Cardiovascular 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.
1. Aspirin.
| 2. Statins.
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?
120 - 200ms.
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
Define shock.
When the cardiovascular system is unable to provide adequate substrate for aerobic cellular respiration.
188
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.
189
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.
190
Classification of shock: describe the vital signs in class 1 e.g. blood loss, pulse, blood pressure, pulse pressure, respiratory rate and urine output.
1. 15% blood loss.
2. Pulse < 100 bpm.
3. Blood pressure - normal.
4. Pulse pressure - normal.
5. Respiratory rate: 14 - 20.
6. Urine output > 30ml/h.
191
Classification of shock: describe the vital signs in class 2 e.g. blood loss, pulse, blood pressure, pulse pressure, respiratory rate and urine output.
1. 15-30% blood loss.
2. Pulse > 100 bpm.
3. Blood pressure - normal.
4. Pulse pressure - decreased.
5. Respiratory rate: 20 - 30.
6. Urine output: 20 - 30ml/h.
192
Classification of shock: describe the vital signs in class 3 e.g. blood loss, pulse, blood pressure, pulse pressure, respiratory rate and urine output.
1. 30-40% blood loss.
2. Pulse > 120 bpm.
3. Blood pressure - decreased.
4. Pulse pressure - decreased.
5. Respiratory rate: 30 - 40.
6. Urine output: 5 - 15ml/h.
193
What can cause cardiogenic shock?
1. Cardiac tamponade.
2. Pulmonary embolism.
3. Acute MI.
4. Fluid overload.
194
What is septic shock?
A systemic inflammatory response associated with an infection (bacterial endotoxins).
195
What is anaphylactic shock?
An intense allergic reaction associated with massive histamine release = haemodynamic collapse. The patient may be breathless, wheezy and have a rash.
196
What is the treatment for anaphylactic shock?
Adrenaline and supportive therapy e.g. O2 delivery, fluid replacement.
197
Give 2 signs of ARDS.
1. Impaired oxygenation.
2. Bilateral pulmonary infiltrates.
3. No cardiac failure.
198
Describe the pathophysiology of ARDS in 3 stages.
1. Exudative phase: increased vascular permeability leads to a platelet, fibrin and clotting factor rich exudate.
2. Proliferative phase: fibroblast proliferation.
3. Fibrotic phase.
199
Give 4 extra-pulmonary causes of ARDS.
1. SEPSIS!
2. Trauma.
3. Shock.
4. Drug reaction.
5. Pancreatitis.
200
Give 3 pulmonary causes of ARDS.
1. Pneumonia.
2. Smoke inhalation.
3. Near drowning.
201
How much serous fluid is there between the visceral and parietal pericardium?
50ml.
202
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.
203
What is the function of pericardium?
It restrains the filling volume of the heart.
204
Describe the aetiology of pericarditis.
1. Viral (common) e.g. enteroviruses.
2. Bacterial e.g. mycobacterium tuberculosis.
3. Autoimmune e.g. RA, sjögren syndrome.
4. Neoplastic.
5. Metabolic e.g. uraemia.
6. Traumatic and iatrogenic.
7. 80-90% are idiopathic.
205
What is acute pericarditis?
An inflammatory pericardial syndrome with or without effusion.
206
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.
207
Give 5 symptoms of pericarditis.
1. Chest pain! Described as severe, sharp and pleuritic. Rapid onset. Pain can radiate to the arm.
2. Dyspnoea.
3. Cough.
4. Hiccups.
5. Skin rash.
208
Why might someone with pericarditis have hiccups?
Because of irritation to the phrenic nerve.
209
What investigations might you do on someone who you suspect to have pericarditis?
1. ECG.
2. CXR.
3. Bloods.
4. Echocardiogram.
210
What might the ECG look like in someone with acute pericarditis?
1. PR depression seen in most leads.
| 2. 'Saddle shaped' concave ST elevation.
211
What is the major differential diagnosis of acute pericarditis?
MI - it is important to rule this out ASAP!
212
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).
213
Why does chronic pericardial effusion rarely cause tamponade?
The parietal pericardium is able to adapt when effusions accumulate slowly and so tamponade is prevented.
214
What is haemopericardium?
Direct bleeding from vasculature through the ventricular wall following MI.
215
What can cause myocarditis?
Viral infection.
216
Name 3 cardiomyopathies.
1. Hypertrophic (HCM).
2. Dilated (DCM).
3. Arrhythmogenic right/left ventricular (ARVC/ALVC).
217
What can cause HCM?
Sarcomeric gene mutations e.g. beta myosin, troponin T mutations. About 1 in 500 people are affected.
218
What can cause ARVC/ALVC?
Desmosome gene mutations.
219
What is the usual inheritance pattern for cardiomyopathies?
Autosomal dominant; off-spring have a 50% chance of being affected.
220
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.
221
Describe the pathophysiology of DCM.
Ventricular dilation and dysfunction = poor contractility.
222
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.
223
Give 3 symptoms of HCM.
1. Angina.
2. Dyspnoea.
3. Syncope.
224
Give 3 symptoms of DCM.
DCM usually presents with symptoms similar to those seen in heart failure:
1. Breathlessness.
2. Tiredness.
3. Oedema.
225
Give a sign of ARVC/ALVC.
Ventricular tachycardia.
226
What might an ECG look like from a person with HCM.
1. Large QRS complexes.
| 2. Large inverted T waves.
227
What might an ECG look like from a person with ARVC/ALVC.
Epsilon waves.
228
What is restrictive cardiomyopathy?
Poor dilation of the heart restricts diastole.
229
What is the commonest cause of restrictive cardiomyopathy?
Amyloidosis (extra-cellular deposition of an insoluble fibrillar protein - amyloid).
230
What are channelopathies?
Mutations in genes coding for ion channels.
231
Name 4 channelopathies.
1. Long QT syndrome.
2. Short QT syndrome.
3. Brugada.
4. CPVT.
232
What ion channel is affected in Brugada?
Sodium channel.
233
What is the commonest symptom of channelopathies?
Recurrent syncope.
234
What might the ECG look like from someone with Brugada?
Characteristic ST elevation in chest leads.
235
What is Brugada?
A channelopathy caused by a mutation in sodium channels.
236
What are the four main features of tetralogy of fallot?
1. Ventricular septal defect.
2. Over-riding aorta.
3. RV hypertrophy.
4. Pulmonary stenosis.
237
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!
238
What is VSD?
An abnormal connection between the two ventricles.
239
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.
240
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.
5. Requires surgical repair.
241
What syndrome might VSD lead on to?
Eisenmengers syndrome.
242
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!
243
What are the risks associated with Eisenmengers syndrome?
1. Risk of death.
2. Endocarditis.
3. Stroke.
244
What is ASD?
An abnormal connection between the two atria; it is fairly common.
245
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.
246
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.
247
What is AVSD?
Atrio-ventricular septal defects. Basically a hole in the very centre of the heart.
248
Give 2 clinical signs of AVSD.
1. Breathless.
| 2. Poor feeding and poor weight gain.
249
What is PDA?
Patent ductus arteriosus.
250
Give 4 clinical signs of PDA.
1. Torrential flow from the aorta to the pulmonary arteries can lead to pulmonary hypertension and RHF.
2. Breathless.
3. Poor feeding, failure to thrive.
4. Risk of endocarditis.
251
Describe the pathophysiology behind coarctation of the aorta.
Excessive sclerosing that normally closes the ductus arteriosus extends into the aortic wall leading to narrowing.
252
What is pulmonary stenosis?
Narrowing of the RV outflow tract.
253
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.
254
Name a congenital heart defect that is cyanotic.
Tetralogy of Fallot.
Right to left shunt.
255
Define cardiac failure.
A complex clinical syndrome of signs/symptoms that suggest the efficiency of the heart as a pump is impaired; the heart is unable to deliver blood at a rate that meets the metabolic demands.
256
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.
257
Give 5 causes of heart failure.
1. Commonest cause: IHD.
2. Hypertension.
3. Cardiomyopathy.
4. Excessive alcohol.
5. Obesity.
258
Why are men more commonly effected by heart failure than women?
Women have 'protective hormones' meaning they are less at risk of developing heart failure.
259
Briefly describe the pathophysiology of heart failure.
When the heart fails, compensatory mechanisms attempt to maintain CO. As HF progresses, these mechanisms are exhausted and become pathophysiological.
260
What are the compensatory mechanisms in heart failure?
1. Sympathetic system.
2. RAAS.
3. Natriuretic peptides.
4. Ventricular dilation.
5. Ventricular hypertrophy.
261
Explain how the sympathetic system is compensatory in heart failure and give one disadvantage of sympathetic activation.
The sympathetic system improves ventricular function by increasing HR and contractility = CO maintained.
BUT it also causes arteriolar constriction which increases after load and so myocardial work.
262
Explain how RAAS is compensatory in heart failure and give one disadvantage of RAAS activation.
Reduced CO leads to reduced renal perfusion; this activates RAAS. There is increased fluid retention and so increased preload.
BUT it also causes arteriolar constriction which increases after load and so myocardial work.
263
Give 3 properties of natriuretic peptides that make them compensatory in heart failure.
1. Diuretic.
2. Hypotensive.
3. Vasodilators.
264
What are the 3 cardinal symptoms of HF?
1. Shortness of breath.
2. Fatigue.
3. Peripheral oedema.
265
Give 3 signs of left heart failure.
1. Pulmonary crackles.
2. Added heart sounds (3rd and 4th) and murmurs.
3. Displaced apex beat.
4. Tachycardia.
266
What investigations might you initially do in someone who has the signs/symptoms suggestive of HF?
1. ECG.
2. CXR - might show cardiac enlargement.
3. Natriuretic peptide levels - raised indicate heart failure.
267
You have done an ECG, CXR and blood tests on a patient who you suspect might have HF. These have come back abnormal. What investigation might you do next?
An echocardiogram.
268
What is the first line treatment for heart failure?
Vasodilator therapy (ACEi, beta blockers) via the neurohumoral blockade (RAAS-SNS).
269
Give an example of an ACE inhibitor that is commonly used in HF.
Perindopril.
270
Name 4 beta blockers that are used in the treatment of heart failure.
1. Metoprolol.
2. Bisoprolol.
3. Carvedilol.
4. Nebivolol.
271
What drugs might you give to someone with HF for symptom relief.
Diuretics: thiazides (bendroflumethiazide) and loop diuretics (furosemide). They promote Na and so H2O excretion.
272
What is cor pulmonale?
RV hypertrophy and dilation due to pulmonary hypertension.
273
What is the WHO clasification of hypertension?
140/90mmHg.
274
On average, by how much does having high blood pressure shorten life?
7 years. Although this depends on onset and severity.
275
Give 5 causes of hypertension.
1. Kidney disease.
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.
276
Name 3 endocrine diseases that can cause secondary hypertension.
1. Conn's syndrome - hyperaldosteronism.
2. Cushing's syndrome - prolonged cortisol exposure -> raised BP.
3. Phaeochromocytoma - adrenal gland tumour, excess NAd and Ad release -> high BP.
277
Give 3 symptoms of phaeochromocytoma?
1. Pallor.
2. Palpitations.
3. Chest pain.
4. Panic.
278
Why might you examine the eyes of someone with hypertension?
Very high BP can cause immediate damage to small vessels, this can be seen in the eyes where there are small exposed blood vessle.s
279
What investigations might you do in someone with hypertension?
1. 24h ambulatory blood pressure monitoring to confirm a diagnosis.
2. ECG and blood tests may be done to identify secondary causes of hypertension.
280
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.
281
If you gave someone 1 blood pressure tablet by how much would you expect their blood pressure to decrease?
1 tablet = 10mmHg reduction in BP.
282
What is the threshold BP for giving treatment to the following:
a) high risk individuals.
b) low risk individuals.
a) High risk - 140/90mmHg.
| b) Low risk - 160/100mmHg.
283
What are the NICE treatment targets for the following:
a) People aged <80?
b) People aged >80?
a) Below 140/90mmHg in those aged less than 80.
| b) Below 150/90mmHg in those aged above 80.
284
Will anti-hypertensives make someone feel better?
Anti-hypertensives won't necessarily make someone feel better as there are few symptoms associated with high BP although headache symptoms may improve.
285
What are the two main types of treatment for hypertension?
1. Lifestyle modification: reduce salt intake, lose weight, reduce alcohol.
2. Drug therapy: ABCD.
286
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.
287
Give 5 potential side effects of rampiril.
Side effects of ACE inhibitors:
1. Hypotension.
2. Acute renal failure.
3. Hyperkalaemia.
4. Teratogenic.
5. Cough, rash, anaphylactoid due to increased kinin production.
288
On what receptor does valsartan act?
AT-1, prevents Ang 2 binding.
289
Give 4 side effects of valsartan.
Side effects of valsartan:
1. Hypotension.
2. Renal dysfunction.
3. Hyperkalaemia.
4. Rash.
5. Contraindicated in pregnancy.
290
Give 5 side effects of bisoprolol.
Side effects of beta blockers:
1. Hypotension.
2. Fatigue.
3. Headaches.
4. Nightmares.
5. Bradycardia.
6. Hypotension.
7. Erectile dysfunction.
8. Cold peripheries.
291
Give 3 side effects of amlodipine.
Side effects of dihydropyridines (CCB):
1. Flushing.
2. Headache.
3. Oedema.
4. Palpitations.
292
Give 3 side effects of verapamil.
Side effects due to being negatively chronotropic:
1. Bradycardia.
2. AV block.
Side effects due to being negatively inotropic:
1. Worsening of cardiac failure.
293
Give 5 side effects of bendroflumethiazide.
Side effects of diuretics:
1. Hypovolemia.
2. Hypotension.
3. Reduced K, Na, Mg, Ca.
4. Hyperuricaemia -> gout.
5. Erectile dysfunction.
294
Name 4 valvular heart diseases.
1. Aortic stenosis.
2. Mitral regurgitation.
3. Mitral stenosis.
4. Aortic regurgitation.
295
Briefly describe aortic stenosis.
A disease where the aortic orifice is restricted and so the LV can't eject blood properly in systole = pressure overload.
296
Describe the aetiology of aortic stenosis.
1. Congenital bicuspid valve.
| 2. Acquired e.g. age related degenerative calcification and rheumatic heart disease.
297
Describe the pathophysiology of aortic stenosis.
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.
298
Give 3 symptoms of aortic stenosis.
1. Exertional syncope.
2. Angina.
3. Exertional dyspnoea.
Onset of symptoms is associated with poor prognosis.
299
Give 3 signs of aortic stenosis.
1. Slow rising carotid pulse and decreased pulse amplitude.
2. Soft or absent heart sounds.
3. Ejection systolic murmur: <> shape.
300
What investigation might you do in someone who you suspect to have aortic stenosis?
Echocardiography.
301
Describe the management for someone with aortic stenosis.
1. Ensure good dental hygiene.
2. Consider IE prophylaxis.
3. Aortic valve replacement or TAVI.
302
Who should be offered an aortic valve replacement?
1. Symptomatic patients with aortic stenosis.
2. Any patient with decreasing ejection fraction.
3. Any patient undergoing CABG with moderate/severe aortic stenosis.
303
What is mitral regurgitation?
Back flow of blood from the LV to the LA during systole - LV volume overload.
304
Describe the aetiology of mitral regurgitation.
1. Myxomatous degeneration.
2. Ischaemic mitral regurgitation.
3. Rheumatic heart disease.
4. IE.
305
What is the pathophysiology of mitral regurgitation?
LV volume overload! Compensatory mechanisms: LA enlargement and LVH and increased contractility. Progressive LV volume overload -> dilatation and progressive HF.
306
Give 2 symptoms of mitral regurgitation.
1. Dyspnoea on exertion.
| 2. HF.
307
Give 3 signs of mitral regurgitation.
1. Pansystolic murmur (always there).
2. Soft 1st heart sound.
3. 3rd heart sound.
In chronic MR the intensity of the murmur correlates with disease severity.
308
What investigations might you do in someone who you suspect to have mitral regurgitation?
1. ECG.
2. CXR.
3. Echocardiogram: estimates LA/LV size and function.
309
Describe the management of mitral regurgitation.
Rate control for AF e.g. beta blockers. Anticoagulation for AF. Diuretics for fluid overload. IE prophylaxis. If symptomatic = surgery.
310
What is aortic regurgitation?
A regurgitant aortic valve means blood leaks back into the LV during diastole due to ineffective aortic cusps.
311
What is the aetiology of aortic regurgitation?
1. Bicuspid aortic valve.
2. Rheumatic.
3. IE.
312
Describe the pathophysiology of aortic regurgitation.
Pressure and volume overload. Compensatory mechanisms - LV dilatation, LVH. Progressive dilation -> HF.
313
Give 3 symptoms of aortic regurgitation.
1. Dyspnoea on exertion.
2. Orthopnea.
3. Palpitations.
4. Paroxysmal nocturnal dyspnea.
314
Give 3 signs of aortic regurgitation.
1. Wide pulse pressure.
2. Diastolic blowing murmur.
3. Systolic ejection murmur.
315
What investigations might you do in someone who you suspect to have aortic regurgitation?
CXR and echocardiogram.
316
Describe the management for someone with aortic regurgitation.
IE prophylaxis. Vasodilators e.g. ACEi. Regular echo's to monitor progression. Surgery if symptomatic.
317
What is mitral stenosis?
Obstruction to LV inflow that prevents proper filling during diastole.
318
Give 3 causes of mitral stenosis.
1. Rheumatic heart disease.
2. IE.
3. Calcification.
319
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.
320
Give 3 symptoms of mitral stenosis.
1. Dyspnea.
2. Haemoptysis.
3. RHF symptoms.
321
Give 3 signs of mitral stenosis.
1. 'a' wave in jugular venous pulsations.
2. Signs of RHF.
3. Pink patches on cheeks due to vasoconstriction.
4. Low pitched diastolic murmur.
5. Loud opening 1st heart sound snap.
322
What investigations might you do in someone who you suspect to have mitral stenosis?
1. ECG.
2. CXR.
3. Echocardiogram - gold standard.
323
Describe the management for mitral stenosis.
If in AF rate control e.g. beta blockers/CCB. Anticoagulation if AF. Balloon valvuloplasty or valve replacement. IE prophylaxis.
324
Why does medication not work for mitral and aortic stenosis?
The problem is mechanical and so medical therapy does not prevent progression.
325
What is infective endocarditis?
Infection of the heart valves or other endocardial lined structure within the heart.
326
Name 4 types of IE.
1. Left sided native IE.
2. Left sided prosthetic IE.
3. Right sided IE (rarely prosthetic).
4. Device related IE e.g. pacemakers, defibrillators.
327
Which type of IE is more likely to spread systemically?
Left sided IE - these are more likely to cause thrombo-emboli.
(Right side IE could spread to the lungs).
328
Give 2 risk factors for IE.
1. Having a regurgitant or prosthetic valve.
| 2. If infectious material is introduced into the blood stream or during surgery.
329
What bacteria are most likely to cause IE?
1. Staph aureus.
2. Staph epidermidis (coagulase negative staph).
3. Strep viridans (alpha haemolytic).
330
Give 3 groups of people who are at risk of IE.
1. Elderly.
2. IVDU.
3. Those with prosthetic valves.
4. Those with rheumatic fever.
331
Describe the pathogenesis of IE.
Microbial adherence (infection) -> vegetation on valve -> cardiac valve distortion -> cardiac failure and septic problems.
332
What is the hallmark of IE?
Vegetation - lumps of fibrin hanging off the heart valves.
333
IE: Name 2 sites where vegetation is likely?
1. Atrial surface of AV valves.
| 2. Ventricular surface of SL valves.
334
Give 3 symptoms of IE.
1. Signs of systemic infection e.g. fever, sweats.
2. Embolisation e.g. stroke, PE, MI.
3. Valve dysfunction e.g. HF, arrhythmia.
335
Give 5 signs of IE.
1. Splinter haemorrhages.
2. Osler's nodes.
3. Janeway lesions.
4. Roth spots.
5. Heart murmurs.
336
What investigations might you do in someone who you suspect to have IE?
1. Blood cultures are essential for diagnosis.
2. Echocardiogram shows endocardial involvement e.g. TTE or TOE.
3. Bloods - raised ESR/CRP.
4. ECG.
337
Give 2 advantages and 1 disadvantage of a trans-thoracic echo (TTE).
1. Safe.
2. Non-invasive, no discomfort.
3. Poor images.
338
Give 1 advantage and 2 disadvantages of a trans-thoracic echo (TTE).
1. Excellent images.
2. Discomfort.
3. Small risk of perforation or aspiration.
339
Describe the treatment for IE.
1. Antibiotics based on cultures.
2. Treat any complications.
3. Surgery.
340
Give 4 indications for surgery in IE.
1. Antibiotics not working.
2. Complications.
3. To remove infected devices.
4. To replace the valve.
5. to remove large vegetations before they embolise.
341
Why is it important to remove large vegetations?
To prevent them embolising and causing a stroke, MI etc.
342
Why might blood cultures be negative in a person with IE?
They may have previously received antibiotics.
343
What is giant cell arteritis?
A common type of vasculitis: localised, chronic and granulomatous inflammation of temporal arteries.
344
What are the signs of giant cell arteritis?
1. Thickened often palpable blood vessels.
| 2. Evidence of granulomatous inflammation.
345
Give a possible consequence of giant cell arteritis.
Blindness if the occular artery is affected.
346
What is the name of the criteria used to diagnose IE?
The duke criteria.
347
Name a disease might cause flattening of the P wave.
1. Hyperkalaemia.
| 2. Obesity.
348
Name a disease that might cause tall P waves.
1. Right atrial enlargement.
349
Name a disease that might cause broad notched P waves.
Left atrial enlargement.
350
What aspect of the heart is represented by leads 2, 3 and aVF?
The inferior aspect.
351
What might ST elevation in leads 2, 3 and aVF suggest?
RCA blockage.
These leads show the activity of the inferior aspect of the heart and the RCA supplies the inferior aspect of the heart with blood.
352
Give 3 effects of hyperkalaemia on an ECG.
1. Tall 'tented' T waves.
2. Flat P waves.
3. Broad QRS.
353
Give 2 effects of hypokalaemia on an ECG.
1. Flat T waves.
2. QT prolongation.
3. ST depression.
4. Prominent U waves.
354
Give an effect of hypocalcaemia on an ECG.
1. QT prolongation.
2. T wave flattening.
3. Narrowed QRS.
4. Prominent U waves.
355
Give an effect of hypercalcaemia on an ECG.
1. QT shortening.
2. Tall T waves.
3. No P waves.
356
What is the main pacemaker in the heart?
The sinus node.
357
What controls the sinus node discharge rate?
The autonomic nervous system.
358
Define sinus rhythm.
Sinus rhythm - a P wave precedes each QRS complex.
359
Give 3 potential consequences of arrhythmia.
1. Sudden death.
2. Syncope.
3. Dizziness.
4. Palpitations.
5. Can also be asymptomatic.
360
Define bradycardia.
< 60 bpm.
361
Define tachycardia.
> 100 bpm.
362
Give the two broad categories of tachycardia.
1. Supra-ventricular tachycardia's.
| 2. Ventricular tachycardia's.
363
Where do supra-ventricular tachycardia's arise from?
They arise from the atria or atrio-ventricular junction.
364
Do supra-ventricular tachycardia's have narrow or broad QRS complexes?
Supraventricular tachycardias are often associated with narrow complexes.
365
Where do ventricular tachycardia's arise from?
The ventricles.
366
Do ventricular tachycardia's have narrow or broad QRS complexes?
Ventricular tachycardias are often associated with broad complexes.
367
Name 5 supra-ventricular tachycardia's.
1. Atrial fibrillation.
2. Atrial flutter.
3. AV node re-entry tachycardia (AVNRT).
4. Accessory pathway.
5. Focal atrial tachycardia.
368
Give 4 causes of sinus tachycardia.
1. Physiological response to exercise.
2. Fever,
3. Anaemia.
4. Heart failure.
5. Hypovolemia.
369
Describe 2 characteristics of an ECG taken from someone with atrial fibrillation.
1. Absent P waves.
| 2. Fine oscillation of the baseline.
370
The ECG taken from someone with atrial fibrillation shows a fine oscillation of the baseline and absent P waves. Why?
The atria fire a lot, it is chaotic. The AV node and ventricles can't keep up -> irregularly irregular pulse.
371
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.
372
What score can be used to calculate the risk of stroke in someone with atrial fibrillation?
CHADS2 VASc.
373
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. Age.
2. Hypertension.
3. Previous stroke/TIA.
4. Diabetes.
5. Female.
A score >2 indicates the need for anticoagulation.
374
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.
375
Atrial fibrillation treatment: what might you give someone to help with rate control?
Beta blockers, CCB and digoxin.
376
Atrial fibrillation treatment: what might you give someone to help restore sinus rhythm (rhythm control)?
Electrical cardioversion or pharmacological cardioversion using flecainide.
377
What is the long term treatment of atrial fibrillation?
Catheter ablation - it targets the triggers of AF.
378
Describe the ECG pattern taken from someone with atrial flutter.
1. Narrow QRS.
| 2. 'sawtooth' flutter waves.
379
The ECG shows a continuous undulating pattern and sawtooth flutter waves. What arrhythmia is this describing?
Atrial flutter.
380
What pathophysiological mechanism can cause atrial flutter?
The re-entry mechanism - there is blockage of the normal circuit. Another pathway forms, takes a different course and re-enters the circuit -> tachycardia.
381
What is the commonest supra-ventricular tachycardia?
AV node re-entry tachycardia (AVNRT).
382
Do you see P waves in AVNRT?
No - the P waves are within the QRS complex.
383
Give 4 symptoms of AVNRT.
1. Sudden onset/offset palpitations.
2. Neck pulsation.
3. Chest pain.
4. Shortness of breath.
384
Describe the acute treatment of AVNRT.
Acute treatment: vagal manoeuvre and adenosine.
385
What drugs might you give to someone to suppress future episodes of AVNRT?
Beta blockers, CCB, flecainide.
386
Describe the pathophysiology of accessory pathway arrhythmias.
Congenital muscle strands connect the atria and ventricles - accessory pathway. This can result in pre-excitation of ventricles.
387
Describe 3 characteristics of an ECG taken from someone with accessory pathway arrhythmia.
1. Delta wave.
2. Short PR interval.
3. Slurred QRS complex.
388
Give an example of an accessory pathway arrhythmia.
Wolff-Parkinson-White syndrome.
389
Describe the pathophysiology of focal atrial tachycardia.
Another area of the atrium becomes more autonomic than the sinus node and so sinus node function is taken over -> focal atrial tachycardia.
390
What might you see on an ECG taken from someone with focal atrial tachycardia.
Abnormal P waves appear before a normal QRS.
391
What is the treatment for ventricular tachycardia in an urgent situation?
DC cardioversion.
392
What is the long term treatment for ventricular tachycardia in high risk patients?
Implantable defibrillator.
393
What are ectopic beats?
Very common, generally benign arrhythmias caused by premature discharge. The patient may complain of symptoms of 'skipped beats'.
394
Give 3 causes of long QT syndrome.
1. Congenital.
2. Electrolyte disturbances e.g. hypokalaemia and hypocalcaemia.
3. A variety of drugs.
395
Give 2 signs of long QT syndrome.
1. Palpitations.
| 2. Syncope.
396
Give 4 causes of sinus bradycardia.
1. Ischaemia.
2. Fibrosis of the atrium.
3. Inflammation.
4. Drugs.
397
Give 3 causes of heart block.
1. CAD.
2. Cardiomyopathy.
3. Fibrosis.
398
What kind of heart block is associated with wide QRS complexes with an abnormal pattern?
RBBB or LBBB.
399
Describe first degree AV block.
Fixed prolongation of the PR interval due to delayed conduction to the ventricles.
400
Describe second degree AV block.
There are more P waves to QRS complexes because some atrial impulses fail to reach the ventricles and so you don't get a QRS complex.
401
Types of second degree AV block: describe Mobitz type 1.
PR interval gradually increases until AV node fails and no QRS is seen.
402
Types of second degree AV block: describe Mobitz type 2.
There is a sudden unpredictable loss of AV conduction and so loss of QRS. PR interval is constant but every nth QRS complex is missing.
403
Describe third degree AV block.
Atrial activity fails to conduct to the ventricles. P waves and QRS complexes therefore occur independently.
404
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.
405
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.
406
Cardiac arrhythmias: what is the treatment of choice in a patient who is hemodynamically unstable due to the underlying rhythm?
DC cardioversion.
407
What is a consequence of peripheral arterial occlusion?
Gangrene.
408
Give 2 diseases that result from stress indicued ischaemia.
1. Exercise induced angina.
| 2. Intermittent claudication.
409
Give 2 diseases that result from ischaemia due to structural/functional breakdown.
1. Critical limb ischaemia.
| 2. Vascular dementia.
410
Give a sign of infarction.
Gangrene.
411
What is intermittent claudication?
A symptom describing muscle pain that is caused by moderate ischaemia. Intermittent claudication occurs when exercising (stress induced) and is relieved with rest.
412
What can intermittent claudication lead on to if left untreated?
Critical ischaemia.
413
Intermittent claudication: is O2 supply normal or low at rest and when you begin exercise?
Normal. Intermittent claudication is stress induced so at rest and when you begin exercise O2 supply is able to meet demand.
414
Intermittent claudication: is O2 supply normal or low when you do moderate/hard exercise?
Low. O2 supply is unable to meet demand -> anaerobic respiration -> lactic acid.
415
Intermittent claudication: is O2 supply normal or low after a short rest?
Low. It takes longer to recover as you're getting rid of the lactic acid. After a long rest however it is normal.
416
Give a symptom of intermittent claudication.
Muscle cramps.
417
What is critical ischaemia?
Blood supply is barely adequate for life. There is no reserve for an increase in demand. Very severe, cells are dying.
O2 supply is ALWAYS low, even at rest!
418
Give 4 signs of critical ischaemia.
1. Rest pain.
2. Classically nocturnal.
3. Ulceration.
4. Gangrene.
419
What can cause acute ischaemia?
Embolism/thrombosis.
420
Give 6 symptoms of acute ischaemia.
1. Pain.
2. Pale.
3. Paralysis.
4. Paraesthesia.
5. Perishing cold.
6. Pulseless.
421
Give 2 examples of acute ischaemia.
1. Stroke.
| 2. MI.
422
Give 5 risk factors for peripheral vascular disease.
1. Hypertension.
2. Hyperlipidaemia.
3. Diabetes.
4. Smoking.
5. Obesity.
423
Give 4 treatments for peripheral vascular disease.
1. Risk factor modification.
2. Vein bypass for critical leg ischaemia.
3. Balloon angioplasty.
4. Stenting of occlusion.
5. Amuptation.
424
Describe 4 steps in the initial management of a STEMI.
1. ABCDE.
2. Morphine.
3. Oxygen (if hypoxic).
4. Nitrates.
5. Aspirin.
425
PCI is the treatment of choice for a STEMI. What might you do instead if you were unable to do PCI?
Thrombolysis using streptokinase.
426
Name a drug that can be used for thrombolysis in the treatment of a STEMI.
Streptokinase.
427
In what type of valvular heart disease would you hear a mid-diastolic murmur and a 1st heart sound snap?
Mitral stenosis.
428
In what type of valvular heart disease would you hear a pan-systolic murmur?
Mitral regurgitation.
429
In what type of valvular heart disease would you hear a ejection systolic murmur?
Aortic stenosis.
430
In what type of valvular heart disease would you see a wide pulse pressure and hear an early diastolic blowing murmur and systolic ejection murmur?
Aortic regurgitation.
431
Name the criteria that is used in the diagnosis of infective endocarditis.
Duke's criteria.
432
Give 2 major points in the Duke's criteria that if present can confirm a diagnosis of IE.
1. Positive blood culture with typical IE microorganism.
| 2. Positive echo showing endocardial involvement.
433
What organism can cause rheumatic fever?
Group A strep e.g. s.pyogenes.
434
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!
435
What type of drug is digoxin?
Digoxin is a cardiac glycoside.
436
What is a typical lesion of atherosclerosis?
Fatty streaks.
437
Write an equation for mAP.
mAP = DP + 1/3 PP.
438
What is the cause of reactive hyperaemia?
When blood flow increases following occlusion to arterial flow.
439
Give the equation for BP.
BP = CO x TPR.
440
Give the equation for stroke volume.
SV = EDV - ESV.
441
Give the equation for cardiac output.
CO = SV x HR.
442
Name the classification system for peripheral vascular disease (PVD).
Fontaine classification.
443
Why does mitral stenosis cause AF?
There is increased LA pressure. This stretches the myocytes in the atria and irritates pacemaker cells -> AF.
444
Why does mitral stenosis lead to a raised JVP?
Pulmonary congestion -> pulmonary hypertension causes a raised JVP.
445
Why might someone with mitral stenosis be breathless? Use Sterling's law in your explanation.
Mitral stenosis means ventricles don't fill completely -> reduced EDV -> reduced SV -> reduced CO and so breathlessness.
446
Give 2 ECG signs of PE.
1. Sinus tachycardia.
| 2. Atrial fibrillation.
447
Name 2 diseases that are due to moderate ischaemia.
1. Angina.
| 2. Intermittent claudication.
448
Name a disease that is due to severe ischaemia.
Critical limb ischaemia.
449
Give 2 signs of RHF.
1. Raised JVP.
| 2. Ascites.
450
Describe the NYHA classification for heart failure.
1. Class 1: heart disease is present but there is no limitation.
2. Class 2: comfortable at rest but slight limitation on activity - mild HF.
3. Class 3: marked limitation - moderate HF.
4. Class 4: SOB at rest, all activity causes discomfort (moderate HF).
451
Give 4 signs you might see on a CXR taken from someone with heart failure.
1. Pleural effusion.
2. Dilated pulmonary arteries.
3. Kerley B lines.
4. Bat's wings.
5. Cardiomegaly.
452
What coronary event might Dressler's syndrome develop after?
Can develop 2-10 weeks after an MI.
453
What is Dressler's syndrome?
Myocardial injury stimulates formation of autoantibodies against the heart. Cardiac tamponade may occur. Dressler's is a secondary form of pericarditis.
454
Give 3 symptoms of Dressler's syndrome.
1. Fever.
2. Chest pain.
3. Pericardial rub.
Occurs 2-10 week after MI.
455
Describe the treatment for an MI.
1. MONA.
2. PCI or streptokinase.
3. Aspirin and clopidogrel.
4. LMWH.
5. Anti-anginals e.g. beta blockers, CCB, nitrates.
6. Preventing a secondary CV event: ACEi, aspirin, statins, RF modification.
456
How does LMWH work?
It activates anti-thrombin, which then inhibits thrombin and factor 10a.
457
Define ischaemia.
Reversible tissue damage as a result of impaired vascular perfusion depriving tissues of nutrients and oxygen.
458
Define infarction.
Irreversible tissue death due to ischaemia.
459
Why might someone with HF feel tired?
Due to reduced CO.
460
Why might someone with HF feel breathless when lying down?
Due to pulmonary oedema.
461
Why might someone with HF have tachycardia?
Due to activation of the sympathetic system.
462
Why might someone with HF have peripheral oedema?
1. Decreased venous pressure.
| 2. RAAS activation -> sodium and H2O retention.
463
Give 3 clinical features of shock.
1. Low blood pressure.
2. Rapid pulse.
3. Low urine output.
4. Pallor.
5. Sweating.
464
Give 5 signs of anaphylactic shock.
1. Breathlessness.
2. Wheeze.
3. Rash.
4. Swollen lips/tongue.
5. Low BP.
6. Chest tightness.
465
Why might someone with anaphylactic shock have a low BP?
1. Vasodilation.
| 2. Increased vascular permeability.
466
State two common allergens responsible for causing anaphylactic shock.
1. Seafood.
2. Nuts.
3. Grains.
