CARDIO Flashcards
1
Q
Name 4 valvular heart diseases.
A
- Aortic stenosis.
- Mitral regurgitation.
- Mitral stenosis.
- Aortic regurgitation.
2
Q
Briefly describe aortic stenosis.
A
A disease where the aortic orifice is restricted and so the LV can’t eject blood properly in systole = pressure overload.
3
Q
Describe the aetiology of aortic stenosis.
A
- Congenital: bicuspid valve.
2. Acquired: age related degenerative calcification/ rheumatic heart disease.
4
Q
Describe the pathophysiology of aortic stenosis.
A
Aortic orifice is restricted e.g. by calcific deposits and so there is a pressure gradient between the LV and the aorta.
LV function is initially maintained due to compensatory hypertrophy.
Overtime this becomes exhausted = LV failure.
5
Q
Give 3 symptoms of aortic stenosis.
A
- Exertional syncope.
- Angina.
- Exertional dyspnoea.
Onset of symptoms is associated with poor prognosis. ( <25% of normal function)
6
Q
Give 3 signs of aortic stenosis.
A
- pulsus tardus + pulsus parvus
- Soft or absent heart sounds.
- Ejection systolic murmur: crescendo/decrescendo (right 2nd intercostal space)
7
Q
What investigation might you do in someone who you suspect to have aortic stenosis?
A
Echocardiography.
8
Q
Describe the management for someone with aortic stenosis.
A
- Ensure good dental hygiene.
- Consider IE prophylaxis.
- Aortic valve replacement or TAVI.
9
Q
Who should be offered an aortic valve replacement?
A
- Symptomatic patients with aortic stenosis.
- Any patient with decreasing ejection fraction.
- Any patient undergoing CABG with moderate/severe aortic stenosis.
10
Q
What is mitral regurgitation?
A
Back flow of blood from the LV to the LA during systole - LV volume overload
11
Q
Describe the aetiology of mitral regurgitation.
A
- Myxomatous degeneration.
- Mitral valve prolapse
- Rheumatic heart disease.
- IE
12
Q
What is the pathophysiology of mitral regurgitation?
A
LV volume overload! Compensatory mechanisms: LA enlargement and LVH and increased contractility. Progressive LV volume overload -> dilatation and progressive HF.
13
Q
Give 2 symptoms of mitral regurgitation.
A
- Dyspnoea on exertion.
2. HF.
14
Q
Give 3 signs of mitral regurgitation.
A
- Pansystolic murmur (always there).
- Soft 1st heart sound.
- 3rd heart sound.
In chronic MR the intensity of the murmur correlates with disease severity.
15
Q
What investigations might you do in someone who you suspect to have mitral regurgitation?
A
- ECG.
- CXR.
- Echocardiogram: estimates LA/LV size and function.
16
Q
Describe the management of mitral regurgitation.
A
- Rate control for AF e.g. beta blockers.
- Anticoagulation for AF.
- Diuretics for fluid overload.
- IE prophylaxis.
- If symptomatic = surgery.
17
Q
What is aortic regurgitation?
A
A regurgitant aortic valve means blood leaks back into the LV during diastole due to ineffective aortic cusps.
18
Q
What is the aetiology of aortic regurgitation?
A
- Bicuspid aortic valve.
- Rheumatic.
- IE.
19
Q
Describe the pathophysiology of aortic regurgitation.
A
Pressure and volume overload. Compensatory mechanisms - LV dilatation, LVH. Progressive dilation -> HF.
20
Q
Give 3 symptoms of aortic regurgitation.
A
- Dyspnoea on exertion.
- Orthopnea.
- Palpitations.
- Paroxysmal nocturnal dyspnea.
21
Q
Give 3 signs of aortic regurgitation.
A
- Wide pulse pressure.
- Diastolic blowing murmur.
- Systolic ejection murmur.
22
Q
What investigations might you do in someone who you suspect to have aortic regurgitation?
A
CXR and echocardiogram.
23
Q
Describe the management for someone with aortic regurgitation.
A
- IE prophylaxis.
- Vasodilators e.g. ACEi.
- Regular echo’s to monitor progression.
- Surgery if symptomatic.
24
Q
What is mitral stenosis?
A
Obstruction to LV inflow that prevents proper filling during diastole.
25
Give 3 causes of mitral stenosis.
1. Rheumatic heart disease.
2. IE.
3. Calcification.
26
Describe the pathophysiology of mitral stenosis.
1. LA dilation -> pulmonary congestion.
2. Increased trans-mitral pressures -> LA enlargement and AF.
3. Pulmonary venous hypertension causes RHF symptoms.
27
Give 3 symptoms of mitral stenosis.
1. Dyspnea.
2. Haemoptysis.
3. RHF symptoms.
28
Give 3 signs of mitral stenosis.
1. low volume pulse
2. Signs of RHF.
3. MALAR FLUSH (Pink patches on cheeks due to vasoconstriction)
4. Low pitched diastolic murmur.
5. Loud opening 1st heart sound snap.
29
What investigations might you do in someone who you suspect to have mitral stenosis?
1. ECG.
2. CXR.
3. Echocardiogram - gold standard.
30
Describe the management for mitral stenosis.
1. If in AF rate control e.g. beta blockers/CCB.
2. Anticoagulation if AF.
3. Balloon valvuloplasty or valve replacement.
4. IE prophylaxis.
31
Why does medication not work for mitral and aortic stenosis?
The problem is mechanical and so medical therapy does not prevent progression.
32
What is the main pacemaker in the heart?
Sino atrial node
33
What controls the sinus node discharge rate?
The autonomic nervous system.
34
Define sinus rhythm.
Sinus rhythm - a P wave precedes each QRS complex.
35
Give 3 symptoms of arrhythmia.
1. Sudden death.
2. Syncope.
3. Dizziness.
4. Palpitations.
5. Can also be asymptomatic.
36
Define bradycardia.
<60 bpm
37
Define tachycardia
>100 bpm
38
Give the two broad categories of tachycardia.
1. Supra-ventricular tachycardia's.
| 2. Ventricular tachycardia's.
39
Where do supra-ventricular tachycardia's arise from?
They arise from the atria or atrio-ventricular junction.
40
Do supra-ventricular tachycardia's have narrow or broad QRS complexes?
NARROW
41
Where do ventricular tachycardia's arise from?
Ventricles (duh)
42
Do ventricular tachycardia's have narrow or broad QRS complexes?
BROAD
43
Name 4 supra-ventricular tachycardia's.
1. Atrial fibrillation.
2. Atrial flutter.
3. AV node re-entry tachycardia (AVNRT).
4. Atrioventricular reciprocating tachycardia (AVRT)
44
Give 4 causes of sinus tachycardia.
1. Physiological response to exercise.
2. Fever,
3. Anaemia.
4. Heart failure.
5. Hypovolemia.
45
Give an example of an Atrioventricular reciprocating tachycardia (AVRT)
Wolff-Parkinson-White syndrome (WPW)
46
Describe 3 characteristics of an ECG taken from someone with atrial fibrillation.
1. ’Irregularly irregular’
2. No clear P waves
3. QRS is rapid and irregular
4. F waves
47
Give 4 causes of atrial fibrillation
1. Heart failure
2. hypertension
3. rheumatic heart disease
4. thyrotoxicosis
48
Give 4 symptoms of atrial fibrillation
1. Palpitations.
2. Shortness of breath.
3. Fatigue.
4. Chest pain.
5. Increased risk of thromboembolism and therefore stroke.
49
What score can be used to calculate the risk of stroke in someone with atrial fibrillation?
CHADS2 VASc.
50
What does the CHADS2 VASc score take into account?
The CHADS2 VASc score is used to calculate the risk of stroke in patients with atrial fibrillation. It considers:
1. Congestive heart failure
2. Hypertension
3. Age >75 (2)
4. DM
5. Stroke/TIA in past. (2)
6. Vascular disease
5. Sex = female.
A score >2 indicates the need for anticoagulation.
51
Describe the treatment for atrial fibrillation.
1. Rate control - beta blockers, CCB and digoxin.
2. Rhythm control - electrical cardioversion or pharmacological cardioversion using flecainide.
3. Flecainide can be taken on a PRN basis in people with infrequent symptomatic paroxysms of AF.
4. Long term - catheter ablation and a pacemaker.
52
Atrial fibrillation treatment: what might you give someone to help with rate control?
Beta blockers, CCB and digoxin.
53
Atrial fibrillation treatment: what might you give someone to help restore sinus rhythm (rhythm control)?
Electrical cardioversion or pharmacological cardioversion using flecainide.
54
What is the long term treatment of atrial fibrillation?
Catheter ablation - it targets the triggers of AF.
55
Describe the ECG pattern taken from someone with atrial flutter.
1. Narrow QRS.
| 2. 'sawtooth' flutter waves.
56
Give 3 extrinsic causes of bradycardia
1. BB/ digoxin
2. hypOthyroidism/hypOthermia
3. raised ICP
57
Give 3 intrinsic causes of bradycardia
1. Acute ischaemia
2. Infarction of SAN
3. Sick sinus syndrome
58
How would you treat bradycardia?
1. Underlying cause if extrinsic
2. ATROPINE if intrinsic
3. Surgery = pacemaker
59
ECG: what might a long PR interval indicate?
Heart block
60
Give 3 causes of heart block.
1. CAD.
2. Cardiomyopathy.
3. Fibrosis.
61
What kind of heart block is associated with wide QRS complexes with an abnormal pattern?
RBBB or LBBB
62
What is 1st degree heart block characterised by?
1. Asymptomatic!
2. Caused by myocarditis/hypokalaemia
3. Delayed AV conduction —> PR interval prolonged >0.2s
63
What are the two types of second degree heart block?
1. Mobitz type 1 (Wenckebach) - progressive prolongation of PR interval
2. Mobitz type 2 - fixed PR interval
(an occasional QRS is dropped)
64
What is 3rd degree heart block?
COMPLETE heart block
| All atrial activity fails to conduct to the ventricles – there is no association between atrial and ventricular activity
65
What would the ECG look like of a patient with 3rd degree heart block?
1. P waves and QRS complex are independent
| 2. Ventricular contractions are sustained by spontaneous escape rhythm
66
What is the treatment for complete heart block
1. IV atropine (acute)
| 2. pacemaker insertion
67
LBBB: what would you see in lead V1 and V6?
A 'W' shape would be seen in the QRS complex of lead V1 and a 'M' shape in V6
WiLLiaM
68
RBBB: what would you see in lead V1 and V6?
A 'M' shape would be seen in the QRS complex of lead V1 and a 'W' shape in V6.
MaRRoW.
69
A patient enters the clinic with BP of 140/90 mmHg. What would you management plan be?
1. Offer 24hr ambulatory BP monitoring
2. Assess end organ damage/ DM/QRISK2
3. Lifestyle advice!
70
What are 7 risk factors for developing hypertension?
1. Family history
2. Old age
3. Male
4. Afro-Carribeans
5. Lack of physical activity
6. Unhealthy diet
7. Obesity
71
What would be the BP of a patient with
- moderate
- severe
HTN?
Moderate = 160/100 mmHg
Severe = 180/110 mmHg
72
What are the two main types of treatment for hypertension?
1. Lifestyle modification: reduce salt intake, lose weight, reduce alcohol.
2. Drug therapy: ABCD.
73
What drugs might you give to someone with hypertension?
A - ACEi e.g. rampiril or ARB e.g. candesartan.
B - beta blockers e.g. bisoprolol.
C - Calcium CB e.g. amlodipine, diltiazem or verapamil.
D - diuretics e.g. bendroflumethiazide or furosemide.
74
A patient with hypertension has come to see you about their medication. You see in their notes that ACE inhibitors are contraindicated. What might you prescribe them instead?
An Angiotensin 2 Receptor Blocker (ARB) e.g. candesartan
75
A patient comes to see you who has recently started taking calcium channel blockers for their hypertension. They complain of constipation. What calcium channel blocker might they be taking?
Verapamil
76
You see a 45 y/o patient who has recently been diagnosed with hypertension. What is the first line treatment?
ACE inhibitors e.g. ramapril or ARB e.g. candesartan.
77
You see a 65 y/o patient who has recently been diagnosed with hypertension. What is the first line treatment?
Calcium channel blockers (as this patient is over 55) e.g. amlodipine.
78
You see a 45 y/o patient who has recently started taking ACE inhibitors for their hypertension. Unfortunately their hypertension still isn't controlled. What would you do next for this patient?
You would combine ACE inhibitors or ARB with calcium channel blockers.
79
You see a 45 y/o patient who has been taking ACE inhibitors and calcium channel blockers for their hypertension. Following several tests you notice that their blood pressure is still high. What would you do next for this patient?
You would combine the ACEi/ARB and calcium channel blockers with a thiazide diuretic e.g. bendroflumethiazide.
80
Give 5 causes of hypertension.
1. Kidney disease (CKD)
2. Genetics and family history.
3. Lifestyle factors e.g. high salt diet, excess alcohol, obesity, stress, caffeine.
4. Recreational drug use e.g. cocaine.
5. Drugs such as OCP and NSAIDS.
6. Hyperaldosteronism.
7. Pregnancy!
81
Name 5 conditions that hypertension is a major risk factor of?
1. MI (IHD).
2. Stroke.
3. Heart failure.
4. Chronic renal disease.
5. Dementia.
82
Give 3 side effects of amlodipine.
Side effects of dihydropyridines (CCB):
1. Flushing.
2. Headache.
3. Oedema.
4. Palpitations.
83
Diuretics: where do in the kidney do thiazides work?
The distal tubule.
84
Name a thiazide.
Bendroflumethiazide.
85
Name 2 loop diuretics.
1. Furosemide.
| 2. Bumetanide.
86
Name a potassium sparing diuretic.
Spironolactone.
87
Why are potassium sparing diuretics especially effective?
They have anti-aldosterone effects too.
88
In what diseases are diuretics clinically indicated?
1. HF
| 2. HTN
89
Give 5 potential side effects of diuretics.
1. Hypovolemia.
2. Hypotension.
3. Reduced serum Na+/K+/Mg+/Ca2+.
4. Increased uric acid -> gout.
5. Erectile dysfunction.
6. Impaired glucose tolerance.
90
What is heart failure?
A complex clinical syndrome of signs and symptoms that suggest the efficiency of the heart as a pump is impaired.
91
What is the most common cause of heart failure?
IHD
92
How do you calculate CO?
CO = HR x SV
93
What hormones does the heart produce?
Atrial natriuretic peptide (ANP)
| Brain natriuretic peptide (BNP)
94
What is the counter regulatory system to RAAS?
ANP/BNP hormones.
95
What are the two broad categories of heart failure?
1. Systolic failure: the ability of the heart to pump blood around the body is impaired.
2. Diastolic failure: the heart is pumping blood effectively but is relaxing and filling abnormally.
96
How does the ejection fraction differ in systolic and diastolic HF?
Systolic: EF <40%
Diastolic: EF>50%
97
Give 3 diseases that cause
- systolic HF
- diastolic HF
Systolic - IHD, MI, cardiomyopathy
| Diastolic - Constrictive pericarditis, cardiac tamponade, hypertension
98
Briefly describe the pathophysiology of heart failure.
1. When the heart fails, COMPENSATORY mechanisms attempt to maintain CO.
2. As HF progresses, these mechanisms are exhausted and become PATHOLOGICAL.
99
What is preload?
1. Left ventricular end-diastolic pressure (LVEDP),
| 2. the amount of ventricular stretch at the end of diastole
100
What is after load?
1. Systemic vascular resistance (SVR)
2. the amount of resistance the heart must overcome to open the aortic valve and push the blood volume out into the systemic circulation
101
Describe low-output HF
Decreased CO, fails to increase with exertion
102
What are 3 causes of low output HF
1. Pump failure
2. Excessive pre-load
3. Chronic increased afterload
103
What is high output HF? What can cause it?
1. Demands of body are too high
| 2. Pregnancy/ anaemia / hyperthyroidism
104
What are the compensatory mechanisms in heart failure?
1. Sympathetic system.
2. RAAS.
3. Inflammation
ALSO
Natriuretic peptides/ Ventricular dilation/Ventricular hypertrophy.
105
Explain how the sympathetic system is compensatory in heart failure and how that can be damaging
1. improves ventricular function by increasing HR and contractility = CO maintained.
2. Increases afterload by causing peripheral vasoconstriction
106
Explain how RAAS is compensatory in heart failure and give one disadvantage of RAAS activation.
1. Reduced CO leads to reduced renal perfusion; this activates RAAS.
2. Increased fluid retention + vasoconstriction = increased preload AND afterload
107
Give 3 properties of natriuretic peptides that make them compensatory in heart failure.
1. Diuretic.
2. Hypotensive.
3. Vasodilators.
108
How do cardiac myocytes change to compensate for HF
1. Ventricular dilation
| 2. Myocyte hypertrophy
109
What are the 3 cardinal symptoms of HF?
1. Shortness of breath.
2. Fatigue.
3. Peripheral oedema.
110
Give 4 signs of left heart failure.
1. Cardiomegaly (displaced apex beat)
2. 3rd and 4th heart sounds
3. Crepitations in lung bases
4. Tachycardia
111
Give 3 symptoms of LHF
1. Exertional dyspnoea
2. Fatigue
3. Paroxysmal Nocturnal Dyspnoea
- pink, frothy sputum
112
Give 4 signs of RHF
1. Raised JVP
2. Hepatomegaly
3. Pitting oedema
4. Ascites
113
What investigations might you initially do in someone who has the signs/symptoms suggestive of HF?
1. ECG.
2. CXR
3. Natriuretic peptide levels - raised BNP (not specific!)
114
What would you observe on a CXR of a patient with heart failure
```
Alveolar oedema (Bat wings)
B Kerley B lines
Cardiomegaly
Dilated prominent upper lobe vessels
E Pleural Effusion
```
115
What is the management for a patient with heart failure?
1. Lifestyle!!
2. (first line) Loop diuretics (furosemide)
3. ACE inhibitor (ramipril) + Beta blocker (bisoprolol)
116
When would the prescription of a beta blocker be contraindicated?
1. ASTHMA
| 2. 2nd and 3rd degree heart block
117
How do you calculate Stroke volume?
EDV-ESV
118
What is ASD?
An abnormal connection between the two atria; it is fairly common.
119
Would a baby born with ASD be cyanotic?
No. There is a higher pressure in the LA than the RA and so blood is shunted from the left to right, therefore not cyanotic.
120
Give 4 clinical signs of a large ASD.
1. Pulmonary flow murmur
2. Fixed split second heart sound (delayed closure of PV because more blood has to get out)
3. CXR - enlarged pulmonary arteries
4. Cardiomegaly
121
Give 2 symptoms of ASD
1. SOBOE
| 2. Inc no. of chest infections
122
What is AVSD?
Atrio-ventricular septal defects. Basically a hole in the very centre of the heart.
123
Give 2 clinical signs of AVSD.
1. Breathless.
| 2. Poor feeding and poor weight gain.
124
What is VSD?
An abnormal connection between the two ventricles.
125
Would a baby born with VSD be cyanotic?
No. There is a higher pressure in the LV than the RV and so blood is shunted from the left to right meaning there is an increased amount of blood going to the lungs; not cyanotic.
126
Give 4 clinical signs of a large VSD.
1. High pulmonary blood flow.
2. Breathless, poor feeding, failure to thrive.
3. Increased respiratory rate,
4. Tachycardia.
127
What syndrome might VSD lead on to?
Eisenmenger's syndrome
128
Briefly describe the physiology of Eisenmengers syndrome.
1. High pressure pulmonary blood flow damages pulmonary vasculature
2. increased resistance to blood flow (pulmonary hypertension)
3. RV pressure increases
4. shunt direction reverses (RV to LV) -> CYANOSIS!
129
What are the risks associated with Eisenmengers syndrome?
1. Death
2. Stroke
3. Endocarditis
130
What is PDA?
Patent Ductus Ateriosus
| - torrential flow from aorta to pulmonary arteries
131
Give 3 clinical signs of PDA.
1. Pulmonary hypertension and RHF.
2. Breathless.
3. Poor feeding, failure to thrive.
132
What can be a complication of having a bicuspid aortic valve?
1. Aortic stenosis
| 2. Aortic regurgitation
133
Describe the pathophysiology behind coarctation of the aorta.
Excessive sclerosing that normally closes the ductus arteriosus extends into the aortic wall leading to narrowing.
134
How would severe correction of the aorta present?
Collapse with heart failure
135
How would mild coarction of the aorta present?
1. Raised BP
2. Systolic murmur (best heard over left scapula, ‘scapula bruit’)
3. Radio-femoral delay, BP in right arm > than left arm
136
How would you manage correction of the aorta?
Surgical repair/Stent
137
What are the four main features of tetralogy of fallot?
1. Ventricular septal defect.
2. Over-riding aorta.
3. RV hypertrophy.
4. Pulmonary stenosis.
138
Would a baby born with tetralogy of fallot be cyanotic?
YES! There is a greater pressure in the RV than the LV and so blood is shunted into the LV -> CYANOSIS!
139
What may be seen on CXR of a child with TOF?
Boot shaped heart
140
Why do children with TOF squat?
1. Increases TPR
| 2. Alleviates R -> L shunt
141
What is pulmonary stenosis?
Narrowing of the RV outflow tract.
142
Name 3 congenital heart defects that are not cyanotic.
1. VSD.
2. ASD.
3. PDA.
Left to right shunt! This is okay but a bit insufficient and there is a risk of Eisenmengers syndrome.
143
Give 3 causes of IHD
1. Reduced blood flow to the heart muscle (clot or atheroma)
2. Increased distal resistance (LV hypertrophy)
3. Reduced O2 carrying capacity (anaemia) or availability (hypoxia)
144
Give 4 modifiable risk factors of IHD
1. Smoking
2. Obesity/ sedentary lifestyle
3. Hypertension
4. diet (High cholesterol = LDL)
145
Give 3 non-modifiable risk factors for IHD
1. age
2. genetics
3. gender (male)
146
Give examples of 2 psychosocial risk factors for IHD
1. High demand, low control jobs (high stress)
| 2. low social interaction and support
147
What is the QRISK2?
Predicts risk of CVD in next 10 years
148
What is the most common manifestation of stable IHD?
Angina pectoris
149
What is the most common cause of angina?
Narrowing of the coronary arteries due to atherosclerosis.
150
Briefly describe the pathophysiology of angina that results from atherosclerosis.
1. On exertion there is increased O2 demand.
2. Coronary blood flow is obstructed by an atherosclerotic plaque
3. Myocardial ischaemia -> angina.
151
Give 5 symptoms of angina.
1. Crushing central chest pain.
2. The pain RAPIDLY RESOLVES with rest or using a GTN spray.
3. The pain is provoked by physical exertion.
4. The pain might radiate to the arms, neck or jaw.
5. Breathlessness.
152
What investigations might you do in someone you suspect to have angina?
GOLD = Coronary Angiography – shows luminal narrowing
ECG – usually normal, may show ST depression and T wave inversion.
Bloods – anaemia?
CXR – check heart size and pulmonary vessels
153
Describe the primary prevention of angina.
1. Risk factor modification.
| 2. Low dose aspirin.
154
Describe the secondary prevention of angina.
1. Risk factor modification.
2. Pharmacological therapies for symptom relief and to reduce the risk of CV events.
3. Interventional therapies e.g. PCI.
155
Name 3 symptom relieving pharmacological therapies that might be used in someone with angina.
1. Beta blockers.
2. Nitrates e.g. GTN spray.
3. Calcium channel blockers.
156
Describe the action of beta blockers.
1. Antagonise sympathetic activation and so are negatively chronotropic and inotropic.
2. Myocardial work is reduced and so is myocardial demand = symptom relief.
157
Give 3 side effects of beta blockers.
1. Bradycardia.
2. Tiredness.
3. Erectile dysfunction.
4. Cold peripheries.
158
When might beta blockers be contraindicated?
1. Asthma
2. Bradycardia
3. Heart block
159
Describe the action of nitrates.
Nitrates e.g. GTN spray are VENODILATORS
1. Venodilators -> reduced venous return -> reduced pre-load -> reduced myocardial work and myocardial demand.
160
Describe the action of Ca2+ channel blockers.
Ca2+ blockers are ARTERODILATORS
Reduced BP -> reduced afterload -> reduced myocardial demand.
161
Name 2 drugs that might be used in someone with angina or in someone at risk of angina to improve prognosis.
1. Aspirin
| 2. Statins
162
How does aspirin work?
Aspirin irreversibly inhibits COX. You get reduced TXA2 synthesis and so platelet aggregation is reduced.
Caution: Gastric ulcers!
163
What are statins used for?
Reduce the amount of LDL in the blood
164
What is revascularisation?
Revascularisation might be used in someone with angina. It restores the patent coronary artery and increases blood flow.
165
Name 2 types of revascularisation.
1. PCI
| 2. CABG
166
Give 2 advantages and 1 disadvantage of PCI.
1. Less invasive.
2. Convenient and acceptable.
3. High risk of restenosis.
167
Give 1 advantage and 2 disadvantages of CABG.
1. Good prognosis after surgery.
2. Very invasive.
3. Long recovery time.
168
What is the common cause of ACS?
Rupture of an atherosclerotic plaque and subsequent arterial thrombosis.
169
Briefly describe the pathophysiology of ACS?
1. Atherosclerosis
2. plaque rupture
3. platelet aggregation
4. thrombosis formation
5. ischaemia and infarction
6. necrosis of cells
7. permanent heart muscle damage and ACS.
170
What are uncommon causes of ACS?
1. emboli
2. coronary vasospasm
3. vasculitis
171
What might the ECG of someone with unstable angina/NSTEMI show?
1. Normal
| 2. May show T wave inversion and ST depression.
172
What might the ECG of someone with STEMI show?
1. ST elevation in the anterolateral leads
2. After a few hours, T waves invert
3. deep, broad, pathological Q waves develop.
173
What would the serum troponin level be like in someone with unstable angina?
Normal
174
What would the serum troponin level be like in someone with NSTEMI/STEMI?
Significantly raised
175
What other cardiac enzymes are indicators for myocyte damage?
1. CK: CK-MB (creatine kinase - muscle/brain) rise within 3-12h of onset of pain
2. Myoglobin: rises within 1-4h of onset of pain, highly sensitive but not specific
176
A raised troponin is not specific for ACS. In what other conditions might you see a raised troponin?
1. Gram negative sepsis.
2. Pulmonary embolism.
3. Myocarditis.
4. Heart failure.
5. Arrhythmias.
177
Give 3 signs of unstable angina.
1. Cardiac chest pain at rest.
2. Cardiac chest pain with crescendo patterns; pain becomes more frequent and easier provoked.
3. No significant rise in troponin.
178
What is unstable angina?
An ACS that is defined by the absence of biochemical evidence of myocardial damage
179
What is a myocardial infarction?
Plaque rupture leads to a clot forming which then occludes one of the coronary arteries causing myocardial cell death and inflammation.
180
What are the symptoms of an MI?
1. acute central chest pain
2. radiating to jaw or shoulder
3. lasting >20 mins
4. nausea
5. SOB
6. palpitations.
181
Give 4 signs of an MI
1. clammy and pale
2. 4th heart sound
3. pansystolic murmur,
4. may later develop peripheral oedema
182
Describe the initial management for ACS.
1. Get into hospital ASAP - call 999.
2. If STEMI, paramedics should call PCI centre for transfer.
3. Aspirin 300mg.
4. Pain relief e.g. morphine/ anti - emetic
5. Oxygen if hypoxic.
6. Nitrates.
183
What is the long term management for an MI?
1. Lifestyle- modifiable risk factors!!
2. B-blocker: metoprolol - if CI then verapamil.
3. ACE-I
4. Statin: reduced cholesterol post MI beneficial
5. Aspirin: 75mg OD
Advice: return to work after 2 months (not all jobs). Encourage exercise and no air travel for 2 months.
184
What are 3 complications that could occur within 24 hours of an MI?
1. Ventricular arrhythmia
2. Bradyarrhythmia (due to AV block)
3. Cardiogenic shock
185
What are 3 complications that can occur within 3 days and 2 weeks of an MI?
1. Mitral regurgitation (due to papillary muscle infarction)
2. Ventricular septal rupture
3. Rupture of left ventricle free wall
186
What are 2 complications that could occur 2 weeks + after an MI?
1. Chronic pericarditis (Dressler syndrome)
| 2. Life threatening arrhythmia (ventricular tachycardia)
187
What are 2 complications that could occur anytime after an MI?
1. AF
| 2. HF
188
What is the DdX for chest pain?
1. Cardiac: ACS, aortic dissection, pericarditis, myocarditis
2. Respiratory: PE, pneumonia, PT, pleurisy, ca. lung
3. Musculoskeletal: rib fracture, chest trauma
Costochondritis
4. GORD/Oesophageal spasm
5. Anxiety/panic attack
189
In which arteries would you be most likely to find atheromatous plaques?
In peripheral and coronary arteries
190
Why is lidocaine an effective treatment for ventricular tachycardias?
It blocks the INactivation gate of the sodium channel
191
Why is digoxin a useful drug in the treatment of supra ventricular tachycardias?
It makes the membrane potential more positive releasing acetylcholine from parasympathetic nerves
192
Which additional property makes propranolol the most useful beta blocker to help control the arrhythmias which occur immediately following a heart attack ?
Is also a sodium channel blocker
193
In the treatment of heart failure, which transport protein or ion channel is inhibited by the loop diuretic, furosemide?
Na/K/2Cl transporter
194
What is the purpose of beta blockers in chronic heart failure?
Block reflex sympathetic responses which stress the failing heart
195
Which CVS drug is most likely to induce POSTURAL HYPOTENSION as a potential side effect?
CCB
196
What is the cardinal symptom of Peripheral Vascular Disease?
Intermittent Claudication
- cramping pain in calves, thighs and buttocks
- brought on by exercise
- relieved by rest!!
197
What can intermittent claudication lead on to if left untreated?
Critical Ischaemia
198
Give 6 symptoms of acute limb ischaemia.
1. Pain.
2. Pale.
3. Paralysis.
4. Paraesthesia.
5. Perishing cold.
6. Pulseless.
199
Give 5 risk factors for peripheral vascular disease.
1. Hypertension.
2. Hyperlipidaemia.
3. Diabetes.
4. Smoking.
5. Obesity.
200
Give 3 signs of Peripheral Vascular Disease
1. absent pulses
2. punched out ulcers
3. postural colour change (Buerger’s Test)
201
What would the Ankle Brachial Pressure Index (ABPI) be in a patient with PVD?
```
Normal = 1 - 1.2
PAD = 0.5 - 0.9
```
202
What investigations would you carry out on a patient with suspected PVD?
1. ECG - check for evidence of CAD
2. Rule out DM, arteritis, anaemia, renal disease
3. ABPI
4. Colour Duplex ultrasound!
5. CT angiography
6. Blood test - CK-MM raised (muscle damage)
203
How would you manage patients with peripheral vascular disease?
1. Risk factor modification
2. Anti-platelet, clopidogrel (1st line).
3. Exercise programmes
- reduce claudication by improving blood flow.
4. PTA or surgery if severely stenosed.
204
Give 4 signs of critical ischaemia (as well as 6 Ps)
1. PAIN AT REST
2. Classically nocturnal.
3. Ulceration.
4. Gangrene.
205
How would you differentiate acute ischaemia from gout/cellultitis?
Acute ischaemia
1. Deep duskiness of limb
2. Sudden deterioration
206
What is shock?
Circulatory failure resulting in inadequate organ perfusion
207
Give 7 signs/symptoms of shock.
1. Pale.
2. Sweaty.
3. Cold.
4. Pulse is weak and rapid.
5. Reduced urine output.
6. Confusion.
7. Weakness/collapse.
208
What would the BP be of someone in shock?
systolic <90 mmHg
209
What can cause hypovolemic shock?
1. Loss of blood e.g. acute GI bleeding, trauma, post-op, splenic rupture.
2. Loss of fluid e.g. dehydration, burns, vomiting, pancreatitis.
210
What is the function of the serous fluid between the visceral and parietal pericardium?
It acts as a lubricant and so allows smooth movement of the heart inside the pericardium.
211
What is the function of pericardium?
It restrains the filling volume of the heart.
212
Describe the aetiology of pericarditis.
1. Idiopathic (80-90%)
2. Infection (more commonly virus)
3. Autoimmune
4. Dressler syndrome (inflammation of pericardium after MI damaging it)
213
How would a patient with acute pericarditis describe their pain?
1. Central pain
2. NOT WORSE on exertion
3. But WORSE on inspiration / lying flat
4. Relieved by sitting forward
214
What would you hear upon auscultation with a stethoscope of a patient with acute pericarditis?
Pericardial friction rub
215
What would you see on the ECG of a patient with acute pericarditis?
1. Concave (saddle-shaped) ST segment elevation in all leads
| 2. PR Depression
216
What is the major differential diagnosis of acute pericarditis?
MI - rule this out ASAP!
217
What is the treatment for pericarditis?
1. Patients are advised to avoid strenuous activity until symptom resolution.
2. NSAID or aspirin - high doses.
3. PPI for gastric protection
3. Colchicine (anti-inflammatory).
218
How does colchicine have an anti-inflammatory effect?
Inhibits migration of neutrophils to site of inflammation
219
Give 2 complications of acute pericarditis
1. Fluid accumulation = PERICARDIAL EFFUSION
| 2. Fibrosis = CHRONIC CONSTRICTIVE pericarditis
220
What can pericardial effusion progress to?
Cardiac tamponade!
221
What 3 signs are cardiac tamponade characterised by?
BECK'S TRIAD
1. Falling BP
2. Rising JVP
3. Muffled heart sounds
222
A lady presents with a tearing pain and is found to have hypertension. A CT scan is done and a 'tennis ball sign' is observed. What is the likely pathology behind the patient's pain?
Aortic dissection!
223
What is the difference between a true and a false aneurysm?
1. True aneurysm:
- Affect all 3 layers (intimal, media, adventitia)
2. False aneurysm:
- A collection of blood under adventitia only
224
Give 3 causes of aneurysms
1. Atheroma (persistent inflammation weakens the arterial wall)
2. Trauma
3. Connective tissue disorders; (eg: Marfan’s, Ehlers-Danlos)
225
How is the screening carried out for AAA?
Aortic Ultra Sound
226
What signs and symptoms would you observe of a patient with AAA
1. Symptoms
- asymptomatic
- sometimes with abdominal / back pain
2. Signs
- Pulsatile (normal; but if >5.5cm suggests unruptured)
- EXPANSILE = abdominal mass (suggests rupture)
227
What is aortic dissection?
1. Blood flows into media
2. Tearing of INTIMA
3. Occlusion of branches of aorta
228
What pain would a patient describe who was experiencing an aortic dissection?
‘Sudden tearing chest pain, radiating to the back’
229
What are the different types of aortic dissection and how would you treat them?
Type A = Involves ascending aorta (surgery)
Type B = Doesn’t involve ascending aorta (surgery/antihypertensives)
230
Name 3 cardiomyopathies.
1. Hypertrophic (HCM).
2. Dilated (DCM).
3. Arrhythmogenic right/left ventricular (ARVC/ALVC).
231
What can cause HCM?
Sarcomeric gene mutations
232
What is the usual inheritance pattern for cardiomyopathies?
Autosomal dominant
233
Describe the pathophysiology of HCM.
1. Systole is normal but diastole is affected
| 2. heart is unable to relax properly due to thickening of the ventricular walls.
234
Describe the pathophysiology of DCM.
Ventricular dilation and dysfunction = poor contractility.
235
Give 3 symptoms of HCM.
SAD ( young)
1. Syncope
2. Angina
3. Dyspnoea
236
What might an ECG look like from a person with HCM.
1. Large QRS complexes
| 2. Large inverted T waves
237
What is restrictive cardiomyopathy?
Poor dilation of the heart restricts diastole.
238
What is the commonest cause of restrictive cardiomyopathy?
Amyloidosis (extra-cellular deposition of an insoluble fibrillar protein - amyloid).
