Cardiology Flashcards
1
Q
How may risk factors be categorised in Atherosclerosis?
Give an example of 3 for each.
A
NM RFs: Older age Family history Male Genetics
M RFs: Smoking Alcohol consumption Poor diet (high sugar and trans-fat and reduced fruit and vegetables and omega 3 consumption) Low exercise Obesity Poor sleep Stress
2
Q
What decision-making tool may be used to assess the risk that a patient will have a CVI in the next 10 years?
A
QRISK
3
Q
What is the QRISK threshold to prescribe a statin?
A
> 10%
4
Q
What monitoring is required for starting a patient on statins in the community?
A
LFTs at 3 months then 12 months
Lipids at 3 months - aim for 40% reduction
5
Q
What secondary prevention is there for Cardiovascular Disease?
A
Mnemonic: ABS
Aspirin/Antiplatelet \+ Beta blocker \+ Statin
6
Q
What is the MOA of statins?
A
HMG-CoA reductase inhibitors thus reduce hepatic cholesterol synthesis
7
Q
What are the side effects of statins?
A
Myopathy…
Myalgia
Myositis
Rhabdomyolysis
8
Q
Give 3 indications for Statins
A
QRisk > 10%
T1DM + over 40 years/10 years Hx/ Nephropathy
CKD Stage 3a
9
Q
What is the gold-standard diagnostic investigation for unstable Angina?
A
CT-CA
10
Q
What is the main difference between stable and unstable angina?
A
Angina is caused by stenosis of the coronary arteries resulting in myocardial ischaemia.
Stable = resolves with rest or GTN within 10 minutes
Unstable = experienced at rest; increases with frequency/severity
11
Q
What are the clinical features of angina?
A
Constricting pain experienced in the chest +/- typical radiation to the arm/neck/jaw
Precipitated by physical exertion
Relieved by rest or GTN within 5 minutes
12
Q
How can you grade Angina? Outline the grades.
A
Canadian Cardiovascular Society (CCS)
Grade I = angina with strenuous exercise
Grade II = angina with moderate activities
Grade III = angina with mild exertion (walk up stairs)
Grade IV = angina at rest
13
Q
What are the criteria for obstructive CAD upon CT-CA?
A
≥70% of stenosis of ≥1 coronary arteries
≥50% stenosis in LAD
14
Q
For how long after PCI should DAPT be conducted?
A
6 months
15
Q
What are the indications for CABG?
A
> 50% stenosis of left main stem
70% stenosis of proximal LAD and circumflex
Triple vessel disease
16
Q
If a patient presents within 12 hours of chest pain, where do you refer them to?
A
RACPC
17
Q
If a patient presents within 12 hours to 72 hours of chest pain, where do you refer them to?
A
Same day referral to hospital
18
Q
If a patient presents 3 days following ACS, what do you do regarding management/referral?
A
ECG + Trops
Then decide on further action
19
Q
Describe the term ACS.
A
Umbrella term for myocardial ischaemia:
Unstable Angina (UA)
NSTEMI
STEMI
20
Q
What are the types of Myocardial Infarction?
A
5 types based on aetiological mechanism
Type 1 = primary coronary event
Type 2 = oxygen supply/demand mismatch
Type 3 = sudden unexpected cardiac death secondary to myocardial ischaemia
Type 4 = associated with PCI or stent complications
Type 5 = Associated with cardiac injury
21
Q
Outline the pathophysiology of atherosclerosis.
A
Endothelial dysfunction: LDL accumulate and become oxidised to Ox-LDL
Plaque formation: Macrophages take up Ox-LDL to form lipid laden foam cells and form fatty streaks
Plaque rupture: Chronic inflammation involves cytokines and either stabilisation (fibrous cap) or destabilisation and subsequent rupture (if TNF-a high) resulting in thrombus/embolus
22
Q
What are the causes of ST elevation?
A
STEMI Pericarditis Coronary vasospasm Bundle branch block Ventricular aneurysm
23
Q
What are the causes of ST depression?
A
NSTEMI Reciprocal change to ST elevation Electrolyte imbalances Digoxin effects Bundle branch blocks
24
Q
What can cause T wave inversion?
A
Myocardial ischaemia
25
Which leads are anteroseptal territory?
V1-V4
26
Which leads are lateral territory?
V5, V6, I, aVL
27
Which leads are inferior?
II, III and aVF
28
Which leads are posterior?
V7-V9
29
What are the changes in an ECG seen over time in a STEMI?
Mins-Hours: Hyperacute T waves
0-12 hours: ST-elevation
1-12 hours: Q-wave development
Days: T wave inversion
Weeks: T wave normalisation and persistent Q waves
30
What is the gold-standard blood test for investigating myocardial necrosis?
Troponin-I/T
31
Give 5 causes of troponin elevation
```
Heart Failure
Hypertensive emergencies
Myocarditis
Cardiomyopathy
Coronary Spasm
Renal dysfunction
Pulmonary Embolism
Structural Heart Disease
```
32
What is the management of acute chest pain suspected to be an ACS?
Mnemonic: MONA
```
Morphine 10mg IV
+
Oxygen high flow non-rebreather mask
+
Nitrates sublingual GTN
+
Aspirin 300mg STAT
```
33
What is the management for a STEMI?
Medical: MONA
± within 120 minutes of being diagnosed with ST elevation (within 12 hours of onset of chest pain)
Intervention: PCI
± Unable to be performed within 120 minutes
Medical: Alteplase
+
Arrange transfer to PCI centre (2-24 hours after fibrinolysis)
34
What may be given in the case of high thrombus burden?
GP IIB/IIIA inhibitor such as Tirofiban
35
What risk stratification tool can be used to guide the management of a patient presenting with chest pain in suspected ACS?
GRACE Score = % 6 month mortality risk in patients with NSTMI/UA
Grace score > 1.5% treat with DAPT + Fondaparinux
Grace score (intermediate/high) then treat with PCI
36
A patient experiences a STEMI. 2 weeks following this, they experience pleuritic chest pain and a low grade fever. O/E there is a pericardial rub heard.
What is your diagnosis?
What is your management?
Dressler Syndrome
Tx:
- Medical: NSAIDs
± Severe
- Steroids: Prednisolone
37
Following a CABG, how soon can a patient drive?
4 week
38
Following insertion of a pacemaker, how soon can someone drive?
1 week
39
How soon after an angioplasty can a patient drive?
1 week
40
If a patient has had sustained ventricular arrhythmia and has an ICD put in, how soon can they drive?
6 months
41
How soon can a patient drive after a successful catheter ablation?
2 days off driving
42
How soon after a heart transplant can a patient drive?
6 weeks, do not need to notify DVLA
43
What are the two types of pericarditis?
Acute: Acute-onset chest pain with ECG features
Chronic: >3 months following acute episode
Complications may be: chronic pericardial effusion and constrictive pericarditis
44
How much fluid is usually present in the pericardial space?
20-50mL
45
What are the 3 functions of the pericardium?
Mechanical (limits cardiac dilation; aids ventricular compliance)
Barrier (reduces external friction; barrier)
Anatomical (fixes in position)
46
What virus commonly causes Pericarditis?
Coxsackie B virus
47
Give 5 causes of pericarditis.
Idiopathic
Viral
Bacterial
TB
Systemic disease (e.g. RA, uraemic pericarditis, hypothyroidism or post-myocardial infarction)
Drugs/Radiotherapy
Trauma
48
What are the features of cardiac tamponade?
Muffled heart sounds
Distended JVP
Pulsus paradoxus (reduced BP > 10mmHg during inspiration)
Hypotension
ECG: Saddle-shaped ST elevation; PR depression
49
How is pericarditis commonly managed?
NSAIDs + colchicine
50
What is the Beck Triad?
Hypotension + Muffled Heart Sounds + Raised JVP
51
What are the complications of pericarditis?
Cardiac tamponade
Chronic pericarditis
52
Muffled heart sounds + Raised JVP + Hypotension are collectively termed?
Beck Triad
53
Give 5 causes of cardiac tamponade.
```
Trauma
Tuberculosis
Malignancy
Iatrogenic
CT disease
Radiation
Uraemia
Post-MI
Aortic dissection
Bacterial infection
```
54
What is the gold-standard investigation to diagnose Cardiac Tamponade?
What may be seen?
Echocardiography
Chamber collapse (early diastolic collapse of RV and late diastolic collapse of RA)
Respiratory variation in volume and flow
IVC Plethora (dilation of IVC and reduced diameter during inspiration)
55
How is cardiac tamponade managed?
Intervention: Urgent needle pericardiocentesis
56
What is the difference between acute and chronic pericarditis?
Timeframe
Acute: Initial episode
Chronic: >3 months following initial event
57
Which cause of pericarditis rarely causes chronic pericarditis?
Acute idiopathic pericarditis
58
What is the gold-standard diagnosis of chronic pericarditis?
Echocardiography
59
How may chronic pericarditis present?
Signs of right heart failure
SOB
Peripheral oedema
Abdominal swelling
Raised JVP
Ascites
Hepatomegaly
60
How is chronic pericarditis managed?
Surgery: Pericardiectomy
61
How may you classify heart failure?
- Acute = Rapid onset of Sx or S/ life-threatening condition requiring urgent care/ acute decompensation of chronic heart failure. E.g.s MI/ Myocarditis/ Acute valvular disease/ Pericardial tamponade
- Chronic = Progressive cardiac dysfunction due to structural and/or functional cardiac abnormalities. This leads to reduced CO and elevated intracardiac pressure at rest or on stress. Chronic HF is precipitated by conditions affecting the muscles (cardiomyopathy), vessels (IHD), valves (aortic stenosis) or conduction (atria fibrillation)
- Left = Left ventricle of heart pumps insufficient blood (CO reduced) due to numerous conditions. May lead to RHF due to increased intrathoracic pressure and pulmonary hypertension
- Right = Right ventricle pumping insufficient blood to lungs (cor pulmonale) which can commonly be due to advanced LHF. Biventricular failure can be referred to as congestive heart failure (CHF). Causes separated into: 2º to pulmonary hypertension; 2º to pulmonary/tricuspid valve pathology or pericardial disease
- Systolic = reduced left ventricle ejection fraction (LVEF) leading to ventricular dilatation and eccentric remodelling
Causes: Contractility/ Volume overload/ Pressure overload
- Diastolic (preserved systolic function) = impaired ventricular relaxation or filling however LVEF is preserved via cardiac remodelling leading to ventricular hypertrophy
Causes: Reduced expansion/ Increased thickness/ Delayed relaxation/ Increased HR
62
Give 5 causes of Heart Failure.
Think in terms of vascular, valvular, muscular, electrical, output
MI
Hypertension
Vasculitides
Stenosis
Regurgitation
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Congenital heart disease
Arrhythmias
```
Hyperthyroid
Septicaemia
Thyrotoxicosis
Anaemia
Liver failure
```
63
Outline the Frank-Starling Law.
stretching of cardiac muscle (within physiological limits) will increase the force of contraction
64
Calculate the MAP.
diastolic blood pressure + 1/3rd of the pulse pressure
65
What factors influence stroke volume?
Preload (venous return + filling time)
Afterload (valve function + vascular resistance)
Contractility (muscular function + ANS)
66
Outline the pathophysiology of heart failure.
The heart fails due to numerous reasons which results in a compensatory mechanism to maintain the cardiac output (amount of blood going through the body per minute).
Should demand > supply, decompensation occurs which is pathophysiological
Compensatory mechanisms:
- RAAS: reduced BP thus increased RAAS output, resulting in water retention, oedema, dyspnoea and sodium retention with potassium excretion
- SNS: reduced BP thus constriction to increase venous return; increase cardiac remodelling and hypertrophy
- Ventricular dilatation and remodelling: increased EDV leading to greater output however cardiomyocytes remodel which leads to hypertrophy, loss of myocytes and interstitial fibrosis causing contractile failure
- BNP/ANP: BP high thus natriuresis encouraged
67
Give some clinical features of HF.
- Dyspnoea: SOBE
- Orthopnoea
- Paroxysmal Nocturnal Dyspnoea (PND)
- Fatigue
- Tachycardia
- Raised JVP
- Cardiomegaly + displaced apex beat
- S3 or S4 heart sounds
- Bi-basal lung crackles
- Pleural effusion
- Oedema: Ankle; Sacral
- Ascites
- Tender hepatomegaly
68
A patient has a ventricular arrhythmia which required a shock. How long can they not drive for?
6 months
69
How do you manage acute heart failure?
Mnemonic: LMNOP
```
Loop diuretic
+
Morphine
+
Nitrates (if severe HTN or valvular disease)
+
Oxygen
+
Position (sit forward)
```
May give...
Inotropes (<85mmHg)
Vasopressors
Mechanical circulatory assistance (Intra-aortic balloon)
70
What are the criteria for HFpEF?
>50%
71
What is the criteria for HFrEF?
<35-40%
72
What does R sided heart failure generally give you?
Mnemonic: Right = rest of body
Peripheral oedema
Raised JVP
Hepatomegaly
Weight gain
Fluid retention
Cardiac cachexia (anorexia)
73
What are the general clinical features of Left sided Heart Failure?
SOB
Orthopnoea
PND
Bibasal crackles
74
What is the first line treatment for a patient with Chronic Heart Failure?
Mnemonic: ABA
ACEi + ß-blocker ± ARB
No long term reduction in mortality for Diuretic but does give symptomatic alleviation
75
What effect does Candesartan have on potassium?
Hyperkalaemia
76
What effect does Ramipril have on potassium?
Hyperkalaemia
77
When should you give Ivabradine?
Sinus rhythm > 75bpm AND HFrEF <35%
78
When can you give sacubitril-valsartan?
HFrEF <35% when symptomatic on ACEi/ARBs
79
When can digoxin be used in HF?
Symptomatic alleviation due to inotropic effect
Used when co-existant AF
80
When may hydralazine be used with a nitrate in HF?
Afro-Carribean patient
81
What vaccines should a patient with Heart Failure be offered?
Annual Flu Vaccine
One-off Pneumococcal
82
No symptoms or limitations would be what NYHA classification?
I
83
Mild symptoms and slight limitation of physical activity would be what NYHA classification?
II
84
Moderate symptoms e.g. marked limitation of physical activity would be what NYHA classification?
III
85
Severe symptoms with features at rest would be what NYHA classification?
IV
86
What is the MOA of Digoxin?
Reduces AVN conduction to slow ventricular rate in AF/AFlut
Inhibits Na+/K+ ATPase pump to increase force of cardiac muscle contraction
Stimulates vagus nerve
87
What are the clinical features of Digoxin toxicity?
Unwell, lethargic, N/V, anorexia, confusion, xanthopsia, gynaecomastia
88
What are the precipitating factors for Digoxin toxicity?
Increased age
MI
Renal failure
Hypokalaemia
Hypomagnesaemia
Hypercalcaemia
Hypernatraemia
Acidosis
Hypothermia
Hypoalbuminaemia
Hypothyroidism
Drugs: Amiodarone; Quinidine; Verapamil; Diltiazem; Spironolactone; Ciclosporine; Thiazides; Loop diuretics
89
How do you manage Digoxin toxicity?
A-E
Digibind
Correct arrhythmias
Monitor potassium
90
What are the CXR finds seen in a patient with HF?
```
Alveolar shadowing
Batwing sign (hilar lymphadenopathy)
Cardiomegaly/Kerley B lines
Diversion
Effusion
```
91
What would contraindicate Eplerenone in HF treatment?
Hyperkalaemia
Hyponatraemia
AKI
92
How do you initiate ACEi treatment in HF?
Ramipril 1.25mg OD
Check U+Es before, repeat in 1-2 weeks
Double dose every 2-4 weeks until symptomatic alleviation achieved
93
How do you initiate ß-blocker treatment in HF?
Bisoprolol 1.25mg OD
Double dose every 4 weeks until target dose achieved
94
What may contraindicate ß-blockers?
Severe asthma
COPD
Pulmonary oedema
Bradycardia
95
What is the 1st line treatment in a patient with HFpEF?
Loop diuretic
96
Give 3 causes of Cor Pulmonale.
COPD
Pulmonary Embolism
Interstitial Lung Disease
Cystic Fibrosis
Primary Pulmonary Hypertension
97
Describe Cor Pulmonale.
RS HF due to respiratory distress which causes increased pressure and resistance in the pulmonary arteries with RV hypertrophy and back pressure to SVC and systemic venous system
98
Give the clinical features of Cor Pulmonale.
Hypoxia
Cyanosis
Raised JVP (due to a back-log of blood in the jugular veins)
Peripheral oedema
Third heart sound
Murmurs (e.g. pan-systolic in tricuspid regurgitation)
Hepatomegaly due to back pressure in the hepatic vein (pulsatile in tricuspid regurgitation)
99
Give 5 causes of Hypertension
Vascular: Atherosclerosis; RAS
Idiopathic
Trauma: Psychological; SIADS; DI
Acquired: Diabetes, Pregnancy, Alcoholism, CLD
Metabolic: Renal disease; Hyperaldosteronism (Conn's); Cushing's; Nephritic Syndromes
Infective (none)
Neoplasia: Pituitary adenoma; Phaeochromocytoma (adrenal cancer);
Congenital: ASD; VSD; Valvulopathies; Polycythaemia
100
How much time is given between a seated and standing Blood Pressure reading?
3 minutes
101
What are the criteria for Orthostatic Hypotension?
3 minutes apart
>20mmHg Systolic drop
>10mmHg Diastolic drop
102
156/92mmHg is what stage hypertension?
Stage 1
103
164/102mmHg is what stage Hypertension?
Stage 2
104
192/124mmHg is what stage of hypertension?
Stage 3
105
What is the management of Hypertension?
Supportive: Low salt diet (<6g/day); reduce caffeine; smoking cessation; exercise; lose weight
± Stage 2 Hypertension/ CKD/ Risk >10%/ Diabetes/ End organ damage
Follow algorithm
Age < 55 years / European/ T2DM = ACEi/ARB
Afro-Carrib = CCB
then follow A + C + D
If potassium is >4.5mmol/L consider alpha/beta blocker
If potassium is <4.5mmol/L consider ARB
106
Who should be referred to a specialist regarding hypertension?
Fail to respond to step 4 measures (resistant hypertension)
107
What are the clinic BP targets for <80 years?
140/90mmHg
108
What are the HBPM targets for <80 years?
135/85mmHg
109
What are the clinic BP targets for >80 years?
150/90mmHg
110
What are the HBPM targets for >80 years?
145/85mmHg
111
Give 3 causes of aortic regurgitation.
Split by valve leaflets or aortic root
Rheumatic heart disease
Infective endocarditis
Connective tissue disease
Bicuspid aortic valve
```
Aortic dissection
CT disease
Aortitis
Syphilis
Hypertension
Spondyloarthropathies
```
112
What is the causative pathogen of Rheumatic Heart Disease?
GAS
113
Describe a water hammer pulse?
Give the other name for this.
Collapsing pulse due to arm being raised + blood emptying very quickly due to gravity with artery emptying back to heart in diastole which increases preload and cardiac output during aortic regurgitation
Corrigan's Pulse
114
What is Quincke's Sign?
Nailbed pulsation
115
What type of murmur is heart in AR?
Early diastolic murmur
Mid-diastolic Austin-Flint murmur in severe AR (partial closure of anterior mitral valve cusps caused by regurgitation streams)
116
What is de Musset's sign?
Head nodding with heartbeat
117
What is Muller's sign in AR?
Pulsation of uvula
118
What is the key diagnostic investigation for AR?
Echocardiogram
119
What is the management of chronic AR?
Treatment indicated: Significant enlargement / Severe AR / Severe AR + LVEF <50%/ Marfan's disease with ascending aorta diameter > 50mm
Valve replacement - TAVI or Open surgery
Mechanical vs Bioprosthetic valve replacement
120
Give 5 causes of aortic stenosis.
Calcification
Bicuspid aortic valve
William's Syndrome (supravalvular aortic stenosis)
Rheumatic fever
HOCM (subvalvular)
121
What are the clinical features of AS?
Mnemonic: SAD
Syncope
Angina
Dyspnoea
```
Ejection systolic murmur
Murmur radiates to carotids
Sustained apex
Slow rising pulse
Narrow pulse pressure
```
```
4th heart sound
Softer S2 (aortic component of second heart sound may become quieter in severe disease as leaflets fail to oppose each other forcefully)
```
122
What is the management for AS?
Asymptomatic = do not treat
Asymptomatic + valvular gradient >40mmHg = consider surgery
Symptomatic = surgery
Valvotomy (open or balloon) or Valve replacement (mechanical vs bioprosthetic)
123
Give 5 causes of MR.
```
Post-MI
CAD
Mitral valve prolapse
Dilated cardiomyopathy (overfilling)
Infective endocarditis
Rheumatic fever
Congenital
Medications (ergotamine; bromocriptine; pergolide)
```
124
What are the clinical features of MR?
Asymptomatic
Symptoms will arise due to HF or arrhythmia
Displaced apex beat
Systolic thrill
Pansystolic murmur
S3 heart sound
HF signs: bibasal crackles; peripheral oedema
125
What is the change in P waves in MR and why does this occur?
P wave broadened due to atrial enlargement
126
What may be seen on CXR in severe MR?
L atrial and ventricular enlargement with double right heart border due to large L atrium
Pulmonary oedema
127
How is MR managed?
Acute vs Chronic
```
Acute
Supportive: Stabilise
+
Medical: Nitroprusside/Inotropes/IA balloon pump
± Severe
Surgery: Valve repair surgery
```
Chronic:
Medical: ACEi/ß-blocker/ARB
± HFrEF <30%
Surgery: Valve repair; LVAD; Heart transplant
128
Give 3 causes of MS.
```
Rheumatic feber
Mucopolysaccharidoses
Carcinoid
Endocardial fibroelastosis
Fabry's disease
Radiation
Mitral annular calcification
Congenital MS (Lutembacher syndrome = ASD + MS)
```
129
Outline the process of Rheumatic Heart Disease.
GAS infection with cross-reactivity of Abs to combat GAS resulting in arthritis and carditis.
130
What is Lutembacher syndrome?
ASD + MS
131
What are the clinical features of MS?
SOB
CX pain
Irregular pulse
Raised JVP
RV heave (pulmonary heave)
Mid-diastolic murmur
Prominent A wave
Peripheral oedema
Hepatomegaly
132
What is the A wave?
RA contracts which creates retrograde pressure thus blood into the IVJ
Mnemonic: A wave is Atrial Contraction wave
133
What is the X descent?
RA relaxes thus blood fills RA from SVC
Following C wave, RV contracts which creates space in pericardium for atria to fill again which causes a drop in the IVJ column
134
What is the C wave?
RV contracts so blood in the pulmonary artery with temporary rise in the RV projecting tricuspid valve into RA and upward force causing a temporary rise in JVP
Mnemonic: C wave is contraction wave
135
What is the V wave?
Relaxation of the RA whilst tricuspid is closed draws blood into the RA
Mnemonic: V wave is venous filling
136
What is the Y descent?
Tricuspid valve opens thus blood fills from RA to RV with reduced blood in JVC column
Mnemonic: Y descent as blood descends from RA to RV
137
What are the CXR signs of MS?
Double right heart border due to L atrial enlargement
Splayed carina (L main bronchus lifted)
138
How is MS managed?
Medical: Anticoagulation (Warfarin)
± Asymptomatic
Supportive: Monitoring with echocardiograms
± Symptomatic
Surgery: Percutaneous mitral balloon valvotomy or Mitral valve replacement
139
What is the most common cause of infective endocarditis?
S aureus
140
Infective endocarditis from dental surgery is most likely to be caused by which pathogen?
A. S aureus
B. S viridans
C. S epidermidis
D. S bovis
E. Lupus
B
141
Infective endocarditis from IVDU is most likely to be caused by which pathogen?
A. S aureus
B. S viridans
C. S epidermidis
D. S bovis
E. Lupus
A
142
Infective endocarditis associated with CRC is most likely to be caused by which pathogen?
A. S aureus
B. S viridans
C. S epidermidis
D. S bovis
E. Lupus
D
143
Infective endocarditis from indwelling lines is most likely to be caused by which pathogen?
A. S aureus
B. S viridans
C. S epidermidis
D. S bovis
E. Lupus
C
144
Libman-Sacks endocarditis is most likely to be caused by which pathogen?
A. S aureus
B. S viridans
C. S epidermidis
D. S bovis
E. Lupus
E
145
Give 3 examples of culture negative infective endocarditis.
Prior ABX use
C burnetii
Bartonella
Brucella
HACEK
146
What are the types of infective endocarditis?
Based on valve type
NVE: Normal valve
PVE: Early (<1 year) or Late (>1 year)
IVDA Endocarditis: Tricuspid valve (50%)
147
Give 7 RFs for Infective Endocarditis.
```
Increased age
Male
IVDU
Indwelling lines
Recent surgery
Poor dentition
```
```
Structural heart disease
Valvular heart disease
Previous IE
Prosthetic heart valves
Autoimmune conditions
CRC
Malignancy
```
Immunosuppressed
Haemodialysis
148
Outline the pathophysiology of Infective Endocarditis.
Turbulent blood flow causes endothelial damage thus platelets and fibrin adhere to underlying collagen surface, resulting in a prothrombotic environment.
Bacteraemia (S. aureus) leads to colonisation of thrombus and precipitates additional fibrin deposition, immunological response (mediated by macrophages and neutrophils) and platelet aggregation (‘vegetation’) causing mature infected vegetation. Vegetation causes destruction locally of valves leading to regurgitant murmurs and subsequent congestive cardiac failure.
149
What is the difference between Janeway lesions and Osler nodes?
Janeway lesions = painLESS erythematous macules on solar surfaces
Osler nodes = PaiNful violaceous nodules on pads of fingers and toes
150
What are roth spots?
Exudative, oedematous haemorrhagic lesions of the retina with a pale centre
151
What criteria is used in the diagnosis of Infective Endocarditis?
Duke's Criteria 2 major or 1 major 3 minor
Major criteria:
- 2 positive blood cultures
- Positive echocardiogram finds (vegetation/abscess/valvulopathy)
Minor criteria:
- IVDU
- PMHx cardiac condition
- Fever >38C
- Vascular phenomenon
- Immunological phenomena
- Microbiological evidence
152
How is infective endocarditis managed?
Depends on the bacteria isolated
Initial blind therapy: Amoxicillin
S. aureus
Flucloxacillin 12g/day in 4-6 doses over 4-6 wks
MRSA
Vancomycin 30-60mg/kg/day in 2-3 doses over 4-6 weeks
If prosthetic valve
+ Rifampicin + Gentamicin for ≥ 6 weeks
153
How do you treat IE caused by S epidermis?
Penicillins for 4-6 wks
154
How do you treat IE caused by a less sensitive streptococci?
Benpen + Gentamicin
155
What are the indications for surgery due to IE?
Severe valvular incompetence
Aortic abscess
Infections resistant to ABX
Cardiac failure refractory to medical Tx
Recurrent emboli following ABX
156
Where is the aortic valve auscultated?
2nd ICS RHS
157
Where is the pulmonary valve heard?
2nd ICS LHS
158
Where is the mitral valve heard?
5th ICS MCL
159
Where is the tricuspid valve heard best?
5th ICS LHS
160
How can you accentuate an aortic murmur?
Sit up and lean forward
Expiration
161
How can you accentuate a mitral murmur?
LHS and listen with bell of stethoscope
162
How do you accentuate a right sided murmur?
Mnemonic: RILE
Right Inspiration
163
How do you accentuate a left sided murmur?
Mnemonic: RILE
Left sided expiration
164
How do you characterise a murmur?
Timing
Character and grade
Where it is heard loudest
Pitch (diaphragm or bell)
Change with position or dynamic manoeuvres
Radiation
165
How do you grade murmurs?
The Levine Scale
Grade 1: Heard by experts
Grade 2: Slight murmur
Grade 3: Moderate, easily heard, no palpable thrill
Grade 4: Loud, palpable thrill
Grade 5: Very loud, palpable thrill
Grade 6: Heard without a stethoscope
166
An ejection systolic murmur is heard which is best heard on expiration.
What is it?
Aortic stenosis
167
An ejection systolic murmur is heard which is best heard on inspiration. What is it?
Pulmonary stenosis
168
A pansystolic murmur is heard over the apex which radiates to the axilla.
What is it?
Mitral regurgitation
169
A pansystolic murmur is heard over the left lower sternal edge. It does not radiate to the axilla. It is best heard on inspiration.
What is it?
Tricuspid regurgitation
170
What is Eisenmenger Syndrome?
reversal of a left-to-right shunt in a congenital heart defect due to pulmonary hypertension. This occurs when an uncorrected left-to-right leads to remodeling of the pulmonary microvasculature, eventually causing obstruction to pulmonary blood and pulmonary hypertension.
171
An early diastolic murmur is heard on expiration with the patient leaning forward.
What is your diagnosis?
Aortic regurgitation
172
A mid-diastolic murmur is heard at the apex with breath held in expiration whilst laying in the left lateral decubitus.
What is your diagnosis?
Mitral stenosis
173
A mid-diastolic murmur is heard which is augmented by inspiration.
What is your diagnosis?
Tricuspid stenosis
174
What is an Austin-Flint murmur?
mid-diastolic rumble seen in severe aortic regurgitation. Its exact aetiology is still debated, but it may be related to vibration of the mitral valve secondary to the regurgitant jet.
175
What is a Graham-Steele murmur?
Early diastolic murmur in pulmonary regurgitation which occurs secondary to pulmonary hypertension caused by mitral stenosis
176
Compare and contrast the choices for heart valves.
Mechanical:
+ Last longer
+ Lower failure rate
- Risk of thrombosis
- Warfarin
Bioprosthetic:
+ Long-term coagulation not needed
- Structural deterioration
177
What are the types of mechanical heart valve?
Tilting disc
St Jude (least risk of thrombus formation)
Starr-Edwards (ball in cage; highest thrombus formation)
178
What proportion of patients undergoing a surgical valve replacement experience infective endocarditis?
2.5%
179
What is the INR target range for a patient with a mechanical heart valve?
2.5-3.5
180
How may AF be classified?
Paroxysmal: Recurrent episodes lasting more than 30 seconds, which terminate spontaneously or within 7 days of intervention
Persistent: AF failing to self-terminate within 7 days; >12 months and it becomes long-standing persistent AF
Permanent: sinus rhythm cannot be restored or maintained and AF accepted in final rhythm
181
Give 5 causes of AF.
```
Hypertension
MI
IHD
Valvular disease
Cardiomyopathy
```
```
COPD/Pneumonia/PE
Hyperthyroidism/DM
Infection
Hypokalaemia/Hypomagnesaemia/Hyponatraemia
Bronchodilators/Thyroxine
Alcohol
Excessive caffeine
Obesity
```
182
What are the clinical features of AF?
Asymptomatic
SOB
Palpitations
Angina
Presyncope
Irregularly irregular pulse
Absent a wave on JVP (≈ atrial contraction)
Tachycardia
Hypotension
HF Features: bibasal crackles, raised JVP and peripheral oedema
183
What risk stratification tool can be used to assess stroke risk in patients with AF?
Outline it.
What is the threshold for anticoagulation?
CHADVASc score
```
CHF
Hypertension
Age ≥75 (2)
Diabetes
Stroke/TIA/VTE (2)
Vascular disease
Age 65-74
Sex category
```
Score ≥2 = DOAC
If DOAC not suitable or tolerated, offer Warfarin
184
What risk assessment tool can be used in major bleeding?
Outline it.
ORBIT Score
```
Age (75+)
Bleeding Hx (2)
Coagulation treatment
Drop in Hb (2)
eGFR
```
0-2 = low risk
3 = medium
4-7 = high risk
185
How is AF managed?
Establish cause - if any? and Tx cause
THEN
Rate or Rhythm control
```
Rate control (1st line)
ß-blocker
or
CCB
or
Digoxin (very little physical exercise or co-existent heart failure
```
Rhythm control
Amiodarone
186
Which patients are suitable for rhythm control in AF?
New-onset AF
Identifiable reversible cause
Heart failure (exacerbated by AF)
Associated Atrial Flutter
Rhythm control determined by clinical judgement
187
What are the complications of AF?
Heart failure
Tachycardia-induced cardiomyopathy
Ischaemia
Sudden cardiac arrest
Thromboembolic events
Collapse
Bleeding events (anticoagulation)
188
When should rhythm control in AF not be offered?
AF has a reversible cause
New-onset AF (<48 hours)
Atrial flutter which is suitable for ablation strategy
Heart failure due to atrial fibrillation
Rhythm control strategy more suitable based on clinical judgement
189
What is the recommended management for patients who have not responded to anti arrhythmic medication in AF?
What impact does this treatment have on the rhythm and the stroke risk?
How long should they be anticoagulated for?
Catheter ablation
Use anticoagulation 4 weeks before and during procedure
Note: Controls rhythm but not reduced stroke risk
Therefore if CHADSVASc = 0, 2 months of anticoagulation
If CHADSVASc >1 = long-term anticoagulation recommended
190
What two cell types aid myocardial contraction?
Autorhtymic cells (1%): Generate APs to drive contractile cells - these are 'pacemaker' cells
Contractile cells (99%): Responsible for myocardial contraction; undergo radical depolarisation driven by auto-rhythmic cells
191
What is the location of the SAN?
Junction of SVC and RA (by the right auricle)
192
Where is the AVN located?
Base of RA near the septum
193
Outline the phases of the action potential of autorhythmic cells
Phase 4 = If channels open thus Na+ in
T-type calcium channels open at -50mV
Phase 0 = L-type calcium channels remain open, continuing depolarisation
Phase 3 = Ik open thus potassium efflux and repolarisation occurs
194
Outline the action potential stages in contractile cardiomyocytes.
Phase 4 = Leaky Ik channels allow K+ efflux and keep RMP at -90mV
Phase 0 = Depolarisation via Ina thus sodium channels open and Na+ in
Phase 1 = Ikto (transient) thus K+ efflux
Phase 2 = Plateau phase due to Ical channels open prolonging repolarisation (L-type calcium channels)
Phase 3 = Ik open thus outward movement of K+ to return to -90mV
195
What are the main types of pacemakers?
Single-chamber: leads to a single chamber - RA if SAN defunct; RV if AVN defunct
Dual-chamber: Leads in both RA and RV - pacemaker synchronises contractions of both atria and ventricles
Biventricular (triple-chamber): RA, RV and LV - used in patients with heart failure to synchronise contractions in these chambers
Also called Cardiac Resynchronisation Therapy (CRT) pacemakers
Implantable Cardioverter Defibrillators (ICDs): Continually monitor the heart and apply defibrillator shock to Cardioverter patient into sinus rhythm - identify a shockable arrhythmia
196
What are the causes of Cardiomyopathy?
Primary: Genetic
Secondary:
Chemotherapy (Doxorubicin) -> Toxicity CM
Infection -> Infective CM
Systemic disease (Amyloidosis/Sarcoidosis) -> Infiltrative/Inflammatory CM
SLE -> Autoimmune CM
Radiation
Malignancy
Alcohol
Diabetes/Acromegaly/Thyrotoxicosis -> Endocrine CM
HH --> Storage CM
Pregnancy -> Peripartum
Stress -> Takotsubo
197
Describe HCM.
increased ventricular wall thickness or mass not caused by pathologic loading conditions.
198
Which mutations can cause HCM?
How is it inherited?
Myosin heavy chain
Troponin I
Troponin T
Inherited by autosomal dominant
199
What are the potential clinical features of HCM?
```
Fatigue
SOB
Orthopnoea
Ankle Swelling
Cx pain
Pre/syncope
Palpitations
```
Heave
Thrill
Ejection systolic murmur
Mid-late systolic murmur (AR)
Potential HF: Raised JVP, crackles, peripheral oedema
200
What is the primary mode of diagnosis of HCM?
What threshold is used?
Echocardiography: ≥15mm LV wall thickness
201
What is the management for HCM?
ß-blockers reduce outflow tract gradient
Surgery: Septal myomectomy
202
Give 5 causes of dilation cardiomyopathy (DCM).
Idiopathic
TTN gene mutation
MYH7 gene mutation
Cardiac: CHD/ Hypertension/ Peripartum cardiomyopathy
MSK: DMD
Infection: Coxsackie B/ Rheumatic Heart Disease/ Chagas disease/ HIV
Autoimmune: Sarcoidosis/ SLE
Toxins: Alcohol; abuse/ Cocaine/ Organic solvents
Malnutrition: Thiamine deficiency/ Selenium deficiency
Radiation
203
What is the management for DCM?
Mirrors heart failure thus use the same treatment
ACEi + ß-blocker ± ARB
± Symptoms
Tx symptoms e.g. Diuretics for Oedema
204
A patient has been experiencing SOBE, fatigue, peripheral oedema and PND.
Echocardiography shows non-dilated, non-thickened ventricles with abnormal ventricular filling.
What is your diagnosis?
Restrictive cardiomyopathy
205
How is RCM managed?
Tx underlying cause
+
Tx symptoms
206
How is Arrhythmogenic Cardiomyopathy managed?
ß-blockers
+
ICD
207
What is ARVD?
Arrhythmia alongside myocardial structural abnormalities
RV myocardium replaced by fibrofatty tissue due to a mutation of genes encoding hemidesmosomes
208
What ECG abnormality may be seen in ARVD?
Epsillon wave with terminal notch in QRS complex
209
What is Naxos disease?
Variant of ARVC.
ARVC + Palmoplantar keratosis + Wooly hair
210
The presence of ARVC, palmoplantar keratosis and wooly hair suggests?
Naxos disease
211
What is seen on echocardiogram in Takotsubo cardiomyopathy?
Transient, apical ballooning whereby hypokinesis of mid and apical segments thus apex balloons but area to base contracts thus appears like the neck of the octopus trap
212
What drugs should be avoided in HOCM?
Nitrates
ACEi
Inotropes
213
Discuss the process of cardioversion in AF.
Cardioversion may be electrical or pharmacological; subject to onset
Onset < 48 hours
LMWH
+
Cardioversion: Electrical (DC) or Pharmacological (Amiodarone if structural; Flecainide if without)
Onset > 48 hours
LMWH for 3/52 AND continue for 4 weeks after at least
+
Electrical cardioversion: DC
± High risk of cardioversion failure
Amiodarone/Sotalol 4 weeks
214
What are the two shockable rhythms?
Ventricular fibrillation
Ventricular tachycardia
215
What are the non-shockable rhythms?
PEA (all electrical activity without pulse, except VT or VF)
Asystole (no significant electrical activity)
216
How may you classify arrhythmias?
Rate: Bradycardia vs Tachycardia
Site: Supraventricular vs Ventricular
217
What causes a sinus arrhythmia?
Respiratory pattern changes e.g. inspiration causes reduction in PSNS thus increase HR
218
What may cause a sinus bradycardia?
```
ß-blockers
Digoxin
Hypothyroidism
Hypothermia
Cholestatic jaundice
Raised ICP
Vasovagal attacks
Carotid sinus syndrome
Anorexia
```
219
How do you treat acute sinus bradycardia?
If symptomatic, Atropine
If persistent
Cardiac pacemaker
220
What is the management for a sinus tachycardia?
ß-blocker: Bisoprolol
221
How is Atrial Flutter managed?
```
Rate or Rhythm control
+
Anticoagulation
+
Tx cause
```
222
What are the treatment steps of managing a stable patient with an SVT?
```
Valsalva
±
Carotid sinus massage
±
Adenosine
±
Verapamil (CCB)
±
DC Cardioversion
```
223
What is the MOA of adenosine?
Slows cardiac conduction via AV node to reset back to rhythm
224
How is adenosine administered?
Check if patient has asthma/COPD/HF/Heart block/Severe hypotension;
Warn patient of impending doom when injected
Fast IV bolus via grey cannula 6mg then 12mg then 12mg (if no improvement)
225
What is the long term management of a patient with an SVT?
Medication: ß-blockers
±
Intervention: Radiofrequency ablation
226
What is WPW Syndrome?
Type of SVT that is a AVRT due to an accessory pathway connecting the atria and ventricles (The Bundle of Kent)
227
What ECG changes are seen in WPW Syndrome?
```
Short PR interval <0.12 seconds
Wide QRS complex >0.12
Axis deviation (L if L accessory or R if R accessory)
```
Delta wave, slow and slurred upstroke on QRS complex
228
What medications may prolong the QT interval?
Antipsychotics
SSRIs
ß-blockers
Amiodarone
Macrolide antibiotics
229
Give 5 causes of sinus tachycardia.
- Emotional
- Exercise
- Fever
- Pain
- Anaemia
- Heart failure
- Thyrotoxicosis
- Acute PE
- Hypovolemia
- Drugs (atropine/ catecholamine)
230
At what part of the ECG is DC Electrical cardioversion synchronised to and why?
Synchronised to R wave to prevent delivery of a shock during vulnerable period of cardiac repolarisation when ventricular fibrillation can be induced
231
Give 5 causes of ventricular ectopics.
- Anxiety
- Sympathomimetics
- ß-agonists
- Excess caffeine
- Hypokalaemia
- Hypomagnesaemia
- MI
232
What is the management for ventricular ectopics?
ß-blockers
233
How may you classify Ventricular Tachycardia?
Morphology: Monomorphic vs Polymorphic
Duration: Sustained vs Non-Sustained
234
What are the ECG signs seen in Ventricular Tachycardia?
Broad QRS complex
AV dissociation (p wave and QRS complex at different rates)
S wave notching in lead III (Josephson's sign)
235
What are the clinical features of Jervell-Lange-Nielsen Syndrome?
Prolonged QT interval
+
Deafness
236
What are the clinical features of Romano-Ward Syndrome?
Prolonged QT interval (congenital)
without deafness
237
Give 5 causes of prolonged QT interval.
```
Amiodarone
Sotalol
TCAs
SSRIs
Chloroquine
Macrolides e.g. Erythromycin
Electrolyte imbalances: hypokalaemia; hypocalcaemia; hypomagnesaemia
Myocarditis
MI
Hypothermia
Subarachnoid haemorrhage
```
Jervell-Lange-Nielsen Syndrome
Romano-Ward Syndrome
238
How is Ventricular Tachycardia managed?
Unstable: Immediate cardioversion
Stable:
Amiodarone (via central line)
Procainamide
If drug therapy fails...
EPS
+
ICD
239
What drug should never be given in VT?
Verapamil
240
Exertional syncope following swimming is a feature of which variant of LQT?
A. LQT1
B. LQT2
C. LQT3
D. Sudden Cardiac Death
A
241
Syncope following emotional stress is a feature of which variant of LQTS?
A. LQT1
B. LQT2
C. LQT3
D. Sudden Cardiac Death
B
242
Cardiac events occurring at night when resting is a feature of which LQTS variant?
A. LQT1
B. LQT2
C. LQT3
D. Sudden Cardiac Death
C
243
How is LQTS managed?
Avoid precipitants
+
ß-blockers
244
Give 5 causes of Ventricular Fibrillation.
4Hs and 4Ts
Hypoxia
Hyperkalaemia
Hypovolaemia
Hypothermia
Thrombosis
Tamponade
Toxins
Tension pneumothorax
245
How do you manage Ventricular Fibrillation?
Defibrillator
+
ICD following resuscitation
246
Give 5 causes of LBBB.
```
MI
Hypertension
Idiopathic fibrosis
Aortic stenosis
Cardiomyopathy
Digoxin toxicity
Hyperkalaemia
```
247
Give 5 causes of RBBB.
```
RV hypertrophy
Cor pulmonale
Ischaemic heart disease
PE
Congenital heart disease
Myocarditis
Rheumatic heart disease
Cardiomyopathy
Idiopathic fibrosis (LLS)
```
248
What is Ebstein's anomaly?
Low insertion of tricuspid valve thus large atrium and small ventricle = 'atrialisation of RV'
249
What are the clinical features of Ebstein's anomaly?
Cyanosis
Prominent a wave
Hepatomegaly
Tricuspid regurgitation: pansystolic murmur; worse on inspiration
RBBB
250
What is the mode of inheritance for Brugada syndrome?
Autosomal Dominant
251
What gene mutation is predominantly responsible for Brugada syndrome?
SCN5A
252
What are the ECG changes observed in Brugada syndrome?
Convex ST segment elevation >2mm in V1-V3 AND negative T wave
Partial RBBB
253
What is the management of Brugada syndrome?
ICD
254
What is a bifascicular block?
Combination of RBBB or LBBB with anterior or posterior hemiblock
255
What classification system can be used for anti arrhythmic drugs?
Vaughan-Williams
256
What V-W class of drug is Disopyramide?
1a
257
What V-W class of drug is Lignocaine?
1b
258
What V-W class of drug is Bisoprolol?
2
259
What V-W class of drug is Amiodarone?
Class 3
260
What is the MOA of Amiodarone?
Blocks KCN thus increases refractory period
261
What is the MOA of Flecainide?
NaCN blocker thus reduces rate of firing and Na+ influx
262
What is the MOA of Verapamil?
Block CCN therefore reduce conduction
263
Which biochemical marker gives the most accurate reflection of an MI in the last 5 days?
CK-MB (up to 5 days)
Trop-I (up to 10 days)
264
What is the eponymous term for Costochondritis?
Tietze Syndrome
265
What is the MOA of aspirin?
COX-i thus prevent TXA2 production and inhibits platelet aggregation to stop clots
266
What is the MOA of Apixaban?
Factor X inhibitor thus stops clotting
267
What is the MOA of bisoprolol?
Antagonist of ß-adreoceptor thus antagonises SNS
268
Give 3 side effects of beta blockers?
Bronchoconstriction
Vasoconstriction
Lethargy
Hyperkalaemia
Erectile dysfunction
Loss of joie de vivre
Nightmares
Headaches
269
When should you consider stopping ACEi?
sCr >20%
Angiooedema
Cough
eGFR drops markedly
270
What is the MOA of Furosemide?
Loop diuretic - inhibiting Na/2Cl/K cotransporter thus increases loss of water and electrolytes
271
What are the side effects of CCBs?
Ankle oedema
Flushes
Headaches
Gingival hypertrophy
272
What is the MOA of Digoxin?
Inhibits Na+/K+ pump
Vagal nerve discharge
273
What ECG sign may be seen in Digoxin toxicity?
Reverse tick sign
ST depression with rapid upstroke back to isoelectric line
274
What is the MOA of Flecainide?
Sodium channel blocker
Class I anti-arrhythmia drug
Useful in AF and SVT with accessory pathways
275
What are the contraindications for Flecainide?
Structural heart disease
Post-MI infarction
Sinus node dysfunction
Atrial flutter
276
What are the side effects of Flecainide?
Negatively inotropic
Bradycardia
Oral paraesthesia
Visual disturbances
277
What is the MOA of Amiodarone?
Class III anti-arrhythmia drug blocking potassium channels to inhibit repolarisation thus prolongs AP
278
What are the adverse effects of Amiodarone?
```
Slate-gray appearance
Corneal deposits
Thyroid derangement (hypo and hyper)
Pulmonary fibrosis/pneumonitis
Liver fibrosis/hepatitis
Thrombophlebitis
Bradycardia
QT interval prolongation
```
279
What is the MOA of statins?
HMG-CoA reductase inhibitors thus reduces cholesterol synthesis
Increased LDL-r expression by hepatocytes thus reduced LDL concentration in blood
280
What are the potential side effects of Statins?
```
Abdo discomfort
Muscle aches
Myositis
Raised CK
Raised transaminases
```
281
What types of angina are there?
Stable
Prinzmetal angina
Decubitus
Unstable
282
What is the management of angina?
Investigate with CT coronary angiography
Do other tests too...FBC; U+Es; LFTs; TFTs; Troponin; HbA1c; ECG
Acute: Morphine + Oxygen + Aspirin + Nitrates
```
Ongoing
Beta blockers or CCB (rate-limiting)
Nitrates
RF modification
Aspirin 75mg
Statins
ACEi (if diabetic or HTN) - or CCBs if needed
```
283
What are the criteria for a STEMI?
>20mins of ECG features in ≥2 contiguous leads showing:
2.5mm ST elevation in leads V2-V3 in men under 40 or 2.0mm ST elevation in V2-V3 in men over 40
1.5mm ST elevation in V2-V3 in women
1mm ST elevation in other leads
New LBBB criteria
284
How is a GRACE score calculated?
```
Age
BP
Cardiac: ECG findings, Troponin, HR
Disability: cardiac arrest?
eGFR: Renal function
```
285
What are the potential complications of an MI?
Cardiac arrest
Cardiogenic shock
Bradyarrhythmia
Tachyarrhythmia
```
Pericarditis
Cardiac tamponade
Mitral regurgitation
VSD
LV aneurysm
```
Dressler syndrome
286
What is bigeminy?
normal QRS followed by ventricular ectopic beat with compensatory pause and repeat
287
Outline the Orbit score.
Mnemonic: ABCDE
```
Age (75+)
Bleeding Hx
Coagulation
Dick? (M or F)
eGFR
```
288
Outline the treatment steps for Hypertension.
<55 y/o or DM give ACEi/ARB
>55y/o or Afro-Carrib give CCB
Add the other
Add a diuretic
[K+] > 4.5 = alpha blocker//beta blocker
[K+] < 4.5 = spironolactone
Beta Blocker
289
When should you treat in Hypertension?
HBPM >135/85mmHg AND 1 of following: end-organ damage; CVD disease; 10-year CV risk >10%
HBPM >150/95mmHg regardless of age
290
What is the most common valve affected in IVDU for endocarditis? Explain why.
Tricuspid valve - this is the first valve receiving venous blood
291
What is the most common valvulopathy associated with PCKD?
Mitral prolapse/regurgitation
292
When might you prescribe nitrates in heart failure?
MI
AR or MS
Hypertension
293
What are the target saturations in a patient with hypoxia in HF?
94-98%
294
List 5 causes of VT.
Congenital: Jervell-Lange-Nielsen Syndrome (with deafness); Romano-Ward Syndrome
Drugs: Macrolides; Amiodarone; Sotalol; TCAs; SSRIs
Electrolytes: Hypocalcemia; Hypokalaemia; Hypomagnesaemia
SAH; Myocarditis
Hypothermia
