Cardio Flashcards
(548 cards)
1
Q
Define atherosclerosis
A
Build up of plaque in the intima of an artery
2
Q
What can an atherosclerotic plaque cause?
A
- Heart attack
- Stroke
- Gangrene
3
Q
Give 4 risk factors for atherosclerosis
A
- Family history
- Increasing age
- Smoking
- High serum cholesterol (LDL)
- Obesity
- Diabetes
- Hypertension
4
Q
What are the constituents of an atheromatous plaque?
A
Lipid core Necrotic debris Connective tissue surrounded by foam cells Fibrous cap Lymphocytes
5
Q
In which arteries would you most likely find an atheromatous plaque?
A
Peripheral and coronary arteries
Focal distribution along the length
6
Q
What histological layer of the artery may be thinned by an atheromatous plaque?
A
Media
7
Q
What is the precursor for atherosclerosis?
A
Fatty streaks
8
Q
What can cause chemoattractant release?
A
Endothelial cell injury
9
Q
What is the function of chemoattractants?
A
Signal leukocytes and produce a concentration gradient
10
Q
What is the function of leukocytes?
A
Leukocytes accumulate and migrate into vessel walls and release cytokines leading to inflammation
11
Q
What inflammatory cytokines are found in plaques?
A
IL-1 IL-6 IFN-y MCP-1 TGF-B
12
Q
Describe the process of leukocyte recruitment
A
- Capture
- Rolling
- Slow rolling
- Adhesion
- Transmigration
13
Q
What types of molecules are present during leukocyte recruitment?
A
- Chemoattractants
- Selectins (1-3)
- Integrins (3-5)
14
Q
Describe the 5 steps of progression of atherosclerosis
A
- Fatty streaks
- Intermediate lesions
- Fibrous plaque
- Plaque rupture
- Plaque erosion
15
Q
At what age do fatty streaks begin to appear?
A
< 10 years old
16
Q
What are the constituents of fatty streaks?
A
Foam cells and T lymphocytes within the intimal layer of the vessel wall
17
Q
What are the constituents of intermediate lesions?
A
Foam cells Smooth muscle cells T lymphocytes Platelet adhesion and aggregation Extracellular lipid pools
18
Q
What are the constituents of fibrous plaques?
A
Fibrous cap overlies lipid core and necrotic debris Smooth muscle cells Macrophages Foam cells T lymphocytes
19
Q
What are fibrous plaques able to do?
A
Impede blood flow and they are prone to rupture
20
Q
Why might a plaque rupture?
A
Fibrous plaques are constantly growing and receding
Fibrous cap has to be resorbed and redeposited in order to be maintained
If balance is shifted in favour of inflammatory condition, the cap becomes weak and the plaque ruptures
Thrombus formation and vessel occlusion
21
Q
What the primary treatment for atherosclerosis?
A
Percutaneous Coronary Intervention (PCI)
22
Q
What is the major limitation of PCI?
A
Restenosis
23
Q
How can restenosis be avoided following PCI?
A
Drug eluting stents –> anti-proliferative and drugs that inhibit healing
24
Q
What drugs can patients be started on following a PCI?
A
Aspirin - antiplatelet
Clopidogrel/Ticagrelor - inhibit P2Y12 ADP receptors on platelets
Statins - cholesterol lowering
Anti-inflammatory drugs - Colchicine, canakinumab
25
What is the key principle behind pathogenesis of atherosclerosis?
It is an inflammatory process
26
Define atherogenesis
The development of an atherosclerotic plaque
27
What is an electrocardiogram?
Representation of electrical events of the cardiac cycle
28
What can ECGs identify?
```
Arrhythmias
Myocardial ischaemia and infarction
Pericarditis
Chamber hypertrophy
Electrolyte disturbances
```
29
What is depolarisation?
Contraction of any muscle associated with electrical changes
30
What is the dominant pacemaker of the heart?
```
Sinoatrial node (SAN)
60-80 bpm
```
31
What are the pacemakers of the heart?
1. Sinoatrial node (dominant)
2. Atrioventricular node
3. Ventricular cells
32
What is the standard calibration of an ECG?
25 mm/S
0.1 mV/mm
Electrical impulse that travels towards the electrode produces a positive deflection
33
What is the route of impulse conduction in the heart?
SAN --> AVN --> Bundle of His --> Bundle branches --> Purkinje fibres
34
What does the P wave represent?
Atrial depolarisation
35
What does the QRS complex represent?
Ventricular depolarisation
36
What does the T wave represent?
Ventricular repolarisation
37
What does the PR interval represent?
Atrial depolarisation and delay in AV junction
38
How long should the PR interval be?
120-200 ms
39
What might a long PR interval indicate?
Heart block
40
How long should the QRS complex be?
< 110 ms
41
What does the ST segment represent?
Time between depolarisation and repolarisation of the ventricles (contraction)
42
What is the J point?
Where the QRS complex becomes the ST segment
43
How many seconds do the following represent on ECG paper?
a) Large squares
b) Small squares
a) 0.2s
| b) 0.04s
44
What is the normal axis of the QRS complex?
-30° to +90°
45
What is the QT interval?
Time from the beginning of ventricular depolarisation to the end of ventricular repolarisation
46
How long should the QT interval be?
0.35-0.45s
47
Where would you place lead I?
From the right arm to the left arm
| At 0°
48
Where would you place lead II?
From the right arm to left leg
| At 60°
49
Where would you place lead III?
From the left arm to left leg
| At 120°
50
Where would you place lead aVF?
From halfway between the left arm and right arm to the left leg
At 90°
51
Where would you place lead aVL?
From halfway between the right arm and left leg to the left arm
At -30°
52
Where would you place lead aVR?
From halfway between the left arm and left leg to the right arm
At -150°
53
Where are the chest electrodes placed?
- V1 = 4th intercostal space, right sternal edge
- V2 = 4th intercostal space, left sternal edge
- V3 = midway between V2 and V4
- V4 = 5th intercostal space, midclavicular line
- V5 = Same horizontal level as V4, left anterior axillary line
- V6 = same horizontal level as V4 and V5, left mid-axillary line
54
What leads show the lateral view of the heart on an ECG?
Lead I
aVL
V5
V6
55
What leads show the inferior view of the heart on an ECG?
Lead II
Lead III
aVF
56
What leads show the septal view of the heart on an ECG?
V1
| V2
57
What leads show the anterior view of the heart on an ECG?
V3
| V4
58
In which leads would you expect the QRS complex to be upright in?
Leads I and II
59
In which lead are all waves negative?
aVR
60
In which leads must the R wave grow?
From chest leads V1 to V4
61
In which leads must the S wave grow?
From chest leads V1 to V3
| Must disappear in V6
62
In which leads should T waves and P waves be upright?
Leads I, II and V2-V6
63
What might tall pointed P waves on an ECG suggest?
Right atrial enlargement
64
What might notched, 'm shaped' P waves on an ECG suggest?
Left atrial enlargement
65
Give 3 signs of abnormal T waves
1. Symmetrical
2. Tall and peaked
3. Biphasic or inverted
66
What happens to the QT interval when HR increases?
QT interval decreases
67
What part of the ECG does the plateau phase of the cardiac action potential coincide with?
QT interval
68
Define angina
Type of ischaemic heart disease
| It is a symptom of O2 supply/demand mismatch to the heart
69
What is the most common cause of angina?
Narrowing of the coronary arteries due to atherosclerosis
70
Give 5 possible causes of angina
1. Impairment of blood flow = narrowed coronary artery (e.g. atherosclerosis)
2. Increased distal resistance (e.g. LV hypertrophy)
3. Reduced O2 carrying capacity of blood (e.g. anaemia)
4. Coronary artery spasm
5. Thrombosis
6. Aortic stenosis
71
How reduced does the diameter of an artery need to be before symptoms occur?
Diameter has to fall below 70%
72
Name 4 types of angina
1. Stable angina
2. Unstable angina
3. Cescendo angina
4. Prinzmetal's angina
5. Microvascular angina (syndrome X)
6. Decubitus angina
73
Name 3 non-modifiable risk factors for angina
1. Increasing age
2. Family history
3. Gender - Male
74
Give 5 modifiable risk factors for angina
1. Smoking
2. Diabetes
3. Hypertension
4. Hypercholesterolaemia
5. Sedentary lifestyle/obesity
6. Stress
75
Name 3 exacerbating factors for angina that effect the supply of O2
1. Anaemia
2. Hypoxaemia
3. Polycythaemia
4. Hypothermia
5. Hyper/hypovolaemia
76
Name 3 exacerbating factors for angina that effect the demand of O2
1. Hypertension
2. Tachyarrhythmia
3. Valvular heart disease
4. Hyperthyroidism
5. Cold weather
6. Heavy meals
7. Emotional stress
77
Briefly describe the pathophysiology of angina that results from atherosclerosis
On exertion there is increase O2 demand
| Coronary blood flow is obstructed by an atherosclerotic plaque --> myocardial ischaemia --> angina
78
Briefly describe the pathophysiology of angina the results from anaemia
On exertion there is increased O2 demand
| In someone with anaemia there is reduced O2 transport --> myocardial ischaemia --> angina
79
Briefly describe the pathophysiology of Prinzmetal's angina
Occurs due to coronary artery spasm
80
How do blood vessels try and compensate for increased myocardial demand during exercise?
When myocardial demand increases, microvascular resistance drops and flow increases
81
Why are blood vessels unable to compensate for increased myocardial demand in someone with cardiovascular disease?
In CVD, epicardial resistance is high meaning microvascular resistance has to fall at rest to supply myocardial demand at rest
When this person exercise, microvascular resistance can't drop anymore and flow can't increase to meet metabolic demand = angina
82
Name 3 differential diagnoses for angina
1. Pericarditis/myocarditis
2. PE
3. Chest infection
4. Dissection of aorta
5. GORD
83
How would you describe the chest pain in angina?
Crushing central chest pain that is heavy and tight
84
What 3 things are used to assess whether it is typical angina, atypical pain or non-anginal pain?
1. Have central, tight, radiation to arms, jaw and neck
2. Precipitated by exertion
3. Relieved by rest or GTN spray
3/3 = Typical angina
2/3 = Atypical pain
1/3 = Non-anginal pain
85
Give 5 symptoms of angina
1. Crushing central chest pain
2. Pain is relieved with rest or GTM spray
3. Pain is provoked by physical exertion
4. Pain may radiate to arms, neck or jaw
5. Dyspnoea
6. Nausea
86
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
87
What investigations might you do in someone you suspect to have angina?
1. ECG - usually normal, sometimes ST depression, flat or inverted T waves
2. Echocardiogaphy
3. CT angiography - high NPV and good at excluding disease
4. Exercise tolerance test - induces ischaemia
5. Invasive angiogram - tells you FFR (pressure gradient across stenosis)
6. SPECT - radio labelled tracer taken up by metabolising tissues
88
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, so is ideal for excluding CAD in younger, low risk patients
89
How can angina be reversed?
Resting - reducing myocardial demand
90
Describe the primary prevention for angina
1. Modify risk factors
2. Treat underlying causes
3. Low dose aspirin
91
Describe the secondary prevention of angina
1. Modify risk facotrs
2. Pharmacological therapies for symptom relief and to reduce the risk of CV events
3. Interventional therapies (e.g. PCI)
92
Name 3 symptom reliving pharmacological therapies the might be used in someone with angina
1. Beta blockers (e.g. atenolol, propranolol, bisoprolol)
2. Nitrates (e.g. GTN spray)
3. Calcium channel blockers
93
Describe the action of beta blockers
Beta 1 specific
Antagonise sympathetic activation and so are negatively chronotropic and inotropic
Myocardial work is reduced and so is myocardial demand = symptom relief
94
Give 3 side effects of beta blockers
1. Bradycardia
2. Tiredness
3. Erectile dysfunction
4. Cold peripheries
95
When might beta blockers be contraindicated?
Someone with asthma or someone who is bradycardic
96
Describe the action of nitrates
Venodilators
| Reduce venous return --> reduced preload --> reduced myocardial work and myocardial demand
97
Describe the action of Calcium channel blockers
Arterodilators
| Reduce BP --> Reduce afterload --> reduced myocardial demand
98
Name 2 drugs that might be use in someone with angina or in someone at risk of angina to improve prognosis
1. Aspirin
2. Clopidogrel
3. Statins
99
How does aspirin work?
Antiplatelet
| Irreversibly inhibits COX --> reduced thromboxane 2 synthesis --> platelet aggregation reduced
100
What is a caution when prescribing aspirin?
Gastric ulceration
101
How does clopidogrel work?
Antiplatelet
| P2Y12 inhibitor --> prevents platelet activation
102
What are statins used for?
To reduce the amount of LDL in the blood
103
What is revascularisation?
Used to restore coronary artery and increase blood flow
104
Name 2 types of revascularisation
1. Percutaneous coronary intervention (PCI)
| 2. Coronary artery bypass graft (CABG)
105
Give 2 advantages and 1 disadvantage of PCI
```
ADVANTAGES
1. Less invasive
2. Convenient and acceptable
DISADVANTAGES
1. High risk of restenosis
```
106
Give 1 advantage and 2 disadvantages of CABG
```
ADVANTAGES
1. Good prognosis after surgery
DISADVANTAGES
1. Very invasive
2. Long recovery time
```
107
Name 2 complications of angina
1. Acute coronary syndromes
2. Congestive cardiac failure
3. Conduction disease
4. Arrhythmia
108
What are acute coronary syndromes?
Encompasses a spectrum of acute cardiac conditions from unstable angina, NSTEMI and STEMI
109
What is the common cause of ACS?
Rupture of an atherosclerotic plaque and subsequent arterial thrombosis
110
What are uncommon causes of ACS?
1. Coronary vasospasm
2. Drug abuse
3. Coronary artery dissection
4. Thoracic aortic dissection
111
Briefly describe the pathophysiology of ACS
Atherosclerosis --> plaque rupture --> platelet aggregation --> thrombus formation --> ischaemia and infarction --> encores of cells --> permanent heart muscle damage and ACS
112
Describe type 1 MI
Spontaneous MI with ischaemia due to plaque rupture
113
Describe type 2 MI
MI secondary to ischaemia due to increased O2 demand
114
What is troponin a marker for?
Cardiac muscle injury
115
Why do you see increased serum troponin in NSTEMI and STEMI?
The occluding thrombus causes necrosis of cells and so myocardial damage causing troponin to be raised
116
Give 3 signs of unstable angina
1. Cardiac chest pain at rest
2. Cardiac chest pain with crescendo pattern
3. No significant rise in troponin
117
Give 4 symptoms of MI
1. Unremitting and usually severe central cardiac chest pain
2. Pain occurs at rest
3. Sweating
4. Breathlessness
5. Nausea and vomiting
118
Give 3 signs of MI
1. Hypo/hypertension
2. 3rd/4th heart sound
3. Signs of congestive heart failure
4. Ejection systolic murmur
119
Name 3 possible differential diagnoses of MI
1. Pericarditis
2. Stable angina
3. Aortic dissection
4. GORD
5. Pneumothorax
120
What investigation would you do on someone you suspect to have ACS?
1. ECG
2. Blood tests - troponin levels and rule out anaemia
3. Coronary angiography
4. Cardiac monitoring for arrhythmias
5. Chest x-ray
121
What might the ECG of someone with unstable angina show?
May be normal, or might show T wave inversion and ST depression
122
What might the ECG of someone with NSTEMI show?
May be normal or might show T wave inversions and ST depression
Might also be R wave regression, ST elevation and biphasic T wave in lead V3
123
What might the ECG of someone with STEMI show?
ST elevation in the anterolateral leads
| After a few hours, T waves inlet and deep, broad, pathological Q waves develop
124
What would the serum troponin level be like in someone with unstable angina?
Normal
125
What would the serum troponin level be like in someone with NSTEMI/STEMI?
Significantly raised
126
A raised troponin is not specific for ACS. In what other conditions might you see a raised troponin?
1. Gram negative sepsis
2. PE
3. Myocarditis
4. Heart failure
5. Arrhythmias
127
Describe the initial management of ACS
1. Get into hospital ASAP - 999
2. If STEMI, paramedic call PCI centre for transfer
3. Aspirin 300 mg
4. Pain relief - opioid
5. Oxygen if hypoxic
6. Nitrates
128
What is the treatment of choice for STEMI?
PCI
129
What is the function of P2Y12?
It amplifies platelet activation
130
Give 2 potential side effect of P2Y12 inhibitors
1. Bleeding
2. Rash
3. GI disturbances - ulceration
131
Describe the secondary prevention therapy for people after having a STEMI
1. Aspirin - antiplatelet
2. Clopidogrel - P2Y12 inhibitor
3. Statins
4. Metoprolol - beta blocker
5. ACE inhibitor - ramipril, lisinopril
6. Modification of risk factors
132
What is involved in antithrombotic therapy?
```
Dual antiplatelet therapy = aspirin and clopidogrel
Anticoagulant = heparin
```
133
Give 5 potential complications of MI
1. Heart failure
2. Rupture of infarcted ventricle
3. Rupture of intraventricular septum
4. Mitral regurgitation
5. Arrhythmias
6. Heart block
7. Pericarditis
134
Give 2 possible sequelae to MI
1. Shock
2. Heart failure
3. Pericarditis
135
What is a DVT?
Blood clot within a blood vessel of the lower limb
136
What are the symptoms of DVT?
Non-specific symptoms
| Pain and swelling
137
What are the signs for DVT?
Tenderness, warmth and discolouration
138
What investigations might be done in order to diagnose a DVT?
1. D-dimer (blood test) - look for fibrin breakdown products --> normal excludes DVT diagnosis (abnormal does NOT confirm)
2. Ultrasound compression test of proximal veins - if you can't squash the vein = clot
139
What is the treatment for DVT?
1. LMW heparin
2. Oral warfarin or direct acting oral anticoagulant (DAOC)
3. Compression stockings
4. Treat the underlying cause (e.g. malignancy or thrombophilia)
140
Name the types of DVT
1. Spontaneous
| 2. Provoked - incidence of recurrence is low if you remove the stimulus
141
Give 5 risk factors for DVT
1. Surgery, immobility, leg fracture
2. Combined oral contraceptive pill, HRT
3. Long haul flights
4. Genetic predisposition
5. Pregnancy
142
How can DVTs and PEs be prevented?
1. Hydration
2. Early mobilisation
3. Compression sticking/pumps
4. Low dose LMW heparin
143
What is low risk thromboprophylaxis treatment?
```
< 40 years
Surgery < 30 mins
Early mobilisation and hydration
No chemical
TED if surgical
```
144
What is high risk thromboprophylaxis?
Hip, knee, pelvis, malignancy, risk factors, prolonged immobility
All immobile medical, many surgical - Dalteparin s/c od
145
What might be the consequence of a dislodged DVT?
Pulmonary embolism
146
Give 2 symptoms of a PE
1. Breathlessness
| 2. Pleuritic chest pain
147
Give 2 signs of a PE
1. Tachycardia
| 2. Tachypnoea
148
What investigations might be done to diagnose a patient with PE?
ECG sinus tachycardia - to exclude cardiac cause
Blood gases - to exclude respiratory causes
D-dimer - normal excludes diagnosis
CTPA spiral with contrast - gaps in dye if PE has occurred
Ventilation/perfusion scan (used in pregnancy)
149
What is the treatment for a PE?
LMW heparin, oral warfarin for 6 months
DOAC - for outpatient with a relatively minor PE
Treat cause if possible
150
If a patient can not be placed on anticoagulation following a PE, what alternative treatment should be considered?
IVC filter - prevents more clot travelling from the leg to the lungs
151
Define thrombosis
Blood coagulation inside a vessel
152
How would you describe an arterial thrombus?
Platelet rich (a 'white thrombosis')
153
How would you describe a venous thrombosis?
Fibrin rich (a 'red thrombosis')
154
What are the potential consequences of an arterial thrombosis?
1. Coronary circulation = MI
2. Cerebral circulation = Stroke
3. Peripheral circulation = Peripheral vascular disease (e.g. gangrene)
155
What investigations would you do to diagnose an arterial thrombosis?
```
MI = history, ECG, cardiac enzymes
Stoke = History and examination, CT/MRI scan
PVD = History and examination, ultrasound, angiogram
```
156
What is the treatment for arterial thrombosis?
1. Aspirin
2. LMW heparin
3. Thrombolytic therapy: streptokinase tissue plasminogen factor
4. Treat risk factors
157
What are the potential consequences of a venous thrombosis?
Deep vein thrombosis
| Pulmonary embolism
158
Name 4 causes of a venous thrombosis
```
Circumstantial
- surgery
- immobilisation
- malignancy
Genetic
- factor V Leiden
- antithrombin deficiency
- protein C or S deficiency
Acquired
- Anti-phospholipid syndrome
```
159
How does heparin work?
Inhibits thrombin and factor Xa
| Indirect thrombin inhibitor - binds to antithrombin and increased its activity
160
How do you monitor heparin?
Activated partial thromboplastin time
| Aim ratio: 1.8-2.8
161
Why is LMW heparin often used instead of normal heparin?
Smaller molecule, less variation in dose and renally excreted
162
How does warfarin work?
Inhibits production of vitamin K dependent clotting factors (2, 7, 9, 10)
Prolongs the prothrombin time
163
What is warfarin an antagonist of?
Vitamin K
164
Why is warfarin difficult to use?
Lots of interactions
Needs almost constant monitoring
Teratogenic
165
How is warfarin measured?
Using International Noramlised Ratio (derived from prothrombin time)
Usual target = 2-3
Higher range = 3-4.5
166
How does Direct Acting Oral Anticoagulant (DAOC) work?
Directly acts on factor 2 (thrombin) or 10
| No blood test or monitoring needed just given od or bd
167
How much serous fluid is there between the visceral and parietal pericardium?
50 ml
168
What is the function of the serious fluid between the visceral and parietal pericardium?
Lubricant and so allows smooth movement of the heart inside the pericardium
169
What is the function of the pericardium?
Restrains the filling volume of the heart
170
Describe the aetiology of pericarditis
1. Viral (common) - e.g. enteroviruses
2. Bacterial - e.g. mycobacterium tuberculosis
3. Autoimmune - e.g. Sjören syndrome
4. Neoplastic
5. Metabolic - e.g. uraemia
6. Traumatic and iatrogenic
7. Idiopathic (90%)
171
Define acute pericarditis
Acute inflammation of the pericardium with or without effusion
172
Give 5 symptoms of pericarditis
1. CHEST PAIN
2. Dyspnoea
3. Cough
4. Hiccups
5. Skin rash
173
Describe the chest pain in acute pericarditis
Severe, sharp, pleuritic, rapid onset, can radiate to arm
174
Why might someone with pericarditis have hiccups?
Due to irritation to the phrenic nerve
175
What is the major differential diagnosis of acute pericarditis?
Myocardial infarction
176
Name 3 differential diagnoses for acute pericarditis
1. MI
2. Angina
3. Pneumonia
4. Pleurisy
5. PE
177
What investigations might you do on someone who you suspect to have pericarditis?
1. ECG
2. CXR
3. Bloods - FBC, ESR and CRP, Troponin
4. Echocardiogram - usually normal, rule out silent pericardial effusion
178
What might the ECG look like in someone with acute pericarditis?
1. Saddle shaped ST elevation
| 2. PR depression
179
What does a raised troponin in acute pericarditis suggest?
Myopericarditis
180
How can acute pericarditis be clinically diagnosed?
Patient has to have at least 2 of the following:
1. Chest pain
2. Friction rub
3. ECG changes
4. Pericardial effusion
181
What is the treatment for pericarditis?
1. Restrict physical activity until symptoms resolve
2. NSAID or aspirin
3. Colchicine - reduces recurrence
4. Treat the cause
182
What is pericardial effusion?
Abnormal accumulation of fluid in the pericardial cavity
183
What is a complication of pericardial effusion?
Cardiac tamponade
184
Why does chronic pericardial effusion rarely cause tamponade?
Parietal pericardium is able to adapt when effusion accumulate slowly and so tamponade is prevented
185
Briefly explain the pathophysiology of cardiac tamponade
Accumulation of pericardial fluid --> increase in intra-pericardial pressure --> poor ventricular filling --> decrease in CO
186
What are the signs of Cardiac tamponade?
Beck's triad:
1. Decreased BP
2. Increased jugular venous pressure
3. Quiet heart sounds
Pulsus paradoxus = pulses fade on inspiration
Kussmaul's sign = rise in jugular venous pressure with inspiration
187
What is the treatment of cardiac tamponade?
Pericardiocentesis (drainage)
188
What is chronic constrictive pericarditis?
Calcification thickens the pericardium and affects cardiac effusion
189
What is the treatment for chronic constrictive pericarditis?
Surgical excision of thickened pericardium
190
Name 3 major predictive markers for complications for pericarditis
1. Fever >38 degree
2. Subacute onset
3. Large pericardial effusion
4. Cardiac tamponade
5. Lack of response to aspirin or NSAIDs after at least 1 week of therapy
191
What is haemopericaridum?
Direct bleeding from vasculature through the ventricular wall following MI
192
What can cause myocarditis?
Viral infection
193
Give 5 risk factors for peripheral vascular disease
1. Hypertension
2. Hyperlipidaemia
3. Diabetes
4. Smoking
5. Obesity
194
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. Amputation
195
What is critical ischaemia?
Blood supply is barely adequate for life
No reserve for an increase in demand
Very severe, cells are dying
O2 is always low, even at rest
196
Give 4 signs of critical ischaemia
1. Rest pain
2. Classically nocturnal
3. Ulceration
4. Gangrene
197
What can cause acute ischaemia?
Embolism/thrombosis
198
Give 6 symptoms of acute ischaemia
1. Pain
2. Pale
3. Paralysis
4. Paraesthesia
5. Perishing cold
6. Pulseless
199
Give 2 examples of acute ischaemia
1. Stroke
| 2. MI
200
What might you do if you are unable to do a PCI for a STEMI?
Thrombolysis
201
Name a drug that can be used for thrombosis in the treatment of a STEMI
Streptokinase
202
Define cardiomyopathy
Group of diseases of the myocardium that affect the mechanical or electrical function of the heart
203
Name 4 cardiomyopathies
1. Hypertrophic (HCM)
2. Dilated (DCM)
3. Arrhythmogenic right/left ventricular (ARVC/ALVC)
4. Restrictive
204
Name 4 risk factors for cardiomyopathy
1. FH
2. High BP
3. Obesity
4. Diabetes
5. Previous MI
205
What can cause Hypertrophic cardiomyopathy?
Sarcomeric gene mutations - Troponin T and B-myosin
206
What is the usual inheritance pattern for cardiomyopathies?
Autosomal dominant (restrictive not familial)
207
Describe the pathophysiology of Hypertrophic cardiomyopathy
Hypertrophic ventricle so impaired diastolic filling resulting in reduced stroke volume and therefore CO
Disarray of cardiac myocytes so conduction is also affected
208
Give 3 symptoms of HCM
1. Angina
2. Dyspnoea
3. Syncope
4. Palpitations
209
Give 3 signs of HCM
1. Cardiac arrhythmia
2. Ejection systolic murmur
3. Jerky carotid pulse
4. Double apex beat
210
What might an ECG look like from a person with HCM?
1. Large QRS complexes
| 2. Progressive T wave inversion
211
Briefly describe treatment for HCM
1. BB - atenolol
2. CCB - Verapamil
3. Amiodarone - anti-arrhythmic
4. Anticoagulants
5. ICD insertion
212
Describe the pathophysiology of DCM
Cytoskeletal gene mutation
| Ventricular dilation and dysfunction leading to poor contractility
213
Name 3 causes of DCM
1. Genetic
2. Alcohol
3. Ischaemia
4. Thyroid disorder
214
Give 3 symptoms of DCM
Presents with symptoms of heart failure
1. SOB
2. Fatigue
3. Oedema
215
What investigations would you do for someone you suspect has DCM?
CXR --> cardiomegaly, pulmonary oedema
ECG --> tachycardia, arrhythmia
ECHO --> dilated ventricles
216
What is the treatment for DCM?
Heart failure and AF treatment
217
What can cause Arrhythmogenic cardiomyopathy?
Desmosome gene mutations
218
Describe the pathophysiology of ARVC/ALVC
Desmosome gene mutation
Cardiac cells not held together properly so myocytes pulled apart and ventricles are replaced with fatty fibrous tissue
Gap junctions are affected too
219
Give 2 signs of ARVC/ALVC
1. Ventricular tachycardia
| 2. Syncope
220
What might an ECG look like from a person with ARVC/ALVC?
Epsilon waves
221
What is the treatment for ARVC/ALVC?
BB - atenolol - non-life threatening arrhythmias
Amiodarone - symptomatic arrhythmias
ICD - high risk
Occasionally heart transplant
222
What is restrictive cardiomyopathy?
Poor dilation of the heart restricts diastole
223
Name 2 causes of restrictive cardiomyopathy
1. Amyloidosis (extra-cellular deposition of an amyloid, a insoluble fibrillar protein)
2. Sarcoidosis
224
What are channelopathies?
Inherited arrhythmias caused by ion channel protein gene mutations
Structurally normal heart but abnormality on an ECG
225
Name 4 channelopathies
1. Long QT syndrome
2. Short QT syndrome
3. Brugada
4. Catecholamine Polymorphic Ventricular Tachycardia (CPVT)
226
What is Brugada?
A channelopathy caused by a mutation in sodium channels
227
What might an ECG look like from someone with Brugada?
Characteristic ST elevation in chest leads
228
What is the commonest symptom of channelopathies?
Recurrent syncope
229
What is familial hypercholesterolaemia?
Inherited abnormality of cholesterol metabolism
| LDL receptor affected
230
Define heart failure
A complex clinical syndrome of signs/symptoms that suggest the efficiency of the heart as a pump is impaired
Heart is unable to deliver blood at a rate that meets the metabolic demands
231
What are the 2 broad categories of heart failure?
1. Systolic failure = ability of heart to pump blood around the body is impaired
2. Diastolic failure = inability of ventricles to relax and fill fully
232
Give 4 risk factors for heart failure
1. >65 y/o
2. African descent
3. Men
4. Obesity
5. Previous MI
233
Why are men more commonly effected by heart failure than women?
Women have 'protective hormones' meaning they are less at risk of developing HF
234
Describe the pathophysiology of heart failure
When the heart fails, compensatory mechanisms attempt to maintain CO
As HF progresses, these mechanism are exhausted and become pathophysiological
235
What are the compensatory mechanisms in heart failure?
1. Sympathetic system
2. RAAS
3. Natriuretic peptides
4. Ventricular dilation
5. Ventricular hypertrophy
236
Explain how the sympathetic system is compensatory in HF and give one disadvantage of sympathetic activation
Improves ventricular function by increasing HR and contractility = CO maintained
BUT it also causes arteriolar constriction which increases afterload and so myocardial work
237
Explain how the RAAS system is compensatory in HF and give one disadvantage of RAAS activation
Reduced CO leads to reduced renal perfusion, this activates RAAS --> increased fluid retention so increased preload
BUT it also causes arteriolar constriction which increase afterload and so myocardial work
238
Give 3 properties of natriuretic peptides that make them compensatory in HF
1. Diuretic
2. Hypotensive
3. Vasodilators
239
Give 5 causes of HF
1. IHD = commonest
2. Hypertension
3. Cardiomyopathy
4. Valvular heart disease
5. Excessive alcohol
240
What are the 3 cardinal symptoms of HF?
1. SOB
2. Fatigue
3. Peripheral oedema
241
Give 3 signs of left HF
1. Pulmonary crackles
2. S3 and S4 and murmurs
3. Displaced apex beat
4. Tachycardia
242
Give 2 signs of right HF
1. Raised JVP
| 2. Ascites
243
Describe the NYHA classification for HF
Class 1 = heart disease present but no limitation = asymptomatic
Class 2 = comfortable arrest but slight limitation on activity = mild HF
Class 3 = marked limitation = moderate HF
Class 4 = SOB at rest, all activity causes discomfort = severe HF
244
What investigations might you do initially do in someone who you suspect has HF?
1. ECG
2. CXR
3. Natriuretic peptide levels - raised indicates HF
245
What 4 signs might you see on a CXR taken from someone with HF?
1. Pleural effusion
2. Bat's wings
3. Cardiomegaly
4. Kerley B lines
5. Dilated prominent upper lobe vessels
246
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
247
What is first line treatment for HF?
Vasodilator therapy = ACEi and BB - via the neurohumoral blockade (RAAS-SNS)
248
Give an example of an ACEi that is commonly used in HF
Ramipril
249
Name 3 BB that are used in treatment of HF
1. Propranolol
2. Bisoprolol
3. Atenolol
4. Carvedilol
250
What drugs might you give to someone with HF for symptomatic relief?
Diuretics - thiazides (bendroflumethiazide) and loop (furosemide)
Promote Na and water excretion so help with fluid overload
251
What might you give to someone with hypertension if they are ACE inhibitor intolerant?
Angiotensin receptor blocker (ARB) - losartan, valsartan, candesartan
252
What is 2nd line treatment for HF?
Anticoagulant therapy and aspirin
Calcium channel blocker - amlodipine
Aldosterone antagonist
Digoxin
253
How can chronic HF be prevented?
```
Stop smoking
Eat more healthy
Exercise
Avoid large meals
Vaccinations
Treat underlying cause - dysarrhythmias or valve disease
```
254
What is the treatment for acute HF?
```
LOON
Loop diuretic = furosemide
Oxygen
Opioid = diamorphine
Nitrates = GTN spray
and Monitor ECG
```
255
What is the clinical diagnosis go hypertension?
BP > 140/90 mmHg
256
Name 4 conditions that hypertension is a major risk factor for
1. Stroke
2. MI
3. HF
4. Chronic renal failure
5. Cognitive decline
6. Premature death
257
On average, by how much does having high blood pressure shorten life?
5-7 years
258
What are the blood pressure readings for someone to be diagnosed with Stage 1 hypertension?
Clinic BP = 140/90
| ABPM = 135/85
259
What are the blood pressure readings for someone to be diagnosed with Stage 2 hypertension?
Clinic BP = 160/100
| ABPM = 150/95
260
What are the blood pressure readings for someone to be diagnosed with severe hypertension?
Systolic BP = >180
| Diastolic BP = >110
261
Name the 2 types of hypertension
1. Essential (primary) hypertension
| 2. Secondary hypertension
262
What causes essential hypertension?
Unknown cause
263
Give 5 causes of secondary hypertension
1. Renal disease
2. Genetics and FH
3. Pregnancy
4. Endocrine
5. Cortication of the aorta
6. Drug therapy - cocaine, OCP, NSAIDs
264
Name 3 endocrine disease that can cause secondary hypertension
1. Conn's syndrome - hyperaldosteronism
2. Cushing's syndrome - excess cortisol --> increase BP
3. Phaemochromocytoma - adrenal gland tumour, excess catecholamines --> high BP
265
Name 5 risk factor for hypertension
1. Increasing age
2. FH
3. Obesity
4. Sedentary lifestyle
5. Alcohol intake
5. High slat intake
6. Diabetes
266
What is the clinical presentation of hypertension?
Usually asymptomatic
| Found on screening
267
Why might you examine the eyes of someone with hypertension?
Very high BP can cause immediate damage to small vessels --> seen in the eyes --> retinopathy
268
What investigations might you do in someone with hypertension?
1. 24 hour ambulatory blood pressure monitoring --> confirm diagnosis
2. ECG and Bloods --> identify secondary causes
269
What are the treatment target for the following:
a) People aged <80?
b) People aged >80?
a) < 140/90 mmHg
| b) < 150/90 mmHg
270
What are the 2 main types of treatment for hypertension?
1. Lifestyle modifications - reduce salt, loss weight, reduce alcohol
2. Drug therapy = ACD
271
Describe the pharmacological intervention for someone with hypertension
1. ACEi - ramipril (or ARB - candesartan if ACEi contraindicated)
2. Calcium channel blocker - amlodipine, diltiazem, verapamil
3. Diuretics - bendroflumethethizaide, furosemide
272
What other pharmacological interventions might you give to someone with hypertension (except ACD)?
Beta blockers - bisoprolol
273
Will anti-hypertensives make someone feel better?
No, usually treating hypertension doesn't relive symptoms except headache
274
If you gave someone 1 BP tablet by how much would you expect their blood pressure to decrease?
1 tablet = 10 mmHg reduction in BP
275
What is cor pulmonale?
RV hypertrophy and dilation due to pulmonary hypertension
276
Write an equation for BP
BP = CO x TPR
277
Name 2 systems that are targeted pharmacologically in the treatment of hypertension
1. RAAS
| 2. Synpathetic nervous system
278
Give 4 functions of angiontensin II
1. Potent vasoconstrictor
2. Activated sympathetic nervous system - increased NAd
3. Activates aldosterone - Na+ retention
4. Vascular growth, hyperplasia and hypertrophy
279
Give 3 ways in which the Sympathetic nervous system (NAd) leads to increased BP
1. Noradrenaline is a vasoconstrictor = increase TPR
2. NAd has positive chronotropic and inotropic effects
3. It can cause increase renin release
280
In what diseases are ACE inhibitors clinically indicated?
1. Hypertension
2. Heart failure
3. Diabetic nephropathy
281
Name 3 ACE inhibitors
1. Ramipril
2. Enalapril
3. Perindopril
4. Trandolapril
5. Lisinopril
282
Give 4 potential side effects of ACE inhibitors due to reduced angiontensin II formation
1. Hypotension
2. Hyperkalaemia
3. Acute renal failure
4. Teratogenic
283
Give 2 potential side effects of ACE inhibitors due to increased kinin production
1. Cough
2. Rash
3. Anaphylactoid reaction
284
Why do ACE inhibitors lead to increased kinin production?
ACE also converts bradykinin to inactive peptides
| So ACE inhibitors lead to build up of kinin
285
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
286
What are ARBs?
Angiotensin II receptor blockers
287
At which receptor do ARB's work?
AT-1 receptor - prevent angiotensin II binding
288
In what diseases are ARBs clinically indicated?
1. Hypertension
2. Heart failure
3. Diabetic nephropathy
289
Name 3 ARBs
1. Candesartan
2. Valsartan
3. Losartan
290
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
291
Give 4 potential side effect of ARBs
1. Hypotension
2. Hyperkalaemia
3. Renal dysfunction
4. Rash
Contraindicated in pregnancy
292
In what diseases are calcium channel blockers clinically indicated?
1. Hypertension
2. IHD
3. Arrhythmia
293
Name 2 calcium channel blockers
1. Amlopipine
2. Felodipine
3. Diltiazem
4. Verapamil
294
Name 2 dihydropyridines and briefly explain how they work
Class of CCBs
Amlodipine and felodipine
Arterial vasodilators
295
Name a calcium channel blocker that acts primarily on the heart
Verapamil
| Negatively chronotropic and inotropic (reduce HR and force of contraction)
296
Name a CCB that acts on the heart and on blood vessels
Diltiazem
297
On what channels do CCB work?
L type Ca2+ channels
298
Give 3 potential side effects that are due to the vasodilatory ability of CCBs
1. Flushing
2. Headache
3. Oedema
4. Palpitations
299
Give 2 potential side effects that are due to the negatively chronotropic ability of CCBs
1. Bradycardia
2. Atrioventricular block
3. Postural hypotension
300
Give a potential side effect that is due to the negatively inotropic ability of CCBs
Worsening cardiac failure
301
Give 4 potential side effects of verapamil
1. Worsening of cardiac failure (-ve inotrope)
2. Bradycardia (-ve chronotrope)
3. Atrioventricular block (-ve chronotrope)
4. Constipation
302
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
303
In what diseases are beta blockers clinically indicated?
1. IHD
2. Heart failure
3. Arrhythmia
4. Hypertension
304
Name 3 beta blockers
1. Bisoprolol (beta 1 elective)
2. Atenolol
3. Propranolol (beta 1/2 nonselective)
305
Give 5 potential side effects of beta blockers
1. Fatigue
2. Headache
3. Sleep disturbances/nightmares
4. Bradycardia
5. Hypotension
6. Cold peripheries
7. Erectile dysfunction
8. Bronchospasm
306
Give 3 conditions in which Beta blockers can worsen them
1. Asthma or COPD
2. PVD
3. Heart failure
307
In what diseases are diuretics clinically indicated?
1. Heart failure
| 2. Hypertension
308
Name 4 classes of diuretics
1. Thiazides
2. Loop
3. Potassium sparing
4. Aldosterone antagonists
309
Where in the kidney do thiazide diuretics work?
The distal tubule
310
Name a thiazide
Bendroflumethethiazide
311
Name a loop diuretic
Furosemide
| Bumetanide
312
Name a potassium sparing diuretic
Spironolactone
| Eplerenone
313
Why are potassium sparing diuretics especially effective?
They have anti-aldosterone effects too
314
Give 5 potential side effects of diuretics
1. Hypovolaemia
2. Hypotension
3. Reduced serum Na+, K+, Mg+, Ca2+
4. Increased uric acid --> gout
5. Erectile dysfunciton
6. Impaired glucose tolerance
315
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
316
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
317
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
318
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
319
What is the counter regulatory system to RAAS?
Atrial Natriuretic Peptide/BNP (ventricular natriuretic peptide) hormones
320
Where are ANP and BNP produced?
The heart
321
What metabolises ANP and BNP?
Neprilysin (NEP)
322
What are the functions of ANP and BNP?
1. Increased renal excretion of Na+ and water
2. Vasodilators
3. Inhibit aldosterone release
323
Why can Neprilysin (NEP) inhibitors work for heart failure treatment?
NEP metabolises ANP and BNP
| NEP inhibitors therefore increase levels of ANP and BNP in the serum
324
In what diseases are nitrates clinically indicated?
1. IHD
| 2. Heart failure
325
Name 2 nitrates that are used pharmacologically
1. GTN spray (short acting)
| 2. Isosorbide mononitrate (long acting)
326
How do nitrates work in the treatment of heart failure?
They are venodilators so reduce preload and therefore BP
327
Give 2 potential side effects of nitrates
1. Headache
2. GTN syncope
3. Tolerance
328
How do anti-arrhythmic drugs work?
Interfere with the action potential of the heart in different phases
329
What classification is used to group anti-arrhythmic drugs?
Vaughan Williams classification
330
Name two class 1 drugs of the Vaughan Williams classification
Class 1 are Na+ channel blockers
1a = disopyramide, quinidine
1b = lidocaine
1c = flecainide (tachycardias)
331
Name three class 2 drugs of the Vaughan Williams classification
Class 2 are Beta blockers
Propranolol
Atenolol
Bisoprolol
332
Name a class 3 drug of the Vaughan Williams classification
Class 3 rugs prolong the action potential
Amiodarone
Side effects are likely with these
333
Name two class 4 drugs of the Vaughan Williams classification
Class 4 drugs are calcium channel blockers (but NOT dihydropyridines as they don't effect the heart)
Verapamil
Dilitiazem
334
How does digoxin work?
Inhibits the Na+/K+ pump therefore making the action potential more positive and ACh is released from parasympathetic nerves
335
What are the main effect of digoxin?
1. Bradycardia
2. Reduced atrioventricular conduction
3. Increased force of contraction (positive inotrope)
336
Give 3 potential side effects of digoxin
1. Nausea
2. Vomiting
3. Diarrhoea
4. Confusion
Also has a narrow therapeutic range
337
In what disease is digoxin clinically indicated?
1. Atrial fibrillation
| 2. Severe heart failure
338
What does furosemide block?
The Na+/K+/2Cl- transporter
339
Why are beta blockers good in chronic heart failure?
They block reflex sympathetic responses which stress the failing heart
340
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
341
What drug might you give to someone with angina caused by coronary artery vasospasm?
Amlodipine
342
How does amiodarone work?
Prolongs action potential by delaying depolarisation
343
Name 4 potential effects of amiodarone
1. QT prolongation
2. Interstitial lung disease
3. Hypothyroidism
4. Abnormal liver enzymes
344
Name a disease that might cause flattening of the P wave
1. Hyperkalaemia
| 2. Obesity
345
Name a disease that might cause tall P waves
Right atrial enlargement
346
Name a disease that might cause broad notched P waves
Left atrial enlargement
347
What aspect of the heart is represented by leads II, III and aVF?
Inferior aspect
348
What might ST elevation in leads II, II and aVF suggest?
RCA blockage
| Leads represent inferior aspect of heart, RCA supplies inferior aspect
349
Give 3 effects hyperkalaemia on an ECG
1. Tall tented T waves
2. Flat P waves
3. Broad QRS
350
Give 2 effects of hypokalaemia on an ECG
1. Flat T waves
2. QT prolongation
3. ST depression
4. Prominent U waves
351
Give an effect go hypocalcaemia on an ECG
1. QT prolongation
2. T wave flattening
3. Narrowed QRS
4. Prominent U waves
352
Give an effect of hypercalcaemia on an ECG
1. QT shortening
2. Tall T wave
3. No P waves
353
What controls the sinus node discharge rate?
Autonomic nervous system
354
Define sinus rhythm
A P wave precedes each QRS complex
355
Define cardiac arrhythmia
Abnormality of cardiac rhythm
356
Give 3 potential consequences of arrhythmia
1. Sudden death
2. Syncope
3. Heart failure
4. Chest pain
5. Palpitations
May also be asymptomatic
357
Define bradycardia
< 60 bpm
358
Define tachycardia
> 100 bpm
359
Give 2 causes of bradycardia
1. Conduction tissue fibrosis
2. Ischaemia
3. Inflammation/infiltrative disease
4. Drugs
360
Give 2 broad categories of tachycardia
1. Supraventricular tachycardias
| 2. Ventricular tachycardias
361
Where do supra-ventricular tachycardia's arise from?
Atria or atrio-ventricular junction
362
Do supra-ventricular tachycardia's have narrow or broad complex QRS complexes?
Narrow QRS complexes
363
Name 3 types of supraventricular tachycardia
1. Atrial fibrillation
2. Atrial flutter
3. AV node re-entry tachycardia
4. AV re-entry tachycardia (accessory pathway)
364
Where do ventricular tachycardia's arise from?
The ventricles
365
Do ventricular tachycardia's have narrow or broad complex QRS complexes?
Broad QRS compelxes
366
What is the commonest supra-ventricular tachycardia?
AV node re-entry tachycardia (AVNRT)
367
Do you see P waves in AVNRT?
Loss of P waves
368
Give 4 symptoms of AVNRT
1. Sudden onset/offset palpitations
2. Neck pulsation
3. Chest pain
4. SOB
369
Describe the acute treatment of AVNRT
Vagal manoeuvre, catheter ablation and adenosine (block AVN to terminate the SVT)
370
What drugs might you give someone to suppress further episodes of AVNRT?
Beta blockers, CCB
371
Describe the pathophysiology of AVRT (accessory) arrhythmias
Congenital muscle strands connect atria and ventricles = accessory pathway
Result in pre-excitaiton of ventricles
372
Describe 3 characteristics of an ECG from someone with accessory pathway arrhythmia
1. Delta wave
2. Short PR interval
3. Slurred QRS complex
373
Give an example of an AVRT (accessory) arrhythmia
Wolff-Parkinson-White Syndrome
374
Give 4 causes of sinus tachycardia
1. Physiological response to exercise
2. Fever
3. Anaemia
4. Heart failure
5. Hypovolaemia
375
Why do ventricular tachycardia's arise?
Extra circuits in ventricles or abnormal muscle depolarisation
Can come from previous MI or cardiomyopathy
376
What ECG changes might you see with someone with ventricular tachycardia?
Crescendo-decrescendo amplitude = torsades de pointes
377
What is the treatment for ventricular tachycardia in an urgent situation?
DC cardioversion
378
What is long term treatment for ventricular tachycardia in high risk patients
Implantable cardioverter defibrillator (ICD)
379
What is the treatment for stable ventricular tachycardia?
IV beta blockers and IV amiodarone
380
Define atrial fibrillation
Chaotic irregular atrial rhythm at 300-600 bpm
381
Give 4 symptoms of atrial fibrillation
1. SOB
2. Chest pain
3. Palpitations
4. Syncope
382
Name 3 causes of atrial fibrillation
1. Idiopathic
2. Hypertension
3. IHD
4. Mitral valve stenosis
5. PE
6. HF
383
Briefly describe the pathophysiology of atrial fibrillation
Chaotic irregular atrial rhythm --> AV response = irregular ventricular rhythm
384
Describe 2 characterics of an ECG taken from someone with atrial fibrillation
1. Absent P aves
2. Irregular QRS complexes
3. Fine oscillation of the baseline
Irregularly irregular
385
What score can be used to calculate the risk of stroke in someone with atrial fibrillation?
CHADS2 VAS
386
What does the CHADS2 VASc score take into account
```
CCF
HTN
Age (>75) = 2 points
DM
Stroke (previous) = 2 points
Vascular disease
Age 65-74
Sex (female)
```
Score >1 = anticoagulation
387
Describe the treatment for atrial fibrillation
1. Treat underlying cause
2. Rate control - BB, CCB and digoxin
2. Rhythm control 0 electrical cardioversion or pharmacological cardioversion using flecainide
3. Felcainide can be taken on a PRN basis in people with infrequent systemic paroxysms of AF
4. Long term - catheter ablation and a pacemaker
388
What might you give someone to help with rate control in atrial fibrillation?
BB, CCB and digoxin
389
What might you give someone to help restore sinus rhythm in atrial fibrillation?
Electrical cardioversion or pharmacological cardioversion using flecainide
390
What is the long term treatment for atrial fibrillation?
Catheter ablation
391
What is atrial flutter?
Fast but organised waves in the atrium
| Atrial rate 250-350 bpm
392
Describe the ECG pattern taken from someone with atrial flutter
1. Narrow QRS
| 2. Saw tooth flutter waves
393
Describe the pathophysiology of atrial flutter
Re-entry mechanism - blockage of normal circuit
| Another pathway forms, takes different course and re-enters the circuit --> tachycardia
394
What are ectopic beats?
Non sustained beats arising from ectopic regions of atria or ventricles
Very common, generally benign arrhythmias caused by premature discharge
395
What are ventricular ectopics?
Extra ventricular contractions --> palpitations/heart missing a beat
396
Give 3 causes of long QT syndrome
1. Congenital
2. Electrolyte disturbances - hypokalaemia, hypocalcaemia
3. Drugs
397
Give 2 signs of long QT syndrome
1. Palpitations
| 2. Syncope
398
Where can heart blocks occur?
1. Block in either AVN or bundle of His = AV block
| 2. Block lower in conduction system = Bundle Branch Block
399
Describe a first degree AV block
Fixed prolongation of the PR interval due to delayed conduction to the ventricles
400
Describe a second degree AV block
There are more P waves to QRS complexes because some atrial impulses fail to reach the ventricles
401
Describe a Mobitz type 1 second degree AV block
PR interval gradually increases until AV node fails and no QRS is seen
402
Describe a Mobitz type 2 second degree AV block
Sudden unpredictable loss of AV conduction and so loss of QRS
PR interval is constant but every nth QRS is missing
403
Describe a third degree AV block
Atrial activity fails to conduct to the ventricles
| P waves and QRS complexes occur independently
404
What are the treatments for AV heart blocks?
1st = asymptomatic, watch and wait --> atropine
Mobitz 1 = no pacemaker
Mobitz 2 = pacemaker
3rd = permanent pacemaker
405
Give 4 causes of heart block
1. Coronary artery disease
2. Cardiomyopathy
3. Fibrosis
4. Previous MI
406
What kind of heart block is associated with wide QRS complexes with an abnormal pattern?
Right bundle branch block (RBBB) and Left bundle branch block (LBBB)
407
Explain the pathophysiology of a BBB
Lack of simultaneous ventricular contractions
LBBB = R before L
RBBB = L before R
408
What changes would you see on an ECG from someone with a LBBB?
A 'W' Shape would be seen in QRS complex of Lead V1
'M' shape seen in V6
WiLLiaM
409
What changes would you see on an ECG from someone with a RBBB?
A 'M' Shape would be seen in QRS complex of Lead V1
'W' shape seen in V6
MaRRoW
410
Cardiac arrhythmias: what is the treatment of choice in a patient who is hemodynamically unstable due to the underlying rhythm?
DC cardioversion
411
Name 4 valvular heart diseases
1. Aortic stenosis
2. Mitral regurgitation
3. Mitral stenosis
4. Aortic regurgitation
412
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
413
Name the 3 types of aortic stenosis
1. Surpavalvular
2. Subvalvular
3. Valvular = most common
414
What are the causes of aortic stenosis?
1. Congenital bicuspid valve
| 2. Acquired --> age related degenerative calcification and rheumatic heart disease
415
Describe the pathophysiology of aortic stenosis
Aortic orifice is restricted by calcific deposits
Pressure gradient develops between LV and aorta
LV function initially maintained due to compensatory hypertrophy
Mechanism become exhausted = LV failure
416
Give 3 symptoms of aortic stenosis
Occur when valve area is 1/4 of normal (normal - 3-4 cm2)
1. Exertional syncope
2. Angina
3. Exertional dyspnoea
417
Give 3 signs of aortic stenosis
1. Slow rising carotid pulse (pulsus tradus) and decreased pulse amplitude (pulsus parvus)
2. Soft or absent heart sounds
3. Ejection systolic murmur - crescendo-decrescendo character
418
What investigation might you do in someone who you suspect to have aortic stenosis?
Echocardiography - assess LV size and function and doppler derived gradient and valve area
High gradient = severe stenosis
419
Describe the management for someone with aortic stenosis
1. Ensure good dental hygiene
2. Consider IE prophylaxis
3. Aortic valve replacement or Transcatheter aortic valve replacement (TAVI)
420
Why does medical intervention have a limited role in aortic and mitral stenosis treatment?
Aortic and mitral stenosis are mechanical problems
421
Who should be offered an aortic valve replacement?
1. Symptomatic patient with AS
2. Any patient with decreasing ejection fraction
3. Any patient undergoing CABG with moderate/severe AS
422
What is mitral regurgitation?
Backflow of blood from the LV to the LA during systole
| LV volume overload
423
What can cause mitral regurgitation?
1. Myxomatous degeneration (mitral valve prolapse)
2. Ischaemic mitral valve
3. Rheumatic heart disease
4. IE
424
Describe the pathophysiology of mitral regurgitation
LV volume overload
Compensatory mechanism = LA enlargement, LVH and increase contractility
Progressive LV volume overload --> dilation and progressive HF
425
Give 2 symptoms of mitral regurgitation
1. Dyspnoea on exertion
2. HF
3. Fatigue and lethargy
426
Give 3 signs of mitral regurgitation
1. Pan-systolic murmur
2. Soft 1st heart sound
3. 3rd heart sound
In chronic MR, intensity of murmur correlates with severity
427
What investigations might you do in someone who you suspect to have mitral regurgitation?
1. ECG
2. CXR
3. Echo - estimates LA/LV size and function
428
What is the management of mitral regurgitation?
```
Rate control for AF - BB, CCB, digoxin
ACEi = vasodilator
Anticoagulation for AF
Diuretics for fluid overload
IE prophylaxis
If symptomatic = surgery
```
429
What is aortic regurgitation?
Leakage of blood into LV from aorta duding diastole due to ineffective coaptation of aortic cusps
430
What causes aortic regurgitation?
1. Bicuspid aortic valve
2. Rheumatic fever
3. IE
431
Describe the pathophysiology of aortic regurgitation
Pressure and volume overload
Compensatory mechanism = LV dilation, LVH
Progressive dilation --> HF
432
Give 3 symptoms of aortic regurgitation
1. Dyspnoea on exertion
2. Orthopnoea
3. Palpitations
4. Paroxysmal nocturnal dyspnea
433
Give 3 signs of aortic regurgitation
1. Diastolic blowing murmur
2. Wide pulse pressure
3. Systolic ejection murmur
434
What investigations might you do in someone who you suspect to have aortic regurgitation?
CXR - cardiomegaly, aortic root enlargement
| ECHO - LV size and function and aortic root evaluation
435
Describe the management for someone with aortic regurgitation
IE prophylaxis
ACEi = vasodilators
Regular echos - motion progression
Surgery if symptomatic
436
What is mitral stenosis?
Obstruction of LV inflow that prevents proper filling during diastole
437
Name 3 causes of mitral stenosis
1. Rheumatic heart disease
2. IE
3. Mitral annular calcification
438
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
439
Give 3 symptoms of mitral stenosis
1. Dyspnoea
2. Haemoptysis
3. RHF symptoms
440
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 systolic murmur
5. Loud opening S1 snap
6. Diastolic murmur
441
What investigations might you do in someone who you suspect to have mitral stenosis?
1. ECG
2. CXR
3. Echo - gold standard for diagnosis
442
Describe the management for mitral stenosis
```
If in AF rate control - BB, CCB
Anticoagulation if AF
Diuretics for fluid overload
Percutaneous mitral balloon valvotomy
Mitral vale replacement
IE prophylaxis
```
443
In what type of valvular heart disease would you hear a mid-diastolic murmur and a 1st heart sound snap?
Mitral stenosis
444
In what type of valvular heart disease would you hear a pan systolic murmur?
Mitral regurgitation
445
In what type of valvular heart disease would you hear an ejection systolic murmur?
Aortic stenosis
446
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
447
What is infective endocarditis?
Infection of heart valve/s or other endocardial lined structure within the heart
448
Name 4 types of IE
1. Left sided native IE
2. Left sided prosthetic IE
3. Right sided IE
4. Device related IE (pacemaker, defibrillators)
449
Which type of IE is more likely to spread systemically?
Left sided IE - more likely to cause thrombo-emboli
| Right sided IE could spread to the lungs
450
Give 2 risk factors for IE
1. Having a regurgitant o prosthetic valve
2. If infectious material is introduced into blood stream (drugs) or during surgery
3. Poor dental hygiene and dental treatment
451
Which bacteria are most likely to cause IE?
1. Staphylococcus aureus
2. Staphlococcus epidermidi (coagulase negative staph)
3. Streptococcus viridian's (alpha haemolytic)
452
Give 3 groups of people who are at risk of IE
1. Elderly
2. IV drug users
3. Those would prosthetic valves
4. Those with rheumatic fever
5. Young with congenital heart disease
453
Describe the pathophysiology of IE
Microbial adherence (infection) --> vegetation on valve --> cardiac valve distortion --> cardiac failure and septic problems
454
What is the hallmark of IE?
Vegetation - lumps of fibrin hanging of heart valves
455
Name 2 sites where vegetation is likely in IE
1. Atrial surface of AV valves
| 2. Ventricular surface of SL valves
456
Give 3 symptoms of IE
1. Signs of systemic infections - fever, sweats etc
2. Embolism - stroke, PE, MI
3. Valve dysfunction - HF, arrhythmia
457
Give 4 signs of IE
1. Splinter haemorrhages
2. Osler's nodes
3. Janeway lesions
4. Roth spots
5. Heart murmurs
458
Name the criteria that I used in the diagnosis of IE
Duke's criteria
459
Give the 2 major points in the Duke's criteria that if presence can confirm a diagnosis of IE
1. Positive blood culture with typical IE micro-organism
| 2. Positive echo showing endocardial involvement
460
What investigations might you do in someone who you suspect to have IE?
1. Blood cultures - essential
2. Echo - TTE ot TOE
3. Bloods - raised ESR and CRP
4. ECG
461
Give 2 advantages and 1 disadvantage of a trans-thoarcic echo (TTE)
```
Advantages:
1. Safe
2. Non-invasive, no discomfort
Disadvantage:
1. Poor images
```
462
Give 1 advantage and 2 disadvantages of a trans-oesophageal echo (TOE)
```
Advantage:
1. Excellent images
Disadvantage:
1. Discomfort
2. Small risk of perforation or aspiration
```
463
Describe the treatment for IE
1. Antibiotics based on cultures
2. Treat any complications
3. Surgery - remove and replace valve
464
Give 4 indications for surgery in IE
1. Antibiotics not working
2. Complications
3. To remove infected devices
4. To replace valve after infection cured
5. To remove large vegetations before they embolism
465
Why is it important to remove large vegetations?
To prevent them embolising and causing a stroke, MI etc
466
Why might blood cultures be negative in a person with IE?
They may have previously received antibiotics
467
Name 2 drugs that can prolong the QT interval
1. Sotalol
| 2 Amiodarone
468
Give 5 potential side effects of drugs that prolong the QT interval
1. Pro-arrhythmic effects
2. Interstitial pneumonitis
3. Abnormal liver function
4. Hyper/hyopthyroidism
5. Sun sensitivity
6. Grey skin discolourations
7. Corneal micro-deposits
8. Optic neuroapthy
469
How do sodium channel blockers work in the treatment of ventricular tachycardia?
Block the inactivation gate of the sodium channel
470
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
471
Define shock
Acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in generalised hypoxia and/or an inability of the cells to utilise oxygen
472
Give 6 symptoms/signs of shock
1. Pale
2. Sweaty
3. Cold
4. Pulse is weak and rapid
5. Reduced urine output
6. Confusion
7. Weakness/collapse
8. Low BP
473
Name 5 types of shock
1. Hypovolaemic
2. Haemorrhagic
3. Septic
4. Anaphylactic
5. Neurogenic
6. Cardiogenic
474
What can cause hypovolaemic shock?
1. Loss of blood = acute GI bleeding, trauma, post-op, splenic rupture
2. Loss of fluid = dehydration, burns, vomiting , pancreatitis
475
What can cause cariogenic shock?
1. Cardiac tamponade
2. PE
3. Acute MI
4. Fluid overload
5. Myocarditis
476
What is septic shock?
A systemic inflammatory response associated with an infection (bacterial endotoxins)
477
What is anaphylactic shock?
An intense allergic reaction associated with massive histamine release = haemodyanmic collapse
Patient may be breathless, wheezy and have a rash
478
What is the treatment for anaphylactic shock?
Adrenaline and supportive therapy - O2 delivery, fluid replacement
479
What is the treatment for shock?
ABC
480
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
481
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
482
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
483
What are the 4 main features of tetralogy of fallot?
1. Ventricular septal defect
2. Over-riding aorta
3. RV hypertrophy
4. Pulmonary stenosis
484
Would a baby born with tetralogy of fallot be cyanotic?
YES
RV pressure higher than LV
Blood passes from RV to LV so patients are blue = cyanosis
485
What is VSD?
Ventricular septal defect = abnormal connection between the 2 ventricles
486
Would a baby born with VSD cyanotic?
NO
High pressure in LV than RV so blood shunted from left to right
Increased amount of blood going to the lungs
Not cyanotic
487
Give 4 clinical sins of a large VSD
1. High pulmonary signs of a large VSD
2. Breathless, poor feeding, failure to thrive
3. Increased respiratory rate
4. Tachycardia
5. Requires surgical repair
488
Give 2 clinical signs of a small VSD
Asymptomatic
No intervention needed
Loud systolic murmur
489
What syndrome might VSD lead on to?
Eisenmengers syndrome
490
Briefly decscribe the pathophysiology if Eisenmengers syndrome
High pressure pulmonary blood flow damages pulmonary vasculature --> increase in resistance to blood flow (pulmonary hypertension) --> RV pressure increase --> shunt direction reverses (RV to LV) = cynanosis
491
What are the risks associated with Eisenmengers syndrome?
1. Risk of death
2. Endocarditis
3. Stroke
492
What is ASD?
Atrial septal defect = abnormal connection between the two atria
493
Would a baby born with ASD be cyanotic?
NO
| Higher pressure in the LA than the RA and so blood is shunted from the left to right
494
Give 5 clinical signs of a large ASD
1. Significant increased flow through right heart and lungs = pulmonary flow murmur
2. Right heart dilation
3. Enlarged pulmonary arteries
4. SOB on exertion
5. Increased chest infections
495
Give 3 signs of a small ASD
Asymptomatic
No right heart dilation
Increases with age but left alone
496
How are ASDs closed?
Surgically
| Percutaneous (key hole)
497
What is AVSD?
Atrio-ventricular septal defects
Basically a hole in the very centre of the heart
Involves the ventricular septum, atrial septum and the mitral and tricuspid valves
Can be complete or partial
498
What happens to the AV valves in AVSD?
Instead of 2 separate AV valves there is 1 big malformed one
| Usually leaks to a greater or lesser degree
499
Give 2 clinical signs of AVSD
1. Breathlessness
| 2. Poor feeding and weight gain
500
Does a AVSD need surgical repair?
Complete AVSD needs repair
| Partial can be left alone if no right heart dilation
501
What is PDA?
Patent ductus arteriosus = persistent communication between proximal left pulmonary artery and descending aorta
502
Give 4 clinical signs of PDA
1. Torrential flow from aorta to pulmonary arteries can lead to hypertension and RHF
2. Breathless
3. Poor feeding, failure to thrive
4. Risk of endocarditis
503
Describe the pathophysiology behind coarctation of the aorta
Excessive sclerosing that normally closes the ductus arteriosus extends into the aortic wall leading to narrowing
504
What happens with severe coarctation of the aorta?
Complete or almost complete obstruction to aortic flow
Collapse with heart failure
Needs urgent repair
505
How does mild coarctation of the aorta present?
Presents with hypertension
Incidental murmur
Should be repaired to try to prevent problems in the long term
506
What long term problems can occur due to coarctation of the aorta?
Hypertension - early CAD, early stroke, subarachnoid haemorrhage
Re-coarctation requiring repeat intervention
Aneurysm formation at the site of repair
507
What is pulmonary stenosis?
Narrowing of the RV outflow tract
508
How does a patient present with pulmonary stenosis?
```
Right ventricular failure
Collapse
Poor pulmonary blood flow
RVH
Tricuspid regurgitation
```
509
How is pulmonary stenosis treated?
Ballon valvuloplasty
Open valvotomy
Open trans-annular patch
Shunt (to bypass blockage)
510
What are 3 problems with a bicuspid aortic valve?
1. Degenerate quicker than normal valves
2. Become regurgitant earlier than normal valves
3. Associated with coarctation and dilation of ascending aorta
511
Name 3 congenital heart defect that are not cyanotic
1. VSD
2. ASD
3. PDA
Left to right shunt
512
Name a congenital heart defect that is cyanotic
1. Tetralogy of Fallot
| Right to left shunt
513
Why does mitral stenosis cause AF?
Increased LA pressure
| Stretches myocytes in the atria and irritates pacemaker cells --> AF
514
Why does mitral stenosis lead to a raised JVP?
Pulmonary congestion --> pulmonary hypertension causing a raised JVP
515
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
516
Give 3 symptoms of Dressler's syndrome
1. Fever
2. Chest pain
3. Pericardial rub
Occurs 2-10 weeks after MI
517
Write an equation for mAP
mAP = DP + 1/3PP
518
Give the equation for stroke volume
SV = EDV - ESV
519
What is a consequence of peripheral arterial occlusion?
Gangrene
520
Give 2 diseases that result from stress induced ischaemia
1. Exercise induced angina
| 2. Intermittent claudication
521
Give 2 disease that result from ischaemia due to structural/functional breakdown
1. Critical limb ischaemia
| 2. Vascular dementia
522
Give a sign infarction
Gangrene
523
Name the classification system for Peripheral vascular disease (PVD)
Fontaine classification
524
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
525
What can intermittent claudication lead on to if left untreated?
Critical ischaemia
526
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
527
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
528
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 = normal
529
Give a symptom of intermittent caludication
Muscle cramps
530
Name 2 diseases that are due to moderate ischaemia
1. Angina
| 2. Intermittent claudication
531
Name a disease that is due to severe ischaemia
Critical limb ischaemia
532
Name 3 causes of an aneurysm
1. Atherosclerotic (most common)
2. Ateriomegaly
3. Collagen disease - Marfans, vascular Ehlers Danlos
533
How do you treat peripheral vascular disease?
```
Risk factor modification
- Stop smoking
- lower cholesterol
- control BP, diabetes
- Aspirin = antiplatelets
Revascularisation for critical ischaemia
- Stent
- Bypass
Open aneurysm repair
Amputation is very severe
```
534
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
535
Name 2 types of aortic aneurysm
1. Abdominal aortic aneurysm (AAA)
| 2. Thoracic abdominal aneurysm (TAA)
536
What classifies as an Abdominal aortic aneurysm?
> 3 cm
| Dilation affects all 3 layers of the vascular tunic
537
Describe the pathophysiology of a thoracic abdominal aneurysm
Aorta loses distensibility so that a rise in BP can excess arterial wall strength and many trigger dissection or rupture
538
Describe the pathophysiology of an aortic dissection
Tear in intimal lining of aorta --> column of blood under pressure enters aortic wall forming haematoma --> separates intima from adventitia --> false lumen
False lumen extends --> intimal tears
539
Mr newton, a 64-year-old male attends a GP complaining that this week he’s started experiencing some chest pain when he’s out birdwatching. It’s in the centre of his chest and eases off if he sits down for a few minutes. Which of the following would you expect to see on a stress ECG?
a. Saddle shaped ST with PR depression
b. Tall tented T waves and pathological Q waves
c. ST elevation
d. ST depression
e. Absent P waves
What are the others ECG traces for?
= ANGINA so...
d. ST depression = Angina
a. Saddle shaped ST with PR depression = Pericarditis
b. Tall tented T waves and pathological Q waves = Hyperkalaemia
c. ST elevation = STEMI
d. ST depression = Angina
e. Absent P waves = AF (irregularly irregular)
540
She has acute pericarditis pain; how does she describe the pain?
a. Sitting --> standing
b. When leaning forward alleviated by lying down
c. When lying down alleviated by leaning forward
d. On inspiration
e. On exertion
c. When lying down alleviated by leaning forward
541
Mitral regurgitation, what murmur do you hear?
a. Early diastolic murmur
b. Early systolic click murmur
c. Ejection systolic crescendo-decrescendo murmur
d. End diastolic murmur
e. Pansystolic murmur
What are the others murmurs of?
e. Pansystolic murmur = occurs throughout duration of systole = Mitral regurgitation
a. Early diastolic murmur = Mitral stenosis
b. Early systolic click murmur = Mitral valve replacement (click = replacement as metal)
c. Ejection systolic crescendo-decrescendo murmur = Aortic stenosis
d. End diastolic murmur
e. Pansystolic murmur = occurs throughout duration of systole = Mitral regurgitation
542
```
Trystan, a 54-year old Caucasian gentleman, attends his annual diabetes check with the nurse practitioner. His BP is 143/82. He’s currently on metformin and simvastatin but reckons three’s a charm and wants another pill. Which is the appropriate anti-hypertensive to give him?
a. Amlodipine
b. Bendroflumethiazide
c. Candesartan
d. Diltiazem
e. Isomorbide mononitrate (GTN spray)
What type of drugs are the others?
```
c. Candesartan = ACEi/ARB first line for younger than 55 non afro-Caribbean’s patients with
a. Amlodipine = CCB
b. Bendroflumethiazide = thiazide like diuretic
c. Candesartan = ACEi/ARB first line for younger than 55 non afro-Caribbean’s patients with hypertension
543
What is the mechanism of action of Heparin?
a. Increases cGMP and reduces intracellular Ca2+ concentration
b. Inhibits COX reducing production of thromboxane A2
c. Inhibits production of vitamin K dependent clotting factors
d. Inhibits thrombin and factor Xa
e. Induces vagal nerve stimulation
What are drugs are the other mechanisms of actions?
d. Inhibits thrombin and factor Xa = Heparin
a. Increases cGMP and reduces intracellular Ca2+ concentration = CCB
b. Inhibits COX reducing production of thromboxane A2 = NSAIDs (Ibuprofen, Aspirin)
c. Inhibits production of vitamin K dependent clotting factors = Warfarin
d. Inhibits thrombin and factor Xa = Heparin
544
Infective endocarditis, which would you not see on the patient’s hands?
a. Roth spots
b. Janeaway lesion
c. Oslar nodes
d. Splinter haemorrhages
e. Clubbing
a. Roth spots
| Seen in the eye, not on the hands
545
Ellie’s boyfriend commented that she had fat calves. Over the past 2 days she has noticed her left calf has become swollen and red compared to the right. You have conducted a wells score which gives a score less than 4. This is a medium risk. What test would you request too further investigate this case?
a. Full blood count
b. CRP
c. D-dimer
d. Tropomyosin I
e. Anti-phospholipid antibody
c. D-dimer
546
What is the definition of BP?
a. CO x Total vascular resistance
b. HR x SV
c. Diastolic + pulse pressure
d. End diastolic volume – end systolic volume
a. CO x Total vascular resistance
547
```
What is the diagnostic test for heart failure?
a. Troponin I
b. ANP
c. BNP
d. CK-MB
e. FBC
When do the others increase?
```
c. BNP = increased in ventricular dysfunction
a. Troponin I = MI
b. ANP = produced in problem with atrium
c. BNP = increased in ventricular dysfunction
d. CK-MB = MI, increases when there is damage to the heart
548
A 43-year-old male is started on an ACE inhibitor as part of his management for angina. He presents to your clinic complaining of a cough which he thinks he’s has since his last visit with you. The GP changes the ACEi for an ARB. Which substance is responsible for the cough?
a. ACH
b. Bradykinin
c. Histamine
d. IgE
e. Prostaglandin
b. Bradykinin
