Cardio 2 Flashcards
(135 cards)
1
Q
list 3 viral causes of acute pericarditis
A
Coxsackie B Influenza EBV Mumps Varicella HIV
2
Q
list 3 bacterial causes of acute pericarditis
A
Pneumonia Rheumatic fever TB Streps Staphs
3
Q
list 5 causes, other than bacterial/viral infection, of acute pericarditis
A
Fungi, MI, uraemia, rheumatoid arthritis, SLE, myxoedema, trauma, surgery, malignancy, radiotherapy, sarcoidosis, idiopathic + drugs
4
Q
describe the pain seen in acute pericarditis
A
sharp, central chest pain - worse on inspiration or lying flat, relieved by leaning forward
5
Q
what might be heard on auscultation of a patient with pericarditis?
A
pericardial friction rub
6
Q
what investigation would you carry out to diagnose acute pericarditis? what would you see?
A
ECG - concave upwards (saddle-shaped) ST segment elevation in all leads
7
Q
how would you treat acute pericarditis?
A
treat underlying cause.
NSAIDs for analgesia.
colchicine if relapsing.
8
Q
what is constrictive pericarditis?
A
heart is encased in a rigid fibrotic pericardium - prevents diastolic filling of ventricles.
9
Q
what causes constrictive pericarditis?
A
most common in UK = idiopathic.
globally = TB.
also occurs after any pericarditis.
10
Q
what are the clinical features of constrictive pericarditis?
A
those of right-sided heart failure - raised JVP, oedema, hepatomegaly, ascites, pulsus paradoxus, diffuse apex beat
11
Q
what two investigations would you carry out in constrictive pericarditis and what would you find?
A
CXR - normal/small heart + pericardial calcification.
CT/MRI - pericardial thickening/calcification
12
Q
how would you treat constrictive pericarditis?
A
surgical excision of pericardium
13
Q
what is the definition of hypertension?
A
> 140/90mmHg based on 2+ readings on separate occasions
14
Q
what are the criteria for treating hypertension?
A
ALL with sustained >160/100mmHg.
those with sustained >140/90 that are at high risk of coronary events, have diabetes or end-organ damage
15
Q
list 3 causes of secondary hypertension
A
renal disease - diabetic nephropathy, chronic glomerulonephritis, PKD, chronic tubulointerstitial nephritis.
endocrine disease - Conn’s, phaeochromocytoma, Cushing’s, acromegaly.
Coarctation of the aorta.
pregnancy.
steroids.
the Pill.
16
Q
give 3 risk factors for hypertension
A
age, FHx, male gender, African or Caribbean origin, high salt intake, sedentary lifestyle, overweight/obese, smoking, excess alcohol intake.
17
Q
what investigations would you carry out on a patient presenting with a high blood pressure reading?
A
take blood pressure again, on at least 1 other occasion.
24h ambulatory BP monitoring (ABPM) - exclude white coat effect
18
Q
give 3 examples of non-pharmacological measures you would encourage a patient with hypertension to take
A
weight reduction. Mediterranean diet - oily fish, low saturated fat, low salt. limit alcohol consumption. exercise. smoking cessation. increase fruit and veg intake.
19
Q
what drug would you prescribe for a 45yo caucasian patient with hypertension with no other medical history?
A
ACE inhibitor - ramipril. if CI (cough) - ARB - losartan
20
Q
what drug would you prescribe a 67yo Afro-Caribbean man with hypertension?
A
calcium channel blocker - amlodipine
21
Q
if first line treatment is failing to control a patient’s hypertension, what drug regime would you prescribe them? and if this fails?
A
ACE inhibitor + CCB or ACE inhibitor + thiazide.
all 3 if a combination of 2 fails to control.
22
Q
how do calcium channel blockers work to reduce hypertension?
A
decrease calcium entry into vascular smooth muscle cells - vasodilation of arterial smooth muscle, lowering arterial pressure.
23
Q
what are the side effects of CCBs?
A
bradycardia, headaches, flushing
24
Q
what is the most common cardiac arrhythmia?
A
atrial fibrillation
25
what is AF?
chaotic, irregular atrial rhythm at 300-600bpm.
AV node is conducting some of the atrial impulses - irregular ventricular response.
irregularly irregular pulse.
26
list 4 causes of atrial fibrillation
heart failure/ischaemia, hypertension, MI, PE, mitral valve disease, pneumonia, hyperthyroidism, caffeine, alcohol, hypokalaemia, hypomagnaesaemia
27
what ECG features would you see in atrial fibrillation?
absent P waves
irregular QRS complexes
atrial rate 300bpm
28
give 3 forms of treatment you would give a patient with atrial fibrillation
warfarin - anticoagulation.
beta blockers/CCBs - rate control.
Cardioversion - rhythm control.
29
describe what you would see on an ECG trace in atrial flutter
saw tooth flutter waves between QRS complexes
30
what is the difference between atrial fibrillation and atrial flutter?
atrial fibrillation = irregular ventricular conduction of atrial beats.
atrial flutter = atrial rate of 300bpm (same as AF), but ventricles conduct every other atrial beat - 150bpm
31
name 2 common causes of heart block
coronary artery disease, cardiomyopathy, fibrosis of conducting tissue
32
what is first degree AV block? how does it appear on ECG?
delayed AV conduction.
| prolonged PR interval (>0.22s).
33
how does Mobtiz type I (second degree) AV block appear on ECG? aka Wenckebach phenomenon
progressive PR interval prolongation until a P wave fails to conduct - PR interval then returns to normal, then begins to get longer again.
34
how is Mobitz type II (second degree) AV block seen on ECG?
dropped QRS waves aren't preceded by progressive PR prolongation. wide QRS complex.
35
what is 2:1 or 3:1 advanced second degree AV block?
every second or third P wave conducts to ventricles
36
what is third degree AV block? how are ventricular contractions maintained?
all atrial activity is failing to conduct to ventricles - atrial and ventricular activity completely dissociated (shown in P and QRS waves).
ventricular contractions are being maintained by spontaneous escape rhythms from below site of block.
37
describe the ECG features seen in RBBB
secondary R waves in V1.
| slurred S in V5 and V6
38
list 2 causes of RBBB
PE, RVH, IHD, congenital heart disease, idiopathic
39
describe the ECG features seen in LBBB
opposite to RBBB.
secondary R waves in left ventricular leads (I, AVL, V4-V6).
slurred S in V1 and V2.
40
list 2 causes of LBBB
IHD, LVH, aortic valve disease, post-op
41
give 3 causes of sinus tachycardia
physiological - exercise/excitement.
| fever, anaemia, heart failure, thyrotoxicosis, acute PE, hypovolaemia, drugs.
42
what causes atrioventricular junctional tachycardias?
re-entry circuits - two separate pathways for impulse conduction
43
what are the ECG changes seen in supraventricular tachycardia?
absent or inverted P wave after QRS
44
name 2 things that may aggravate a supraventricular tachycardia
exertion, coffee, tea, alcohol
45
what is the 1st line management of a supraventricular tachycardia?
vagal manoeuvres - breath holding, valsalva manoeuvre, carotid massage
46
what drugs may be used to treat a supraventricular tachycardia?
IV adenosine.
| if fails - verapamil/atenolol.
47
what is the long-term management of a supraventricular tachycardia?
radiofrequency ablation of accessory pathway via catheter.
48
what are ventricular ectopic premature beats?
a premature beat arising from an ectopic focus in the ventricles - this focus depolarises before the SAN, leading to a premature and inefficient beat.
49
describe the clinical and ECG features of a premature ventricular ectopic beat
broad, abnormal QRS complex before you would expect it.
| patient complains of extra/missed beats/heavy beats - palpitations
50
how would you treat a symptomatic ventricular ectopic beat? what are patients with ventricular ectopic beats at a higher risk of?
beta blockers.
| ventricular fibrillation.
51
what are the ECG features of a ventricular tachycardia?
rapid ventricular rhythm with broad abnormal QRS complexes
52
list 3 causes of prolonged QT
congenital, hypokalaemia, hypocalcaemia, hypomagnesaemia, tricyclics, macrolides
53
what causes Wolff-Parkinson-White?
congenital accessory conduction pathway between atria and ventricles
54
describe the features of a resting ECG in a patient with WPW
short PR interval, wide QRS complex due to slurred upstroke (delta wave)
55
what is an aneurysm? how might they cause symptoms?
permanent localised dilation of an artery.
pressure effects on local structures, or vessel rupture.
can be a source of emboli.
56
how might an abdominal aortic aneurysm be discovered?
a pulsatile mass palpated on abdo exam.
calcification on a plain XR.
rupture.
epigastric or back pain due to pressure effects.
57
what is the difference between a true and false aneurysm?
true aneurysm has the wall of the artery forming a capsule around the aneursym.
false aneurysm wall is made up of surrounding tissue.
58
how would a ruptured AAA present?
sudden severe epigastric pain radiating to back leading to hypovolaemic shock - collapse
59
how would a ruptured AAA be repaired?
endovascular repair with stent insertion, or surgical replacement of aneurysmal section
60
describe the pain of a dissecting aortic aneurysm
abrupt onset of severe, tearing central chest pain radiating through back
61
how is a dissecting aortic aneurysm managed?
urgent BP control - lanetalol IV.
| surgical repair.
62
give 3 risk factors for peripheral arterial disease
hypertension, smoking, diabetes, diet, sedentary lifestyle, obesity, hyperlipidaemia, age, male gender, FHx
63
what causes peripheral artery disease?
atherosclerosis causing stenosis of arteries
64
describe the clinical features of intermittent claudication
cramping pain in calf/thigh/buttock after walking a given distance (shorter=more severe) - relieved by rest
65
describe the clinical features of critical ischaemia
ulceration, gangrene, pain at rest.
| burning foot pain at night relieved by hanging legs over the side of the bed
66
what are the 4 stages in the Fontaine classification of peripheral artery disease?
asymptomatic - intermittent claudication - ischaemic rest pain - ulceration/gangrene (critical ischaemia)
67
give 3 signs of peripheral artery disease
absent femoral, popliteal or foot pulses.
| cold, white leg(s), atrophic skin, punched out ulcers, postural colour change, capillary refill prolonged
68
what are the 5 Ps of acute limb ischaemia?
```
Paraesthesia
Perishingly cold
Pallor
Paralysis
Pain
```
69
what diagnostic tests would be performed in peripheral artery disease?
Ankle-brachial pressure index (ABPI) - ratio of ankle and brachial systolic pressures.
colour duplex USS.
MR/CT angiography.
70
describe conservative treatment of limb ischaemia
exercise, quit smoking, lose weight, manage diabetes and hypertension.
clopidogrel (antiplatelet) to prevent progression and reduce risk.
71
how would intermittent claudication be managed, beyond conservative risk reduction treatments?
revascularisation - percutaneous transluminal angioplasty (PTA) or surgical reconstruction/arterial bypass graft.
72
what are some risk factors for infective endocarditis?
```
congenital - valve defects, VSD, PDA.
prosthetic valves.
IVDU.
poor dental hygiene.
soft tissue infections.
```
73
name the most common causative organism in infective endocarditis?
Streptococcus viridans
74
give 3 organisms (apart from Strep viridans) that can cause infective endocarditis
enterococci, staph aureus/epidermidis, diphtheroids, Haemophilus, actinobacillus, Coxiella burnetii, chlamydia.
fungi - Candida, aspergillus, histoplasma.
75
what is an infective endocarditis patient at risk of?
stroke - vegetations.
| destruction of valve - regurgitation - worsening heart failure.
76
describe the clinical features of infective endocarditis
systemic features of infection - malaise, fever, night sweats, weight loss, anaemia.
heart failure + new murmurs.
vascular events - embolism ± metastatic abscesses.
immune complex deposition - petechial haemorrhages under skin, splinter haemorrhages under nails, Roth's spots, arthrlagia, acute glomerulonephritis.
77
what investigations should you carry out in suspected endocarditis?
3 sets of blood cultures, at different times and sites.
bloods - anaemia, neutrophilia, high ESR/CRP.
transthoracic echocardiography (TTE) - just standard echo.
78
describe the Duke criteria for diagnosis of IE
2 major or 1 maj + 3 min, or 5 min.
Major criteria - persistently +ve blood culture. endocardium involvement seen on +ve echo, new murmur.
Minor criteria - fever, vascular/immunological signs, +ve blood culture/echo that doesn't meet major.
79
how would you treat infective endocarditis?
before results of culture - IV benzylpenicillin + gentamicin.
then tailor to cultures and sensitivity.
80
what is shock?
acute circulatory failure with inadequate or inappropriately distributed tissue perfusion - prolonged oxygen deprivation leads to necrosis, organ failure and death
81
list the different types of shock
hypovolaemia, cardiogenic, sepsis, anaphylaxis, neurogenic shock
82
give 3 causes of hypovolaemia shock
haemorrhages - GI bleed, trauma, AAA dissection etc.
| fluid loss - burns, diarrhoea, intestinal obstruction.
83
give 3 causes of cardiogenic shock
(= pump faillure).
| ACS, arrhythmias, aortic dissection, PE, tension pneumothorax, cardiac tamponade, endocarditis
84
give 3 signs of hypovolaemic shock
pale grey skin, slow capillary refill, sweating, weak pulse, tachycardia
85
name 2 precipitating factors of anaphylactic shock
penicillin, contrast, latex, dairy, nuts, insect stings
86
describe the clinical features of anaphylactic shock
onset within 5-60mins of exposure.
| warm peripheries, hypotension, urticarial, angio-oedema, wheezing, upper airway obstruction.
87
how would you manage septic shock?
take blood cultures before abx - then co-amoxiclav and tazocin IV
88
how would you manage anaphylactic shock?
remove cause. O2. IM adrenaline. IV chlorphenamine and hydrocotisone.
89
how would you manage hypovolaemic shock?
raise legs. fluid bolus - repeat if shock improves.
90
what risk score is used to determine stroke risk in AF patient?
```
CHA2DS2-VASc score:
Congestive heart failure.
Hypertension.
Age >75yrs. (2 points, that's why it's A2).
Diabetes mellitus.
S2 - prior stroke (2pts).
V - vascular disease
Age - 65-74.
Sex category - female sex.
```
91
what is the enzyme that breaks down bradykinin?
angiotensin converting enzyme - excess bradykinin (since it's not being broken down) is the reason why some patients on ACEi get a persistent dry cough
92
explain how ACE inhibitors work
ACE inhibitors inhibit conversion of angiotensin I to angiotensin II in the lungs - this prevents it from acting on the adrenals to increase aldosterone secretion and thus cause water and sodium retention at the kidneys.
angiotensin II is also a vasoconstrictor, so ACEi act as vasodilator, and causes sodium and water excretion - lower blood volume, lowers BP.
93
how do angiotensin receptor blockers produce a similar effect to ACEi? give two examples of ARBs
by blocking angiotensin II receptors, so its actions cannot be exerted.
losartan, candesartan.
94
give 2 examples of ACEis
ramipril, lisinopril
95
why do you get hyperkalaema as a side effect of angiotensin 2 receptor blockers?
ARBs cause a direct effect on aldosterone production in the adrenals - aldosterone works on the distal convoluted tubules of kidney by causing sodium to be reabsorbed in return for potassium excretion - ARBs reverse this transfer, so there's potassium retention.
96
calcium channel blockers are negatively inotropic and negatively chronotropic, what does this mean?
inotropic - reduces the contraction.
| chronotropic - lowers the heart rate.
97
how do calcium channel blockers work? give some examples.
decrease calcium entry into vascular and cardiac cells. intracellular calcium is lower - relaxation and vasodilation of arterial smooth muscle.
reduce myocardial contractility and suppress cardiac conduction, particularly at AV node.
this reduces myocardial oxygen demand - important in angina.
dihydropyridines (amlodipine, nifedipine) - selective for vasculature.
non-dihydropyridines (diltiazem, verapamil)- selective for heart
98
what clotting factors does warfarin work on?
2, 7, 9, 10 by inhibiting vitamin K synthesis - so anticoagulates by inhibiting coagulation factor synthesis
99
statins are given to correct hyperlipidaemia, what enzyme do they act on? name 2 statins.
HMG-CoA reductase - involved in making cholesterol.
so they reduce the cholesterol production in liver and increase clearance of LDL-cholesterol from blood.
simvastatin, atorvastatin, pravastatin.
100
amiodarone is used for pharmacological cardioversion, but it also chemically resembles a hormone made naturally by the body - what is this and what can this cause?
thyroxine - can cause hyperthyroidism
101
in supraventricular tachycardia, adenosine is administered IV to bring the heart back into normal rhythm, how does it work on the heart? what type of arrhythmias should it be used for?
it works via the A1 receptor, which reduces cAMP - so causes cell hyperpolarisation by pushing potassium out of the cell.
also relaxes the smooth muscle of the heart causing vasodilation.
only used for ventricular tachycardias.
102
why do you need to warn the patient that they may get a sense of 'impending doom' after you administer adenosine?
because it induces transient heart block in the AV node so the heart stops for a beat or so
103
atropine is derived from the deadly nightshade, but what heart arrhythmia is it used for and how does it help?
it is used for any severe bradycardia - it blocks the action of the vagus nerve/parasympathetic system by being a competitive antagonist of muscarinic ACh receptors.
dilates pupils, increases heart rate and reduces salivation.
104
if you have a patient that comes in with unstable angina but tells you he is allergic to aspirin, what is then your first line of treatment after giving GTN?
clopidogrel monotherapy
105
give an example of a short and a long acting nitrate
short - glyceryl trinitrate (GTN).
| long - isosorbide mononitrate
106
how do nitrates work to reduce the pain of angina?
converted to NO, which is a vasodilator - relaxation of capaticance vessels reduces cardiac preload + LV filling, which reduces cardiac work and myocardial oxygen demand.
107
give 2 possible side effects of nitrates
flushing, headaches, light headedness, hypotension
108
name 3 beta blockers
bisoprolol, atenolol, propranolol, metoprolol
109
how do beta blockers work to improve symptoms of ischaemic heart disease?
they reduce force of contraction and speed of conduction in the heart via beta 1 receptors - reducing cardiac work and oxygen demand.
110
how do beta blockers work as a treatment for AF?
slow the ventricular rate by prolonging the refractory period at the AV node
111
list the indications for beta blockers
IHD - symptoms and improve prognosis.
chronic heart failure.
AF and other SVTs - reduce rate, maintain sinus rhythm.
hypertension - only if other medicines are insufficient.
112
how do beta blockers work as a treatment for hypertension?
reduce renin secretion from the kidney, which is mediated by beta1 receptors.
113
give some possible SEs of beta blockers
fatigue, cold extremities, headache, nausea, sleep disturbance, ED in men.
114
what major disease is a contraindication to the use of beta blockers?
ASTHMA - can cause life-threatening bronchospasm due to blockade of beta2 adrenoreceptors in airways
115
name an aldosterone antagonist
spironolactone, epleronone
116
what cardiac indication do aldosterone antagonists treat?
chronic heart failure - as an addition to beta blocker and ACEi/ARB
117
name a LMWH. name a drug that is very similar to LMWHs
dalteparin, enoxaparin.
| similar drug - fondaparinux.
118
how do LMWHs work?
inhibit factor Xa by inhibiting antithrombin
119
how does fondaparinux work?
inhibits factor Xa.
120
how does aspirin work in prevention of thrombosis?
it irreversibly inhibits cyclooxygenase (COX) to reduce production of pro-aggregation factor thromboxane from arachidonic acid - reduces platelet aggregation and risk of arterial occlusion.
121
give some examples of antiplatelet drugs, apart from aspirin
clopidogrel, new oral anticoagulants, glycoprotein IIb/IIIa inhibitors
122
how does clopidogrel work?
prevents platelet aggregation by binding irreversibly to adenosine diphosphate receptors on surface of platelets
- independent of COX pathway, so can be taken with aspirin
123
how do glycoprotein IIb/IIIa inhibitors work?
prevent platelet aggregation by inhibiting the GPIIb/IIIa receptor on platelet surface
124
name 2 fibrinolytic (thrombolysis) drugs
alteplase, streptokinase
125
how do fibrinolytic drugs work?
catalyse the conversion of plasminogen to plasmin which acts to dissolve fibrinous clots and re-canalise occluded vessels.
- allows reperfusion of tissues, preventing/limiting tissue infarction.
126
name a loop diuretic
furosemide, bumetanide
127
give a cardiac indication of loop diuretics
symptomatic treatment of fluid overload in chronic heart failure
128
describe the mechanism of loop diuretics
act on ascending limb of loop of Henle to inhibit the Na/K/2CL cotransporter that transports the ions into the cell - water follows these ions, so they have a potent diuretic effect.
also - cause dilation of capaticance vessels - reduces preload + improves contractile function of the heart.
129
what are potassium sparing diuretics used for? name an example.
used as part of combination therapy, to treat hypokalaemia arising from loop/thiazide diuretic use.
amiloride.
130
how do potassium sparing diuretics work?
weak diuretics.
act on distal convoluted tubules in kidney - inhibit sodium and water reabsorption by acting on epithelial sodium channels - causes potassium retention.
131
give an example of a thiazide/thiazide like diuretic
bendroflumethiazide, indapamide, chlortalidone
132
describe the mechanism of action of thiazide diuretics
inhibit the Na/Cl cotransporter in the distal convoluted tubule of the nephron, preventing reabsorption of sodium and water.
also cause vasodilation.
133
how does digoxin work in AF/atrial flutter?
reduces heart rate and increases force of contraction (-vely chronotropic, +vely inotropic).
works via indirect pathway - increased vagal tone, reduced contraction at AVN and preventing dome impulses travelling to the ventricles.
134
for what cardiac problem might sildenafil be prescribed? what class of drug is this?
primary pulmonary hypertension.
| phosphodiesterase type 5 (PDE5) inhibitor
135
how does sildenafil work as a treatment of pulmonary hypertension?
causes arterial vasodilation by increasing cGMP (normally broken down by PDE5).
