Cardiology Flashcards
1
Q
Define atherosclerosis.
A
A hardened plaque in the intima of an artery. It is an inflammatory process.
2
Q
What can an atherosclerotic plaque cause?
A
- Heart attack.
- Stroke.
- Gangrene.
3
Q
What are the constituents of an atheromatous plaque?
A
- Lipid core.
- Necrotic debris.
- Connective tissue.
- Fibrous cap.
- Lymphocytes.
4
Q
Give 5 risk factors for atherosclerosis.
A
- Family history.
- Increasing age.
- Smoking.
- High levels of LDL’s.
- Obesity.
- Diabetes.
- Hypertension.
5
Q
In which arteries would you be most likely to find atheromatous plaques?
A
In the peripheral and coronary arteries.
6
Q
Which histological layer of the artery may be thinned by an atheromatous plaque?
A
The media.
7
Q
What is the precursor for atherosclerosis.
A
Fatty streaks.
8
Q
What can cause chemoattractant release?
A
A stimulus such as endothelial cell injury.
9
Q
What are the functions of chemoattractants?
A
Chemoattractants signal to leukocytes. Leukocytes accumulate and migrate into vessel walls -> cytokine release e.g. IL-1, IL-6 -> inflammation!
10
Q
Describe the process of leukocyte recruitment.
A
- Capture.
- Rolling.
- Slow rolling.
- Adhesion.
- Trans-migration.
11
Q
Describe in 5 steps the progression of atherosclerosis.
A
- Fatty streaks.
- Intermediate lesions.
- Fibrous plaque.
- Plaque rupture.
- Plaque erosion.
12
Q
Progression of atherosclerosis: what are the constituents of fatty streaks?
A
Foam cells and T-lymphocytes. Fatty streaks can develop in anyone from about 10 years old.
13
Q
Progression of atherosclerosis: what are constituents of intermediate lesions?
A
- Foam cells.
- Smooth muscle cells.
- T lymphocytes.
- Platelet adhesion.
- Extracellular lipid pools.
14
Q
Progression of atherosclerosis: what are the constituents of fibrous plaques?
A
- Fibrous cap overlies lipid core and necrotic debris.
- Smooth muscle cells.
- Macrophages.
- Foam cells.
- T lymphocytes.
Fibrous plaques can impede blood flow and are prone to rupture.
15
Q
Progression of atherosclerosis: why might plaque rupture occur?
A
Fibrous plaques are constantly growing and receding. The fibrous cap has to be resorbed and redeposited in order to be maintained. If balance shifted in favour of inflammatory conditions, the cap becomes weak and the plaque ruptures. Thrombus formation and vessel occlusion.
16
Q
What is the treatment for atherosclerosis?
A
Percutaneous coronary intervention (PCI)
17
Q
What is the major limitation of PCI?
A
Restenosis.
18
Q
How can restenosis be avoided following PCI?
A
Drug eluting stents: anti-proliferative and drugs that inhibit healing
19
Q
What is the key principle behind the pathogenesis of atherosclerosis?
A
It is an inflammatory process!
20
Q
Define atherogenesis.
A
The development of an atherosclerotic plaque.
21
Q
Define angina.
A
Angina is a type of IHD. It is a symptom of O2 supply/demand mismatch to the heart experienced on exertion.
22
Q
What is the most common cause of angina?
A
Narrowing of the coronary arteries due to atherosclerosis.
23
Q
Give 5 possible causes of angina.
A
- Narrowed coronary artery = impairment of blood flow e.g. atherosclerosis.
- Increased distal resistance = LV hypertrophy.
- Reduced O2 carrying capacity e.g. anaemia.
- Coronary artery spasm.
- Thrombosis
24
Q
Give 5 modifiable risk factors for angina.
A
- Smoking.
- Diabetes.
- High cholesterol (LDL).
- Obesity/sedentary lifestyle.
- Hypertension.
25
Give 3 non-modifiable risk factors for angina.
1. Increasing age.
2. Gender, male bias.
3. Family history/genetics.
26
Briefly describe the pathophysiology of angina that results from atherosclerosis.
On exertion there is increased O2 demand. Coronary blood flow is obstructed by an atherosclerotic plaque -> myocardial ischaemia -> angina.
27
Briefly describe the pathophysiology of angina that results from anaemia.
On exertion there is increased O2 demand. In someone with anaemia there is reduced O2 transport -> myocardial ischaemia -> angina.
28
How do blood vessels try and compensate for increased myocardial demand during exercise.
When myocardial demand increases e.g. during exercise, microvascular resistance drops and flow increases!
29
Why are blood vessels unable to compensate for increased myocardial demand in someone with CV disease?
In CV disease, epicardial resistance is high meaning microvascular resistance has to fall at rest to supply myocardial demand at rest. When this person exercises, the microvascular resistance can't drop anymore and flow can't increase to meet metabolic demand = angina!
30
How can angina be reversed?
Resting - reducing myocardial demand.
31
How would you describe the chest pain in angina?
Crushing central chest pain. Heavy and tight. The patient will often make a fist shape to describe the pain.
32
Give 5 symptoms of angina.
1. Crushing central chest pain.
2. The pain is relieved 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.
33
What tool can you use to determine the best investigations and treatment in someone you suspect to have angina?
Pre-test probability of CAD. It takes into account gender, age and typicality of pain.
34
What investigations might you do in someone you suspect to have angina?
1. ECG - usually normal, there are no markers of angina.
2. Echocardiography.
3. CT angiography - has a high NPV and is good at excluding the disease.
4. Exercise tolerance test - induces ischaemia.
5. Invasive angiogram - tells you FFR (pressure gradient across stenosis).
35
A young, healthy, female patient presents to you with what appears to be the signs and symptoms of angina. Would it be good to do CT angiography on this patient?
Yes. CT angiography has a high NPV and so is ideal for excluding CAD in
younger, low risk individuals.
36
Describe the primary prevention of angina.
1. Risk factor modification.
| 2. Low dose aspirin.
37
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.
38
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.
39
Describe the action of beta blockers.
Beta blockers are beta 1 specific. They antagonise sympathetic activation and so are negatively chronotropic and inotropic. Myocardial work is reduced and so is myocardial demand = symptom relief.
40
Give 3 side effects of beta blockers.
1. Bradycardia.
2. Tiredness.
3. Erectile dysfunction.
4. Cold peripheries.
41
When might beta blockers be contraindicated?
They might be contraindicated in someone with asthma or in someone who is bradycardic.
42
Describe the action of nitrates.
Nitrates e.g. GTN spray are venodilators. Venodilators -> reduced venous return -> reduced pre-load -> reduced myocardial work and myocardial demand.
43
Describe the action of Ca2+ channel blockers.
Ca2+ blockers are arterodilators -> reduced BP -> reduced afterload -> reduced myocardial demand.
44
Name 2 drugs that might be used in someone with angina or in someone at risk of angina to improve prognosis.
Name 2 drugs that might be used in someone with angina or in someone at risk of angina to improve prognosis.
45
How does aspirin work?
Aspirin irreversibly inhibits COX. You get reduced TXA2 synthesis and so platelet aggregation is reduced.
Caution: Gastric ulcers!
46
What are statins used for?
They reduce the amount of LDL in the blood.
47
What is revascularisation?
Revascularisation might be used in someone with angina. It restores the patent coronary artery and increases blood flow.
48
Name 2 types of revascularisation.
1. PCI.
| 2. CABG.
49
Give 2 advantages and 1 disadvantage of PCI.
1. Less invasive.
2. Convenient and acceptable.
3. High risk of restenosis.
50
Give 1 advantage and 2 disadvantages of CABG.
1. Good prognosis after surgery.
2. Very invasive.
3. Long recovery time.
51
What are acute coronary syndromes (ACS)?
ACS encompasses a spectrum of acute cardiac conditions including unstable angina, NSTEMI and STEMI.
52
What is the common cause of ACS?
Rupture of an atherosclerotic plaque and subsequent arterial thrombosis.
53
What are uncommon causes of ACS?
1. Coronary vasospasm.
2. Drug abuse.
3. Coronary artery dissection.
54
Briefly describe the pathophysiology of ACS?
Atherosclerosis -> plaque rupture -> platelet aggregation -> thrombosis formation -> ischaemia and infarction -> necrosis of cells -> permanent heart muscle damage and ACS.
55
Describe type 1 MI.
Spontaneous MI with ischaemia due to plaque rupture.
56
Describe type 2 MI.
MI secondary to ischaemia due to increased O2 demand.
57
Why do you see increased serum troponin in NSTEMI and STEMI?
The occluding thrombus causes necrosis of cells and so myocardial damage. Troponin is a sensitive marker for cardiac muscle injury and so is significantly raised in reflection to this.
58
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.
59
Give 6 signs/symptoms of MI.
1. Unremitting and usually severe central cardiac chest pain.
2. Pain occurs at rest.
3. Sweating
4. Breathlessness.
5. Nausea/vomiting.
6. 1/3 occur in bed at night.
60
Give 5 potential complications of MI.
1. Heart failure.
2. Rupture of infarcted ventricle.
3. Rupture of interventricular septum.
4. Mitral regurgitation.
5. Arrhythmias.
6. Heart block.
7. Pericarditis.
61
What investigations would you do on someone you suspect to have ACS?
1. ECG.
2. Blood tests; look at serum troponin.
3. Coronary angiography.
4. Cardiac monitoring for arrhythmias.
62
What might the ECG of someone with unstable angina show?
The ECG from someone with unstable angina may be normal or might show T wave inversion and ST depression.
63
What might the ECG of someone with NSTEMI show?
The ECG from someone with NSTEMI may be normal or might show T wave inversion and ST depression. There also might be R wave regression, ST elevation and biphasic T wave in lead V3.
64
What might the ECG of someone with STEMI show?
The ECG from someone with STEMI will show ST elevation in the anterolateral leads. After a few hours, T waves invert and deep, broad, pathological Q waves develop.
65
What would the serum troponin level be like in someone with unstable angina?
Normal.
66
What would the serum troponin level be like in someone with NSTEMI/STEMI?
Significantly raised.
67
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.
68
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.
5. Oxygen if hypoxic.
6. Nitrates.
69
What is the treatment of choice for STEMI?
PCI.
70
What is the function of P2Y12?
It amplifies platelet activation.
71
Give 3 potential side effects of P2Y12 inhibitors.
1. Bleeding.
2. Rash.
3. GI disturbances.
72
Describe the secondary prevention therapy for people after having a STEMI.
1. Aspirin.
2. Clopidogrel (P2Y12 inhibitor).
3. Statins.
4. Metoprolol (beta blocker).
5. ACE inhibitor.
6. Modification of risk factors.
73
ECG: what is the J point?
Where the QRS complex becomes the ST segment.
74
ECG: what is the normal axis of the QRS complex?
-30° -> +90°
75
ECG: what does the P wave represent?
Atrial depolarisation.
76
ECG: how long should the PR interval be?
ECG: how long should the PR interval be?
77
ECG: what might a long PR interval indicate?
Heart block.
78
ECG: how long should the QT interval be?
0.35 - 0.45s.
79
ECG: what does the QRS complex represent?
Ventricular depolarisation.
80
ECG: what does the T wave represent?
Ventricular repolarisation.
81
ECG: where would you place lead 1?
From the right arm to the left arm with the positive electrode being at the left arm. At 0°.
82
ECG: where would you place lead 2?
From the right arm to the left leg with the positive electrode being at the left leg. At 60°.
83
ECG: where would you place lead 3?
From the left arm to the left leg with the positive electrode being at the left leg. At 120°.
84
ECG: where would you place lead avF?
From halfway between the left arm and right arm to the left leg with the positive electrode being at the left leg. At 90°.
85
ECG: where would you place lead avL?
From halfway between the right arm and left leg to the left arm with the positive electrode being at the left arm. At -30°.
86
ECG: where would you place lead avR?
From halfway between the left arm and left leg to the right arm with the positive electrode being at the right arm. At -150°.
87
What is the dominant pacemaker of the heart?
The SA node. 60-100 beats/min.
88
How many seconds do the following represent on ECG paper?
a) small squares.
b) large squares.
a) 0.04s.
| b) 0.2s.
89
How long should the QRS complex be?
Less than 110 ms.
90
In which leads would you expect the QRS complex to be upright in?
Leads 1 and 2.
91
In which lead are all waves negative?
aVR.
92
In which leads must the R wave grow?
From chest leads V1 to V4.
93
In which leads must the S wave grow?
From chest leads V1 to V3. It must also disappear in V6.
94
In which leads should T waves and P waves be upright?
Leads 1, 2, V2 -> V6.
95
What might tall pointed P waves on an ECG suggest?
Right atrial enlargement.
96
What might notched, 'm shaped' P waves on an ECG suggest?
Left atrial enlargement.
97
Give 3 signs of abnormal T waves.
1. Symmetrical.
2. Tall and peaked.
3. Biphasic or inverted.
98
What happens to the QT interval when HR increases?
The QT interval decreases.
99
What part of the ECG does the plateau phase of the cardiac action potential coincide with?
QT interval.
100
What are the symptoms of DVT?
Non-specific symptoms, pain and swelling. Tenderness, warmth and slight discolouration.
101
Briefly describe the investigations might be done in order to diagnose a DVT.
1. D-dimer; looks for fibrin breakdown products. If normal, you can exclude DVT. Abnormal does not confirm diagnosis however.
2. Ultrasound compression scan; if you can't squash the vein = clot.
102
What is the treatment for DVT?
1. LMWH.
2. Oral warfarin or DOAC.
3. Compression stockings.
4. Treat the underlying cause e.g. malignancy or thrombophilia.
103
Give 5 risk factors for DVT.
1. Surgery, immobility, leg fracture.
2. OCP, HRT.
3. Long haul flights.
4. Genetic predisposition.
5. Pregnancy.
104
How can DVT's be prevented?
1. Hydration.
2. Mobilisation.
3. Compression stockings.
4. Low does LMWH.
105
What might be the consequence of a dislodged DVT?
Pulmonary embolism.
106
How would you describe an arterial thrombosis?
Platelet rich - a 'white thrombosis'.
107
How would you describe a venous thrombosis?
Fibrin rich - a 'red thrombosis'.
108
What are the potential consequences of arterial thrombosis?
1. MI.
2. Stroke.
3. Peripheral vascular disease e.g. gangrene
109
What are the potential consequences of venous thrombosis?
Pulmonary embolism.
110
What is the treatment for arterial thrombosis?
1. Aspirin.
2. LMWH.
3. Thrombolytic therapy.
111
How does warfarin work?
It produces NON-functional clotting factors 2, 7, 9 and 10.
112
What is warfarin the antagonist of?
Vitamin K.
113
Why is warfarin difficult to use?
1. Lots of interactions!
2. Teratogenic.
3. Needs almost constant monitoring.
114
What is infective endocarditis?
Infection of the heart valves.
115
What is the clinical diagnosis of hypertension?
BP ≥ 140/90mmHg.
116
How can hypertension be treated?
1. Lifestyle modification e.g. reduce salt intake.
| 2. Anti-hypertensive drugs.
117
Write an equation for BP.
BP = CO X TPR.
118
Name 2 systems that are targeted pharmacologically in the treatment of hypertension.
1. RAAS.
| 2. Sympathetic nervous system (NAd).
119
Give 4 functions of angiotensin 2.
1. Potent vasoconstrictor.
2. Activates sympathetic nervous system; increased NAd.
3. Activates aldosterone = Na+ retention.
4. Vascular growth, hyperplasia and hypertrophy.
120
Give 3 ways in which the sympathetic nervous system (NAd) lead to increased BP.
1. Noradrenaline is a vasoconstrictor = increased TPR.
2. NAd has positive chronotropic and inotropic effects.
3. It can cause increased renin release.
121
Name 3 ACE inhibitors.
1. Ramapril.
2. Enalapril.
3. Perindopril.
122
In what diseases are ACE inhibitors clinically indicated?
1. Hypertension.
2. Heart failure.
3. Diabetic nephropathy.
123
Give 4 potential side effects of ACE inhibitors.
1. Hypotension.
2. Hyperkalaemia.
3. Acute renal failure.
4. Teratogenic.
124
Why do ACE inhibitors lead to increased kinin production?
ACE also converts bradykinin to inactive peptides. Therefore ACE inhibitors lead to a build up of kinin.
125
ACE inhibitors: give 3 potential side effects that are due to increased kinin production.
1. Dry chronic cough.
2. Rash.
3. Anaphylactoid reaction.
126
You see a patient who is taking ramipril. They say that since starting the medication they have had a dry and persistent cough. What might have caused this?
ACE inhibitors lead to a build up of kinin. One of the side effects of this is a dry and chronic cough.
127
What are ARBs?
Angiotensin 2 receptor blockers.
128
At which receptor do ARB's work?
AT-1 receptor.
129
Name 3 ARBs?
1. Candesartan.
2. Valsartan.
3. Losartan.
130
In what diseases are ARBs clinically indicated?
1. Hypertension.
2. Heart failure.
3. Diabetic nephropathy.
131
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 ARB e.g. candesartan.
132
Give 4 potential side effects of ARBs.
ARBs have similar side effects to ACEi:
1. Hypotension.
2. Hyperkalaemia.
3. Renal dysfunction.
4. Rash.
Contraindicated in pregnancy.
133
Name 4 Calcium channel blockers.
1. Amlodipine.
2. Felodipine.
3. Diltiazem.
4. Verapamil.
134
Name 2 dihydropyridines and briefly explain how they work.
Dihydropyridines are a class of calcium channel blockers. Amlodipine and felodipine are examples of dihydropyridines. They are arterial vasodilators.
135
Name a calcium channel blocker that acts primarily on the heart.
Verapamil - it is negatively chronotropic and inotropic.
136
Name a calcium channel blocker that acts on the heart and on blood vessels.
Diltiazem - acts on the heart and the vasculature.
137
In what diseases are calcium channel blockers clinically indicated?
1. Hypertension.
2. IHD.
3. Arrhythmia.
138
On what channels do calcium channel blockers work?
L type Ca2+ channels.
139
Give 3 potential side effects that are due to the vasodilatory ability of calcium channel blockers.
1. Flushing.
2. Headache.
3. Oedema.
140
Give a potential side effect that is due to the negatively inotropic ability of calcium channel blockers.
Worsening caridac failure.
141
Give 2 potential side effects that are due to the negatively chronotropic ability of calcium channel blockers.
1. Bradycardia.
| 2. Atrioventricular block.
142
Give 4 potential side effects of verapamil.
1. Worsening cardiac failure (-ve inotrope).
2. Bradycardia (-ve chronotrope).
3. Atrioventricular block (-ve chronotrope).
4. Constipation!
143
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.
144
Name 3 beta blockers.
1. Bisoprolol (beta 1 selective).
2. Atenolol.
3. Propanolol (beta 1/2 non selective).
145
In what diseases are beta blockers clinically indicated?
1. IHD.
2. Heart failure.
3. Arrhythmia.
4. Hypertension.
146
Give 5 potential side effects of beta blockers.
1. Fatigue.
2. Headache.
3. Nightmares.
4. Bradycardia.
5. Hypotension.
6. Cold peripheries.
7. Erectile dysfunction.
8. Bronchospasm.
147
Diuretics: where do in the kidney do thiazides work?
The distal tubule.
148
Name a thiazide.
Bendroflumethiazide.
149
Name 2 loop diuretics.
1. Furosemide.
| 2. Bumetanide.
150
Name a potassium sparing diuretic.
Spironolactone.
151
Why are potassium sparing diuretics especially effective?
They have anti-aldosterone effects too.
152
In what diseases are diuretics clinically indicated?
1. Heart failure.
| 2. Hypertension.
153
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.
154
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.
155
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.
156
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.
157
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.
158
What is heart failure?
A complex clinical syndrome of signs and symptoms that suggest the efficiency of the heart as a pump is impaired.
159
What is the most common cause of heart failure?
Ischaemic heart disease.
160
What might you give to someone with hypertension if they are ACE inhibitor intolerant?
ARB.
161
What hormones does the heart produce?
ANP and BNP.
162
What metabolises ANP and BNP?
NEP.
163
Why can NEP inhibitors work for heart failure treatment?
NEP metabolises ANP and BNP. NEP inhibitors can therefore increase levels of ANP and BNP in the serum.
164
What are the functions of ANP and BNP?
1. Increased renal excretion of Na+ and therefore water.
2. Vasodilators.
3. Inhibit aldosterone release.
165
What is the counter regulatory system to RAAS?
ANP/BNP hormones.
166
Name 2 nitrates that are used pharmacologically.
1. Isosorbide mononitrate.
| 2. GTN spray.
167
How do nitrates work in the treatment of heart failure?
They are venodilators. They reduce preload and so BP.
168
Give 3 potential side effects of nitrates.
1. Headache.
2. Syncope.
3. Tolerance.
169
What classification is used to group anti-arrhythmic drugs?
Vaughan Williams classification.
170
Vaughan Williams classification: name 3 class 1 drugs.
Class 1 are Na+ channel blockers. There are 3 sub-divisions in this group.
1a: disopyramide.
1b: lidocaine.
1c: flecainide.
171
Vaughan Williams classification: name 3 class 2 drugs.
Class 2 are beta blockers:
1. Propranolol.
2. Atenolol.
3. Bisoprolol.
172
Vaughan Williams classification: name a class 3 drug.
Class 3 drugs prolong the action potential. E.g. amiodarone. Side effects are very likely with these drugs.
173
Vaughan Williams classification: name 2 class 4 drugs.
Class 4 drugs are calcium channel blockers but NOT dihydropyridines as these don't effect the heart.
1. Verapamil.
2. Diltiazem.
174
How does digoxin work?
It inhibits the Na+/K+ pump therefore making the action potential more positive and ACh is released from parasympathetic nerves.
175
What are the main effects of digoxin?
1. Bradycardia.
2. Reduced atrioventricular conduction.
3. Increased force of contraction (positive inotrope).
176
Give 4 potential side effects of digoxin.
1. Nausea.
2. Vomiting.
3. Diarrhoea.
4. Confusion.
177
In what diseases is digoxin clinically indicated?
Atrial fibrillation and severe heart failure.
178
Name 2 drugs that can prolong the QT interval.
1. Sotalol.
| 2. Amiodarone.
179
Give 5 potential side effects of drugs that prolong the QT interval.
1. Pro-arrythmic effects.
2. Interstitial pneumonitis.
3. Abnormal liver function.
4. Hyper/hypothyroidism.
5. Sun sensitivity.
6. Grey skin discolouration.
7. Corneal micro-deposits.
8. Optic neuropathy.
180
How do sodium channel blockers work in the treatment of ventricular tachycardia?
They block the inactivation gate of the sodium channel.
181
What additional property makes propranolol the most useful beta blocker to help control the arrhythmias which occur immediately following a heart attack ?
It can also block sodium channels.
182
What does furosemide block?
The Na+/K+/2Cl- transporter.
183
Why are beta blockers good in chronic heart failure?
They block reflex sympathetic responses which stress the failing heart.
184
Doxazosin can be used in the treatment of hypertension. How does this drug work?
It is an alpha 1 receptor antagonist.
185
How do beta blockers provide symptom relief in angina?
1. They reduce O2 demand by slowing heart rate (negative chronotrope).
2. They reduce O2 demand by reducing myocardial contractility (negative inotrope).
3. They increase O2 distribution by slowing heart rate.
186
What drug might you give to someone with angina caused by coronary artery vasospasm?
Amlodipine.
187
How much serous fluid is there between the visceral and parietal pericardium?
50ml.
188
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.
189
What is the function of pericardium?
It restrains the filling volume of the heart.
190
Describe the aetiology of pericarditis.
1. Viral (common) e.g. enteroviruses.
2. Bacterial e.g. mycobacterium tuberculosis.
3. Autoimmune e.g. RA, sjogren syndrome.
4. Neoplastic.
5. Metabolic e.g. uraemia.
6. Traumatic and iatrogenic.
7. 80-90% are idiopathic.
191
What is acute pericarditis?
An inflammatory pericardial syndome with or without effusion.
192
How can acute pericarditis be clinically diagnosed?
Acute pericarditis can be clinically diagnosed if the patient has at least 2 of the following:
1. Chest pain.
2. Friction rub.
3. ECG changes.
4. Pericardial effusion.
193
Give 5 symptoms of pericarditis.
1. Chest pain - Described as severe, sharp and pleuritic; rapid onset; possible radiation to arm.
2. Dyspnoea.
3. Cough
4. Hiccups.
5. Skin rash.
194
Why might someone with pericarditis have hiccups?
Because of irritation to the phrenic nerve.
195
What investigations might you do on someone who you suspect to have pericarditis?
1. ECG.
2. CXR.
3. Bloods.
4. Echocardiogram.
196
What might the ECG look like in someone with acute pericarditis?
1. PR depression seen in most leads.
| 2. 'Saddle shaped' concave ST elevation.
197
What is the major differential diagnosis of acute pericarditis?
MI - It is important to rule this out asap.
198
What is the treatment for pericarditis?
1. Patients are advised to avoid strenuous activity until symptom resolution.
2. NSAID or aspirin - high doses.
3. Colchicine (anti-inflammatory).
199
Why does chronic pericardial effusion rarely cause tamponade?
The parietal pericardium is able to adapt when effusions accumulate slowly and so tamponade is prevented.
200
What is haemopericardium?
Direct bleeding from vasculature through the ventricular wall following MI.
201
What can cause myocarditis?
Viral infeciton.
202
Name 3 cardiomyopathies.
1. Hypertrophic (HCM)
2. Dilated (DCM)
3. Arrhythmogenic right/left ventricular. (ARVC/ALVC)
... Yes these can cause heart failure.
203
What can cause HCM (hypertrophic cardiomyopathy)
1. Sarcomeric gene mutations are the main cause e.g. beta myosin, troponin T mutations. (1/500 affected)
2. High blood pressure and ageing.
204
What can cause ARVC/ALVC?
Desmosome gene mutations.
205
What is the usual inheritance pattern for cardiomyopathies?
Autosomal dominant. Offspring will therefore have a 50% chance of being affected
206
Describe the pathophysiology of HCM.
Systole is normal but diastole is affected; the heart is unable to relax properly due to thickening of the ventricular walls.
Will this affect preload then?
207
Describe the pathophysiology of DCM.
Ventricular dilation and dysfunction = poor contractility.
208
Describe the pathophysiology of ARVC/ALVC.
Desmosomes attach cells via their intermediate filaments. Desmosome mutations lead to myocytes being pulled apart and ventricles are replaced with fatty fibrous tissue. Gap junctions are affected too.
209
Give 3 symptoms of HCM.
1. Angina. (think due to increased resistance of small vessels)
2. Dyspnoea.
3. Syncope.
210
Give 3 symptoms of DCM.
DCM usually presents with symptoms similar to those seen in heart failure:
1. breathlessness.
2. Tiredness.
3. Oedema.
211
Give a sign of ARVC/ALVC.
Ventricular tachycardia.
212
What might an ECG look like from a person with HCM.
1. Large QRS complexes.
| 2 Large inverted T waves.
213
What might an ECG look like from a person with ARVC/ALVC.
Epsilon waves.
214
What is restrictive cardiomyopathy?
Poor dilation of the heart restricts diastole.
215
What is the commonest cause of restrictive cardiomyopathy?
Amyloidosis (extra-cellular deposition of an insoluble fibrillar protein - amyloid).
(Different to HCM as no hypertrophy)
216
What are channelopathies?
Mutations in genes coding for ion channels.
217
Name 4 channelopathies.
1. Long QT syndrome.
2. Short QT syndrome.
3. Brugada.
4. CPVT.
218
What ion channel is affected in Brugada?
Sodium channel.
219
What is the commonest symptom of channelopathies?
Recurrent syncope.
220
What might the ECG look like from someone with Brugada?
Characteristic ST elevation in chest leads.
221
What is Brugada?
A channelopathy caused by a mutation in sodium channels.
222
What are the four main features of tetralogy of fallot?
1. Ventricular septal defect.
2. Over-riding aorta.
3. RV hypertrophy.
4. Pulmonary stenosis.
223
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.
224
What is VSD (ventricular septal defect)
An abnormal connection between the two ventricles.
225
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... (I'm guessing there is no deoxygenated blood getting into systemic circulation).
226
Give 4 clinical signs of a large VSD.
1. High pulmonary blood flow.
2. Breathlessness, poor feeding, failure to thrive.
3. Increased resp rate.
4. Tachycardia.
(requires surgical repair)
227
What syndrome might VSD lead on to?
Eisenmengers syndrome.
228
Briefly describe the physiology of Eisenmengers syndrome.
High pressure pulmonary blood flow damages pulmonary vasculature --> there is increased resistance to blood flow (pulmonary hypertension) --> RV pressure increases --> shunt direction reverses (RV to LV) --> cyanosis!
229
What are the risks associated with Eisenmengers syndrome?
1. Risk of death.
2. Endocarditis.
3. Stroke.
230
What is ASD?
An abnormal connection between the two atria. It is fairly common.
231
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 the right (therefore no deoxy blood in systemic circulation)
232
Give 5 clinical signs of a large ASD.
1. Significant increase in blood flow through the right heart and lungs - pulmonary flow murmur.
2. Enlarged pulmonary arteries.
3. Right heart dilatation.
4. SOBOE
5. Increased chest infection.
233
What is AVSD?
Atrio-ventricular septal defects. Basically a hole in the very centre of the heart.
234
Give 2 clinical signs of AVSD.
1. Breathlessness.
| 2. Poor feeding and poor weight gain.
235
What is PDA?
Patent ductus arteriosus.
236
Give 4 clinical signs of PDA.
1. Torrential flow from the aorta to the pulmonary arteries can lead to pulmonary hypertension and RHF.
2. Breathlessness.
3. Poor feeding, failure to thrive.
4. Risk of endocarditis.
237
Describe the pathophysiology behind coarctation of the aorta.
Excessive sclerosing (to become hardened) that normally closes the ductus arteriosus extends into the aortic wall leading to narrowing.
238
What is pulmonary stenonsis?
Narrowing of the RV outflow tract.
239
Name 3 congenital heart defects that are not cyanotic.
1. VSD.
2. ASD.
3, PDA.
- Left to right shunt means no cyanosis
- There is risk of Eisenmengers however.
240
Name a congenital heart defect that is cyanotic.
1. Tetraology of Fallot.
| 2. Right to left shunt.
