Cardio Flashcards

1
Q

How does a first degree AV block present (clinically and ECG)

A

Consistent prolongation of the PR interval (>0.2 seconds), due to delayed AV node conduction. No dropped QRS complexes. Regular rhythm, every P wave present. Usually asymptomatic and not progress to higher class of AV blocks

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2
Q

How does a second degree, Mobitz type I, AV block present? (clinically and ECG)

A
  • progressive prolongation of PR interval until atrial impulse is not conducted. Regular pattern, irregular rhythm. All P waves present, not all QRS. Usually benign
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3
Q

How does a second degree, Mobitz type II, AV block present? (clinically and ECG)

A
  • irregular. More P wavs than QRS. Intermittently dropped QRS waves, with no progressive elongation of PR interval before
  • pathological
  • can experience syncope, regular irregular pulse
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4
Q

What AV blocks are benign and which require rapid treatment?

A
  • 1st degree and mobitz type 1: normally benign. May have slight increased risk of AF
  • Mobitz type 2 and third degree: require immediate treatment
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5
Q

How does a third degree, AV block present? (clinically and ECG)

A
  • ECG: no electrical communication between atria and ventricles. Variable rhythm. P wave presence, but no association with QRS
  • palpitations, syncope, shortness of breath
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6
Q

How does AF present on an ECG and clinical?

A
  • ECG: irregular rhythm, no p wave, variable ventricular rate, thinner QRS
  • clinical: tachycardia, irregular HR. Reduced exercise tolerance and heart failure. Dyspnoea, angina, palpitations, dizziness.
  • SYNCOPE = RARE
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7
Q

What is the aetiology and mnemonic for AF?

A

PIRATES

  • P: pulmonary, post operative, pericarditis
  • I: idiopathic, IHD
  • R: rheumatic heart disease
  • A: alcohol, anaemia
  • T: thyroid disease
  • E: elevated BP (HTN)
  • S: sepsis, sleep apnoea
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8
Q

What is the treatment for AF?

A

Beta-blockers and calcium channel blockers are first-line agents for rate control in AF. These drugs can be administered either intravenously or orally.

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9
Q

What is the ECG presentation for atrial flutter?

A
  • narrow complex tachycardia
  • regular atrial activity
  • flutter waves
  • regular QRS
  • regularly irregular pulse
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10
Q

What is atrial flutter?

A

Supraventricular tachycardia caused by a re-entry circuit to RA. AV node can’t keep up, so blocks some impulses

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11
Q

What is long QT syndrome?

A

Represents time taken from ventricular repolarisation to repolarisation. Inversely proportional to heart rate. Shorter when faster. Abnormally prolonged can risk ventricular fibrillation

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12
Q

What is Wolf Parkinson White syndrome? How does it present on ECG?

A

Pre excitation syndrome. Combination of congenital accessory pathway and episodes of tachyarrhythmia. Impulses bypass AV node vis the accessory pathway.

  • ECG: short PR interval, delta wave (slow slurring rise of QRS), QRS prolonged
  • form of supra ventricular tachycardia
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13
Q

What are the four forms of supraventricular tachycardia and what pathophysiology do they all have in common?

A
  • AF, atrial flutter, wolf parkinson white syndrome, PVST

- all tachycardia that originate above the level fo the bundle of His

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14
Q

What is a fusion beat (and what is is also known as?

A
  • Dressler’s beat

- when P wave starts during VT

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15
Q

What view of the heart do leads I, aVL and V5-V6 give, and if there is ST elevation in these leads, where is the MI located?

A

lateral views. Left circumflex

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16
Q

What view of the heart do leads II, III and aVF give, and if there is ST elevation in these leads, where is the MI located?

A

inferior view. Right coronary artery

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17
Q

What view of the heart do leads V1-V4 give, and if there is ST elevation in these leads, where is the MI located?

A

anterior/sepal view. Left anterior descending artery

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18
Q

What marker is used for HF?

A

B-type natriuretic peptide. Due to ventricle stretch

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19
Q

What is the most common cause of right axis deviation? What leads would be most positive and negative?

A
  • right ventricular hypertrophy
  • III = most positive
  • I = most negative
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20
Q

What is the most common cause of left axis deviation? What leads would be most positive and negative?

A
  • electrical conduction issues

- I is most positive

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21
Q

What is the treatment for SVT?

A
  • young: Valsalva manoeuver: stimulates vagus nerve

- amiodarone: broad complex tachycardia

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22
Q

What time period does one large square represent on ECG?

A

0.2 seconds

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23
Q

How long is the average PR interval?

A

120-200 m/s

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24
Q

How long should QRS complex be?

A

<110m/s

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25
Q

What is the J point?

A

Point between QRS and ST segment

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26
Q

What murmur is heard in mitral stenosis? Where is it heard? Does it radiate?

A

Diastolic.
Apex.
No radiation

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27
Q

What murmur is heard in mitral regurg? Where is it heard? Does it radiate?

A
  • pan systolic murmur
  • heard at the apex
  • radiates to the axilla
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28
Q

What murmur is heard in aortic stenosis? Where is it heard? Does it radiate?

A
  • ejection systolic (crescendo-decrescendo)
  • heart at 2nd line intercostal space, sternal edge
  • radiates to the carotid artery
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29
Q

What murmur is heard in aortic regurg? Where is it heard? Does it radiate?

A
  • early diastolic
  • heard at left sternal edge, 4th intercostal space
  • no radiation
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30
Q

What does aortic stenosis cause, and consequently what is the clinical presentation?

A
  • decreased cardiac output, due to obstruction of the left ventricular outflow
  • decreased CO leads to syncope on exertion, dyspnoea on exertion, angina
  • LV hypertrophy seen on ECG
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31
Q

What symptoms are seen with mitral regurgitation?

A

fatigue, oedema, dyspnoea on exertion

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32
Q

What is the preload?

A

stretching of myocytes before contraction. Relates to ventricular filling

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33
Q

What is afterload?

A

amount of resistance needed to open aortic valve and push blood out

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34
Q

What are the four compensatory mechanisms of the heart in heart failure?

A
  1. RAAS system activation
  2. natriuretic peptides release
  3. ventricular dilation
  4. activation of the sympathetic nervous system
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35
Q

What are common causes of heart failure in the developing world?

A

HTN, IHD, dilated cardiomyopathy

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36
Q

What is the pharmacological reatment for heart failure?

A
  1. Vasodilation: ACE-I (excrete salt and water, which increases cardiac output and reduces afterload). Beta blocker (blocks chronically activated sympathetic system. Decreases arteriolar constriction)
  2. Diuretics: get rid of renal overload
  3. Digoxin: rhythm control in HF and AF
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37
Q

What biomarkers are used in MI Dx?

A
  • increased CK (creatinine kinase)

- increased troponin I and T (released from myocardium)

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38
Q

What is seen on a ECG for a MI?

A
  • ST elevation: peaked T waves, T wave inversion
  • new LBBB
  • pathological Q waves
  • can also see ST depression in NSTEMI
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39
Q

When is O2 indicated in an MI?

A

When oxygen sats are <94%

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40
Q

What are the CXR findings in heart failure?

A

ABCDE

  • alveolar odema
  • Kerley B lines (represent interstitial oedema)
  • cardiomegaly
  • dilation of upper lobe vessels
  • effusions
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41
Q

What is CHAD2 used for?

A

Risk of MI with AF

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42
Q

What us QRISK3?

A

risk of developing a heart attack/stroke in the next 10 years

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43
Q

What does JVP provide information on?

A

right atrium filling/pressures

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44
Q

What is Prinzmetal’s angina? What causes it? What us seen on an ECG?

A
  • at rest, coronary artery spasm.
  • causes: stress, vasoconstriction, cocaine
  • ST elevation on ECG
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45
Q

What is Decubitus angina?

A
  • angina when lying down, due to increased strain on the heart
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46
Q

How does GTN spray work?

A
  • vasodilation of venous return

- decreases preload and dilates coronary arteries

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47
Q

What is the general aetiology of heart block?

A
  • cardiomyopathy, fibrosis of conducting tissue, coronary artery disease
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48
Q

What symptoms are seen in mitral stenosis?

A

Pink frothy sputum, malar flush due to increased CO2

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49
Q

What valve is most commonly affected by rheumatic heart disease?

A

Mitral valve: stenosis.

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50
Q

What causes rheumatic heart disease?

A

Group A streptococcus

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51
Q

What vavular heart disease do Marfan’s and Ehler’s Danlos relate to?

A

mitral regurg

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52
Q

When might a third heart sound be heard?

A

mitral regurg

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53
Q

When are symptoms seen with aortic stenosis?

A

When the valve is 1/4 of what is should be

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54
Q

What is the most commony cause of aortic stenosis?

A

Calcification of the aortic valve with age

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55
Q

Which valvular heart disease might have an associated Austin Flint Murmur?

A

Aortic Regurg. Fluttering of cusps due to blood flow stream

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56
Q

What are the four features of Fallot’s tetralogy?

A

ventricular septal defect, pulmonary valve stenosis, RV hypertrophy, overriding aorta

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57
Q

What is the direction of the shunt in Fallot’s tetralogy?

A

right to left

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58
Q

What is seen on investigation of Fallot’s tetralogy?

A
  • RV hypertrophy with RBBB

- CXR: boot shaped heart.

59
Q

What is eisenmenger’s complex?

A
  • initial left to right shunt due to ventricular septal defects
  • leads to pulmonary HTN
  • increasing right heart pressure, until they exceed left. then , shunt reversal.
  • cyanosis: less blood enters systemic system
60
Q

What are the two types of atrial septal defect, and which is more common?

A
  • ostrium secondum and ostrium primum

- secondum = more common

61
Q

What murmur is heard in ventricular septal defect?

A

Pansystolic murmur

62
Q

What is coartication of the aorta?

A

Congenital narrowing of the descending aorta. Level of the ductus arteriosus (origin of left subclavian artery)

63
Q

What are the four stages of heart failure (New York Heart Association)

A

A: no symptoms
B: comfortable at rest, symptoms with exercise
C: minor exercise triggers
D: symptoms at rest

64
Q

What is the treatment for heart failure?

A

LOON

  • L; loop diuretics
  • O: O2
  • O: opioids
  • PN: nitrates
65
Q

What are the symptoms of left sided heart failure?

A

dyspnoea, tachypnoea, crackles at lung base, wheezing, cyanosis. laterally displaced apex beat

66
Q

What are the symptoms of right heart sided heart failure?

A

ascites, oedema, increased JVP, liver enlargement

67
Q

What is the definition of shock?

A
  • BP: systolic below 90 mmHg
  • severe lactic acidosis
  • decreased urine
68
Q

What are the 5 types of shock?

A
  • haemorrhagic
  • neurogenic (sympathetic innervation lost due to CNS damage)
  • cardiogenic
  • anaphylaxis
  • sepsis
69
Q

What are the symptoms of neurogenic shock?

A

instantaneous hypotension, bradycardia, warm flushed skin, priprism

70
Q

What is peripheral vascular disease?

A

narrowing of arteries distal to aortic arch

71
Q

What are the 6 p’s of critical limb ischaemia?

A

The classic presentation of limb ischemia is known as the “six Ps,” pallor, pain, paresthesia, paralysis, pulselessness, and poikilothermia

72
Q

What are the four types of cardiomegaly?

A
  1. dilated
  2. hypertrophic
  3. arrythmogenic RV
  4. restrictive
73
Q

What is the aetiology of dilated cardiomyopathy?

A

genetic: dominant heterogenous mutation fo the cytoskeleton

74
Q

What is the cause of hypertrophic cardiomyopathy?

A

loss of normal myocyte arrangement: myofibrillar disarray. Also, fibrosis present

75
Q

What is hypertrophic cardiomyopathy?

A

hyperdynamic contraction of the heart due to thickening of walls and IV septum. Impaired relaxation. Leads to LV hypertrophy, impaired diastole, reduce stroke volume and abnormal mitral valve. Causes dnyamic obstruction of LV outflow

76
Q

What are the symptoms of hypertrophic cardiomyopathy?

A

forceful apex beat, late ejection systolic murmur, jerky carotid pulse, alpha wave in JVP, AF.

77
Q

What is cardiomyopathy?

A

disease of cardiac muscle

78
Q

What is restrictive cardiomyopathy?

A

normal left ventricular cavity size and systolic function, increased myocardial stiffness. This restricts diastolic filling, and leads to ventricular incompliance

79
Q

What is the aetiology of restrictive cardiomyopathy?

A

infiltrative myocardial disease. Amyloid heart disease. Sarcoidosis

80
Q

What is the most common cause of sudden cardiac death?

A

hypertrophic cardiomyopathy

81
Q

What is arrhythmogenic RV cardiomyopathy?

A

Associated with desmosomes. Fibrofatty replacement of RV myocytes. Leads to loss of function and decreased streak volume and cardiac output

82
Q

What is Naxos disease?

A

Form of arrhythmogenic RV cardiomyopathy. symptoms: wooly hair, white soles of feet. Due to consanguinity

83
Q

What is the most common cause of infective endocarditis?

A

S.aureus

84
Q

What is used to assess severity of infective endocarditis?

A

Modified Dukes Criteria

85
Q

What are the signs of infective endocarditis?

A

Roth Spots, Osler’s nodes, Janeway lesions, splinter haemorrhages, fever

86
Q

What is acute pericarditis?

A

Inflammation of the pericardium: with or without pericardial effusion

87
Q

What are the symptoms of pericarditis?

A

Chest pain (dull, sharp, burning, pressing). Rapid onset. Radiates to neck and shoulders due to phrenic nerve. Aggravated by swallowing, coughing, or laying flat. Relieved by sitting up. Pericardial rub heard. Tachycardia, tachypnoea

88
Q

What is the aetiology pericarditis?

A
  • viral: enterovirus, coxsackie virus, adenovirus, parvovirus
  • bacterial: mycobacterium tuberculosis
  • autoimmune: Sjogrens, rheumatoid, scleroderma, systemic vasculitis
  • neopastic
  • metabolic
  • trauma
  • post MI, some drugs
  • most idiopathic
89
Q

what is the potential compx of pericarditis?

A

If effusion, can become haemorrhagic and lead to cardiac tamponade

90
Q

What is Beck’s triad?

A

Beck triad is a collection of three clinical signs associated with pericardial tamponade which is due to an excessive accumulation of fluid within the pericardial sac. The three signs are: low blood pressure (weak pulse or narrow pulse pressure) muffled heart sounds. raised jugular venous pressure.

91
Q

How do you distinguish chronic effusive and chronic constrictive pericarditis?

A

cardiac catheterisation

92
Q

What is chronic constrictive pericarditis?

A

Occurs with 1% of people with acute pericarditis. Calcification thickens pericardium and affects function. Due to prolonged damage

93
Q

What is the presenation of chronic constrictive pericarditis?

A

Kaussmaul’s sign, dyspnoea, oedema, increased JVP, pulsatile hepatomegaly, hx of cardiac surgery

94
Q

What is an aortic dissection?

A

Tear in intima. blood between layers of the aortic wall: false lumen. Can present with migrating pain

95
Q

What is lidocaine used to treat?

A

ventricular fibrillation. Inactivates gate of the sodium channel

96
Q

How does digoxin work?

A

makes membrane potential more positive, releasing ACh from parasympathetic nerves

97
Q

What transporter does furosemide block?

A

Na/K/2Cl

98
Q

What is a s/e of calcium antagonists?

A

postural hypotension

99
Q

What percentage of vessel must be slerosied for symptoms of angina?

A

70-80%

100
Q

What is the gold standard diagnosis for angina?

A

CT coronary angiography

101
Q

What is the pathophysiology of an NSTEMI?

A

partial occlusion: subendothelial infarct

102
Q

What group of people are most likely to have a silent infarct?

A

Diabetics

103
Q

What management should be done within 120 minutes of a STEMI? If this doesn’t happen, what’s the next step?

A

PCI.

If not, fibrinolysis

104
Q

What is the GRACE score?

A

assess risk of further cardiac events in a NSTEMI

105
Q

What are possible post MI complications?

A
Mnemonic: DREAD:
D: death
R: rupture of heart septum, papillary muscles
E: edema
A: aneurysm
A: arrhythmia
D: Dresslers syndrome
106
Q

What are the causes of secondary hypertension?

A

ROPE:

  • R: renal disease
  • O: obesity
  • P: pregnancy
  • E: endocrine (eg, Conn’s)
107
Q

How can peripheral thrombolisms occur in aortic aneurysms?

A

thrombi form due to turbulent flow

108
Q

What is an aortic dissection?

A

tear in the intimal layer of the aorta which leads to a collecting of blood between intima and medial layers

109
Q

What is a asymmetric BP a sign on?

A

aortic dissection

110
Q

What is the definite diagnosis of aortic dissection?

A

CT

111
Q

What disease can the ankle brachial pressure index be used for, and what would the result be?

A
  • peripheral vascular disease

- <0.90

112
Q

Which valvular heart disease can have increased prevalence in connective tissue disorders?

A

Regurg disorders

113
Q

What is the most common valve defect?

A

aortic stenosis

114
Q

What are the signs of heart failure?

A
  • tachycardia
  • increased JVP
  • cardiomegaly
  • 3rd/4th heart sound
  • ascites
  • tender hepatomegaly
  • displaced apex beat
  • bi basal crackles
  • pleural effusion
115
Q

What is cor pulmonale caused by?

A

right sided HF caused by pulmonary arterial HTN. Can be caused by chronic lung disease, pulmonary vascular disorders, neuromuscular and skeletal disorders

116
Q

what murmur can be heard in cor pulmonale?

A

pan systolic murmur

117
Q

What are saw tooth pattern (f-waves) diagnostic of?

A

atrial flutters

118
Q

What does IV amidarone do?

A

restore sinus rhythm

119
Q

What are the causes of RBBB?

A

PE, IHD, atrial ventricular septal defect

120
Q

What are the causes. of LBBB?

A

IHD, aortic valve disorder

121
Q

What does IV atropine treat?

A

Bradycardia

122
Q

What is sick sinus syndrome?

A

inability of hearts pacemaker to keep rhythm

123
Q

What are hyperkalaemia, hypocalcaemia, drugs (amiodarone, tricyclic antidepressants) and bradycardia, causative factors of?

A

Prolonged QT syndrome and Wolf PArkinson white syndrome

124
Q

What is the most common cause of pericarditis in people who are immunocompromised?

A

histoplasma Spp.

125
Q

What are signs of pleural effusion?

A

bronchial breathing out at left base, muffled heart sounds

126
Q

What is seen on an ECG for pericarditis?

A

Saddle shaped ST elevation. PR depression

127
Q

What can colchicine reduce the recurrence of (as well as gout)

A

pericarditis

128
Q

What inheritance is hypertrophic cardiomyopathy, and what is the most common presenting feature?

A

Autosomal dominant.

Sudden cardiac death :-)

129
Q

What is the mutation to in cardiomyopathy?

A

sarcomere protein

130
Q

What is the fever + new murmur until proven otherwise?

A

IE

131
Q

What is the common causative organisms of I.E

A

s.aureus, pseudomonas auroginosa, streptococcus viridans, enterococci, coxiella burnetti

132
Q

What is the treatment for s.aureus. What is added if it is MRSA?

A
  1. flucoxacillin, macrolides

2. add vancomycin

133
Q

What causes rheumatic fever (and an example)

A

Lancefield Group A-B haemolytic streptococci. EG, pyogenes

134
Q

What is the presentation of rheumatic fever?

A

chorea, fatigue, SOB, arthritis, fever

135
Q

What rash can be seen in rheumatic fever?

A

erythema maginatum (red rash with raised edges and clear centre on trunk, thighs, arms)

136
Q

What is the diagnostic tool for Rheumatic fever?

A

Jones Criteria

137
Q

what is often the first ECG change in an MI?

A

Tall T waves

138
Q

Which artery is likely occluded in a complete heart block?

A

Right coronary

139
Q

What does S4 indicate?

A

forceful atrial contraction

140
Q

first line tx for HF?

A

ACE-I and BB

141
Q

How is postural hypotension diagnosed?

A

Measure BP lying down and standing up. If drop in >20mmHg in systolic pressure, or below 90 = diagnosis

142
Q

What indicates severe aortic stenosis?

A

small volume and slow rising pulse

143
Q

What is the most common cause of heart failure?

A

IHD