
225
What are the 2 types of dilated cardiomyopathy?
Familial and sporadic
226
Aetiology of familial dilated cardiomyopathy
Cytoskeleton proteins mutations such as TTN which codes for titin protein
227
Aetiology of sporadic dilated cardiomyopathy
Coxsackievirus
Haemochromatosis
Sarcoidosis
Ischaemia
Cocaine
228
Pathophysiology of Dilated Cardiomyopathy
Dilation of ventricular chambers
Causes systolic dysfunction, poor contraction & heart failure.
229
Clinical Presentation of Dilated Cardiomyopathy
Heart failure
Arrhythmias
Oedema
230
Investigation of dilated cardiomyopathy
ECG
Echocardiogram
231
What can an ECG show with DC?
Arrythmias
Sinus tachycardia
232
What can can echocardiogram show with DC?
LV + RV dilation (thin walls) with poor contraction.
233
Management of dilated cardiomyopathy
Standard heart failure treatment.
Na+ restriction
ACE inhibitors/ARBs,
β-blockers, diuretics, mineralocorticoid
receptor blockers (eg, spironolactone), digoxin
ICD, heart transplant.
234
Aetiology of Arrythmogenic Cardiomyopathy
AD mutations in genes coding for desmosomes.
Naxos syndrome, Carvajal’s syndrome (recessive forms)
235
Pathophysiology of Arrhythmogenic Cardiomyopathy
Atrophy of mainly right ventricular myocardium.
Replaced by fibrous-fatty tissue.
236
Clinical Presentation of Arrhythmogenic Cardiomyopathy
Ventricular arrhythmias
Syncope
Sudden death
237
Investigation of Arrythmogenic Cardiomyopathy
ECG
238
What can an ECG show in arrythmogenic cardiomyopathy?
Epsilon waves after QRS complex
T-wave inversion in V1-V3 since they look at right ventricle.
239
Management of Arrhythmogenic Cardiomyopathy
Beta blockers e.g bisporolol, metoprolol.
K+ channel blockers e.g Amiodarone, sotalol - symptomatic
ICD for refractory, life threatening arrhythmias.
240
Aetiology of restrictive cardiomyopathy
Post-radiation fibrosis
Loffler's endocarditis
Endomyocardial fibrosis
Amyloidosis
Sarcoidosis
Haemochromatosis
241
Pathophysiology of Restrictive Cardiomyopathy
Bi-atrial enlargement with decreased ventricular volume.
Impaired ventricular filling (diastole).
242
Clinical Presentation of Restrictive Cardiomyopathy
Dyspnoea, Fatigue
243
Examination of Restrictive Cardiomyopathy
Freidrich’s sign
Kussmaul’s sign
244
What is Freidrich's sign?
Elevated JVP with diastolic collapse.
245
What is Kussmaul's sign?
Increase in venous pressure upon inspiration
246
Investigation of Restrictive Cardiomyopathy
ECG
247
Management of Restrictive Cardiomyopathy
Manage the heart failure and potential embolisation
248
What are the inherited arrhythmias?
Long QT syndrome
Brugada syndrome
Catecholaminergic Polymorphic VT (CPVT)
Wolff-Parkinsone White syndrome
Progressive conduction disease
Idiopathic ventricular fibrillation
249
Aetiology of inherited arrythmias
Channelopathies - mutations in channel proteins.
250
Aetiology of long QT syndrome
Caused by mutations of KCNQ1 a potassium channel protein.
Congenital: Romano-Ward syndrome
Jervell and Lange-Nielsen syndrome
Acquired: Hypocalcaemia, Amiodarone, MI.
251
Features of Romano-Ward syndrome
Autosomal dominant, no deafness.
252
Features of Jervell and Lange-Nielsen syndrome
Autosomal recessive, sensorineural deafness.
253
Pathophysiology of long-QT syndrome
Problems with repolarization.
254
Aetiology of Brugada syndrome
Autosomal dominant loss of function mutation of Na+ channels.
255
How would Brugada syndrome look on an ECG?
Pseudo right bundle branch block and ST-segment elevations in leads V1-V2 on ECG.
256
Aetiology of Marfan’s Syndrome
Autosomal dominant FBN1 gene mutation on chromosome 15 affecting fibrillin-1 protein.
257
Pathophysiology of Marfan’s Syndrome
FIbrillin-1 is a glycoprotein that forms a sheath around elastin and sequesters TGF-β, a growth factor for connective tissue.
Lack of connective tissue structure and growth.
258
Clinical Presentation of Marfan’s Syndrome
Very tall, lanky people
Armspan greater than chest
Chest wall deformity
Tendency to have aortic dilation at the root
259
Why does aortic root dilation occur in Marfan's syndrome?
Because more fibrillin is present there since the energy of ventricular contraction is applied there.
260
What are examples of chest wall deformities that can occur with Marfan's syndrome?
Pectus carinatum (pigeon chest)
Pectus excavatum (deep indentation at and around sternum)
261
Pathophysiology of familial hypercholesterolism
Decreased LDL signalling due to cholesterol regulatory protein mutatations.
262
What is an example of a protein that can be mutated to cause familial hypercholestrolism?
PCSK9
263
Clinical Presentation of FH
Cholesterol deposits in eyes and skin.
264
What is the source of oxygen for a foetus inside a mother's womb?
Placenta
265
What vessels carry oxygenated blood from the placenta?
Umbilical veins
266
Where does the umbilical vein lead?
Liver
267
What is the foetal shunt present in the liver and what does it do?
Ductus venosus, shunts oxygenated blood into the IVC
268
What shunt does the blood from the IVC go to once it reaches the heart?
Foramen ovale
269
What does the foramen ovale do?
Shunts blood from right to left atrium.
270
What vessel does deoxygenated blood pass through to recieve placental oxygen?
Umbilical arteries.
271
What happens to the blood entering the RA from the SVC?
2/3 gets shunted to the LA, 1/3 enters the RV
272
What shunt is present at the pulmonary artery?
Ductus arteriosus
273
What is the function of the ductus arteriosus?
Shunts blood from pulmonary artery into aorta, away from the lungs.
274
What is a ventricular septal defect?
Abnormal connection between the two ventricles
275
What type of a shunt is in a VSD?
Left to right shunt.
276
Why does blood flow from the left to right ventricle?
LV is at higher pressure.
277
What happens as a result of a VSD?
Increased pulmonary artery blood pressure.
278
What can happen with a small VSD?
Small increase in pulmonary blood flow only
Risk of endocarditis.
279
What can happen with a large VSD?
Very high pulmonary blood flow in infancy
Can lead to irreversible pulmonary hypertension due to Eisenmanger's syndrome.
280
Pathophysiology of Eisenmanger's syndrome
High pressure pulmonary blood flow causes pulmonary vessel remodeling and increased pulmonary resistance.
This causes increase in RV pressure.
At a point, RV pressure can become suprasystemic (>LV).
The shunt direction reverses causing deoxygenated blood to be pumped out.
281
What are some consequences of Eisenmanger's syndrome
Cyanosis
Irreversible pulmonary hypertension.
282
Clinical presentation of a small VSD
Asymptomatic
Loud pan-systolic murmur
283
Clinical presentation of a large VSD
Small, skinny baby
Can be cyanosed and have signs of clubbing.
Increased respiratory rate
Tachycardia
284
What can be heard upon examination of a baby with a small VSD?
Pan-systolic murmur
285
Investigation of large VSD
Left heart dilation/cardiomegaly on CXR
Echocardiogram
286
Managment of VSD
Surgical repair.
287
What are 3 types of atrial septal defects?
Ostium secundum defects
Patent forman ovale
Ostium primum defects
288
What is the shunt direction in ASD?
Left to right
289
Pathophysiology of a large ASD
Significant increased flow through the right heart and lungs in childhood
Right heart dilation
290
Pathophysiology of a small ASD
Only a small increase in blood flow.
No right heart dilation
291
Clinical signs of a large ASD
Dyspnoea upon exertion
Increased chest infections
292
Clinical signs of a small ASD
Asymptomatic
293
Examination of a large ASD
Systolic ejection murmur
Fixed, split S2 due to (delayed closure of PV because more blood has to get out)
294
Investigation of a large ASD
X-ray: Large pulmonary arteries and cardiomegaly
Echocardiogram
295
Management of ASD
Surgical closure or percutaenous (interventional) closure.
Perctutaneous Mainly for secundum defects.
296
What is a patent ductus arteriosus?
When ductus arteriosus remains open.
297
Pathophysiology of PDA
Due to increased aortic pressure after birth, some blood flows from aorta to PA during systole.
Can cause increased pulmonary hypertension and lead to Eisenmenger's syndrome if left untreated.
298
What is the shunt direction in PDA?
Left to right shunt
299
Clinical presentation of large PDA
Machinery like murmur
Dyspnoea
Central cyanosis (ES)
Toe clubbing (ES)
300
Management of PDA
Surgical closure.
301
What genetic condition is associated with atrioventricular septal defects?
Trisomy 21.
302
What is an atrioventricular septal defect?
Defect that involves the interatrial + invterentricular septum and the tricuspid and mitral valves.
303
Pathophysiology of AVSD
Can result in a common atrioventricular valve.
Can result in high pulmonary blood flow.
304
Clinical presentation of a complete AVSD
Breathless as neonate
Poor weight gain
Poor feeding
305
Clinical presentation of a partial AVSD
Can present in adulthood
Can present as if small ASD/VSD
306
Management of AVSD
Needs repair or PA band in infancy
307
What is icoarctation of the aorta and what condition is associated with it?
Narrowing of the aorta at the site of insertion of the ductus arteriosus.
Turner's syndrome
308
Pathophysiology of severe aortic coarctation
Complete or almost complete obstruction to aortic flow
Can cause heart failure
Blood gets diverted through aortic arch and upper body.
With age, intercostal arteries enlarge in order to provide collateral aortic circulation.
Associated with bicuspide aortic valve.
309
Clinical presentation of aortic coarctation
Higher blood pressure in arms vs legs
Weak pulse and radial-femoral pulse delay in lower extremities.
310
Examination of aortic coarctation
Scapular bruit upon auscultation - buzzes heard over scapulae
311
Investigation of aortic coarctation
CXR - notched ribs due to dilated intercostal vessels.
CT coronary angiogram
312
Management of aortic coarctation
Surgical repair
313
Complications of aortic coarctation
Hypertension
Subarachnoid haemhorrage (berry aneurysm)
Re-coarctation
Aneurysm formation and rupture.
Heart failure
314
What is the normal formation of the aortic valve?
Tricuspid
315
Pathophysiology of bicuspid aortic valves
Bicuspid valves generate turbulence and are not as efficient as tircuspid valves.
They can degenerate faster than normal valves.
Can become regurgitate quicker than normal valves.
Can cause ascending aortic aneurysms
316
What is pulmonary stenosis?
Narrowing of the right ventricular outflow tract
317
What are the types of pulmonary stenosis?
Valvular, sub valvular and supravalvular.
318
Pathophysiology of severe pulmonary stenosis
Right ventricular failure as neonate
Poor pulmonary blood flow
RV hypertrophy
Tricuspid regurgitation
319
Pathophysiology of mild pulmonary stenosis
RV hypertrophy mainly
320
Management of pulmonary stenosis
Balloon valvuloplasty
Open valvotomy
Open trans-annular patch
Shunt (to bypass the blockage)
321
Aetiology of tetralogy of Fallot
Caused by anterosuperior displacement of the
infundibular septum which separates right and left ventricular outflow tracts.
322
Components of tetralogy of Fallot
Pulmonary stenosis
Right ventricular hypertrophy (as a response to pulmonary stenosis)
Ventricular septal defect
Overriding aorta
323
Pathophysiology of tetralogy of Fallot
Pulmonary stenosis causes suprasystemic RV pressure
Results in RV hypertrophy
There is right-left shunting through the VSD.
324
Clinical presentation of tetralogy of Fallot
Early cyanosis of babies.
325
Investigation of tetralogy of Fallot
Boot shaped heart on CXR.
326
Management of tetralogy of Fallot
Surgery to reopen the RVOT and patching of the VSD.
327
What can cause right to left shunts?
1. Truncus arteriosus (1 vessel)
2. Transposition (2 switched vessels)
3. Tricuspid atresia (3 = Tri)
4. Tetralogy of Fallot (4 = Tetra)
5. TAPVR (5 letters in the name)
328
What type of shunt can result in Eisenmenger's syndrome?
Untreated left to right shunts.
329
What conditions have left to right shunts?
VSD, ASD, PDA
330
What physical activity can be used to relieve cyanosis?
Squatting, it increases PVR and reduces efficiency of righ to left shunt.
331
What is a univentricular heart?
Heart with only 1 ventricle.
332
Aetiology/risk factors for secondary hypertension
ROPE
Renal disese
Obesity
Pregnancy
Endocrine - hyperaldosteronism, cushing's
High salt diet
Increasing age
Male gender
333
Classification of hypertension
No hypertension: <135/85
Stage 1: 135/85
Stage 2:150/95
334
Types of BP measurement methods
Office/surgery measurement
Ambulatory measurement
At home self-measurement
335
What is malignant hypertension?
Sudden onset of high BP that can cause end organ damage.
336
Clinical presentation of malignant hypertension
Retinal haemhorrages.
337
Complications of hypertension
Ischaemic heart disease (MI)
Heart failure
Kidney failure/CKD
Stroke
Dementia
PVD
338
Treatment Thresholds for HTN
For patients at low CV risk, treatment started if above 160/100 mmHg.
For patients at high CV risk, treatment started if above 140/90 mmHg.
Treatment will be lifelong.
339
Target range for BP treatment
Routine : <14/90
Prev. stroke: <130/80
Heavy proteinuria: <130/80
CKD & diabetes: <130/80
Older patients: <150/90
340
Why is the BP threshold for older patients higher?
If its too low then increased risk of falling over/collapse.
341
Lifestyle management for hypertension
Low salt diet.
Weight decrease.
Increased exercise.
Lower alcohol intake.
342
What is the first-line antihypertensive drug for patients under the age of 55 or diabetic?
ACE inhibitors e.g ramipril
OR ARB e.g candesartan
343
What is the first-line antihypertensive drug for non-diabetic patients above the age of 55 or of Afro-Carribean descent?
CCB ex. amlodipine, verapamil
344
What is the second line antihypertensive treatment?
If ACEi/ARB given first, add CCB.
If CCB given first, add ACEi/ARB
345
What is third line antihypertensive treatment?
Addition of a thiazide, ex. benzoflumethiazide, hydrochlorothiazide, indapamide.
346
Reasons for resistant hypertension despite treatment
Lack of drug concordance for patients.
Lifestyle changes like increased weight gain, drug usage.
Progression of underlying cause of HTN in secondary HTN.
347
General contraindication for antihypertensives
General anaesthesia - anaesthetics can cause hypotension, and antihypertensives can interfere with efforts to raise the BP to normal.
348
Drugs with side effects of increased HTN
NSAIDs
SNRI
Corticosteroids
Oestrogen containing oral contraceptives
Stimulants like methylphenidate
Anti anxiety drugs e.g gabapentin
Anti TNFs
349
What are the types of aortic stenosis?
Supravalvular
Subvalvular
Valvular
350
Congenital aetiology of aortic stenosis
Congenital aortic stenosis
Congenital bicuspide valve
351
Acquired aetiology of aortic stenosis
Degenerative calcification
Rheumatic heart disease
Congenital bicuspid valves
352
Pathophysiology of aortic stenosis
Increased ESV causes increased LV pressure and afterload.
Causes ventricular hypertrophy as a compensatory mechanism.
Long term stenosis can result in LV failure.
Reduced stroke volume.
353
Clinical Presentation of Aortic Stenosis
Exertional syncope
Exertional angina: (increased myocardial oxygen demand; demand/supply mismatch)
Exertional dyspnoea due to heart failure (systolic and diastolic)
354
Examination of aortic stenosis
Slow rising carotid pulse (pulsus tardus) & decreased pulse amplitude (pulsus parvus) - slow rising small volume pulse.
Soft or absent second heart sound since valve becomes rigid and doesnt move
S4 gallop due to LVH.
Crescendo-decrescendo jection systolic murmur radiating to carotids.
355
Investigation of aortic stenosis
CXR
ECG
Echocardiography
356
What would be expected on an X-ray for aortic stenosis?
Dilated ascending aorta
357
What could be seen on an ECG for aortic stenosis
ST-segment depression and T-wave inversion for leads orientated towards LV (I, aVL, V5-V6).
358
General management of aortic stenosis
Fastidious dental hygiene / care
Consider IE prophylaxis in dental procedures
359
What medication is contraindicated in aortic stenosis?
Vasodilators are relatively contraindicated in severe AS
360
Interventional management of aortic stenosis
Aortic valve replacement surgery
TAVI – Transcatheter Aortic Valve Implantation
361
What are the indications for interventional treatment of aortic stenosis?
Any SYMPTOMATIC patient with severe AS (includes symptoms with exercise)
Any patient with decreasing EF (<50%).
Any patient undergoing CABG
If asymptomatic but adverse features on exercise testing.
362
What is aortic regurgitation?
Leakage of blood from aorta into LV during diastole due to ineffective coaptation of the aortic cusps.
363
Aetiology of Aortic Regurgitation
Bicuspid aortic valve
Rheumatic fever
Infective endocarditis
Marfan's syndrome
364
Pathophysiology of Aortic Regurgitation
Combined pressure and volume overload
Compensatory Mechanisms: LV dilation, LVH.
Progressive dilation leads to heart failure
365
eExamination of Aortic Regurgitation
Early diastolic murmur
Austin flint murmur (apex) - low pitched late diastolic murmur.
Corrigan's pulse - bounding carotid pulses.
366
Investigation of aortic regurgitation
CXR: enlarged cardiac silhouette and aortic root enlargement
ECHO: Evaluation of the AV and aortic root with measurements of LV dimensions and function (cornerstone for decision making and follow up evaluation)
367
General management of aortic regurgitation
Consider IE prophylaxis
368
Medical management of aortic regurgitation
Vasodilators (ACEI’s potentially improve stroke volume and reduce regurgitation but indicated only in CCF or HTN
Serial Echocardiograms: to monitor progression.
369
Surgical management of aortic regurgitation
Valve replacement
370
Indication for surgery treatment of aortic regurgitation
ANY Symptoms at rest or exercise
Asymptomatic treatment if:
EF drops below 50% or LV becomes dilated > 50mm at end systole
371
What is mitral valve stenosis?
Obstruction of LV inflow that prevents proper filling during diastole
372
What is the normal mitral valve area?
4-6 cm^2
373
At what lower mitral valve area threshold do patients become symptomatic?
2 cm^2
374
Aetiolgy of mitral stenosis
Rheumatic heart disease
Infective endocarditis
Mitral annular calcification
375
Pathophysiology of Mitral Stenosis
To maintain CO, LA pressure is increased causing LA hypertrophy.
Results in PV, PA and RA pressure increasing.
Can cause hemoptysis through bronchial vessel rupturing due to increased pulmonary pressure.
376
Clinical Presentation of Mitral Stenosis
Progressive dyspnoea
Malar rash - pink/purple patches on cheeks due to vasoconstriction.
Jugular venous distension
Palpitations
377
Examination of mitral stenosis
A wave in venous jugular pulsations.
Low-pitched mid-diastolic rumble most prominent at the apex.
Loud opening S1 snap: heard at the apex when leaflets are still mobile
378
Investigation of Mitral Stenosis
ECG: may show atrial fibrillation and LA enlargement
CXR: LA enlargement and pulmonary congestion. Occasionally calcified MV
ECHO: The GOLD STANDARD for diagnosis. Asses mitral valve mobility, gradient and mitral valve area
379
Medical management of mitral stenosis
Serial echocardiography (frequency proportional to severity)
B-blockers, CCBs, Digoxin which control heart rate and hence prolong diastole for improved diastolic filling
Furosemide for fluid overload
380
Surgical management of mitral stenosis
Percutaneous mitral balloon valvotomy.
ANY SYMPTOMATIC Patient with NYHA Class III or IV Symptoms
Asymptomatic moderate or Severe MS with a pliable valve suitable for PMBV
381
What is mitral regurgitation?
Backflow of blood from the LV to the LA during systole
382
Aetiology of Mitral Regurgitation
Myxomatous degeneration (MVP)
Ischemic heart disease
Rheumatic heart disease
Infective Endocarditis
Marfan's
383
Pathophysiology of acute mitral regurgitation
Regurgitation causes left atrial dilation and pressure.
Can lead to increased PV pressure and pulmonary hypertension /oedema + RVH.
Decreaed EDV causing VH to increase SV to maintain cardiac output.
384
Clinical Presentation of Mitral Regurgitation
Exertional dyspnoea/ orthopnea
Fatigue, lethargy
385
Examination of Mitral Regurgitation
Pansystolic high-pitched murmur at the apex radiating to the axilla
Prominent S3 (CHF/LA overload)
386
Investigation of Mitral Regurgitation
ECG: LV hypertrophy, atrial fibrillation
CXR: LA, LV, PA enlargement.
ECHO: Estimation of LA, LV size and function. Valve structure assessment, papillary muscle rupture.
387
Medical Management of Mitral Regurgitation
Rate control for atrial fibrillation with B-blockers, CCB, digoxin
Anticoagulation in atrial fibrillation and flutter
Nitrates / Diuretics in acute MR
Serial echos
I.E prophylaxis.
388
Surgical management of Mitral Regurgitation
ANY Symptoms at rest or exercise (repair if feasible)
Asymptomatic:
If EF <60%, LVES Dimension >40mm
If new onset atrial fibrillation/raised PAP >50 mmHg
389
Aetiology/Risk Factors for infective endocarditis
Dental procedures/lack of dental hygiene.
Abnormal native valves
Prosthetic valve replacement
Intravenous drug use
Previous history of I.E
GI/GU procedures
Device implantation such as pacemakers, etc.
390
What organism is most likely to cause infection from dental procedures/lack of dental hygiene.
S.viridans - a-haemolytic, optochin resistant
391
What organisms are most likely to cause infection from abnormal native valves & prosthetic valve replacement
S.aureus, s.epidermidis
392
What organism is most likely to cause infection from IV druge use?
S.aureus, pseudomonas aeruginosa, Candida fungi.
393
What organism is most likely to cause infection from GI/GU procedures?
Enteroccoci
394
What organism is most likely to cause infection from device implantation?
S.aureus, s.epidermidis
395
What side of the heart is most likely to be infected with IV drug use?
Right side since circulating blood with infection comes through right atrium.
396
Pathphysiology of infective endocarditis
Damaged endocardium promotes platelet and fibrin deposition, which allows organisms to adhere and grow, leading to an infected vegetation.
397
Which valve is ost commonly affected in infective endocarditis?
Tricuspid valve
398
Clinical presenetation of infective endocarditis
Signs of systemic infection (fever, sweats, etc)
Embolisation: stroke, P.E, osteomyelitis.
Valve dysfunction
Petechiae
Splinter hemorrhages
Osler’s nodes
Janeway lesions
Roth spots on fundoscopy.
399
What are petechiae?
Tiny, round spots that appear on the skin as a result of subcutaenous bleeding
400
What are splinter haemhorrages?
Thin reddish lines of blood under the nails.
401
What are Osler's nodes?
Small, tender, painful, purple, raised nodules usually found on the fingers and toes.
402
What are Janeway lesions?
Painless flat lesions on palms/soles.
403
What ar Roth spots?
Retinal haemorrhagic lesions with pale centers
404
What are the 2 major criteria in the modified dukes criteria?
Pathogen grown from blood cultures
Evidence of endocarditis on echo, or new valve lea
405
What are the 5 minor criteria in the modified dukes criteria?
Predisposing factors
Fever
Vascular phenomena
Immune phenomena
Equivocal blood cultures
406
Investigation of infective endocarditis
Blood cultures - raised c-reactive protein.
Echocardiography - visualize vegetation.
407
Management of infective endcarditis
Antibiotics to treat the infection
Treating any rhythm issues
Surgery
408
Indications for surgery for infective endocarditis
The infection cannot be cured with antibiotics (ie recurs after treatment, or CRP doesn’t fall)
Complications (aortic root abscess, severe valve damage
To remove infected devices (always needed)
To replace valve after infection cured (may be weeks/months/years later
To remove large vegetations before they embolise
409
Complications of infective endocarditis
Arrythmias
Pulmonary embolism
Stroke
Cataract
410
What organism can cause cataracts in infective endcoarditis?
Candida fungi
411
What can cause P.Es, stroke and cataracts ininfective endocarditis?
Vegetation breaking off and floating as an embolus in circulation.
412
What antibiotic treatment would be used for a s.aureus infective endocarditis?
Flucloxacillin and gentamicin
413
What antibiotic treatment would be used for a MRSA infective endocarditis?
Vancomycin and gentamicin
414
What antibiotic treatment would be used for a s.viridans/s.epidermidis infective endocarditis?
Penicillin and gentamicin
415
What antibiotic treatment would be used for a enterococcus infective endocarditis?
Amoxicillin and gentamicin
416
Aetiology of atrial fibrillation
Hypertension, heart failure, rheumatic heart disease, hyperthyroidism, alcohol intoxication.
417
How would atrial fibrillation present on an ECG?
Irregularly irregular atrial rhythm, absent P waves.
418
Pathophysiology of atrial fibrillation
Rapid atrial firing results in no mechanical coordination.
Irregula/rapid ventricular response.
419
Management of atrial fibrillation
If unstable - DC cardioversion
If stable:
If symptoms < 48 hours, rhythm/rate control
If symptoms >48 hours, rate control + anticoagulation
420
What are the 2 types of cardioversion?
Electric and pharmacological (amiodarone, fleicanide)
421
What is the guideline of cardioversion for atrial fibrillation?
Immediate cardioversion if presenting within 48 hours.
If presenting after 48 hours - anticoagulate, give beta blockers for 3 weeks then cardioversion.
Done to prevent risk of AF thrombus formation.
422
What drugs could be used for rate control in atrial fibrillation?
Calcium channel blockers
Beta blockers
Cardiac glycosides - digoxin
423
What could be done for rhythm control in atrial fibrillation?
Amiodarone and fleicanide.
DC cardioversion
424
Pharmacodynamics of class Ia antiarrhythmic drugs
Moderate sodium channel blockers
425
Examples of class Ia antiarrhythmic drugs
Quinidine, procainamide, disopyramide
426
Pharmacodynamics of class Ib antiarrhythmic drugs
Weak sodium channel blockers
427
Examples of class Ib antiarrhythmic drugs
Lidocaine, phenytoin
428
Pharmacodynamics of class Ic antiarrhythmic drugs
Strong sodium channel blockers
429
Examples of class Ic antiarrhythmic drugs
Flecainide, propafenone
430
Pharmacodynamics of class II antiarrhythmic drugs
Beta blockers
431
Pharmacodynamics of class III antiarrhythmic drugs
Potassium channel blockers
432
Examples of class III antiarrhythmic drugs
Amiodarone, sotalol
433
Pharmacodynamics of class IV antiarrhythmic drugs
Calcium channel blockers
434
Examples of class III antiarrythmic drugs
Verapamil, diltiazem.
435
What score isued to calculate the risk of stroke after atrial fibrillation?
CHA2DS2-VASc score
436
If the CHA2DS2-VASc score is >1 or 2, what treatment should be considered?
Administratin of direcot oral anticoagulants (DOACs) or warfarin.
437
How would atrial flutter appear on an ECG?
Regularly irregular rhythm.
Sawtooth like rhythm between QRS complexes.
438
Pathophysiology of atrial flutter
Increased automaticity causes constant atrial firing.
439
Interventional mangement of atrial flutter and atrial fibrillation
Catheter ablation
440
Clinical presentation of atrial fibrillation/flutter
Palpitations, dyspnoea, fatigue, lightheadedness.
441
What are the 2 types of supraventricular tachycardia?
Atrioventricular nodal re-entrant tachycardia (AVNRT)
Atrioventricular re-entrant tachycardia (AVRT)
442
Pathophysiology of AVNRT
Slow conduction through AV node but fast conduction when coming back up form the ventricles to AV node.
443
How would AVNRT look on an ECG?
Absent P-waves, thin QRS complex.
444
Aetiology of AVRT
Accessory pathway (bundle of Kent)
445
Pathophysiology of AVRT
Accessory pathway allows bypassing of AV node to cause pre-excitation of ventricles.
446
How would AVRT look on a ECG?
Short PR interval
B roader QRS complexes
Slurred beginning of QRS complex known as delta wave.
447
Example of AVRT
Wolff-Parkinson-White syndrome
448
Management of supraventricular tachycardias?
Vagal manoeuvres
IV adenosine
449
What are examples of vagal maneouvres?
Carotid massage
Valsalva manoeuvre
450
Pathophysiology of isolated ectopic atrial beats
Origin of beat is not in SAN, can result in early beats being present.
451
How would isolated ectopic atrial beats look on an ECG?
Series of normal PQRST complexes with one occassionally having differently shaped P-wave.
452
Aetiology of isolated ectopic atrial beats
Secondary to adrenergic drive, so caffiene consumption.
453
Pathophysiology of isolated ectopic ventricular beats
Beat origin is outside of the His-Purkinje system and can cause slighly slower but earlier ventricular depolarization.
454
How would an isolated ventricular ectopic beat look on an ECG?
Wider QRS, no P wave, between normal QRS complexes.
455
Aetiology of isolated ventricular ectopic beats
Underlying heart disease, e.g MI
456
What is ventricular tachycardia?
Abnormally fast beating of the ventricles in a regular manner.
457
Pathophysiology of ventricular tachycardia
Shortened diastole does not allow for adequarte ventricular filling.
458
How would ventricular tachycardia look on an ECG?
Regularly irregular, broad QRS complexes
459
Clinical presentation of ventricular tachycardia
Angina, palpitations, dyspnoea.
460
Management of ventricular tachycardia
Beta blockers - esmolol
DC cardioversion if still unstable.
461
What is ventricular fibrillation?
This involves very rapid and irregular ventricular activation with no cardiac output.
462
How would ventricular fibrillation look on an EG?
Disorganized rhythm with no identifiable waves.
463
Pathphysiology of ventricular fibrillation
Lack of CO results in patients going into cardiac arrest if left untreated.
464
Management of ventricular fibrillation
Electrical defibrillation
465
Aetiology of ventricular fibrillation
MI, cardiomyopathy,
466
What is torsades de pointes?
Polymorphic ventricular tachycardia.
467
Aetiology of torsades de pointes
Drug-induced long QT syndrome
468
How would Torsades de pointes look on an ECG?
Shifting sinusoidal waveforms.
469
Management of long QT syndrome and torsades de pointes
IV Magnesium sulfate.
470
When would unsynchronized and synchronized DC cardioversion be used?
Unsynch: VF, or pulseless
471
What would a first degree heart block look like on an ECG?
PR interval >200ms
472
Aetiology of first degree heart block
Hypokalaemia, inferior MI, myocarditis
473
What are the classifcations of 2nd degree heart block?
Mobitz type 1 and tye 2
474
How would a mobitz type 1 heart block look on an ECG?
Progressive lengthening of PR interval until a p wave with no QRS complex.
475
How would a mobitz type 2 heart block look on an ECG?
Uniform PR interval with some p waves without QRS complexes.
476
Where would a lesion be for a mobitz type 1 heart block?
AV node
477
Where would a lesion be for a mobitz type 2 heart block?
Bundle of His
478
Which Mobitz block type has a higher risk of progressing to complete heart block?
Mobitz type 2
479
What is third degree heart block?
Complete heart block
480
Pathophysiology of third degree heart block
Atrial activity does not conduct to ventricles.
Ventricles contract through spontaenous escape rhythm.
Can be caused by RCA infarct since it supplies AV node.
481
How would third degree heart block look on an ECG?
Dissocated P waves and QRS complexes. Atrial rate > ventricular rate.
482
Aetiology of Mobitz type 1 block
Inferior MI, AV blocking drugs (CCB, BB, digoxin)
483
Aetiology of Mobitz type 2 block
Anterior MI, rheumatic fever, lyme disease.
484
Aetiology of third degree heart block
Structural heart disease, hypertension, endocarditis.
485
Interventional management for second and third degree heart block
Pacemaker insertion
486
Medical management for bradycardia
IV atropine 500mg
487
How would hyperkalaemia present in an ECG?
Tall, tented T- waves, small P-waves, wide QRS complex.
488
How would hypokalaemia present in an ECG?
Small T waves, PR elongation, ST depression,
489
What is an electrical storm?
3 more sustained episodes of VF/VT.
490
Management of electrical storm
– Correct any provoking factors e.g. electrolyte
(K/Mg), ischaemia, infection, heart failure
– Beta blockers, sedation
– Amiodarone +/- lignocaine
491
What is heart failure?
An inability of the heart do deliver blood and O2 at a rate commensurate with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures.
492
Aetiology of heart failure
IHD
Excess alcohol consumption
Dilated cardiomyopathy
Valvular heart disease
493
Types of heart failure
Systolic heart failure (heart failure with reduced ejection fraction, EF<40%)
Diastolic heart failure (heart failure with preserved ejection fraction, EF>50%)
Right systolic heart failure
494
Aetiology of heart failure
495
Symptoms of heart failure
Exertional dyspnoea, orthopnea, fatigue, weight gain, paroxysmal nocturnal dyspnoea, pink frothy sputum.
496
Examination of heart failure
Elevated JVP, peripheral oedema, ascites.
497
What would be heard upon auscultation of heart failure?
Displaced apex beat, third and fourth heart sounds, bi-basal crackles.
498
What is the NYHA classifcation of heart failure?
Class I: No limitation (Asymptomatic)
Class II: Slight limitation (mild HF)
Class III: Marked limitation (Symptomatically moderate HF)
Class IV: Inability to carry out any physical activity without discomfort (symptomatically severe HF)
499
Which clinical presentations are specific to left heart failure?
Orthppnoea, paroxysmal nocturnal dyspnoea, pulmonary oedema
500
Which clinical presentations are specific to right heart failure
Congestive hepatomegaly, jugular venous distension, peripheral oedema.
501
Management of heart failure
Symptomatic - loop diuretic
Guideline:
ACE inhibitor/ARB
Beta blocker
Mineralocorticoid receptor antagonist - spironolactone
SGLT2 inhibitor - osmotic diuresis so reduces preload.
502
Investigation of heart failure
FL: Brain natriuretic peptide - elevated in HF
FBC, U + E, LFT, TFT
CXR - ABCDE
ECG
Transthoracic echo - GOLD STANDARD DIAGNOSTIC
503
What are signs of heart failure in a CXR?
A: alveolar oedema (perihilar/bat-wing opacification)
B: Kerley B lines (interstitial oedema)
C: cardiomegaly (cardiothoracic ratio >50%) – may be difficult to assess on an AP film
D: dilated upper lobe vessels
E: effusions (i.e. pleural effusions – blunted costophrenic angles with meniscus sign)
504
Clinical presentation of heart blocks
Dizziness, syncope, fatigue, dyspnoea.
505
Pharmacodynamics of thiazide like diuretics
Inhibits on the NaCl co-transporter in the DCT
506
Examples of thiazide like diuretics
Benzoflumethiazide, hydrochlorothiazide, indapamide.
507
Pharmacodynamics of loop diuretics
Inhibits the NKCC transporter in the thick ascending loop of henle.
508
Examples of loop diuretics
Furosemide, torsemide
509
Examples of potassium-sparing diuretics
Spironolactone, eplerenone
510
Side effects of diuretics
Hypotension
Hyponatraemia
Hypokalaemia
Raised uric acid - gout
511
Side effects of spironolactone
Gynaecomastia
512
What drug options are available for people with resistant hypertension (HTN despite 3 drugs)
Beta blockers - not for those on aspirin
Spironolactone
513
Investigation of cardiac tamponade
CXR: Cardiomegaly
ECG: Low voltage QRS
Echocardiogram (GS) - late diastolic atrial collapse
514
Management of cardiac tamponade
Pericardiocentesis
515
What is the threshold of diagnosis of hypertension in clinic?
Over 140/90 mmHg
515
Exmination of HC
Ejection systolic murmur- can be due to mitral valve obstruction
S4 sound due to LVH
