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Phase 2A > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Function of a ECG

A

representation of the electrical events of the cardiac cycle

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2
Q

Function of the SA node?

A

dominant pacemaker with an intrinsic rate of 60-100 bpm

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3
Q

Function of the AV node?

A

backup pacemaker with an intrinsic rate of 40-60 bpm

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4
Q

Another pacemaker besides the two nodes?

A

ventricular cells - intrinsic rate of 20-45 bpm

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5
Q

Impulse conduction pathway of the heart with ECG phase

A

Sinoatrial node - AV node (flat between P&Q)- bundle of His - bundle branches - Purkinje fibres (all QRS)

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6
Q

Standard calibration & how to determine pos / neg of wave?

A
  • 25 mm/s or 0.1 mV/mm calibration

- impulses that travel towards the node causes an upright positive deflection, goes away causes a negative deflection

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7
Q

To determine heart rate from ECG graph

A

300 / # large sq between 2 R waves

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8
Q

If heart rate is irregular

A

count # QRS complex on the strip, usually a strip is 10 seconds long so multiply number of complexes by 6

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9
Q

What does the P wave represent in the heart cycle?

A

atrial depolarisation, electrical summation within the atrium

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10
Q

features of the P wave in ECG

A

normally
<120 ms wide, <0.3 mV tall
<3 s. sq wide, <2.5-3 small sq tall

always positive in lead I, II
always negative in lead aVR

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11
Q

How would atrial enlargement show up on the ECG?

A

Right AE - tall P wave (P pulmonale)

Left AE - bifid, broad notched P wave (P Mitrale)

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12
Q

What does the PR interval represent in the heart cycle?

A

= start of P to start of QRS

sinoatrial depol, atrial depol, conduction of AV junction so from A to V (node & bundle of His) (in which there is a delay)

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13
Q

Pathological principles of PR interval

if shorter .. if longer ..

A

Longer: disorders of the AV node and specialised conduction tissues

Shorter: in younger patients and preexcitation

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14
Q

One cause of short PR interval

A

Wolff Parkinson White Syndrome - extra conduction pathway causing rapid heartbeat with short PR and slurred QRS

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15
Q

One cause of long PR interval

A

first degree heart block

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16
Q

What does the QRS complex represent in the heart cycle

A

= start of Q to end of S

  • ventricular depolarisation (& purkinje and bundle branches)
  • also when atrial repolarisation occurs
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17
Q

Features of the QRS complex in ECG

A

normal <120ms
size of complex relates to myocardial mass

predominantly neg S wave in V1, transition to positive R by V6

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18
Q

Pathological principles of QRS complex

if broader .. if smaller .. if taller …

A

Broad QRS = ventricular conduction delay or bundle branch block

Smaller = obese patient, pericardial effusion, infiltrative cardiac disease

Taller QRS = thin patient, LV hypertrophy (S wave in V1 and R wave in V5/V6 > 35mm)

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19
Q

Features of hypertrophies of the ventricles

A
  • deeper waves (best seen in 1 and 6!)
  • S wave in V1 and R wave in V5/V6 > 35mm or R wave is 11-13
  • due to hypertension or valvular disease
  • diagnose using sokolow & lyon criteria
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20
Q

What does the ST segment represent in the heart cycle

A

interval between ventricular depolarization and repolarization

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21
Q

Features of a ST segment

A

flat = isoelectric

so elevated or depressed = pathology but 1mm or more is normal in V1 and V2

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22
Q

Diseases in which ST segment is elevated

A

Early repolarisation, myocardial ischaemia, inflammation, pericarditis or myocarditis

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23
Q

What does the T wave represent in the heart cycle

A

ventricular repolarisation

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24
Q

Features of a T wave

A

normal = asymmetrical, first half having a gradual slope than second
12.5% - 66% of amplitude of R but < 10mm

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25
Q

Abnormal T wave can represent (3)

A

Nonspecific pathology, but can indicate

  • ischaemia or infarction
  • myocardial strain (hypertrophy)
  • myocardial disease (cardiomyopathy)
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26
Q

What does a QT interval represent in the heart cycle

A

= start of QRS to end of T

time taken for ventricular depolarisation and repolarisation

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27
Q

Features of QT interval

A

= 0.35-0.45s corrected for heart rate

Should not be extended to halfway point of two QRS complexes

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28
Q

Causes of QT pathology

A
  • drugs, congenital, electrolyte disturbances
  • excessively rapid or low repol can be arrhythmogenic
  • long QT or short QT syndromes
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29
Q

What is a U wave?

A

follows after T wave, small round and symmetrical

origin unknown but more common when HR <65bpm

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30
Q

Features of a U wave (abnormal and normal)

A

should be <25% of T wave voltage, max 1-2mm

abnormal when prominent or inverted

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31
Q

What is the QRS axis

A

overall direction of the heart’s electrical activity

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32
Q

Abnormalities of QRS axis may be due to ..

A

As QRS = L&R ventricular depolarisation, abnormalities will show

  • ventricular hypertrophy
  • conduction blocks or infarction
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33
Q

How to determine the QRS axis

A

By looking at the nature of Lead I and lead aVF, combine and determine, confirm through lead II

(I)     (aVF)
pos  pos   normal
pos  neg   LAD
neg  pos   RAD
neg  neg   indeterminate axis
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34
Q

What do arrhythmias show

A

Ion channels that conduct the action potentials are affected

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35
Q

What affects the amplitude of deflection as shown on the ECG?

A

mass of myocardium

ventricle has a larger wave than atrium

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36
Q

What affects the width of deflection as shown on the ECG?

A

speed of conduction

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37
Q

Causes of tachycardia

A

> 100 bpm

atrial fibrillation, atrial flutter

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38
Q

Causes of bradycardia

A

< 60 bpm

  • conduction tissue fibrosis / wear and tear
  • ischaemia
  • inflammation / infiltrative disease
  • drugs
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39
Q

Causes of diseased ventricular rhythm

A

caused by cell to cell propagation

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40
Q

Causes of diseased sinus rhythm

A
  • disease of the sinus node
    • sinus pause - lack of cardiac output during the time
  • AV node / distal conduction problems
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41
Q

How is AV block classified

A

For every QRS wave, there should be a P wave preceding it (1:1)

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42
Q

Define 1st degree AV block

A

longer PR interval

still 1:1 P:QRS

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43
Q

Define 2nd degree AV block

A

2:1
One conduct and one doesnt

Two subtypes, Mobitz I and II

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44
Q

Define Mobitz type I 2nd degree AV block

A

gradual increase in length of PR intervals until it eventually drops, no conduction to QRS

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45
Q

Define Mobitz type II 2nd degree AV block

A
  • sudden unpredictable loss of AV conduction and loss of QRS
  • PR interval randomly seen // alternating with no R
  • due to loss of conduction in bundle of His, purkinje fibres
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46
Q

Define 3rd degree AV block

A

no influence of atria at all on ventricle (complete heart block)

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47
Q

How to identify bundle branch blocks

A

identify through V1 and V6 M or W pattern - wiLLiam maRRow

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48
Q

Features of left bundle branch block

A

wilLLiam

  • W in V1
  • LL - left!!
  • M in V6
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49
Q

Features of right bundle branch block

A

maRRow

  • m in V1
  • RR - right!
  • W in V6
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50
Q

Signs of ischaemia and infarction

A
  • flattening of T wave
  • ST segment depression
    (STemi and non stemi)
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51
Q

Signs of a full infarction

A
  • SR segment elevation
  • Inversion of T
  • isoelectric ST, T still inversed
  • Q wave - old infarction
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52
Q

Define atherosclerosis

A

degenerative disease where atherosclerotic plaques form in the intima or L&M arteries. rupture will lead to thrombus formation, partial / complete arterial blockage / heart attack

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53
Q

Cause or risk of atherosclerosis

A

obesity / age / family history

  • systemic hypertension
  • smoking
  • diabetes m
  • elevated serum cholesterol / hyperlipidemia
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54
Q

What triggers the formation of the atherosclerotic plaque (2 physical properties)

A
  • fatty streaks in children to AP
  • injuries to endothelium or arterial wall (turbulent flow at bifurcations / neointima formation)
  • tissue response of vascular wall to injurious agents
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55
Q

Predecessor of atherosclerotic plaques

A

fatty streaks - may disappear or progress

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56
Q

What is the fatty streak made of and where is it found

A
  • lipid laden macrophages / T lymphocytes

- intimal linings, in children

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57
Q

Composition of atherosclerotic plaques

A
  • endothelial surface
  • fibrous cap
  • degenerate material / necrotic core
  • (platelet derived) growth factor
  • lipid
  • inflammatory cells - lymphocytes
  • connective tissue
  • calcification / damage to local wall
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58
Q

Complications of plaque presence

A

occlude vessel lumen: restrict blood so angina, chronic narrowing of blood vessel, dissection

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59
Q

Briefly outline the development of plaques

A
  1. fatty streaks / injury to endothelium
  2. Injury to endothelial cells → endothelial dysfunction → signal sent to circulating leukocytes → leukocyte accumulate & migrate into vessel wall → inflammation, with:
    - LDL causes endothelial dysfunction → response to injury hypothesis where chemoattractants & neutrophils are released e.g. IL 1, 6, 8 and CRP
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60
Q

What is a fibrous cap

A

layer of connective tissue full of collagens (strength) and elastin(flexibility) laid by smooth muscle cell that overlies lipid core and necrotic debris

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61
Q

Features of the smooth muscle cell in the atherosclerotic lesion

A

can move around

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62
Q

Outline how an atherosclerotic plaque may rupture

A
  • fibrous cap has to be resorbed and redeposited for maintenance
    • if balance shifts: increased enzyme activity (inflammatory conditions) : chew away the plaque and led blood in to the wall: cap becomes weak and plaque ruptures leading to thrombosis
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63
Q

Other growth mechanism of the plaque

A

Haemorrhage - results from rupture or leakage of microvessels within

(the other one is platelet drived growth factors)

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64
Q

Presentation of atherosclerosis

A
  • angina - worse in exercise, stress or comorbid
  • MI
  • chronic congestive heart failure
  • sudden death
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65
Q

Complications of plaque rupture

A
  • acute occlusion
  • chronic & significant narrowing of blood vessel
  • aneurysm
  • thrombosis: could impact downstream esp to feet, toes & leg
  • dissection
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66
Q

Pharmacological treatments for atherosclerosis

A
  • *canakinumab**: inhibit interleukin-1 (big boss for inflammation):
  • *aspirin** !! both as management and prevention
  • *clopidogrel**- inhibit platelets
  • *statins** - inhibit HMG CoA reductase, reduce cholesterol synthesis
  • *PCSK9 inhibitors** if statins don’t work

colchicine:low dose anti inflam

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67
Q

procedural treatment for atherosclerosis

A

if coronary artery disease:
Percutaneous Coronary Intervention = stenting

  • uses drugs such as sirolimus or rapamycin to inhibit regrowth
68
Q

define aneurysm

A

if there is a permanent dilatation of the artery TWICE the normal diameter

69
Q

normal diameter of the aorta?

A

2cm - but increases with age

70
Q

classification of aneurysms

A

true or false

aortic aneurysms classified as abdominal or thoracic

71
Q

define a true aneurysm

A
  • all layers of arterial wall involved in abnormal dilatation

most commonly 2 aorta (abdominal and thoracic), the 3 legs (iliac, popliteal and femoral arteries)

72
Q

define a false aneurysm

A

aka pseudoaneurysm

  • only the outer layer = adventitia is involved in collection of blood, often after traumaor a perforating injury
73
Q

how are aortic aneurysms classified?

A

abdominal or thoracic

74
Q

cause & risk of abdominal aortic aneurysms

A

atherosclerosis (and factors)

male, smoke, HT, COPD, HL, age (>60) !

75
Q

present of unruptured abdominal aortic aneurysms

A
  • pain in abdomen, back, loin or groin (due to impaired blood flow to lower body)
  • pulsatile abdominal swelling - less pronounced!
76
Q

present of ruptured abdominal aortic aneurysms

A
  • IM/cont abdominal pain - radiate to back, iliac fossa or groin
  • pulsatile abdominal swelling
  • collapse, hypotension, tachy, profound anemia, death
77
Q

invest of abdominal aortic aneurysms

A
  • abdominal ultrasound! - assess aorta to degree of 3mm

- CT or MRI angiography

78
Q

treat of abdominal aortic aneurysms

A
  • monitor small <5.5cm
  • treat cause, modify risk (smoke / BP / lipid)
  • open surgical or endovascular - stent via femoral or iliac arteries for those <5.5cm
79
Q

epidem of thoracic abdominal aneurysm

A

ascending, arch or descending thoracic aorta may become aneurysmal

ascending - Marfan or hypertension
descending or arch - secondary to atherosclerosis and rarely syphilis

80
Q

risk factors for thoracic abdominal aneurysm

A
  • genetic influence
  • hypertension, age, smoking, COPD
  • atherosclerosis
  • previous aortic aneurysm repair
  • bicuspid or unicuspid valves
81
Q

normal size of mid-descending thoracic aorta

A

26-28mm

82
Q

patho of thoracic abdominal aneurysm

A

inflammation / proteolysis & reduced survival of the smooth muscle cells in aortic wall

once aorta reaches a crucial diameter (6 up 7 down) it loses all distensibility so a rise in BP can trigger dissection or rupture

83
Q

Present of thoracic abdominal aneurysm

A
  • most are asymptomatic
  • pain in chest, neck, upper -mid back, epigastrium
  • aortic regurgitation
  • fever if infective, symptoms from compression
84
Q

how would you diagnose thoracic abdominal aneurysm

A

CT, MI
aortography may be helpful in finding the position

echocardiography for aortic dissection
ultrasound

85
Q

how would you treat thoracic abdominal aneurysm

A 
Ruptured = immediate surgery
Symptomatic = surgery regardless of size;
  • regular monitoring by CT or MRI every 6 months
  • rigorous BP control using beta blockers e.g. bisoprolol
  • smoking cessation and treat cause
86
Q

how does an aortic dissection form?

A

blood is forced through a tear in the aortic intima, through the medial layer and flows between the layers of the aorta. Layers are forced apart resulting in dissection

87
Q

Where would blood in the dissecting aneurysm flow

A

layers in the aortic media (through the aortic intima)

88
Q

Classification of aortic dissection

A

according to timing of diagnosis from the origin of symptoms

  • acute less than 2 weeks
  • subacute 2-8 weeks
  • chronic more than 8 weeks
89
Q

causes of aortic dissection

A
  • trauma: shearing stress in TA
  • inflammatory, degenerative e.g. Marfan’s
  • atherosclerotic
  • hypertension!!
  • inherited
  • connective tissue disorders
90
Q

Briefly detail how an aortic dissection forms

A
  • tear in intimal lining of the aorta
  • a column of blood under pressure enters the aortic wall, forming a haematoma which separates intima from adventitia
  • false lumen is created, extends in either direction: anterograde = to bifurcations, retrograde = to aortic foot
91
Q

2 most common sites of intimal tears

A
  • within 2-3cm of aortic valve
  • distal to the left subclavian artery in the descending aorta
    (perhaps also at turbulent flows and bifurcations?)
92
Q

present - aortic dissection

A
  • sudden onset of severe and central chest pain that radiates to the back and down the arms
  • pain often tearing in nature and may be migratory
  • hypertension
  • pain is maximal from time of onset unlike MI where pain increases in intensity
  • potential absence of peripheral pulse
  • potential neurological symptoms & shock: loss of blood supply in spinal cord
  • potential aortic regurg, coronary ischaem, cardiac tamponade
  • distal extension may produce acute kidney failure, acute lower limb ischaem or visceral ischaem
93
Q

how would you diagnose aortic dissection

A
  • CXR for widened mediastinum

- CT MRI to see clearly (urgent)

94
Q

treatment for aortic dissection

A

aim: contain propagating haematoma by reducing arterial pressure and immediate surgical repair

  • urgent antihypotensive - IV beta blockers: metoprolol or vasodilators e.g. IV GTN
  • analgesia and surgical repair or stent
  • long term follow up with CT or MRI
95
Q

what is peripheral vascular disease

A

essentially lower limb ischaemia - partial blockage of peripheral vessels by an atherosclerotic plaque / thrombus resulting in insufficient perfusion of the leg

96
Q

symptoms of mild peripheral ischaemia

A
  • stress induced physiological malfunction
  • exercise induced angina
  • intermittent claudication: cramping pain induced by exercise and relieved by rest
  • pain is distal to site of atheroma due to lactic acid production
  • caused by inadequate O2 supply
  • limb is usually cold, leg pulses often absent
97
Q

symptoms of moderate peripheral ischaemia

A
  • ischaemic cardiac failure
  • critical limb ischaemia:
    • rest pain is typically nocturnal
  • limb is cold, often pulseless
    • chronic and most severe becomes peripheral vascular disease
98
Q

Differential diagnosis of peripheral vascular disease

A
  • osteoarthritis of hip/ knee if knee pain at rest

- peripheral neuropathy if tingling

99
Q

how would you diagnose peripheral vascular disease

A
  • 1st line color duplex ultrasound
  • for severity Ankle Brachial Pressure Index (ABPI):
  • 0.5 - 0.9 = intermittend claud
  • < 0.5 = critical leg ischaemia
  • MR/CT angiograpy to assess extent, location and quality of distal vessels

Exclusion principle

  • ESR / CRP for arteritis (= raised)
  • FBC to exclude anemia (= raised RBC)
  • ECG for cardiac ischaemia
100
Q

How does an ABPI work?

A

Ankle Brachial Pressure Index

  • compares between the cuff pressure in ant/post tibial arteries vs the brachial artery
  • Doppler ultrasound used
101
Q

Numeral criteria on an ABPI to diagnose leg ischaemia

A

0.5-0.9 - intermittent claudication

< 0.5 - critical leg ischaemia

102
Q

What is acute lower limb ischaemia?

A

sudden decrease in limb perfusion that threatens the viability of the limb

occurs either due to embolic disease or thrombotic disease (or trauma)

103
Q

Examples of embolic disease

A
  • cardiac thrombus, arrhythmias
  • rheumatic fever
  • may also occur secondary to aneurysm thrombus or thrombus on athero plaque
104
Q

Examples of thrombotic disease

A
  • usually forms on a chronic atherosclerotic stenosis in patient w/ prev claudication
  • also in normal vessels in individuals who are hypercoagulable bc of maliganancy or thrombophilia defects
  • popliteal aneurysms: may thro/embose distally!
105
Q

Symptoms of thrombotic disease!

A

6P’s

  • Pain
  • Pallor
  • Perishing cold
  • Pulseless
  • Paralysis
  • Paraesthesia (tingling / prickling, pins & needles)
  • the more P’s the more sudden and complete the ischaemia
106
Q

Treatment of thrombotic disease?

A
  • Risk factor modification
    • smoke: bl supp reduce
    • treat HP, HL, diabetes, exercise
    • antiplatelet - clopidogrel to prevent progression
  • depends if acute or critical limb ischaemia, treat accordingly
107
Q

Treatment for acute limb ischaemia?

A
  • if patient loses use of side of body and fast irregular pulse
  • nature is similar to MI

surgical emergency!
requires revascularisation 4-6hrs to save limb
- angioplasty (widens artery with a balloon)
- intra aterial thrombolysis
- surgical removal of embolus if present

108
Q

Treatment for critical ischaemia?

A
  • Revascularisation for critical ischaemia
    • percutaneous transluminal angioplasty (squash plaque and increase perfusion to reduce ischaemia
    • bypass
    • amputate if severe
109
Q

What is intermittent claudication?

A

Tissue is suffering not dying

  • Oxygen debt when doing mild / moderate exercise = build up of lactic acid resulting in pain
  • physiological pain is the same as it is in you
110
Q

What is critical ischaemia? - symptoms and pathology

A
  • severe pain in all toes of the foot relieved by hanging foot over the edge of bed (gravity to perfuse)
  • non healing painful ulcer on big toe with no trauma

Tissue is dying! and suffering at rest

  • blood supply is inadequate: basal metabolism
  • no reserve available for increased demand
  • there is resting pain: typically nocturnal
  • gangrene / infection risk
111
Q

Berry aneurysms

  • what are they
  • where are they mostly found
A
  • normal muscular arterial wall is replaced by fibrous tissue
  • points of branching, e.g. circle of willis - A/P communicating artery, middle cerebral artery
112
Q

Cause of berry aneurysms

A
  • long standing hypertension: damage to wall of blood vessels
  • connective tissue disorders: collagen synthesis issues - vessel wall dilated until it pops
  • focal area of weakness within the arterial substructure: branching points of circle of willis
113
Q

Presentation berry aneurysm

A
  • pronounced neurological deficit: recoverable and persistent
114
Q

Complication berry aneurysm

A
  • subarachnoid haemorrhage risk

- burst = sudden death

115
Q

Which aneurysm is associated with hypertension and diabetic vascular disease?

A

Capillary microaneurysm (Carcot Bouchard aneurysm)

116
Q

Where are capillary microaneurysm mostly found

A

branches of the middle cerebral artery in hypertension, particularly the lenticulostriate

117
Q

Complications of capillary microaneurysm

A

primary hypertensive intracerebral haemorrhage in basal ganglia, cerebellum or brainstem

118
Q

What are mycotic aneurysms

A
  • weakening of the arterial wall due to bacterial or fungal infection (enter thru bloodstream)
  • commonest in cerebral arteries
  • bacterial endocarditis = most common underlying infection
119
Q

Hypertension definition

A

BP is more than 140/90 mmHg

120
Q

Stage 1 Hypertension

A

140/90 to 159/99 mmHg

subsequent ABPM daytime average or HBPM average ranging from 135/85 mmHg to 149/94 mmHg.

121
Q

Stage 2 Hypertension

A

160/100 to 179/119 mmHg

subsequent ABPM daytime average or HBPM average 150/95 mmHg or higher.

122
Q

Stage 3 Hypertension

A

> 180/120 mmHg

123
Q

Commonest consequence of hypertension

A

cardiac failure
atherosclerosis
cerebral haemorrhage

124
Q

Classification of hypertension

A

Essential or secondary

125
Q

Cause of primary hypertension

A

Multifactorial:

  • genetics, excessive sympathetic nervous activity
  • high salt intake & abnormal Na/K membrane transport
  • abnormal renin-angiotensin -aldosterone system
126
Q

Cause of secondary hypertension

A
  • *Renal disease**
  • chronic kidney disease, esp diabetes
  • renal artery stenosis, glomerulonephritis (less common) - negative cycle
  • *Endocrine causes**
  • adrenal tumors - cortical or medullary
  • cushing’s, conn’s
  • coarctation of aorta
  • drugs: corticosteroids, oral contraceptives
127
Q

Risk factors for hypertension

A
  • age
  • race - more common in blacks
  • fam hist
  • obese, lack of ex
  • smoking, alcohol, diabetes
  • salt in diet
  • stress
128
Q

Impact of hypertension on various systems

  • vascular
  • heart
  • nervous
  • kidney
A
  • *Vascular**:
  • thickening of media of arteries
  • accelerate atherosclerosis
  • endothelial cell dysfunction
  • *Heart**
  • increase risk for ischaemic heart disease
  • *Nervous**
  • intracerebral haemorrhage causing death
  • *Kidneys**
  • cause/result renal disease
  • kidney size reduced, intimal thickening & medial hypertrophy of small vessels
  • sclerotic glomeruli increased
129
Q

What is malignant hypertension

A

Markedly raised diastolic BP, usually >120 mmHg and progressive renal disease
Quite rare!

130
Q

Present malignant hypertension

A
  • Diastole > 120mmHg
  • Progressive renal disease
  • Can occur in previously fit individuals, often black males 30-40’s
  • Prominent renal vascular changes
  • Acute haemorrhage
  • Papilloedema (optic disk swelling caused by increased intercranial pressure)
131
Q

Consequences of malignant hypertension

A
  • cardiac failure with LV hypertrophy and dilatation
  • blurred vision due to papilloedema and retinal hae
  • haematuria and renal failure
  • severe headache and cerebral haemorrhage
132
Q

Briefly outline the Renin-Angiotensin-Aldosterone system?

A

Prorenin’s amino acid hinge, cleaved → Renin, through enzymatic cleavage of angiotensinogen → angiotensin I, through Angiotensin-Converting Enzyme (ACE) → Angiotensin II = vasoconstrictor, can induce hypertension

133
Q

What is ABPM

A

Ambulatory Blood Pressure Monitor

  • 24 hour BP monitoring and to calculate average BP
  • takes a measurement every 20 minutes during the day and less (hourly) during the night
  • used to confirm HT diagnosis for those with BP in between 140/90 mmHg and 180/120 mmHg
134
Q

What is HBPM

A

Home Blood Pressure Monitor

  • for patient to bring home and to calculate average BP
  • twice a day for 4-7 days
  • two reading per sit down, a minute apart
135
Q

Treatment goal and principles for hypertension

A

140/90 mmHg (150/90 mmHg in over 80’s) ± 5/5 for average

  • rarely is one med enough so stack step by step until goal is reached
  • based on if patient has DM and ethnicity & age; varied 1st & 2nd line then 2rd & 4th same
136
Q

1st & 2nd line treatment for

  • patient with Type 2 DM
  • Under 55 & No Type 2 DM
A
  1. ACE inhibitor or Angiotensin Receptor Blocker

2. Repeat (1) + CCB or thiazide like diuretic

137
Q

Treatment steps for

  • patient over 55, no DM
  • Black African / African Caribbean origin any age
A
  1. CCB

2. Repeat (1) + ACE inhibitor or thiazide like diuretic

138
Q

If 1st and 2nd line treatment fails for hypertension, next step would be …

A
  1. ACEi or ARB with CCB and diuretic
    (mind connecting words!)
  2. If resistant hypertension: confirm through A/HBPM, check postural hypertension and discuss adherence.
    Add:
    • low-dose spironolactone if blood potassium level is ≤4.5 mmol/l
    • alpha-blocker or beta-blocker if blood potassium level is >4.5 mmol/l
    Seek expert help if 4 drugs and still uncontrolled BP
139
Q

Examples of ACE inhibitors

A

Ramipril or Enalapril

Side effect cough!

140
Q

Main side effect of ACEi / Ramipril

A

cough (15%)

141
Q

if ACEi contraindicated or not tolerated, another choice as first line

A

Angiotensin Receptor Blocker (ARBi)

142
Q

Example of ARBi

A

Cadesartan or Losartan

143
Q

Example of Calcium Channel Blocker

A

Nifedipine or Amlodipine

Side effect oedema!

144
Q

Main side effect of CCB / amlodipine

A

oedema

145
Q

Example of diuretics

A

Bendroflumethiazide: thiazide (distal tube, less potent)
Furosemide: loop of henle diuretic, more potent
Indapamide:

146
Q

Example of beta blockers

A

bisoprolol or metoprolol

consider in young people esp if intolerant to ACEi or ARB

147
Q

What is the white coat effect?

A

a discrepancy of more than 20/10 mmHg between clinic and A/HBPM measurements. in 15-30% of people. tackle: use A/HBPM

148
Q

Where does the first heart sound come from?

A
  • mitral and tricuspid valve closure
149
Q

Where does the second heart sound come from

A
  • aortic and pulmonary valve closure
150
Q

When would there be a 3rd heart sound and what is it associated with?

A
  • early diastole during rapid ventricular filling
  • normal in children and pregnant women
  • associated with mitral regurg and heart failure
151
Q

When would there be a 4th heart sound and what is it associated with?

A
  • ‘gallop’, in late diastole
  • produced by blood being forced into a stiff hypertrophic ventricle
  • associated with left ventricular hypertrophy
152
Q

What is angina?

A

chest pain or discomfort as a result of reversible myocardial ischaemia

153
Q

Pathophysio angina

A

narrowing of one or more of coronary arteries due to
- atheroma / stenosis of coronary arteries thereby impairing blood flow
- valvular disease
aortic stenosis
arrhythmia
anaemia = thus less O2 transported
or ischaemic metabolites including adenosine stimulating nerve endings and producing pain

154
Q

risk factors for angina

A
  • smoking
  • obesity and umbrella: HP, DM, sedentary lifestyle, hypercholesterolaemia
  • age, family history, genetics
155
Q

Types of angina

A
  • Stable angina: induced by effort and relieved by rest
  • Unstable (crescendo) angina: angina or recent onset (less than 24 hours) / deterioration in previously stable angina & symptoms ar rest / angina with increasing freq & severity even at rest or minimal exertion = acute coronary syndrome!
  • Prinzmetal’s angina: caused by coronary artery spasm (rare)
156
Q

Presentation angina

A
  • central chest tightness or heaviness
  • provoked on exertion? after meal / cold windy weather / anger / excitement
  • relieved by rest? or GTN spray?
  • radiation of pain to arms? neck? jaw or teeth?
  • dyspnoea, nausea, sweatiness and faintness
157
Q

Angina scoring

A

Out of 3

  • Central, tight, radiation to arms, jaw & neck
  • precipitated by exertion
  • relieved by rest or GTN spray

Out of 3
3/3 = typical angina
2/3 = atypical pain
1/3 = non-anginal pain

158
Q

How would you diagnose angina

A

ECG

  • often normal
  • ST depression, flat or inverted T
  • look for signs of past MI

Treadmill / exercise ECG

  • trying to induce ischaemia
  • ST depression is late-stage ischaemia
  • bundle branch block not suitable

CT scan calcium scoring
- if atherosclerosis in the arteries then the calcium will light up white, if significant calcium then = angina

Catheterisation
SPECT / myoview = radio-labelled tracer injected into patient, take (light) up where good blood supply
- no light after exercise = myocardial ischaemia

159
Q

How would you diagnose angina

A

ECG

  • often normal
  • ST depression, flat or inverted T
  • look for signs of past MI

Treadmill / exercise ECG

  • trying to induce ischaemia
  • ST depression is late-stage ischaemia
  • bundle branch block not suitable

CT scan calcium scoring
- if atherosclerosis in the arteries then the calcium will light up white, if significant calcium then = angina

Catheterisation
SPECT / myoview = radio-labelled tracer injected into patient, take (light) up where good blood supply
- no light after exercise = myocardial ischaemia

160
Q

A treatment plan for angina

A
  • Treat active attacks PLUS anti-anginal drug PLUS drug for secondary prevention of cardiovascular disease
  • modify risk factors through lifestyle changes
  • treat underlying conditions
161
Q

1st line pharmacological PREVENTION for angina (2)

A

First line
Beta Blockers
- act on B1 receptors in the heart & reduce force of contraction of heart (heart rate, LV contractility, cardiac output)
→ bisoprolol & atenolol
- SE tiredness, nightmares, brady, erectile dysfunc & cold hands and feet
- CONTRAINDICATED asthma, heart failure/block, hypotension & bradyarrhythmias

Calcium Channel Blockers
- arterodilators: dilates systemic arteries resulting in BP drop, thus reduces
1) afterload on heart
2) energy required for same cardiac output
3) work on heart and O2 demand
→ verapamil
- CONTRAINDICATED BETA BLOCKER, AF, HEART BLOCK AND FAILURE, patient with MI history, LV dysfunc

162
Q

1st line pharmacological TREATMENT for angina (1)

A

Glyceryl Trinitrate (GTN) spray

  • used for active attacks
  • venodilator: dilates systemic veins thereby reducing venous return to right heart, also dilates coronary arteries
  • reduces preload thus work of heart and O2 demand
  • SE profuse headache immediately after use
163
Q

Differences between verapamil and amlodipine

A

both CCBs
Verapamil mainly acts on Ventricles and Amlodipine mainly acts on Arteries.

Amlodipine = dihydropyridines (DHP)

  • potent vasodilators
  • act mainly on vascular smooth muscle, relaxes them and dilates arteries
  • more dilating less depressing

Verapamil = non-DHP

  • acts mainly on the heart
  • potent myocardial depressants (inotropic)
  • depress cardiac contractility
  • depress conduction rate through SA node and slow AV node: useful for SVT, AF
  • more depressing less dilating
164
Q

Inotropic - meaning

A

modifying the force or speed of contraction of muscles

165
Q

2nd line for pharmacological PREVENTION of angina

A

a long-acting nitrate
- GTN is short acting
- Isosorbide mono/dinitrate dose
or

ivabradine [CI resting HR <70 bpm, preg, cardiac his] or

nicorandil or
[CI hypo, G6PD deficient, pulmonary oedema, heart failure (no cardiac MI! good to go]

ranolazine [CI renal or hepatic impairment]

166
Q

Supplementary drugs for PREVENTION of cardiac events (for angina)

A

Aspirin
- antiplatelet in coronary arteries (COX inhibitor: reduces prostaglandin synthesis) thereby reduces platelet thrombosis
→ salicylate

Statins

  • HMG-CoA reductase inhibitor - reduces cholesterol production by liver
  • reduce events and LDL cholesterol
  • anti-atherosclerotic
167
Q

Revascularising procedures for angina

A

= to restore patient coronary artery and increase flow reserve
= if medical fails or high risk disease identified

Percutaneous Coronary Intervention

  • dilating coronary atheromatous obstruction by inflating balloon with stent
  • expanding plaque = make artery bigger
  • less invasive, convinient, short recovery and repeatable
  • risk of stent thrombosis, not good for complex disease

Coronary Arter Bypass Graft (CABG)

  • Left Internal Mammary Atery used to bypass proximal stenosis (narrowing) in LAD artery
  • good prognosis, deals with complex disease
  • invasive, risk of stroke or bleeding, long recovery & one time

Phase 2A (12 decks)

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