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Cardiology Flashcards

1
Q

what is angina pectoris?

A

chest pain arising from the heart as a result of myocardial ischaemia

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2
Q

name 3 types of angina

A

classic/stable, unstable/crescendo, Prinzmetal’s.
decibitus, nocturnal.

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3
Q

what are the differences between stable and unstable angina

A

stable angina is induced by effort + relieved by rest.
unstable angina occurs at rest.

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4
Q

what is Prinzmetal’s (variant) angina?

A

angina that occurs without provocation, usually at rest - due to coronary artery spasm.

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5
Q

what causes angina?

A

atheroma of coronary arteries leading to myocardial ischaemia

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6
Q

give 5 risk factors for angina

A

diabetes, smoking, hyperlipidaema, hypertension, family history, lack of exercise

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7
Q

list the differential diagnoses of central chest pain

A

angina, ACS, pericarditis, myocarditis, aortic dissection, massive PE, musculoskeletal, GORD

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8
Q

describe the presentation of angina

A

central, crushing, retrosternal chest pain - comes on with exertion, relieved by rest.
may radiate to arms and neck

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9
Q

list some things that can exacerbate angina

A

exercise, cold weather, anger, excitement, heavy meals

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10
Q

give some clinical features, apart from pain, of angina

A

dyspnoea, nausea, sweating, faintess

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11
Q

what investigation would you carry out on a patient with angina? what would you find?

A

exercise ECG test - ST depression, flat/inverted T waves

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12
Q

how would you manage stable angina?

A

modify risk factors.
secondary prevention - aspirin, statins.
symptomatic treatment - GTN spray, CCBs, beta blockers, nitrates.

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13
Q

how does aspirin work as a method of secondary prevention in angina?

A

inhibits COX2 and formation of thromboxane A2 - a platelet aggregating agent.
reduces risk of coronary events.

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14
Q

name an alternative to aspirin in secondary prevention of coronary events.

A

clopidogrel

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15
Q

give some examples of beta-blockers

A

bisoprolol, atenolol, propranolol, metoprolol

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16
Q

describe the mechanism of action of beta blockers in improving symptoms of angina

A

by acting on beta1 receptors in the heart, they reduce the force of contraction and speed of conduction in the heart - relieves myocardial ischaemia by reducing cardiac work and oxygen demand

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17
Q

what is the major contra-indication of beta-blockers? why?

A

asthma - beta blockers also act on beta2-receptors which are found in the smooth muscles of airways - cause bronchoconstriction!

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18
Q

give some examples of calcium channel blockers

A

diltiazem, amlodipine, nifedipine, verapamil

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19
Q

describe the mechanism of action of calcium channel blockers in controlling symptoms of stable angina

A

they decrease calcium entry into vascular and cardiac cells. they reduce myocardial contractility and suppress cardiac conduction - reduce heart rate, contractility and afterload - reduces myocardial oxygen demand - prevents angina.

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20
Q

what are the major side effects of calcium channel blockers?

A

postural hypotension/dizziness, headache, ankle oedema - due to systemic vasodilation

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21
Q

describe the mechanism of action of short-acting (GTN) nitrates and long-acting nitrates in acute angina

A

Nitrates are converted to NO, which increases cGMP and reduces intracellular calcium in vascular smooth muscle cells - vasodilation of venous capacitance vessels reduces preload and LV filling.
reduced cardiac work and myocardial oxygen demand - relieve angina

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22
Q

what interventions may be used in worsening angina?

A

Percutaneous coronary intervention (PCI) - balloon used to dilate atheromatous arteries (stents can be placed) - via catheter.
Coronary artery bypass grafting (CABG)

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23
Q

what is involved in a coronary artery bypass graft (CABG)?

A

internal mammary artery used to bypass stenosis in the LAD or RCA.

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24
Q

what does the term acute coronary syndromes (ACS) include?

A

unstable angina.
NSTEMI.
STEMI.

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25
how would you differentiate between NSTEMI and unstable angina?
NSTEMI involves enough occlusion to cause myocardial damage - elevation of serum troponin and creatinine kinase. unstable angina doesn't cause myocardial damage.
26
describe the common pathology behind acute coronary syndromes
1) rupture/erosion of fibrous cap of an atheroma plaque in a coronary artery 2) platelet-rich clot forms 3) vasoconstriction due to chemicals released by platelets
27
name 3 non-modifiable risk factors for ACS
age. male gender. FHx of IHD
28
name 3 modifiable risk factors for ACS
smoking, hypertension, DM, hyperlipidaemia, obesity, sedentary lifestyle, cocaine use
29
list 3 symptoms and 3 signs of ACS
symptoms - central chest pain, sweating, dyspnoea, palpitations. signs - sweating, anxiety, tachycardia, pallor.
30
what biochemical markers would you test for in ACS?
troponin, creatinine kinase, myoglobin
31
what would you expect to see on a 12 lead ECG in ACS?
hyperacute (tall) T waves ST elevation (STEMI) or ST depression (NSTEMI/unstable angina). new LBBB. after hrs-days - T wave inversion, Q waves.
32
what would be your immediate management of ACS?
MONA: Morphine, Oxygen, Nitrates, Aspirin ± clopidogrel/ticragelor
33
what drugs might a patient be put on after an ACS, for secondary prevention?
beta-blockers, ACE inhibitors, statins, aspirin
34
what might the non-medical management of ACS be?
PCI - percutaneous coronary intervention
35
list some possible complications following a MI
heart failure, rupture of interventricular septum, mitral regurg, arrhythmias, heart block, pericarditis, thromboembolism, ventricular aneurysm
36
give 3 causes of heart failure
ischaemic heart disease; valvular disease; pericarditis; pericardial effusion; alcohol; cocaine; myocarditis; arrhythmias; cardiomyopathies; anaemia; pulmonary hypertension
37
what are the types of heart failure?
systolic/diastolic, low output/high output, left/right
38
what compensatory mechanisms are activated as the heart begins to fail?
sympathetic nervous system, RAAS, ventricular dilatation, ventricular remodelling
39
what causes the oedema and dyspnoea seen in heart failure?
activation of the RAAS by decreased renal perfusion (due to low CO) - salt/water retention - peripheral/pulmonary congestion
40
describe the ventricular remodelling seen in heart failure
initial dilatation. hypertrophy, loss of myocytes, increased interstitial fibrosis.
41
what is the difference between systolic and diastolic failure?
systolic = inability of ventricles to contract normally diastolic = inability of ventricles to relax and fill normally
42
give 3 symptoms of heart failure
exertional dypnoea, orthopnoea (SOB on lying down), paroxysmal nocturnal dyspnoea, fatigue, oedema, weight loss, wheeze
43
give 5 signs of heart failure
cold peripheries, cyanosis, displaced apex, wheeze, RV heave, valve disease, hypotension, pleural effusion, oedema, ascites
44
what are 5 features of heart failure seen on CXR?
ABCDE: Aleveolar oedema (bats wings) Kerly B lines (interstitial oedema) Cardiomegaly Dilated upper lobe vessels pleural Effusion
45
list 2 major criteria on the Farmingham criteria for heart failure diagnosis
SAW PANIC S3 heart sound - gallop. Acute pulmonary oedema. Weight loss Paroxysmal nocturnal dyspnoea Abdominojugular reflux Neck vein distension Increased cardiac shadow on CXR (cardiomegaly) Crepitations (crackles heard in lungs)
46
list 2 minor criteria on the Farmingham criteria for heart failure diagnosis
HEART ViNo: Hepatomegaly Effusion, pleural Ankle oedema bilaterally exeRtional dyspnoea Tachycardia Vital capacity decrease by 1/3rd Nocturnal cough
47
describe the NHYA classification of heart failure
class I = no limitation class II = mild limitation (comfort at rest, fatigue and dyspnoea on normal physical activity) class III = marked limitation (comfort at rest, dyspnoea on gentle physical activity) class IV = symptomatic at rest, exacerbated by any physical activity
48
what investigations would you do in heart failure?
ECG - underlying cause. CXR. Bloods - BNP (B type natriuretic peptide - if normal, HF is excluded). echocardiography.
49
describe the medical management of heart failure
loop diuretics (furosemide) ± spironolactone ± thiazide. ACE inhibitors (or ARB). beta blockers. ± digoxin, vasodilators (e.g. hydralazine)
50
name 2 ACE inhibitors
ramipril, lisinopril
51
what causes the common cough side effect of ACE inhibitors? what drug class are a good alternative?
increased levels of bradykinin, which is usually inactivated by ACE. ARBs
52
how do ACE inhibitors act?
prevent conversion of angiotensin I to angiotensin II. Angiotensin II is a vasoconstrictor and stimulates aldosterone secretion - blocking this reuces afterload, lowering BP.
53
name 2 angiotensin receptor blockers (ARBs)?
losartan, candesartan
54
how do angiotensin receptor blockers work?
block action of angiotensin II on the AT1 receptor. similar effects as ACE inhibitors.
55
give 3 causes of mitral stenosis
rheumatic heart disease (most), congenital, cardial fibroelastosis, malignant carcinoid, prosthetic valve.
56
what is mitral stenosis?
thickening and immobility of valve leaflets - leads to obstruction of blood flow from left atrium to left ventricle.
57
give 3 symptoms of mitral stenosis
exertional dyspnoea, fatigue, palpitations, chest pain, systemic emboli, haemoptysis
58
what is the heart murmur heard in mitral stenosis?
rumbling mid-diastolic murmur
59
what diagnostic tests would you perform in mitral stenosis? what would you see?
ECG - AF, bifid P waves. CXR - LA enlargement, pulmonary oedema, mitral valve calcification. Echo - diagnostic.
60
how would mitral stenosis be treated?
diuretics - decrease pre load. balloon valvuloplasty / valve replacement.
61
give 2 complications of mitral stenosis
pulmonary hypertension. emboli (dilated LA). pressure from large LA on local structures e.g. hoarseness due to compression of L recurrent laryngeal
62
give 3 causes of mitral regurgitation
prolapsing mitral valve + rheumatic heart disease = most common. infective endocarditis, annular calcification, LV dilatation, ruptured chordae tendinae, papillary muscle rupture. connective tissue disorders (Ehlers-Danos, Marfan's). cardiomyopathy, congenital.
63
give 3 symptoms of mitral regurgitation
dyspnoea, fatigue, palpitations, infective endocarditis
64
what murmur is heard in mitral regurgitation?
pansystolic murmur
65
what does a bifid P wave indicate on ECG?
bifid P waves = p mitrale - mitral valve disease
66
what investigations would you perform in valvular heart disease?
ECG, CXR, echo ± cardiac catherization
67
what would you see on CXR in mitral regurgitation?
enlarged LA and LV, mitral valve calcification, pulmonary oedema
68
how would you treat mitral regurgitation?
asymptomatic = echo every 1-5yrs. anticoagulate with warfarin if - AF, hx of embolism, prosthetic valve, additional mitral stenosis. diuretics. surgery - valve replacement or repair.
69
give 3 causes of aortic stenosis
degeneration and calcification of normal valve (in the elderly). calcification of congenital biscuspid valve (middle age). rheumatic heart disease.
70
what is the classical triad of symptoms in aortic stenosis?
SAD: Syncope Angina Dyspnoea - heart failure
71
what murmur is heard in aortic stenosis?
ejection systolic murmur
72
what would you expect to see on an ECG in aortic stenosis?
p mitrale, LVH with strain pattern (depressed ST and T wave inversion in I, AVL, V5 and V6)
73
what would you see on a CXR of a patient with aortic stenosis?
normal heart size, prominent ascending aorta, valvular calcification
74
how would you treat aortic stenosis?
prompt valve replacement
75
what are the most common causes of aortic regurgitation?
rheumatic fever and infective endocarditis
76
give 3 causes of acute aortic regurgitation
infective endocarditis, acute rheumatic fever, dissection of the aorta, AAA dissection, prosthetic valve failure
77
give 3 causes of chronic aortic regurgitation
chronic rheumatic heart disease, syphilis, rheumatoid arthritis, severe hypertension, biscupid aortic valve, aortic endocarditis, Marfan's, osteogenesis imperfecta
78
give 3 symptoms of aortic stenosis
exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, palpitations, angina, syncope, CCF
79
what murmur is heard in aortic regurgitation?
early diastolic murmur. "at L sternal edge in 4th intercostal space"
80
what would you see on CXR/ECG in aortic regurgitation?
CXR - cardiomegaly and dilatation of the ascending aorta, pulmonary oedema. ECG - LVH.
81
how would you treat aortic regurgitation?
reduce systolic hypertension - ACE inhibitors. echo every 6-12/12. valve replacement.
82
what are the 3 main cardiomyopathies?
hypertrophic (HCM), dilated (DCM) and restrictive
83
what is hypertrophic cardiomyopathy?
ventricular hypertrophy in absence of abnormal loading conditions - LV outflow tract obstruction.
84
what causes hypertrophic cardiomyopathy?
50% = autosomal dominant 50% = sporadic.
85
what is the major consequence of hypertrophic cardiomyopathy?
sudden cardiac death in young people
86
name 2 clinical features of hypertrophic cardiomyopathy
can be asymptomatic. angina, syncope, sudden death, systolic thrill.
87
what investigations might you carry out in cardiomyopathy?
CXR, ECG, echo. cardiac MR.
88
how would you treat hypertrophic cardiomyopathy?
beta blockers/CCBs to control symptoms. anticoagulate to prevent emboli. implantable defib.
89
give 3 causes of dilated cardiomyopathy
alcohol, hypertension, haemachromatosis, viral infection, autoimmune, congenital.
90
give 3 clinical features of dilated cardiomyopathy
dyspnoea, emboli or arrhythmia, displaced apex beat, S3 gallop, pleural effusion, oedema, jaundice, ascites.
91
how would you treat dilated cardiomyopathy?
bed rest. diuretics, digoxin, ACE inhibitors. biventricular pacing/implantable cardiac defibs. heart transplant.
92
what is restrictive cardiomyopathy?
rigid myocardium restricting diastolic ventricular filling.
93
give 2 causes of restrictive cardiomyopathy
amyloidosis. haemachromatosis. sarcoidosis. scleroderma. idiopathic.
94
give 3 clinical features of restrictive cardiomyopathy
constrictive pericarditis. raised JVP. oedema, ascites, features of RVH.
95
what investigation would you perform in order to diagnose restrictive cardiomyopathy?
cardiac catheterisation.
96
what are the 2 causes of ventricular septal defect?
congenital. acquired post-MI.
97
how might a ventricular septal defect present?
severe heart failure in infancy. OR - asymptomatic, detected later in life
98
does a smaller ventricular septal defect produce louder or quieter murmurs?
louder
99
what murmur is heard in VSD?
harsh pansystolic murmur at left sternal edge, with systolic thrill
100
give 2 complications of a ventricular septal defect
aortic regurgitation, infundibular stenosis, IE, pulmonary hypertension, Eisenmenger's complex.
101
what is seen on a CXR of someone with a ventricular septal defect?
Small VSD - normal sized heart ± enlarged pulmonary blood vessels. Large VSD - cardiomegaly, large pulmonary arteries, marked enlargement of pulmonary vessels.
102
how would you manage a ventricular septal defect?
medical support until spontaneous closure. OR - surgical patch repair or device closure.
103
what are the different types of atrial septal defect?
ostium secundum defects - most common - present in adulthood. ostium primum defects - associated with AV valve abnormalities - present early.
104
give 3 clinical features of an atrial septal defect
pulmonary hypertension, cyanosis, arrhythmia, haemoptysis, chest pain, AF, raised JVP. pulmonary ejection systolic murmur.
105
what investigations are used to diagnose most structural heart defects?
echo. cardiac catheter.
106
how would you treat an ASD?
transcatheter or surgical closure
107
what genetic disorder is associated with atrioventricular septal defects?
Downs syndrome
108
what structures are involved in an atrioventricular septal defect?
atrial septum, ventricular septum, mitral and tricuspid valve
109
what are the clinical features and management of a complete AVSD?
breathless neonate, failure to thrive, poor feeding, torrential pulmonary blood flow. repair with PA band.
110
what are the clinical features and management of a partial AVSD?
presents in adulthood, similar to small ASD/VSD. treatment not necessary.
111
what is a patent ductus arteriosus?
persistent communication between left pulmonary artery and descending aorta - L to R shunt. normally the ductus arteriosus closes within hrs of birth.
112
what are the clinical features of a PDA?
3 classic signs: bounding pulse, 'machinery murmur', pulmonary hypertension. also - breathless, poor feeding, failure to thrive, Eisenmenger's syndrome
113
how would you treat a PDA?
indometacin (prostaglandin) can stimulate closure. if large - surgical or percutaneous closure.
114
what is Eisenmenger's syndrome?
cyanosis - clubbed and blue toes, pink not clubbed fingers.
115
what is coarctation of the aorta?
congenital narrowing of the descending aorta
116
what are the clinical features of coarctation of the aorta? name 2 complications.
radiofemoral delay, weak femoral pulse, high BP, systolic murmur. heart failure + IE.
117
how would you treat coarctation of the aorta?
surgery or balloon dilation ± stenting
118
what are the consequences of a biscupid aortic valve?
go on to develop aortic stenosis - requiring valve replacement. higher risk of IE.
119
give some clinical features of pulmonary stenosis
RV failure as neonate. collapse. poor pulmonary blood flow. RVH. tricuspid regurg.
120
how would you treat pulmonary stenosis?
ballon valvuloplasty. open vavlotomy.
121
what are the 4 features of tetralogy of Fallot?
1 - VSD. 2 - pulmonary stenosis. 3 - RVH. 4 - aorta overriding the VSD
122
what causes tetralogy of Fallot?
abnormalities in separation of truncus arteriosus into the aorta and pulmonary arteries early in gestation
123
describe the presentation of tetralogy of Fallot
acyanotic at birth. gradually become cyanotic. Fallow (hypoxic) spells - go blue, restless, inconsolable crying - toddlers may squat.
124
what is the characteristic feature of a CXR in tetralogy of Fallot?
boot shaped heart
125
how is tetralogy of Fallot managed?
oxygen. knee-chest position. morphine. long-term beta blockers. surgery at less than 12 months.
126
list 3 viral causes of acute pericarditis
Coxsackie B Influenza EBV Mumps Varicella HIV
127
list 3 bacterial causes of acute pericarditis
Pneumonia Rheumatic fever TB Streps Staphs
128
list 5 causes, other than bacterial/viral infection, of acute pericarditis
Fungi, MI, uraemia, rheumatoid arthritis, SLE, myxoedema, trauma, surgery, malignancy, radiotherapy, sarcoidosis, idiopathic + drugs
129
describe the pain seen in acute pericarditis
sharp, central chest pain - worse on inspiration or lying flat, relieved by leaning forward
130
what might be heard on auscultation of a patient with pericarditis?
pericardial friction rub
131
what investigation would you carry out to diagnose acute pericarditis? what would you see?
ECG - concave upwards (saddle-shaped) ST segment elevation in all leads
132
how would you treat acute pericarditis?
treat underlying cause. NSAIDs for analgesia. colchicine if relapsing.
133
what is constrictive pericarditis?
heart is encased in a rigid fibrotic pericardium - prevents diastolic filling of ventricles.
134
what causes constrictive pericarditis?
most common in UK = idiopathic. globally = TB. also occurs after any pericarditis.
135
what are the clinical features of constrictive pericarditis?
those of right-sided heart failure - raised JVP, oedema, hepatomegaly, ascites, pulsus paradoxus, diffuse apex beat
136
what two investigations would you carry out in constrictive pericarditis and what would you find?
CXR - normal/small heart + pericardial calcification. CT/MRI - pericardial thickening/calcification
137
how would you treat constrictive pericarditis?
surgical excision of pericardium
138
what is the definition of hypertension?
>140/90mmHg based on 2+ readings on separate occasions
139
what are the criteria for treating hypertension?
ALL with sustained >160/100mmHg. those with sustained >140/90 that are at high risk of coronary events, have diabetes or end-organ damage
140
list 3 causes of secondary hypertension
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.
141
give 3 risk factors for hypertension
age, FHx, male gender, African or Caribbean origin, high salt intake, sedentary lifestyle, overweight/obese, smoking, excess alcohol intake.
142
what investigations would you carry out on a patient presenting with a high blood pressure reading?
take blood pressure again, on at least 1 other occasion. 24h ambulatory BP monitoring (ABPM) - exclude white coat effect
143
give 3 examples of non-pharmacological measures you would encourage a patient with hypertension to take
weight reduction. Mediterranean diet - oily fish, low saturated fat, low salt. limit alcohol consumption. exercise. smoking cessation. increase fruit and veg intake.
144
what drug would you prescribe for a 45yo caucasian patient with hypertension with no other medical history?
ACE inhibitor - ramipril. if CI (cough) - ARB - losartan
145
what drug would you prescribe a 67yo Afro-Caribbean man with hypertension?
calcium channel blocker - amlodipine
146
if first line treatment is failing to control a patient's hypertension, what drug regime would you prescribe them? and if this fails?
ACE inhibitor + CCB or ACE inhibitor + thiazide. all 3 if a combination of 2 fails to control.
147
how do calcium channel blockers work to reduce hypertension?
decrease calcium entry into vascular smooth muscle cells - vasodilation of arterial smooth muscle, lowering arterial pressure.
148
what are the side effects of CCBs?
bradycardia, headaches, flushing
149
what is the most common cardiac arrhythmia?
atrial fibrillation
150
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.
151
list 4 causes of atrial fibrillation
heart failure/ischaemia, hypertension, MI, PE, mitral valve disease, pneumonia, hyperthyroidism, caffeine, alcohol, hypokalaemia, hypomagnaesaemia
152
what ECG features would you see in atrial fibrillation?
absent P waves irregular QRS complexes atrial rate 300bpm
153
give 3 forms of treatment you would give a patient with atrial fibrillation
warfarin - anticoagulation. beta blockers/CCBs - rate control. Cardioversion - rhythm control.
154
describe what you would see on an ECG trace in atrial flutter
saw tooth flutter waves between QRS complexes
155
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
156
name 2 common causes of heart block
coronary artery disease, cardiomyopathy, fibrosis of conducting tissue
157
what is first degree AV block? how does it appear on ECG?
delayed AV conduction. prolonged PR interval (>0.22s).
158
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.
159
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.
160
what is 2:1 or 3:1 advanced second degree AV block?
every second or third P wave conducts to ventricles
161
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.
162
describe the ECG features seen in RBBB
secondary R waves in V1. slurred S in V5 and V6
163
list 2 causes of RBBB
PE, RVH, IHD, congenital heart disease, idiopathic
164
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.
165
list 2 causes of LBBB
IHD, LVH, aortic valve disease, post-op
166
give 3 causes of sinus tachycardia
physiological - exercise/excitement. fever, anaemia, heart failure, thyrotoxicosis, acute PE, hypovolaemia, drugs.
167
what causes atrioventricular junctional tachycardias?
re-entry circuits - two separate pathways for impulse conduction
168
what are the ECG changes seen in supraventricular tachycardia?
absent or inverted P wave after QRS
169
name 2 things that may aggravate a supraventricular tachycardia
exertion, coffee, tea, alcohol
170
what is the 1st line management of a supraventricular tachycardia?
vagal manoeuvres - breath holding, valsalva manoeuvre, carotid massage
171
what drugs may be used to treat a supraventricular tachycardia?
IV adenosine. if fails - verapamil/atenolol.
172
what is the long-term management of a supraventricular tachycardia?
radiofrequency ablation of accessory pathway via catheter.
173
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.
174
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
175
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.
176
what are the ECG features of a ventricular tachycardia?
rapid ventricular rhythm with broad abnormal QRS complexes
177
list 3 causes of prolonged QT
congenital, hypokalaemia, hypocalcaemia, hypomagnesaemia, tricyclics, macrolides
178
what causes Wolff-Parkinson-White?
congenital accessory conduction pathway between atria and ventricles
179
describe the features of a resting ECG in a patient with WPW
short PR interval, wide QRS complex due to slurred upstroke (delta wave)
180
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.
181
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.
182
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.
183
how would a ruptured AAA present?
sudden severe epigastric pain radiating to back leading to hypovolaemic shock - collapse
184
how would a ruptured AAA be repaired?
endovascular repair with stent insertion, or surgical replacement of aneurysmal section
185
describe the pain of a dissecting aortic aneurysm
abrupt onset of severe, tearing central chest pain radiating through back
186
how is a dissecting aortic aneurysm managed?
urgent BP control - lanetalol IV. surgical repair.
187
give 3 risk factors for peripheral arterial disease
hypertension, smoking, diabetes, diet, sedentary lifestyle, obesity, hyperlipidaemia, age, male gender, FHx
188
what causes peripheral artery disease?
atherosclerosis causing stenosis of arteries
189
describe the clinical features of intermittent claudication
cramping pain in calf/thigh/buttock after walking a given distance (shorter=more severe) - relieved by rest
190
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
191
what are the 4 stages in the Fontaine classification of peripheral artery disease?
asymptomatic - intermittent claudication - ischaemic rest pain - ulceration/gangrene (critical ischaemia)
192
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
193
what are the 5 Ps of acute limb ischaemia?
Paraesthesia Perishingly cold Pallor Paralysis Pain
194
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.
195
describe conservative treatment of limb ischaemia
exercise, quit smoking, lose weight, manage diabetes and hypertension. clopidogrel (antiplatelet) to prevent progression and reduce risk.
196
how would intermittent claudication be managed, beyond conservative risk reduction treatments?
revascularisation - percutaneous transluminal angioplasty (PTA) or surgical reconstruction/arterial bypass graft.
197
what are some risk factors for infective endocarditis?
congenital - valve defects, VSD, PDA. prosthetic valves. IVDU. poor dental hygiene. soft tissue infections.
198
name the most common causative organism in infective endocarditis?
Streptococcus viridans
199
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.
200
what is an infective endocarditis patient at risk of?
stroke - vegetations. destruction of valve - regurgitation - worsening heart failure.
201
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.
202
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.
203
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.
204
how would you treat infective endocarditis?
before results of culture - IV benzylpenicillin + gentamicin. then tailor to cultures and sensitivity.
205
what is shock?
acute circulatory failure with inadequate or inappropriately distributed tissue perfusion - prolonged oxygen deprivation leads to necrosis, organ failure and death
206
list the different types of shock
hypovolaemia, cardiogenic, sepsis, anaphylaxis, neurogenic shock
207
give 3 causes of hypovolaemia shock
haemorrhages - GI bleed, trauma, AAA dissection etc. fluid loss - burns, diarrhoea, intestinal obstruction.
208
give 3 causes of cardiogenic shock
(= pump faillure). ACS, arrhythmias, aortic dissection, PE, tension pneumothorax, cardiac tamponade, endocarditis
209
give 3 signs of hypovolaemic shock
pale grey skin, slow capillary refill, sweating, weak pulse, tachycardia
210
name 2 precipitating factors of anaphylactic shock
penicillin, contrast, latex, dairy, nuts, insect stings
211
describe the clinical features of anaphylactic shock
onset within 5-60mins of exposure. warm peripheries, hypotension, urticarial, angio-oedema, wheezing, upper airway obstruction.
212
how would you manage septic shock?
take blood cultures before abx - then co-amoxiclav and tazocin IV
213
how would you manage anaphylactic shock?
remove cause. O2. IM adrenaline. IV chlorphenamine and hydrocotisone.
214
how would you manage hypovolaemic shock?
raise legs. fluid bolus - repeat if shock improves.
215
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.
216
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
217
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.
218
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.
219
give 2 examples of ACEis
ramipril, lisinopril
220
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.
221
calcium channel blockers are negatively inotropic and negatively chronotropic, what does this mean?
inotropic - reduces the contraction. chronotropic - lowers the heart rate.
222
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
223
what clotting factors does warfarin work on?
2, 7, 9, 10 by inhibiting vitamin K synthesis - so anticoagulates by inhibiting coagulation factor synthesis
224
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.
225
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
226
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.
227
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
228
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.
229
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
230
give an example of a short and a long acting nitrate
short - glyceryl trinitrate (GTN). long - isosorbide mononitrate
231
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.
232
give 2 possible side effects of nitrates
flushing, headaches, light headedness, hypotension
233
name 3 beta blockers
bisoprolol, atenolol, propranolol, metoprolol
234
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.
235
how do beta blockers work as a treatment for AF?
slow the ventricular rate by prolonging the refractory period at the AV node
236
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.
237
how do beta blockers work as a treatment for hypertension?
reduce renin secretion from the kidney, which is mediated by beta1 receptors.
238
give some possible SEs of beta blockers
fatigue, cold extremities, headache, nausea, sleep disturbance, ED in men.
239
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
240
name an aldosterone antagonist
spironolactone, epleronone
241
what cardiac indication do aldosterone antagonists treat?
chronic heart failure - as an addition to beta blocker and ACEi/ARB
242
name a LMWH. name a drug that is very similar to LMWHs
dalteparin, enoxaparin. similar drug - fondaparinux.
243
how do LMWHs work?
inhibit factor Xa by inhibiting antithrombin
244
how does fondaparinux work?
inhibits factor Xa.
245
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.
246
give some examples of antiplatelet drugs, apart from aspirin
clopidogrel, new oral anticoagulants, glycoprotein IIb/IIIa inhibitors
247
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
248
how do glycoprotein IIb/IIIa inhibitors work?
prevent platelet aggregation by inhibiting the GPIIb/IIIa receptor on platelet surface
249
name 2 fibrinolytic (thrombolysis) drugs
alteplase, streptokinase
250
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.
251
name a loop diuretic
furosemide, bumetanide
252
give a cardiac indication of loop diuretics
symptomatic treatment of fluid overload in chronic heart failure
253
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.
254
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.
255
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.
256
give an example of a thiazide/thiazide like diuretic
bendroflumethiazide, indapamide, chlortalidone
257
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.
258
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.
259
for what cardiac problem might sildenafil be prescribed? what class of drug is this?
primary pulmonary hypertension. phosphodiesterase type 5 (PDE5) inhibitor
260
how does sildenafil work as a treatment of pulmonary hypertension?
causes arterial vasodilation by increasing cGMP (normally broken down by PDE5).
261

What HR is considered sinus tachycardia?

>100bpm

262

Name some causes of sinus tachycardia

Anxiety, dehydration, recent exercise, sepsis, pneumonia etc etc

263

What lead(s) would you look in to assess sinus bradycardia/tachycardia?

any - rhythm strip is best

264

What HR is considered sinus bradycardia?

<60bpm

265

List some causes of left axis deviation

left anterior hemiblock

 WPW syndrome

inferior MI

ventricular tachycardia

LVH

266

What is the most likely cause of right axis deviation? List any alternative causes

RVH is most likely

normal variant - tall thin people

lateral MI

WPW syndrome

dextrocardia or R/L arm lead switch

left posterior fascicular block

267

How would you detect left axis deviation?

Look for lead I and II "Leaving" each other - small lead I, negative lead II and III

268

What is a more likely cause of left axis deviation, conduction issues or LVH?

conduction issues

269

What is the mechanism of atrial flutter?

a re-entry circuit within right atrium

270

List some causes of AF

ischaemic heart disease

thyrotoxicosis (hyperthyroidosis)

sepsis

valvular heart disease

alcohol excess

PE

hypokalaemia/hpomagnesaemia

271

What is the mechanism of atrial tachycardia?

A single ectopic focus, outside the SAN that's triggering rapid depolarisation of the atria

272

List causes of atrial tachycardia

digoxin toxicity

atrial scarring

catecholamine excess

congenital abnormatlities

273

What is the mechanism of junctional tachycardia?

AV junctional pacemaker rhythm exceeds that of SAN. There is increased automaticity in AVN coupled with decreased automaticity in SAN.

274

List causes of first degree heart block

increased vagal tone

athletic training

inferior MI

mitral valve surgery

Myocarditis (Lyme disease)

electrolyte disturbances (e.g. hyperkalaemia)

AV nodal blocking drugs:

beta blockers

CCBs

digoxin

amiodarone

275

Describe the ECG trace in Mobitz type I 2nd degree heart block (Wenckebach phenomenon)

progressive lengthening of PR interval, followed by absent QRS (a non-conducted P wave), then cycle repeats

PR interval is longest just before dropped beat, and shortest just after

276

What is the mechanism of Mobitz I 2nd degree heart block?

usually due to reversible conduction block at AVN - malfunctioning AVN cells progressively fatigue until they fail to conduct an impulse (dropped beat)

277

List causes of Mobitz I 2nd degree heart block

Drugs: beta blockers CCBs digoxin amiodarone

Increased vagal tone (e.g. athletes)

inferior MI

myocarditis

cardiac surgery

278

Describe the ECG trace in Mobitz type II 2nd degree heart block

intermittent non-conducted P waves without progressive prolongation of PR interval

P waves 'march through' at constant rate

279

What is the mechanism of Mobitz II 2nd degree heartblock?

usually due to failure of conduction at His-Purkinje system

generally due to structural damage to conducting system "all-or-nothing"

- no progressive fatigue like in Mobitz I, instead His-Purkinje cells suddenly and unexpectedly fail to conduct

280

List causes of Mobitz II 2nd degree heart block

Anterior MI (septal infarction wiht necrosis of bundle branches)

Idiopathic fibrosis of conducting system

cardiac surgery

inflammatory conditions (rheumatic fever, myocarditis, Lyme disease)

autoimmune (SLE, systemic sclerosis)

infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis)

hyperkalaemia

Drugs: beta blockers CCBs digoxin amiodarone

281

List causes of complete heart block

inferior MI

AVN blocking drugs - CCBs, beta blockers, digoxin

Idiopathic degeneration of conducting system

282

In what lead(s) is complete heart block best seen?

II and V1

283

What is the mechanism of complete heart block?

there is complete absence of AV conduction - end point of second degree heart block.

Either progressive fatigue of AVN cells (mobitz I) or due to sudden onset of complete conduction throughout His-Purkinje system (mobitz II)

284

What is the clinical significance of complete heart block? How would it be treated?

high risk of sudden cardiac death - urgent admission for cardiac monitoring, backup temporary pacing followed by permanent pacemaker insertion

285

Describe what is seen:

Complete heart block.

atrial rate is 60bpm

ventricular rate is 27bpm

slow ventricular escape rhythm

286

Describe what is seen:

2:1 heart block

287

Describe what is seen:

3:1 heart block

288

Describe what is seen:

Mobitz II second degree heart block

Intermittent P waves without progressive lengthening of PR interval

289

Describe what is seen:

Mobitz I second degree heart block

aka Weckebach phenomenon

progressive lengthening of PR interval until a QRS fails to conduct (dropped beat)

290

Describe what is seen:

First degree heart block

PR >0.2s (5 small squares)

291

Describe what is seen:

Right axis deviation

leads I and II reaching towards each other

292

Describe what is seen:

Left axis deviation

Leads I and II are leaving each other

293

Describe what is seen:

atrial fibrillation

irregularly irregular, absent P waves

294

Describe what is seen:

Atrial fibrillation

irregularly irregular

absent P waves

295

Describe what is seen:

Atrial flutter

"saw tooth P waves" at c300bpm

 

296

Describe what is seen:

atrial tachycardia

narrow complex tachycardia at 120bpm

each QRS is preceded by an abnormal p wave

297

Describe what is seen:

junctional tachycardia

narrow QRS

retrograde P waves before, during or after QRS

 

298

Describe what is seen:

RBBB

broad QRS

M complex in V1-3

W complex in V6 (slurred S waves)

299

Describe what is seen

LBBB

broad QRS

dominant S in V1 - W

broad R in lateral leads - M

300

Describe what is seen:

ST elevation in I and aVL (high lateral leads)

reciprocal ST depression in III and aVF (inferior leads)

 

acute MI localised to superior part of lateral wall -

high lateral STEMI

occluded first branch of LAD

301

Describe what is seen

ST elevation in inferior (II, III, aVF) leads and lateral (I, V5-V6) leads

ST depression in V1-V3 suggests associated posterior infarction

acute anterolateral STEMI with posterior extension

occlusion of proximal circumflex

302

Describe the ECG changes seen in right bundle branch block

broad QRS >120ms

RSR pattern in V1-3 ('m' shaped complex)

wide, slurred S waves in lateral leads (I, aVL, V5-6) giving a 'W' shaped complex in V6

(MarroW - M in V1, W in V6, rr = right)

possible ST depression in precordial leads (V1-3)

303

Describe what is seen:

ST elevation in leads II, III and aVF

Q-wave formation in III and aVF

reciprocal ST depression and T wave inversion in aVL

inferior STEMI

circumflex occlusion - ST elevation in lead II = lead III

304

Describe what is seen:

marked ST elevation in leads II, III and aVF

reciprocal changes in aVL

inferior STEMI

RCA occlusion as ST elevation in lead III> lead II

305

What is the mechanism in RBBB?

activation of R ventricle is delayed as depolarisation has to spread across septum from left ventricle due to blockage of R bundle of Purkinje fibres

 

left ventricle is activated normally, so early part of QRS is unchanged, but delayed R ventricle activation produces a secondary R wave in V1-3 and a slurred S wave in lateral leads

306

What does this V2 lead trace suggest?

posterior MI

horizontal ST depression

upright T wave

dominant R wave (R/S ratio >1)

307

List causes of RBBB

RVH / cor pulmonale

PE

IHD

rheumatic heart disease

myocarditis or cardiomyopathy

degenerative disease of conduction system

congenital heart disease

308

Describe the ECG changes seen in left bundle branch block

broad QRS >120ms

dominant S wave in V1 - W

broad, notched R wave in V6 - M

(WilliaM - W in V1, M in V6, ll = left)

no Q waves in lateral leads (I, V5-6, small Q waves in aVL)

prolonged R wave peak time >60ms in V5-6

309

List causes of LBBB

aortic stenosis

ischaemic heart disease

dilated cardiomyopathy

anterior MI

primary degnerative disease (fibrosis) of the conducting system

hyperkalaemia

digoxin toxicity

310

Describe the mechanisms in LBBB?

septum is activated R to L instead of L to R

spreads via right bundle branch, and then via septum to left bundle branch

this extends the QRS duration and removes Q waves in lateral leads

as the venrticles are activated sequentially, broad R waves are produced

311

Describe what is seen:

 ST elevation is maximal in anteroseptal leads (v1-V4)

Q waves present in septal leads (V1-2)

hyperacute (peaked) T waves in (V2-4)

hyperactute anteroseptal STEMI

312

Describe what is seen:

ST elevation in V1-6 + I and aVL

minimal reciprocal depression in III and aVF

anterior STEMI

313

Describe the ECG changes seen in junctional escape rhythms

no p waves, or p waves completely unrelated to QRS 

normal QRS, maybe slightly narrow

slow HR

 

314

What is the mechanism of junctional escape rhythms?

there are pacemaker cells at various points in the conduction system

junctional escape rhythm occurs when the rate of AV node depolarisation is less than the intrinsic rate of an ectopic pacemaker

315

list causes of junctional escape rhythms

severe sinus bradycardia

sinus arrest

sino-atrial exit block

high-grade second degree heart block (4:1, 5:1 etc)

complete heart block

hyperkalaemia

drugs:

beta blockers

CCBs

digoxin poisoning

316

Describe the ECG changes seen in a ventricular escape rhythm

ventricular rhythm of 20-40bpm

broad QRS complexes, possibly with a LBBB or RBBB morphology

317

Describe what is seen:

ventricular fibrillation

318

what arteries are likely to be blocked in a lateral STEMI

LAD and LCx

319

Describe what is seen:

sinus rhythm

broad QRS with slurred upstroke - delta wave

dominant R wave in V1

Wolff-Parkinson-White 

320

Describe the ECG changes seen in a lateral STEMI

ST elevation in the lateral leads

(I, aVL, V5-6)

reciprocal ST depression in inferior leads (III and aVF)

321

Describe what is seen

Digoxin effect

"sagging" ST segements

hockey stick T waves

322

Describe the ECG changes seen in an inferior MI

ST elevation in II, III and aVF

progressive development of Q waves in II, III and aVF

reciprocal depression in aVL (±lead I)

 

323

Describe what is seen:

pericarditis

widespread concave ST elevation and PR depression throughout V2-V6 and I, II, aVL, aVF

reciprocal ST depression and PR elevation in aVR

324

Which artery most commonly causes an inferior STEMI?

right coronary artery

(more ST elevation in lead III than II)

LCx can cause it less commonly

(ST elevation in lead II = lead III)

 

325

Describe the ECG changes seen in posterior MI

In V1-V3:

horizontal ST depression

tall, broad R waves

upright T waves

dominant R wave in V2

326

Occlusion of what artery causes an anterior STEMI?

LAD

327

Describe the ECG changes seen in anterior STEMI

ST elevation with Q wave formation in the precordial leads (V1-6) ± the high lateral leads (I and aVL)

reciprocal ST depression in the inferior leads (mainly III and aVF)

328

In what leads would ST elevation be maximal in a septal STEMI?

V1-2

329

In what leads would ST elevation be maximal in an anterior STEMI?

V2-5

330

In what leads would ST elevation be maximal in an anteroseptal STEMI?

V1-4

331

In what leads would ST elevation be maximal in an anterolateral STEMI?

V3-6, I + aVL

332

What is seen in an NSTEMI?

pathological Q waves only

333

Describe the ECG changes that may be seen in a ventricular tachycardia

very broad QRS (>160ms)

no p waves

T waves difficult to identify

rate > 200bpm

 

334

Describe the ECG changes seen in ventricular fibrillation

chaotic irregular deflections of varying amplitude

no identifiable P waves, QRS complexes or T waves

rate 150-500bpm

 

335

Causes of VF

myocardial iscahemia/infarction

electrolyte abnormalities

cardiomyopathy (dilated, hypertrophic, restrictive)

Long QT

Brugada syndrome

Drugs

environmental - electrical shock, drowing, hypothermia

PE

cardiac tampnoade

blunt trauma

 

336

Describe the ECG changes seen in Wolff-Parkinson-White syndrome

sinus rhythm

right axis deviation

short PR interval

sluured upstroke of the QRS complex, best seen in V3 and V4 - wide QRS due to this delta wave

dominant R wave in V1

 

337

what is the mechanism in Wolff-Parkinson-White?

accessory pathway, usually from left atria, allows direct transmission of signal, bypassing AVN (hence short PR)

 

 

338

Describe the "digoxin effect"

downsloping ST depression with "sagging" appearance

flattened, inverted or biphasic T waves - hockey stick

shortened QT

339

What is the mechanism behind the digoxin effect?

shortening of atrial and ventricular refractory periods - producing short QT

increased vagal effects at AVN - prolonged PR interval

340

Describe the ECG changes seen in pericarditis

widespread concave ST elevation and PR depression

Reciprocal ST depression and PR elevation in aVR

 

341

What is P Pulmonale?

peaked P waves

342

What is seen in p mitrale?

bifid p waves

343

list causes of p pulmonale

anything that cause right atrial enlargement

e.g. tricuspid stenosis, pulomnary hypertension

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