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Cardiology Flashcards

1
Q

Essential hypertension

A

95% of HTN cases

A combination of environmental and genetic factors that result in a hypertensive phenotype

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2
Q

Secondary hypertension

A

Caused by an identifiable cause (usually endocrine), e.g. coarctation, Conn’s syndrome**, etc.

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3
Q

Clinical features of hypertension

A

Asymptomatic till end organ damage

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4
Q

Malignant hypertension

A

Uncontrolled HTN
Retinal changes
Progressive renal failure

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5
Q

Hypertension end-organ damage

A

CVD - Thrombotic and haemorrhagic stroke
Vascular disease
LVH - Compensatory response to chronically elevated BP
Renal failure - Renovascular damage/glomerular loss

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6
Q

What is isolated systolic HTN?

A

Common in the elderly (above 70 y.o)

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7
Q

Drugs of choice in isolated systolic HTN

A

Thiazides

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8
Q

Investigations in HTN

A

Repeated BP/Ambulatory BP
Assess for secondary cause (renal disease, Conn’s etc.)
Assess end-organ damage (echo, cardiac US, renal function)

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9
Q

Stages of HTN

A

Stage 1:
140/90 (135/90 now..)

Stage 2: 160/100 in clinic or 150/95 average

Severe:
BP >180/110

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10
Q

Management of severe HTN

A

If severe HTN:
Immediate management. Signs of papilloedema/retinal haemorrhages - same day assessment by specialist

Refer if phaeochromocytoma is suspected (labile/postural hypotension, headache, palpitations, pallor, diaphoresis)

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11
Q

Management of HTN <55 years or DM

A

ACE inhibitor or angiotension II receptor blocker

Ramipril

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12
Q

Management of HTN >55 years, no T2DM or afro-caribbean

A

Calcium channel blocker

Amlodipine

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13
Q

HTN if refractive after first line treatment

A

ACEi + Calc. channel blocker (ARB not ACE if Afro-caribbean)

OR

ACE inhibitor + Diuretic

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14
Q

HTN if refractive after second line treatment

A

A + C + D

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15
Q

HTN management if refractive after A+C+D

A

If potassium <4.5
Add low dose spironolactone

If potassium >4.5
Add alpha or beta blocker

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16
Q

Management of malignant HTN

A

Admit
Oral agents
Lower slowly (otherwise risk of stroke?)

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17
Q

Hyperlipidaemia

A

Elevated cholesterol + triglycerides

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18
Q

What transports cholesterol and triglycerides in the blood

A

Lipoproteins

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19
Q

What controls the signalling of lipid transport

A

Apoproteins (phospholipids and proteins)

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20
Q

Where is cholesterol metabolised

A

The liver

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21
Q

What is the balance between for blood cholesterol levels

A

Blood uptake
Cholesterol production
GI excretion (bile acids)

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22
Q

What secondary causes are there of hyperlipidaemia?

A 
DM
Hypothyroidism
Renal failure
Liver disease (esp. alcoholic)
Biliary obstruction
Steroids/oestrogens
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23
Q

Genetic causes of hyperlipidaemia

A

Familial hypercholesterolaemia
Apoprotein E genotype
Lipoprotein lipase deficiency

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24
Q

Lipids in atherosclosis (CAD)

A

> 6.5 doubles risk of lethal CAD

>7.8 gives 4 times the risk of lethal CAD

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25
Q

Which lipids are most important for indicating CAD

A

LDL cholesterol
HDL is protective

LDL:HDL ratio is a good indicator (>4 is high risk)

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26
Q

Lipid lowering

A

Diet:
Reduce fat intake (eggs, red meat, dairy products)

Reduce body weight

Lipid lowering drugs:
Statins are effective for lowering cholesterol (QRISK2)

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27
Q

How does hyperlipidaemia cause atherosclerosis?

A

Elevated cholesterol (especially oxidises LDL) damages the endothelium early in atherosclerosis and is taken up into the lipid core of established plaques by macrophages (foam cells)

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28
Q

Diagnosis of myocardial ischaemia

A

Tight retrosternal chest pain - radiation to the neck/down left arm
Pains occurring for >4 weeks, strong relation to exercise

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29
Q

How long can episodes of myocardial ischaemia be before infarction

A

If longer than 20-30 minutes, infarction has definitely occurred

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30
Q

When should you not do an x-ray in chest pain?

A

If patient has STEMI and needs to be treated with PCI and this would be delayed by x-ray

Do the x-ray immediately after

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31
Q

Markers of myocardial necrosis

A

Creatinine kinase
Aspartate aminotransferase
Lactate dehydrogenase
Troponin

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32
Q

Causes of raised troponin

A 
Chronic/acute renal dysfunction
Severe congestive heart failure
HTN crisis
Tachy/bradyarryhthmias
PE
Myocarditis
Stroke etc.
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33
Q

Haemolgobin in myocardial ischaemia

A

Consider whether ischaemia could be a result of anaemia

Is the patient bleeding? Would antiplatelet therapy make this worse?

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34
Q

Infection and MI

A

Infection increases the risk of MI by up to 3 times - check the WCC and CRP

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35
Q

What should we check if you see a raised cholesterol

A

Thyroid levels

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36
Q

STEMI Pathology

A

Rupture or erosion of a coronary plaque leading to intracoronary thrombosis

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37
Q

Difference betwen STEMI and NSTEMI

A

STEMI - coronary artery has occluded entirely

NSTEMI - coronary artery either not entirely occluded or only transient in its occlusion (<20 minutes)

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38
Q

STEMI Ix features

A

Prolonged ST elevation

Troponin elevated

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39
Q

‘Threatened Q wave MI’

A

Where a STEMI, in the absence of treatment, progresses to Q wave or full thickness MI

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40
Q

What causes angina

A

Gradual narrowing of the coronary arteries due to the build up of fatty plaques within their walls

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41
Q

ECG leads anterior

A

V1-V4

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42
Q

ECG leads inferior

A

II, III, aVF

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43
Q

ECG leads lateral

A

I, V5-V6

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44
Q

Lateral infarct

A

Left circumflex

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45
Q

Inferior infarct

A

Right coronary

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46
Q

Anterior infarct

A

Left anterior descending

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47
Q

Management of ACS

A

MONA

Morphine
Oxygen
Nitrates
Aspirin

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48
Q

STEMI management

A

Revascularisation:

Give second antiplatelet drug in addition to the aspirin from MONA
Clopidogrel, prasugrel and ticgrelor are options

PCI - angioplasty with a stent (catheter via radial/femoral artery)

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49
Q

Risk stratification in NSTEMI

A

GRACE

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50
Q

NSTEMI and coronary angiography

A

Coronary angiography may be performed during the admission if the patient is considered high risk (using GRACE)
Otherwise will have coronary angiography as an outpatient

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51
Q

Secondary prevention of ACS

A 
Aspirin
Second antiplatelet (e.g. clopidogrel)
Beta blocker
ACE inhibitor
Statin
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52
Q

When should we give O2 in STEMI?

A

<94%

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53
Q

Management of NSTEMI

A

MONA
Antithrombin - fondaparinux (if coronary angiography or high creatinine, give unfr. heparin instead)

Ticagrelor and prasugrel are now preferred to clopidogrel as the second antiplatelet

IV glycoprotein IIb and IIa receptor antagonists: eptifibatide or tirofiban (only if patient have a high risk of CVS events)

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54
Q

Ix findings NSTEMI

A

Raised troponin

Non-raised ST segment

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55
Q

Ix findings unstable angina

A

ST depression/T wave inversion

No rise in troponin

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56
Q

Angina pectoris presentation

A

Constricting discomfort in the front of chest, neck, shoulders, jaw or arms

Precipitated by physical exertion

Relieved by rest or GTN in <5 minutes

Typical angina has all 3. Atypical angina does not

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57
Q

Coronary angiography

A

Passing a catheter through radius or femoral into the ascending aorta and then into the coronary artery.

Radio-opaque dye is injected into the artery

X-ray is then taken

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58
Q

Management of angina pectoris

A

Aspirin + statin

Sublingual glyceryl trinitrate (for attacks)

Beta blocker/calcium channel blocker (depending on comorbidities etc.) (verapamil or diltiazem should be used as they have rate-limiting effects also)

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59
Q

Other causes of ST elevation

A 
Old infarct
Pericarditis
Bundle branch block
Hyperkalaemia
Brugada syndrome
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60
Q

Left bundle branch block

A

If ST elevation and LBBB, still have very high suspicion of an MI

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61
Q

Thrombolysis in STEMI

A

Only if PCI unavailable for whatever reason.

Use tPA tissue plasminogen activator

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62
Q

Immediate (<24 hours) complications of STEMI

A

Ventricular arrhythmias (VT, VF)
AF
Failed reperfusion

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63
Q

STEMI complications (days after)

A 
Cardiac rupture (into the pericardium)
Re-infarction

HF

Cardiogenic shock (where the cardiac output can't maintain arterial BP):
Severe impairment of LV function
Infarction of the right ventricle
Mechanical catastrophe - Vent. septal rupture, papillary muscle rupture
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64
Q

STEMI complications (weeks after)

A

Thromboembolism
Chronic heart failure
VT
Dressler’s

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65
Q

What is Dressler’s syndrome

A

Autoimmune pericarditis weeks after full thickness MI

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66
Q

How do we treat Dressler’s syndrome

A

NSAIDs

Occasionally requires steroids

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67
Q

Stratifying the risk of another MI

A

Lifestyle measures - stop smoking, alcohol, high intensity exercise, weight

LV function - usually measured by echo weeks after MI

Extent of coronary disease - angiography

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68
Q

Nitrate side effects

A

Hypotension
Tachycardia
Headaches
Flushing

Nitrate tolerance - reduced efficacy after a while of using it

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69
Q

Aortic dissection

A

Sudden tear in the tunica intima of the aorta

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70
Q

Risk factors for aortic dissection

A 
HTN
Trauma
Bicuspid aortic valve
Marfan's, Ehler's Danlos
Pregnancy
Syphilis
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71
Q

Heart failure

A

A syndrome in which inadequate cardiac output is compensated for by compensatory mechanisms (e.g. vent. dilation) which eventually become maladaptive

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72
Q

Three aspects of pathophysiology in heart failure

A

Neurohormonal activation

Cytokine activation

Ventricular dilation

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73
Q

Neurohormonal activation in HF

A

Increased vasoconstrictors (renin, angiotensin II, catecholamines etc.) provoke water and salt retention, increasing afterload

These decrease LV emptying further

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74
Q

B-type Natriuretic peptide (BNP)

A

Normal level excludes HF (it is a neurohormone activated in most HF in response to strain)

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75
Q

Cytokine activation in HF

A

IL-6 and TNF-alpha raised in HF

This pathology underlines the anaemia in chronic HF

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76
Q

Ventricular dilation in HF

A

Impaired systolic function (reduced ejection fraction) and fluid retention (dilation) increase the ventricular volume, making contraction less efficient

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77
Q

Law of Laplace

A

Describes the law in which a dilated heart is mechanically inefficient

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78
Q

Acute heart failure

A

Life-threatening emergency as a result of sudden onset or worsening of heart failure symptoms

Can happen in existing or non-existing HF, is usually the result of a functional/structural abnormality

79
Q

De-novo acute HF

A

Usually a result of ischaemia

Can also be due to:
Viral myopathy
Toxins
Valve dysfunction

80
Q

Decompensated acute heart failure

A

Most common reason for AHF

Precipitating causes:
ACS
HTN crisis
Acute arrhythmia
Valvular disease
81
Q

Clinical features of AHF

A 
Symptoms:
Breathlessness
Reduced exercise tolerance
Oedema
Fatigue
Signs:
Cyanosis
Tachycardia
Elevated JVP
Displaced apex beat
S3 Heart sound
Bibasal crackle or wheeze
82
Q

Diagnostic work up for AHF

A

Blood tests - underlying abnormality (e.g. infection, anaemia, abnormal electrolytes)
CXR - Pulmonary venous congestion, interstitial oedema, cardiomegaly
Echo - pericardial effusion, tamponade
BNP - >100mg/litre

83
Q

BP in AHF

A

Usually normal or slightly raised

84
Q

Management of AHF

A

POD MAN

Position (sit up)
Oxygen
Diuretic (furosemide) fluid restriction

Morphine
Anti-emetic
Nitrates (GTN infusion is SBP >110, 2 puffs GTN spray if >90)

85
Q

How do we classify HF

A

New York Heart Association (NYHA) classification

Class I: No symptoms

Class II: mild symptoms (ordinary activity results in fatigue, palpitations, dyspnoea)

Class III: moderate symptoms (less than ordinary activity results in symptoms)

Class IV: severe symptoms (unable to carry out activity without discomfort)

86
Q

Diagnosing chronic HF

A

BNP

If high (>400):

Transthoracic echo within 2 weeks

If raised (100-400):

Transthoracic echo within 6 weeks

87
Q

Chronic HF clinical features

A 
Dyspnoea
Cough (pink/frothy sputum)
Orthopnoea
Paroxysmal nocturnal dyspnoea
Wheeze
Weight loss
Bibasal crackles on examination

RHF signs:
Raised JVP
Ankle oedema
Hepatomegaly

88
Q

Management of CHF

A

First line:
ACEi + beta blocker (start one at a time)
+ furosemide if oedema as well

Second line:
Aldosterone antagonist (spironolactone, eplerenone), angiotensin II receptor blocker or hydralazine with nitrate

Third line:
Digoxin

89
Q

Congestive heart failure

A

Biventricular failure

90
Q

LHF to CHF

A

LHF results in secondary pulmonary HTN which results in RHF

91
Q

LHF

A

Breathlessness, worse when lying down (orthopnoea)
Paroxysmal nocturnal dyspnoea
Gallop rhythm
Bibasilar crepitations

92
Q

RHF

A

Fluid retention in the legs
Ascites (if severe)
Raised JVP

93
Q

Pericardial constriction

A

Ascites more prominent than leg oedema, rare condition

94
Q

CHF valves

A

Mitral/tricuspid regurgitation common

95
Q

Common causes of HF

A 
CAD
HTN
Age
Obesity
Alcohol related disease
Valvular heart disease
96
Q

HF complications

A 
VTE
AF
Pump failure
Ventricular arrhythmias
Sudden cardiac death
97
Q

Causes of aortic stenosis

A

Congenital aortic stenosis

Premature calcification of a congenitally bicuspid aortic valve <65 y.o

Calcific aortic stenosis

98
Q

Calcific aortic stenosis

A

Common
>65 y.o
At age 80 about 10% of the population have this

Renal failure/hypercholesterolaemia can make this occur earlier

99
Q

Triad of symptoms with aortic stenosis

A

SAD
effort Syncope
effort Angina
effort Dyspnoea

All are exertional and all are progressive

100
Q

Aortic stenosis rare symptom

A

Sudden cardiac death - becomes more likely as other symptoms develop

101
Q

Murmur in aortic stenosis

A

Ejection systolic murmur

Harsh and loud

Soft/absent S2

Left sternal edge usually

102
Q

Echo in aortic stenosis

A

Allows assessment of LV function and valve structure, as well as severity of stenosis

103
Q

Features of aortic stenosis

A 
Narrow pulse pressure
Slow rising pulse
Soft/absent S2
S4
Thrill
LVH or LVHF
104
Q

Management of aortic stenosis

A

If asymptomatic - observation

Symptomatic - valve replacement

105
Q

What comorbidities should you assess for in aortic stenosis?

A

Renal failure
DM
Cholesterol +/- angiogram - CAD
FBC to check for iron (vWD can be a result of AS)

106
Q

Aortic regurgitation causes

A 
Disease affecting the valve:
Rheumatic heart disease
Endocarditis
SLE
Aortic stenosis
Disease resulting in aortic root dilation (and thus the aortic valve ring):
HTN
Marfan's
Ankylosing spondylitis
Syphilis
Aortic dissection (acutely)
107
Q

Symptoms in AR

A

If gradual onset, can be no symptoms

If the leak worsens:
LV decompensation
Exertional dyspnoea

108
Q

Signs of AR

A

Collapsing pulse

Hyperdynamic apex beat - due to volume overloaded left ventricle

109
Q

Signs of wide pulse pressure (as seen in severe AR)

A

Corrigan’s sign
De Musset’s
Quinke’s sign
Traube’s phenomenon

110
Q

Corrigan’s sign

A

Visible carotid pulsations

111
Q

De Mussett’s sign

A

Head bobbing

112
Q

Quinke’s sign

A

Nail-bed pulsations

113
Q

Traube’s phenomenon

A

Also called pistol shot femorals:

Auscultation of femoral arteries causing loud sounds during systole

114
Q

Murmur in AR

A

Early diastolic murmur

Left sternal edge

Can accentuate by leaning forward and holding breath

115
Q

Ix in AR

A

Echo/ECG:
LVH

Chest x-ray:
Enlarged heart
Aortic aneurysm potentially

Coronary angiography

116
Q

Treatment of AR

A

For LVH function:
ACEi
Diuretics

Aortic valve replacement (though can’t do this if AR is the result of root dilation of course)

117
Q

Aortic valve replacement

A

Open

Percutaneous (place new over old, via femoral artery)

118
Q

Mitral stenosis causes

A 
Rheumatic fever (99% of cases)
SLE
119
Q

Symptoms of mitral stenosis

A

Progressive exertional dyspnoea (as a result of HF)

Sudden symptoms usually a result of concurrent AF leading to high risk of thromboemboli

120
Q

Mitral stenosis signs

A 
Mitral facies (malar flush)
Chronic HF signs (raised JVP, oedema)
AF
Right ventricular heave
Tapping apex beat
121
Q

Murmur in mitral stenosis

A

Mid-diastolic murmur

Low-pitched

Rumbling

Opening snap precedes murmur

122
Q

Ix in mitral stenosis

A 
Echo:
Confirms diagnosis (usually shows rheumatic valve [thickened and distorted])

Chest x-ray:
Left atrial enlargement
Cardiomegaly

123
Q

Mitral stenosis treatment

A

Medical:
Diuretics, digoxin and warfarin

Surgical:
Mitral valvotomy
Mitral valve replacement

124
Q

Mitral valve prolapse (Barlow’s syndrome)

A

Mitral valve is larger than usual/chordae are too long

Mitral valve prolapses back into atria during systole as a result

125
Q

Mitral valve prolapse features

A

Without mitral regurg. often does not cause any symptoms

With mitral regurg., ‘click’ mid-systole
Predisposes to bacterial endocarditis

126
Q

Mitral regurgitation causes

A

Extremely common condition with two pathologies:

Intrinsic valve disease:
Myxomatous degeneration
Rheumatic heart disease
Infective endocarditis

Secondary (functional):
Stretching of the valve ring when dilated (usually from LHF)

127
Q

Symptoms of mitral regurgitation

A

Heart failure symptoms:
Breathlessness
Effort intolerance
Fatigue

128
Q

Mitral regurgitation murmur

A

Loud pansystolic murmur at the apex

129
Q

Treatment of mitral regurgitation

A

Medical:
Diuretics
Angiotensin converting enzyme inhibitors

If intrinsic valve disease, can perform surgery to repair/replace

130
Q

Dilated cardiomyopathy

A

Most common form of cardiomyopathy, accounting for 90% of cases

Dilated heart leading to predominately systolic dysfunction

All 4 chambers are dilated (L>R)

Eccentric hypertrophy

Mitral regurgitation + AF are common

131
Q

Cardiomyopathy

A

Primary heart muscle diseases that are classified according to the echo findings

132
Q

Treatment of dilated cardiomyopathy

A

As per heart failure:

First line:
ACEi + beta blocker (start one at a time)
+ furosemide if oedema as well

Second line:
Aldosterone antagonist (spironolactone, eplerenone), angiotensin II receptor blocker or hydralazine with nitrate

Third line:
Digoxin

If patient is young, consider heart transplant

133
Q

Causes of dilated cardiomyopathy

A 
Idiopathic
Hypothyroid, thyrotoxicosis
Coxsackie B, HIV, diphtheria
Alcohol
Haemochromatosis
Sarcoid
Familial DCM or Duchenne's muscular dystrophy
134
Q

Hypertrophic cardiomyopathy

A

Genetic condition characterised by asymmetrical hypertrophy of the LV, especially the septum

Causes an outflow tract obstruction and diastolic dysfunction

Secondary MR

135
Q

Symptoms of hypertrophic cardiomyopathy

A

Breathlessness
Dizziness
Chest pain

Sudden death (due to vent. arrhythmias)

136
Q

How do we treat hypertrophic cardiomyopathy

A

Exertional symptoms:
Beta blockers
Calcium channel antagonists

High risk of vent. tachy:
Amiodarone

Genetics/family screening + counselling

137
Q

Restrictive cardiomyopathy

A

Causes cong. HF
Due to infiltration of the myocardium (e.g. by amyloid)

Treat with diuretics (though is usually refractive)

138
Q

Acute pericarditis features

A

Pleuritic chest pain
Often positional (relieved by sitting forward)
Cough, dyspnoea, tachycardia, tachypnoea
Pericardial rub may be heard

139
Q

Acute pericarditis ECG features

A

Saddle shaped ST elevation, widespread

PR depression

140
Q

Ix in pericarditis

A

ECG

Transthoracic echo

141
Q

Causes of pericarditis

A 
Viral infections (coxsackie)
TB
Uraemia
Trauma
Dressler's syndrome
Hypothyroid
Malignancy
Connective tissue disease
142
Q

Treatment of pericarditis

A

Treat underlying cause

NSAIDs
Colchicine

143
Q

When do we use CABG

A

We can use this in CAD to reduce angina symptoms as well as reduce risk of an MI

Involves using the saphenous vein

144
Q

What is cardiac tamponade

A

Accumulation of pericardial effusion to the point where there is impaired heart function/filling

145
Q

Features of cardiac tamponade

A

Beck’s triad:
Hypotension
Raised JVP
Muffled heart sounds

Dyspnoea
Tachycardia
Pulsus paradoxus
Kussmaul’s sign

146
Q

What is pulsus paradoxus

A

An abnormally large drop in BP during inspiration

147
Q

What is Kussmaul’s sign

A

Paradoxical rise in JVP on inspiration - indicative of limited right vent. filling

148
Q

Treatment of cardiac tamponade

A

Urgent pericardiocentesis

149
Q

Constrictive pericarditis features

A

Progressive exertional dyspnoea
Peripheral oedema
Ascites

150
Q

Constrictive pericarditis

A

Recurrent pericarditis can cause pericardial fibrosis sufficient enough to constrict the heart and impede cardiac filling/emptying

151
Q

Treatment of constructive pericarditis

A

Diuretics or surgery

152
Q

Causes of a pericardial effusion

A

Exudates:
Metastatic malignancy
Acute pericarditis

Haemopericardium:
Aortic dissection
Trauma

Transudates:
Heart/liver failure
Nephrotic syndrome
Myxoedema

153
Q

Infective endocarditis

A

An infection of the lining of the heart, usually the valves

154
Q

Pathology of infective endocarditis

A

Blood-borne organisms settle on a heart valve causing fibrin deposits to accumulate there alongside microorganisms and form vegetations

You get symptoms due to:
Valve damage (causing heart failure)
Embolisation of infected material (abscesses, vital organ infarctions)
Immune response to chronic infection (renal failure)

155
Q

Sources of infective endocarditis infections

A

Dental procedures/abscesses
Skin infections
GI infections
IVDU

156
Q

Risk factors for infective endocarditis

A

Prosthetic valves
Rheumatic valve disease
Cong. heart defects

157
Q

Causative organisms in IE

A 
Staph aureus (skin infection)
Staph epidermidis (following surgery)
Strep viridans (dental)
158
Q

Modified Duke’s criteria

A

IE if:
2 major criteria
1 major, 3 minor
5 minor

159
Q

Major criteria in Duke’s

A

Positive blood cultures

Evidence of endocardial involvement (echocardiogram or new valvular regurgitation)

160
Q

Minor criteria in Duke’s

A 
Predisposing heart condition
Fever >38
Vascular phenomena (signs peripherally)
Predisposing heart condition
IVDU
Glomerulonephritis etc.
161
Q

Ix in IE

A 
Blood culture (>12 hours apart 3 times)
Blood tests
Urine dipstick (haematuria)
Echocardiogram
Transoesophogeal echo
162
Q

Management of IE

A

Amoxicillin initially
Vancomycin (if prosthetic valve)

Flucloxacillin (if staph)

Benzylpenicillin (if strep. e.g. strep viridans)

Occasionally surgery

163
Q

Prophylaxis of IE

A

If you have valvular problems and are undergoing a procedure with a high risk of bacteraemia, give prophylactic abx

164
Q

Myocarditis

A

Inflammation of the heart muscle caused by:
Viral infections - coxsackie
Bact. infections
Radiation exposure.

165
Q

Myocarditis features

A

Acute HF
Tachycardia out of proportion to the severity of HF
Sudden cardiac death

166
Q

Treatment of myocarditis

A

No specific treatment

HF therapies

167
Q

Supraventricular arrhythmias

A

Originate in the atria or around the AV node

168
Q

Ventricular arrhythmias

A

Originate in the ventricles

169
Q

AV-reciprocating tachycardias (paroxysmal SVT)

A

A re-entrant circuit set up by an accessory pathway. Can be between:

Atria and the ventricles
(AV re-entrant tachycardia)

Between the atrium and AV node (AV nodal re-entrant tachycardia) - most common type

170
Q

SVT ECG diagnosis

A

Regular narrow QRS tachycardia
Can have abnormal P waves that are activated retrogradely

If AVNRT - can be upside down and following the QRS complex

171
Q

Wolff-Parkinson White

A

A congenital accessory conducting pathway
Get a ‘delta’ wave before the QRS complex
Can get axis deviation (left or right)

172
Q

Treatment of SVT

A

Vasovagal maneuvres:
Valsalva maneuvre - blow out through nose with eyes shut and holding nose
Carotid sinus massage
Swallow a cold drink

Drugs:
IV adenosine (6mg > 12mg > 12mg)
Beta blockers (verapamil, flecanide)

Radiofrequency ablation

173
Q

Atrial fibrillation different types

A

Paroxysmal AF - Where attacks terminate spotaneously
Persistent AF - where attacks do not terminate without medical intervention
Permanent AF - AF considered to be permanent with/without intervention

174
Q

AF pathology

A

Atria depolarise spontaneously in a rapid uncoordinated fashion, bombarding the AV node with signals

175
Q

Causes of AF

A

Cardiac - Ischaemic heart disease, hypertensive heart disease, mitral valve disease, pericarditis

Metabolic - Thyrotoxicosis, alcohol

Pulmonary - PE, pneumonia, COPD, cor pulmonale

Idiopathic

176
Q

Treatment of AF

A

Rate control - beta blockers, calcium channel blockers, digoxin

Rhythm control - Sotalol, amiodarone, flecainide

Cardioversion:
Electrical cardioversion if haemodynamically unstable
Amiodarone or flecainide

177
Q

When to rate, when to rhythm control in AF

A

Rate:
>65 y.o
Hx of IHD

Rhythm:
<65
Symptomatic
First presentation
Cong. heart failure
178
Q

Anticoagulation in AF

A

CHA2DS2VASc score

0 = no treatment
1 = consider anticoagulation
2 = offer anticoagulation
179
Q

Atrial flutter

A

Atria depolarise in a rapid coordinated fashion as a result of macro re-entry circuits

180
Q

Atrial flutter ECG

A

Sawtooth appearance

Atrial rate may be 300, though depending on degree of AV block you may see a ventricular rate of half that

181
Q

Treatment of atrial flutter

A

Cardioversion

Radiofrequency ablation

182
Q

Ventricular tachycardia

A

Broad QRS with abnormal shape

Suspect when there is heart disease (e.g. heart failure damage)

Can be pulseless or haemodynamically stable VT

183
Q

Pulseless VT management

A

DC cardiovert

Immediate anaesthesia

184
Q

Haemodynamically stable VT management

A

IV lidocaine (one drug only - don’t combine)
Amiodarone (one drug only)
DC cardioversion

185
Q

Two types of VT

A

Monomorphic - most commonly caused by MI

Polymorphic - caused by prolonged QT interval

186
Q

Causes of a prolonged QT interval

A 
Drugs:
Amiodarone
Antiarrhythmic drugs
Tricyclic antidepressants
Fluoxetine
Chloroquine
Erythromycin
Other:
Bradycardia
Congenital
Hypocalcaemia
Hypokalaemia
Hypomagnesaemia
MI
Myocarditis
Hypothermia
Subarachnoid haemorrhage
187
Q

Polymorphic VT management

A

DC cardiovert
IV magnesium
Correction of metabolic cause

188
Q

Long-term management of VT

A

Beta blockers, amiodarone, sprinolactone etc.

Revascularisation (if coronary artery disease)

ICD

189
Q

Ventricular fibrillation

A 
Caused by:
IHD
Cardiomyopathies
Channelopathies (Brugada's etc.)
WPW etc.
190
Q

Which are the shockable rhythms

A

VT

VF

191
Q

Stokes-Adams attack

A

Sudden onset syncope
Lasts <60 seconds
Pale and still as if dead
Recovery back to normal rapidly

Classical syncope in bradyarrhythmias

192
Q

Aetiology of bradyarrhythmias

A

Sinoatrial node disease

Atrioventricular block

193
Q

AV block types

A

Impaired electrical conduction between atria and ventricles

First degree:
PR interval >0.2 seconds
Asymptomatic

Second degree:
Mobitz type 1 (Wenckeback) - progression prolongation of PR interval till dropped beat
Mobitz type 2 - PR interval constant but P wave not always followed by a QRS complex

Third degree:
No association between P waves and QRS

194
Q

Treatment of AV block

A

Mobitz type 2 + complete heart block:

Pacemaker

Pass Medicine (24 decks)

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