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FINALS medicine > Cardio > Flashcards

Cardio Flashcards

1
Q

Which is the only valve that is normally bicuspid?

A

mitral

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2
Q

What carotid character do you get in aortic stenosis?

A

Slow rising

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3
Q

Murmur in aortic stenosis

A

Ejection systolic

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4
Q

Sequelae of aortic stenosis?

A

Concentric LVH due to higher pressure needed to open valve

Heart failure

Lack of blood to end organs

+turbulent flow

+microangiopathic haemolytic anaemia- haemoglobinuria

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5
Q

3 cardinal symptoms of aortic stenosis

A

syncope

angina

dyspnoea

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6
Q

Does a mechanical or bio valve last longer?

A

Mechanical

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7
Q

Alternative to valve replacement in AS?

A

Balloon valvuloplasty

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8
Q

50% aortic regurg caused by whaT?

A

Aortic root dilation

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9
Q

What causes aortic root dilation?

A

Idiopathic

aortic dissection

aneurysm

Syphilis

Marfan’s/ED

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10
Q

Murmur aortic regurg?

A

Early decrescendo diastolic

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11
Q

What finding do you get in aortic regurg o/e?

A

Large pulse pressure leading to hyperdynamic circulation

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12
Q

Why do you get a large pulse pressure in aortic regurg?

A

Blood volume in ventricle is increased so higher SV so systolic BP high

Blood volume in aorta is decreased so in diastole get a low BP

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13
Q

What are the signs of hyperdynamic circulation

A

waterhammer pulse

bounding pulse

Head bobbing

Quincke’s sign- pulsating fingernail capillary beds

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14
Q

Other sequelae of aortic regurg?

A

Eccentric LVH

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15
Q

Most common cause of mitral regurg

A

prolapse of valve

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16
Q

What causes mitral valve prolapse?

A

Myxomatous degeneration of the papillary muscles (e.g. due to Marfan’s/ED)

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17
Q

Which valve leaflet’s chordae tendinae are most likely to rupture in mitral prolapse

A

posterior

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18
Q

Symptoms of mitral prolapse

A

mostly asymptomatic

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19
Q

Murmur of mitral prolapse?

A

Systolic murmur with a mid systolic click

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20
Q

What manoeuvres can change the mitral prolapse murmur?

A

Squatting increases venous return so click is later (more space for the valve to move in) and murmur shorter

Standing/valsalva makes the click earlier and murmur longer

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21
Q

What are other causes of mitral regurg?

A

Damage to papillary muscles post MI

LHF leading to LV dilation

Rheumatic fever

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22
Q

Murmur of (non prolapse) mitral regurg

A

Pansystolic ‘blowing’ murmur

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23
Q

Sequelae of mitral regurg

A

LHF- extra work is created for the heart as the blood keeps draining back- LA and LV volume overload - eccentric hypertrophy –> HF

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24
Q

Most common cause mitral stenosis

A

Rheumatic fever

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25
Q

What is rheumatic fever

A

antibodies post strep-A throat infection

Commissural fusion of the valve

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26
Q

Murmur in mitral stenosis

A

Systolic snap and diastolic rumble

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27
Q

Sequelae of mitral stenosis

A

High pressure can = atrial dilation

Backs up into pulmonary circulation- pul oedema and dyspnoea

Pul HTN- strain on RH –> RVH –> RHF

Increased risk AF and therefore thrombus risk

Can also get dysphagia

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28
Q

Malar flush is sign of which valve disease?

A

Mitral stenosis

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29
Q

What pulse pressure do you get in AS?

A

Narrow

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30
Q

Radio-radial and radio-femoral delay are sign of what?

A

Coarctation of the aorta

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31
Q

Left sided murmurs (M&A) are louder on

A

Held expiration

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32
Q

Right sided murmurs (T&P) are louder on

A

Held inspiration

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33
Q

What could a pansystolic murmur indicate

A

Mitral regurg

VSD

Tricuspid regurg

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34
Q

would a VSD murmur alter on position/breathing?

A

No

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35
Q

When is a tricuspid regurg louder?

A

Held inspiration sitting forwards

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36
Q

What sign do you get in tricuspid regurg?

A

large V waves on JVP

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37
Q

What do large A waves mean on JVP?

A

Anything that makes blood flow RA to RV more difficult e.g. RVH (due to pulmonary HTN or pulmonary stenosis) or tricuspid stenosis

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38
Q

What do absent A waves mean on JVP

A

AF

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39
Q

How is heart failure diagnosed?

A

Framingham criteria- 2 major OR 2 minor + 1 major

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40
Q

What can be used as a measure of prognosis in heart failure?

A

Ejection fraction

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41
Q

What categories can heart failure be split into?

A

Normal ejection fraction

Reduced ejection fraction

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42
Q

what is ‘congestive’ heart failure?

A

Both R and L ventricles

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43
Q

Pulmonary oedema is a sign of which sided heart failure?

A

Left

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44
Q

Why does LHF lead to RHF?

A

pulmonary hypertension

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45
Q

What are signs of RHF?

A

Peripheral oedema

Hepatic congestion

(systemic venous congestion)

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46
Q

What is the role of BNP in heart failure?

A

To stratify patients in primary care

> 2000 refer to cardio 2ww

400-200 non urgent referral

<400 consider alt dx

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47
Q

What does BNP do physiologically?

A

body’s natural defence against hypervolaemia- natriuresis, diuresis and vasodilation

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48
Q

Does a normal CXR exclude heart failure?

A

No

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49
Q

5 xray findings of heart failure?

A

Alveolar oedema (bat wing)

Kerley B lines

Cardiomegaly

Dilated upper lobe vessels

Pleural effusion

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50
Q

Which heart failure patients get an echo?

A

All w susp heart failure

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51
Q

How is heart failure classified?

A

NYHA - how much functional limitation

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52
Q

What is the most common arrhythmia that heart failure patients develop?

A

AF

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53
Q

What dietary change is made in severe heart failure?

A

Fluid restriction to <1.5L/day

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54
Q

What are the two main drugs you give in heart failure?

A

ACEi and beta blocker- start at different times (use clinical judgement about which you start first.)

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55
Q

Mechanism of ACEi in heart failure treatment?

A

Vasodilation, reduces afterload and fluid retention- slows LV disease progression and improves neuroendocrine abnormalities

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56
Q

Mechanism of beta blockers in heart failure?

A

reduce afterload + HR (so tackles arrhythmias)

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57
Q

3 cardio C/Is to beta blockers

A

2/3rd degree heart block

Sick sinus syndrome

Sinus bradycardia

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58
Q

What other drugs could you consider for symptom control in heart failure?

A

Diuretics for fluid overload. Once improved may be able to maintain euvolaemia with fluid and salt restriction.

Digoxin if refractory to other Rx

Amiodarone if arryth

CCB

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59
Q

Do diuretics improve LT outcome in heart failure?

A

No only spironolactone does

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60
Q

What type of diuretic is first line in heart failure?

A

Loop

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61
Q

Which CCBs can you use in heart failure?

A

Amlodipine only

62
Q

Which drugs should be avoided in heart failure?

A

TCAs

Li

NSAIDs

Corticosteroids

QT prolonging Rx

Flecainide (an antiarrhythmic)

63
Q

Is the treatment for diastolic HF the same?

A

No - ionotropic effect is the aim

Early CCBs ± B blockers

Avoid diuretics and strong vasodilators

Caution ACEi

64
Q

What is diastolic heart failure?

A

AKA preserved ejection fraction

LV is stiff so can’t fill properly in diastole leading to reduced amount of blood going to body.

Symptoms of HF with normal ejection fraction

65
Q

How does acute heart failure occur and what can it lead to?

A

Due to e.g. MI/arryth

Lead to cardiogenic shock

66
Q

Alternative to ACEi if heart failure pt can’t tolerate ACEi?

67
Q

Can you give ACEi in valvular heart disease?

A

Avoid unless specialist input

68
Q

name the layers of the wall of the heart and pericardium

A

Endocardium

Myocardium

Epicardium (surface of heart + visceral layer pericardium)

Pericardial space (lubricant)

Parietal layer pericardium

Fibrous pericardium

69
Q

Where do the coronary vessels drain into?

A

Coronary sinus in the RA

70
Q

What prevents backflow in AV valves? (mitral and tricuspid)

A

Valve leaflets attached to papillary muscles via the chordae tendineae

71
Q

What has higher resistance systemic or pulmonary circulation?

72
Q

Name the three layers of blood vessels

A

Tunica intima

Tunica media

Tunica externa

73
Q

Which layer of the blood vessel contains smooth muscle and elastin?

74
Q

What additional structure do large blood vessels have in their tunica externa?

A

Vasa vasorum (own blood vessels)

75
Q

What layers do capillaries have?

A

tunica intima ± basement membrane

76
Q

Blood flow =?

A

volume/time

Q

77
Q

Velocity of blood =?

A

Distance/time

Or flow/area (Q/A)

V

78
Q

What is mean arterial pressure?

A

1/3 SBP + 2/3 DBP

79
Q

What is Reynold’s number?

A

How laminar/turbulent blood flow is

80
Q

What are two features unique to skeletal muscle cells?

A

Multinucleated

Sarcoplasm contains myofibrils

81
Q

What is in a myofibril?

A

Sarcomere containing thick myosin filaments and thin actin filaments

82
Q

CO=?

83
Q

Normal CO?

A

about 5L/min

84
Q

How much blood in a human body?

85
Q

How do you work out SV?

A

End diastolic vol - end systolic vol

86
Q

ejection fraction = ?

A

stroke volume/end diastolic volume

87
Q

What is normal ejection fraction?

A

Around 50-65%

88
Q

Which organ receives the most blood per gram?

89
Q

cardiac work =?

A

mean aortic pressure x stroke volume

90
Q

Does cardiac work correlate well with cardiac output?

A

No e.g aortic stenosis- lot of work for little output.

91
Q

What is preload?

A

Ventricle wall stress at the end of diastole

92
Q

What is a law not used in practice to determine wall stress?

A

Law of Laplace

93
Q

What is a surrogate used for preload?

A

End diastolic LV volume

94
Q

What is preload affected by?

A

Venous pressure and rate of venous return

Atrial contraction

Resistance from valves

Ventricular compliance

HR

95
Q

What is afterload?

A

Ventricle wall stress during systole i.e. the amount of resistance ventricles must overcome during systole.

96
Q

What is afterload affected by?

A

SVR

Aortic pressure

Valve disease

97
Q

What cells start the action potential in the heart?

A

Pacemaker cells

98
Q

What is special about pacemaker cells?

A

Autoarrhythmic

99
Q

Where is the SA node located?

100
Q

Action potentials move ___ through pacemaker cells and ____ through myocytes (fast/slow)

101
Q

How does the action potential reach the other atrium?

A

Atrial internodal tracts (Bachmann’s bundle)

102
Q

How and why does conduction slow at the AV node?

A

Smaller diameter of cells and slower ion channels (calcium not sodium)

This delay allows the ventricles to fill

103
Q

Does the action potential move quickly or slowly through the His-Purkinje system? Why?

A

Quick so that there is a co-ordinated contraction

104
Q

What is the firing rate of the SA node

A

60-100 BPM

105
Q

What if the SA node fails to fire?

A

Then other parts of the heart take over pacing- other parts of atria > AV node > ventricular pacemaker cells (each has a slower and slower rate)

(ectopic foci)

106
Q

Where is the AV node?

A

RA just inferior to coronary sinus

107
Q

what is the carotid sinus?

A

Major baroreceptor site at the base of the internal carotid artery just superior to the bifurcation of the common carotid

108
Q

How do cardiomyocytes contract?

A

Small amount of calcium influx from neighbouring cell

Enters T tubules to allow it to go deep into the cell

Binds to ryanodine receptors on sarcoplasmic reticulum

Even more calcium released

Calcium binds to Troponin C which is attached to tropomyosin

(tropomyosin is draped around actin to cover the myosin head binding sites)

When calcium binds this moves the tropomyosin to expose the binding site

Myosin-actin cross bridge formed–> power stroke –> contraction

109
Q

Big box in ECG = how long?

110
Q

Small box in ECG = how long?

111
Q

How to calculate rate on ECG

A

300 divided by number big squares

OR

Number of R waves on strip x 6 (strip is 10s)

112
Q

In which leads is T wave inversion normal?

A

III, aVR, V1

113
Q

What ECG change might be seen in stable angina?

A

Widespread ST depression

114
Q

What ECG changes are seen in an NSTEMI?

A

ST depression

T wave inversion

115
Q

Difference between ischaemia and infarct

A

Infarct when cell death occurs due to ischaemia

116
Q

ECG changes in STEMI (transmural infarct)

A

T wave inversion

Hyperacute T waves

ST elevation

Pathological Q waves

117
Q

What is the criteria for ST elevation on ECG

A

> 1mm in 2 adjacent leads except V2 and V3 where must be >2mm

118
Q

Other causes of ST elevation

A

Coronary artery vasospasm

LVH

Pericarditis

119
Q

Pathological Q waves in V1 and V2- infarct location?

120
Q

Pathological Q waves in V3 and V4 - infarct location?

121
Q

Pathological Q waves in V3-6, I and aVL - infarct location?

A

Anterolateral wall

122
Q

Which lead is not a reliable one to look at for pathological Q waves?

123
Q

Causes of pathological Q waves other than STEMI?

124
Q

How long does it take for each ECG change to resolve post STEMI?

A

ST elevation days

T wave inversion weeks/months

Pathological Q waves stay for longer

125
Q

What would a large P wave in V1 and 2 (and II, III, aVF)

A

RA enlargement

126
Q

What are the ECG signs of RV hypertrophy?

A

Dominant R wave in V1 and dominant S wave V5/6

R axis deviation

Narrow QRS (i.e. not due to RBBB)

127
Q

Main ECG signs LVH

A

Deep S wave V1 and v big R wave V5/6. Add up to >35mm

128
Q

Additional ECG signs in LVH

A

R wave duration longer (>50ms)

ST elevation V1

ST depression V5/6

T wave inversion V5/6

129
Q

What do bifid P waves in Lead II and biphasic P waves in lead V1 mean?

A

LA enlargement

130
Q

What is it called when blood flow to a muscle increases disproportionately due to vasodilation in those blood vessels?

A

(functional) hyperaemia

131
Q

What are the two ways total peripheral resistance is controlled

A

Intrinsic and extrinsic factors

132
Q

What are the intrinsic controls of total peripheral resistance?

A
  1. Level of metabolites in the surrounding tissue- adenosine and CO2 = vasodilation of arterioles
  2. Autoregulation: BP decrease = arteriole dilation
  3. Active hyperaemia: increased organ perfusion as required when it is more active
133
Q

What is the extrinsic control of total peripheral resistance

A

Sympathetic NS and endocrine system control vascular smooth muscle contraction

134
Q

What type of blood vessel is the primary site of vascular resistance?

A

Arterioles

135
Q

What is the Starling equation (basically)

A

fluid movement is based on hydrostatic pressure and oncotic pressure

Also includes a filtration co-efficient which = the water permeability of the capillary wall

136
Q

Left coronary artery splits into which arteries?

A

Left anterior descending

Left circumflex

137
Q

Right coronary artery splits into what?

A

Right marginal

Posterior descending

138
Q

What are the four cardiac veins?

A

Great

Middle

Small

Anterior

139
Q

Which cardiac vein bypasses the coronary sinus and drains straight into the RA?

140
Q

With which artery does the great cardiac vein run?

141
Q

With which artery does the middle cardiac vein run?

142
Q

With which artery does the small cardiac vein run?

A

R marginal

143
Q

With which artery does the anterior cardiac vein run?

A

right coronary

144
Q

ST elevation in leads V1-4- where is the infarction and which artery?

A

Anterior/septal

LAD

145
Q

ST elevation in leads V5,6 I and aVL- where is the infarction and which artery?

A

Lateral

Left circumflex

146
Q

ST elevation in leads II, III, aVF- where is the infarction and which artery?

A

Inferior

RCA

147
Q

ST depression in leads V1-4- where is the infarction and which artery?

A

Posterior

PDA/RCA

148
Q

Mnemonic to remember reciprocal changes in ST elevation?

A

PAILS (arrow under the L)

149
Q

What is R wave progression?

A

V1 has a deeper S wave and v small R wave, as you move along to V6 there is a more and more dominant R wave and a smaller S wave

150
Q

Sensitivity/specificity of BNP?

A

Sensitive but not specific

Useful in ruling out HF but positive can = a lot of things.

151
Q

If suspect an inferior MI what can you do to check?

A

Right sided leads ECG

ST elevation in V4R (5th ICS MCL) is high sens and spec for RV MI.

152
Q

IF suspect posterior MI what can you do to check?

A

Posterior leads (V7,8,9)

FINALS medicine (8 decks)

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