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Year 6 > Cardio > Flashcards

Cardio Flashcards

1
Q

What ECG changes are associated with hyperkalaemia?

A

peaked or ‘tall-tented’ T waves (occurs first)
loss of P waves
broad QRS complexes
sinusoidal wave pattern

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2
Q

What are Stokes Adams attacks?

A

A sudden loss of consciousness, usually without warning and lasting for a few seconds, due to an abnormal heart rhythm (especially complete atrioventricular block).

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3
Q

What causes cannon A waves?

A

occur in conditions with atrioventricular dissociation and right atrial contraction against a closed tricuspid valve

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4
Q

How does pericarditis usually present?

A
  • pleuritic chest pain (sharp retrosternal pain caused by inflammation of te parietal pleura, aggravated by swallowing , coughing or deep inspiration)
  • pain improves on sitting and leaning forward
  • low grade intermittent fever
  • non-productive cough
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5
Q

What investigation findings are seen in pericarditis?

A

ECG changes: diffuse ST elevations and PR segment depression; T-wave inversion

Echo: effusion may be present, often normal

CXR: usually normal

WCC: leukocytosis

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6
Q

Management of acute pericarditis

A

often self-limiting

NSAID (with gsastroprotection)

can consider colchicine

consider prednisone

surgical management is pericariectomy

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7
Q

What is Dressler syndrome

A

post-myocardial infarction syndrome

occurring 2-10 weeks post MI without an infective cause

(thought to be due to circulating antibodies against cardiac muscle cells -> autoimmune aetiology -> immune complex deposition -> inflammation)

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8
Q

Differences in the shape of ST elevation in pericarditis and MI

A

concave upwards ST elevation is associated with pericarditis

convexity in ST elevation is seen in MI

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9
Q

What viruses commonly cause pericarditis?

A

Coxsackie B virus group

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10
Q

What bacteria can cause pericarditis?

is bacterial or viral more common

A

viral is more common (Coxsackie B)

Bacterial may be due to staphylococcus spp., streptococcus spp., M tuberculosis

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11
Q

What is Eisenmenger’s syndrome

A

reversal of a left-to-right shunt (associated with VSDs, ASD and a PDA)

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12
Q

Classification systems for aortic dissection

A

Stanford (type A and B)

DeBakey (I, II, III)

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13
Q

What is the anticoagulation of choice in patients with AF?

A

DOAC
- apixaban
- dagibatran
- edoxaban
- rivaroxaban

Warfarin is second line (where DOAC is contraindicated or not tolerated)

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14
Q

List the reversible causes of cardiac arrest

A

The 4 Hs and 4 Ts

Hypoxia
Hypovolaemia
Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
Hypothermia
(+heroin +hypoglycaemia)

Thrombosis (coronary or pulmonary)
Tension pneumothorax
Tamponade - cardiac
Toxins

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15
Q

Acute management of heart block

A

-IV loop diuretics (furosemide, bumetanide)

+/- oxygen (aim 94-98%)
+/- vasodilators (nitrates; main contraindication/SE is hypotension)
+/- CPAP if resp failure

in patients with hypotension:
- inotropic agents e.g. dobutamine
- vasopressors (e.g. norepinephrine)
- mechanical circulatory assistance (e.g. intra-aortic balloon counterpulsation or ventricular assist devices)

may need to stop b-blockers if:
- >50 bpm
- 2nd/3rd degree AV block
- shock

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16
Q

What type/location of MI most commonly predisposes you to AV block?

A

Inferior

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17
Q

What system is used in the classification of chronic heart failure?

A

NYHA classification

new york heart association classification

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18
Q

Duration of management of an unprovoked PE

A

6 months (DOAC e.g. rivaroxaban)

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19
Q

inheritance pattern of HOCM

A

AD

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20
Q

what classifications are used for aortic dissection?

A

Stanford

   (A and B)

DeBakey (I, II, IIIa, IIIb)

-> emergency surgery is needed in Stanford A and DeBakey I and II.

A(S) and I and II (D) affecting the ascending aorta.

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21
Q

Signs and sx of aortic dissection

A
  • sudden onset, severe pain, radiating to the chest/abdomen/back
  • tearing/ripping pain
  • anterior chest (ascending) or back (descending)
  • interscapular or retrosternal pain
  • asymmetrical BP and pulse readings on both sides
  • syncope
  • diaphoresis
  • confusion
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22
Q

Definition of aortic dissection

A
  • tear in the inner layer of the aorta that leads to a progressively growing hematoma in the intima-media space.
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23
Q

RFs for aortic dissection

A
  • HTN
  • age
  • smoking
  • people with connective tissue diseases may be affected at a younger age (30-50) as opposed to 60-80
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24
Q

Investigations for ?aortic dissection

A
  • obs (incl. bilateral pulse and BP)
  • ECG
  • CXR (often normal but can have widened mediastinum)
  • CT angio (may see double lumen) - in stable patients
  • MRA
  • Transoesophageal Echo (in unstable patients or in renal insufficiency/contrast allergy)
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25
Q

Management of aortic dissection

A

If Stanford A / DeBakey I or II -> IMMEDIATE SURGERY
- open surgery
- endovascular treatment (only in type B dissections and if the open operative risk is too high)

Otherwise treat conservatively, unless complications occur.

Medical Therapy:
- if hypotensive: aim MAP 70 or euvolaemia with IV fluids +/- vasopressor support; AVOID INOTROPES as they can worsen aortic wall stress
- Hypertensive: BP control! srart with IV beta blocker followed by vasodlator)
- supportive care: pain management (morphine)

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26
Q

complications of aortic dissection

A
  • aortic rupture, acute blood loss, shock -> EMERGENCY SURGERY

Type A complications
- MI
- aortic regurg
- cardiac tamponade progressing to cardiogenic shock
- stroke

Complications of type A and type B
- arterial occlusion followed by ischemia of the
-> renal arteries -> AKI
-> spinal arteries -> weakness of the lower extremities due to paraplegia

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27
Q

What can you see on CTA/MRA in aortic dissection?

A

double lumen

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28
Q

Beck’s triad of cardiac tamponade

A

Hypotension
Muffled heart sounds
Raised JVP

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29
Q

what are the pros and cons of bioprosthetic and mechanical heart valves?

A

bioprosthetic
- higher failure rate (structural deterioration and calcification)
+ don’t usually require anticoagulation (if needed, they get warfarin for 3 months and then long term low dose aspirin)

mechanic
+ low failure rate
- increased risk of thrombosis -> require long-term anticoagulation with warfarin

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30
Q

Where do bioprosthetic heart valves commonly come from?

A

porcine and bovine

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31
Q

target INR for aortic and mitral valves in mechanical valve replacement

A

aortic: 3.0
mitral: 3.5

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32
Q

What is the most common cause of death in patients following a myocardial infarction?

A

ventricular fibrillation

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33
Q

During what part of the cardiac cycle is the heart perfused?

A

diastole

(during systole the blood is sent to the rest of the body)

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34
Q

Law of flow in relation to radius

A

Poiseuille’s Law

flow is proportional to r^4

(halving radius would decrease the flow 16x)

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35
Q

main features of angina

A
  • central (crushing) pain / constricting discomfort in the front of the chest or in neck, shoulder or arm
  • precipitated by physical exertion
  • relieved by rest or nitrates within 5 minutes
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36
Q

Ix in people with stable angina to assess risk

A
  • bloods: fasting glucose, HbA1c, lipid profile, thyroid function
  • resting and ambulatory ECG
  • resting Echo

-> higher risk and worse sx flavour functional testing +/- invasive angiography

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37
Q

MoA of dobutamine

A

beta 1 agonist

(enhances cardiac contractility etc.)

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38
Q

how is a stress echo done?

A

it is a functional test

after exercise or giving someone dobutamine before (beta 1 agonist)

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39
Q

what is the first line Mx of stable angina?

A

non-dihydropyridine CCB e.g. dilitazem

or BB

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40
Q

What should all patients with stable angina be prescribed?

A

aspirin with PPI
statin

GTN

BB or non-DHP CCB

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41
Q

2nd line meds for stable angina?

A

long acting nitrates

ivabradine
ranolazine
nicorandil

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42
Q

name of syndrome of pericarditis following MI

A

Dressler syndrome

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43
Q

Causes of pericarditis

A

infection (viral e.g. coxsackie, TB)
malignancy
connective tissue (RA, SLE)
Dressler’s syndrome
uraemia

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44
Q

Mx of pericarditis

A

1st line: NSAIDs + colchicine
2ns: add steroids
3rd: azathioprine

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45
Q

Where on the leg would you find a scar from a CABG procedure?

A

saphenous vein runs medially, therefore the scar for a CABG would be on the medial aspect of the leg/calf

Keep in mind thata now often the LIMA is used for CABG.

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46
Q

indication for a CABG

A

multi vessel CAD
angina not responding to optimal medical management

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47
Q

CABG - where can you get the graft from?

A

arterial graft harvesting in the arm
venous graft harvesting from the leg

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48
Q

What do you want to know in someone who had an MI?

A

What happened when the MI occurred?
What were the consequences of the MI
How is the MI being treated

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49
Q

Wellen syndrome

A

critical stenosis of LAD
-> high risk of anterior wall MI within the next days/weeks

pts pain might have resolved at the time of presentation and cardiac enzymes may be normal or minimally elevated

-> management: admission and coronary intervention

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50
Q

ECG findings in Wellen syndrome

A
  • biphasic or deep T wave inversion in V2-V3
  • minimal ST elevation
  • no Q waves
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51
Q

SA & AV nodes - what do they do?

A

SA node: impulse initiation issues
AV node: impulse propagation

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52
Q

commonest cause of ventricular arrythmia

A

ischaemic heart disease

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53
Q

commonest cause of SA node dysfunction

A

age

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54
Q

sick sinus syndrome

A

Sinus node dysfunction

= an abnormality in sinus node acrion potential generationor conduction

causes:
- intrinstic (SA node fibrosis/degeneration/ischaemia
- extrinsic (hypothyroidism, negative chronotropes)

pts present with signs and symtpoms of end-organ hypoperfusion due to bradycardia (fatigue, dyspnoea, SOBOE), +/- Stokes Adams attacks

tachycardia bradycardia syndrome is a subtype of SND with an increased risk of cardiovascular events and mortality

Dx: ECG and stress test

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55
Q

what is a junctional rhythm?

A

rhythm coming from the AV node or below

this will be at a lower rate

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56
Q

What is a 3rd-degree heart block?

A

completeheart block

no conduction between atria and ventricles

P waves and QRS have thor own rhythms but bear no relationship to each other

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57
Q

Management of a symptomatic 2nd degree type 2 heart block?

A

follow the adult bradycardia algorithm

you are worried about 2nd degree type 2 ad a type 3 AV block - they are dangerous rhythms
- high risk of systole (if it occurs with with end organ dysfunction e.g. syncope, a pacemaker is likely needed)

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58
Q

indication for insertion of a pacemaker in heart block

A

end-organ dysfunction

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59
Q

AVNRT management

A

unstable -> synchronised shock

stable ->

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60
Q

why synchronised shock in AVNRT?

A

the point of synchronisation is for it to occur on the R

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61
Q

where is the defect in atrial fibrillation?

A

pulmonary veins

bulk of the impulse formation in AF is in pulmonary veins
they take over

in advanced AF the pulmonary veins are ablated

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62
Q

how does flecainide work

A

blocks sodium channels (Ic)

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63
Q

classification of anti-arrhythmic drugs

A

Vaughan Williams

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64
Q

mx of a >48 h of AF

A

anticoagulation (based on CHADSVASC and ORBIT score)

Rate/ rhythm control

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65
Q

LAA

A

left atrial appendage
AF predisposes towards LAA thrombus formation which may result in embolic stroke

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66
Q

CO formula

A

HR x SV

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67
Q

bumetanide MoA

A

loop diuretic

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68
Q

dapaglifozin MoA

A

SGLT2i

inhibits proximal sodium and glucose reabsorption

-> glycosuric and natriuretic agent

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69
Q

Which medications do you give in HF?

A

ACE inhibitor
BB

then
MC receptor antagonist

then
dapaglifozin

any congestion -> diuretics
NYHA… -> Entresto
fluid restriction is not recommended by NICE

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70
Q

Why does CPAP work in heart failure?

A

alveoli collapse on themselves because of the water in them
CPAP forces air in the alveoli
CPAP also increases intrathoracic pressure which decreases venous return

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71
Q

management of acute heart failure

A

loop diuretics (ideally continuous) with output monitoring
CPAP if acute pulm oedema and dyspnea
hemofiltration only if

Don’t give morphine
Don’t give beta blockers
nitrates show no improvement in mortality (they don’t cause harm, only advised by NICE in severe HTN/evidence of myocardial iscemia)

C

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72
Q

What does PCI stand for?

A

percutaneous coronary intervention

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73
Q

What are the valves of the heart and how to remember them?

A

RTP
(RA -> tricuspid -> pulmonary artery)

LMA
(LA -> mitral/bicuspid -> aorta)

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73
Q

List the layers of the heart from innermost to outermost

A

endocardium (1 cell thick)
myocardium
visceral pericardium
parietal pericardium
fibrous pericardium

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74
Q

What are the main coronary vessels?

A

RCA (right coronary artery)
LCx (left circumflex)
LAD (left anterior descending)

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75
Q

where is the coronary sinus and where does it drain?

A

sinus itself is situated within the atrioventricular groove on the posterior surface of the heart between the left atrium and ventricle.

drains blood from coronary veins into the right atrium via the coronary sinus orfice

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76
Q

Summarise the Frank Sterling relationship

A

filling of the heart increases the force of contraction

increased diastolic fibre length increases ventricular contraction

ventricles pump greater SV so that, at equilibrium, CO exactly balances the augmented venous return

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77
Q

What is the law of LaPlace?

A

when the pressure within a cylinder is held constant, the tension on its walk increases with increasing radius (T = P x R)

T = (PxR)/h -> when incorporating wall thickness

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78
Q

What are the molecular steps that occur during contraction of the heart?

A
  1. SA node depolatises
  2. AP travels down T-tubules
  3. Ca2+ enters cell
  4. Ca2+ binds to Ryanodine receptor (RyR)
  5. Ca2+ enters cytoplasm from sarcoplastic reticulum (calcium mediated calcium release)
  6. Ca2+ binds to troponin C (leads to conformational changes of troponin I tropomyosin -> opens cross bridge binding sites)
  7. Myosin heads bind to actin
  8. Muscle fibres shorten
  9. Sarcoplasmic endoreticular calcium pump brings Ca2+ back into the sarcoplasmic reticulum for relaxation
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79
Q

What medications can you use for rhythm control in AF?

A

beta blocker (bisoprolol is commonest)
CCB (has to be a rate limiting one, e.g. dilitazem)

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80
Q

b blocker in HF?

A

bisoprolol
xx
ca..olol

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81
Q

What patients would you not give a beta blocker to for rate control? what is the alternative?

A

asthma

can give CCB that rate controls, e.g. dilitazem

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82
Q

How will you assess stroke risk in AF?

A

Chadvasc
ORBIT score
valvular/non-valvular disease
DOAC vs warfarin

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83
Q

what is the ORBIT score for?

A

bleeding risk

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84
Q

what is the biggest risk of AF?

A

stroke

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85
Q

Does DOAC vs warfarin make a difference in valvular disease?

A

in valvular heart disease use warfarin, not DOAC

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86
Q

examples of DOACs

A

apixaban
rivaroxaban
etc

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87
Q

Cardioversion types

A

electrical (DC cardioversion)
pharmacological (e.g. flecainide, sotolol -> these can be CI’d in structural heart disease, then you would have to do electrica lcardioversion)

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88
Q

what medications can be used for pharmacological cardioversion?

A

flecainide
more

89
Q

what is a contraindication for pharmacological cardioversion?

A

structural heart disease

90
Q

reasons to give warfarin rather than DOAC in AF

A

valve disease (esp metallic valve)
antiphospholipid syndrome
severe renal failure (CrCl too low to give DOAC)

91
Q

what is the scoring system to assess bleeding risk

A

ORBIT has now ‘replaced’ HASBLED

92
Q

Is high or low output HF more common?

A

low-output is much more common

refers to cardiac output

93
Q

What is high output cardiac failure?

A

heart is producing normal cardiac output but there is an increase in peripheral metabolic demands that the heart is unable to meet

94
Q

What adverse features of SVT indicate the need of management with synchronised DC shock?

A

HISS

HF
ischaemia
shock
syncope

95
Q

What is the underlying pathology in Brugada syndrome?

A

it is a sodium channelopathy

it predisposes individuals to dangerous arrhythmias and sudden cardiac death

96
Q

inheritance pattern of brugada syndrome

A

AD

97
Q

intractable angina

A

chronic angina that does not respond to medical / surgical intervention

98
Q

What % of pts with stent will come back with angina?

A

30% of pts with stent for angina come back with angina

99
Q

prinzmetal angina

A

Vasospasticangina

caused by transient coronary spasms

not affected by exertion

typically occurs early in the morning

cigarette smoking and the use of stimulants (cocaine, amphetsmines, alcohol, or triptans, stress, exposire to cold, hyperventilation

-> common atherosclerotic RFs do not apply to vasospastic angina

100
Q

MPS

A

myocardial perfusion scan

101
Q

Nicorandil drug class and how it works

A

vasodilator

depolarises SM cells by increasing influx

(K+ channel inhibitor)

102
Q

How to choose anti-anginal therapy?

A

?comorbidities
?asthma -> no beta block

103
Q

treatment options for angina

A

b-blocker
CCB
nitrates (1st line = short acting nitrate spray)
nicorandil
ivabridine
rinolaazione
trimetazadime

104
Q

Summarise NYHA classification

A

NYHA 0: no limitations in ordinary physical activities

NYHA I: mild limitations in physical activity, only in strenuous activities

NYHA II: slight limitation in their ability to perform regular physical activities. Comfortable at rest but may experience fatigue, palpitations, or dyspnea during ordinary activities.

NYHA III: marked limitations in their ability to carry out normal physical activities. They are comfortable at rest but experience significant symptoms with less-than-ordinary exertion.

NYHA IV: discomfort even at rest

105
Q

What ECG can you do to visualise posterior heart?

A

16 lead ECG

106
Q

what information is on the axes of ECG?

A

X - time
Y - voltage (10mm = 1mV)

107
Q

trick to estimate HR on ECG

A

1 - 300 bpm
2 - 150 bpm
3 - 100 bpm
4 - 75 bpm
5 - 60 bpm
6 - 50 bpm

-> count big boxes between QRS

108
Q

normal PR interval

A

<0.2 s

if prolonged: conduction system problem or structural problem

109
Q

where is the PR interval measured?

A

beginning of the P wave to the beginning of the QRS complex

110
Q

types of av block

A

I - prolonged PRi, no dropped QRS

II Mobitz 1: longer longer drops

II Mobitz 2: ratio

III: complete heart block

111
Q

Heart block remember story

A
112
Q

reasons for prolonged QRS

A

bundle branch block
iatrogenic (meds)
dilated heart condition

113
Q

what happens in ECG in hyperetrophy?

A

higher voltage because more cells contract and generate a signal

114
Q

QRS normal duration

A

<0.12 seconds

115
Q

is T wave always upright?

A

T-wave should correspond to the dominant deflection of the QRS complex.

116
Q

why tTTTwave in hyperkalaemia?

A

K+ gets into cell
during repolarisation gets into cell
if high K+, more K+ goes into cell and therefore causes a higher voltage and a bigger T-wave

117
Q

Why can you not see T wave in SVT?

A
118
Q

Sinus tachycardia vs SVT

A

SVT faster (150-250 bpm) compared with ST (100-150)

P wave and T wave are together in SVT (in ST you can see T wave)

119
Q

is SVT always regular?

A

yes

120
Q

types of atrial arrythmia

A

AF
atrial flutter

121
Q

ECG findings in atrial arrythmia

A

P wave disappeared and replaced by F-wave in atrial flutterer f-wave in AF

R-R can be regular or irregular

QRSS wave usually normal

122
Q

difference between atrial

A

AF is faster and irregular

atrial flutter is slower and regular, ventricles can still catch up

In flutter the R-R interval is regular

123
Q

What causes atrial arrythmia?

A
124
Q

Ventricular arrythmia types

A

VT
Vf
VF (most dangerous)

125
Q

classes of arrythmia

A

sinus
atrial
ventricular

?more

126
Q

Key features of ventricular arrythmia?

A

wider QRS complex
rapid regular/irregular PR interval

127
Q

HR in different ventricular arrythmias

A

VT 120-250
Vf 200-250
VF 200-500

128
Q

how to check if ECG leads were placed correctly/

A

AVR should be negative (

129
Q

how to estimate axis deviation

A

I and III up = normal

I up and III down = left axis (because L arm is up)

I down and III up - right axis dev because R arm is up

130
Q

which leads to look at to compare to voltage and check for hypertrophy

A

V4 and V5

check for

131
Q

What is ‘holiday heart’?

A

quite common
experience palpitations following ingestion of alcohol

spontaneous AF which resolved spontaneously

if asymptomatic f/u in 1week (and safety net)

132
Q

CHADSVASC score cut off for anticoag

A

2

133
Q

pathophys of holiday heart

A

alcohol is poison for myocardium and can cause issues with conduction

alcohol causes tachy and will have an effect on condition system

134
Q

normal range for PR interval

A

120-200 ms

135
Q

normal ECG variants in athletes

A
  • sinus bradycardia
  • junctional rhythm
  • first degree heart block
  • Mobitz type 1 (Wenckebach phenomenon)
136
Q

management of torsades de pointes

A

haemodynamically stable: IV Magnesium sulfate

haemodynamically unstable: Defibrillation and CPR

137
Q

What is the complication of torsadess de pointes?

A

can progress to life-threatening ventricular fibrillation

138
Q

NSTEMI antiplatelet choice

A
  • aspirin, plus either:
  • ticagrelor, if not high bleeding risk
  • clopidogrel, if high bleeding risk
139
Q

What is cor pulmonale?

A

RHF that develops secondary to chronic lung diseases

140
Q

What are the 5 types of PH?

A
  • type 1: pulmonary arterial HTN
  • type 2: left heart disease / post capillary PH
  • type 3: chronic lung disease / hypoxia
  • type 4: pulmonary artery obstruction (CTEPH - chronic thromboembolic PH)
  • type 5: unclear multifactorial / miscellaneous PH
141
Q

PAH causes/types?

A

congenital heart diesase
connective tissue disease
idiopathic PAH

liver disease
HIv infection
drugs and toxins

142
Q

Is PAH more common in males or females?

A

PAH is more common in females

143
Q

components of risk stratification in PAH

A

6 min walk test
BNP
WHO functional class

144
Q

when do you see a collapsing pulse?

A

aortic regurgitation

145
Q

contraindications for treatment with warfarin

A

peptic ulcer disease
bleeding d/o
severe HTN
pregnancy (teratogenic)

145
Q

causes of AR

A
  • acute (primarily caused by bacterial endocarditis or aortic dissection)
  • chronic (e.g., due to a congenital bicuspid valve or rheumatic fever)
146
Q

presentation of AR

A
  • acute -> CV collapse (AR leads to rapid deterioration of LV function with subsequent pulmonary edema and cardiac decompensation).
  • Chronic AR -> fatigue and exertional dyspnoea (may remain compensated for a long period of time, becoming symptomatic only when left heart failure develops -> SOB, reduced exercise tolerance, fatigue, exertion dyspnoea)
147
Q

O/E in AR

A
  • Auscultation: S3 and a high-pitched, decrescendo early diastolic murmur.
  • widened pulse pressure
  • Echocardiography is the most important diagnostic tool, both for confirming the diagnosis and determining the severity of disease
148
Q

Mx of aortic regurgitation

A
  • asymptomatic: conservative treatment consists of symptom management and physical activity as tolerated.
  • Symptomatic patients or those with severely reduced LV function require surgical intervention, most commonly aortic valve replacement.
149
Q

indications for pacemaker

A
  • severe heart failure (ejection fraction <35%) not responding to medication
  • complete AV block
  • Mobitz type 2 AV block
  • symptomatic bradycardia
  • symptomatic sick sinus syndrome
  • drug-resistant tachyarrhythmias.
150
Q

When can you use unsynchronised DC cardioversion?

A

Unsynchronised electrical cardioversion is reserved for ALS only, as the R-on-T phenomenon does not apply to ventricular tachyarrhythmias(??surerly there are some tachyarrythmias) i.e. pulseless ventricular tachycardia or ventricular fibrillation

150
Q

R-on-T phenomenon

A

superimposition of the ectopic beat from the cardioversion on the T-wave of the preceding beat generated by the patient’s heart. This can result in sustained ventricular tachyarrhythmias which are dangerous and potentially fatal.

151
Q

CXR findings of pulmonary HTN

A

dilated pulmonary trunk
enlarged heart

…

152
Q

Wheat are the key differences between the RV and LV?

A
  • embryologically different origin
  • shape: LV is round, RV is crescent shaped cavity
153
Q

Outline the management of stable angina

A
  • lifestyle
  • refer to cardio

Medical
- immediate sx relief: GTN spray (vasodilates)
- sx prevention (BB or CCB (or both), or medication prescribed by specialist - long acting nitrates (e.g. ISMN), ivabradine, nicorandil, ranolazine.
- secondary prevention (4As)
Aspirin 75mg OD
Atorvastatin 80mg OD
Atenolol (reminder that BB should be given)
ACEi

surgical -> PCI with coronary angioplasty (stent insertion) or CABG (offered to patients with severe stenosis)

154
Q

What dose of atorvastatin and aspirin in stable angina?

A

80 mg atorvastatin

75mg aspirin

155
Q

which leg vessel is usually used for CABG

A

great saphenous vein

(-> scar would be along the inner calf)

156
Q

Atorvastatin dose for secondary and primary prevention

A

80 mg for secondary

20 mg for primary prevention

157
Q

What type of medication is dagibatran?

A

anticoagulant

158
Q

What is the reversal agent for dagibatran?

A

idarucizumab

-> binds to and inactivates dabigatran and its metabolites.

Its use should be considered in patients with symptomatic intracranial bleeding or uncontrolled bleeding with haemodynamic instability.

159
Q

How long after MI can pt drive?

A

1 week if successful angioplasty

4w If unsuccessful angioplasty or if no angioplasty

160
Q

ventricular aneurysms post MI timeline

A

3-14 days?

up to 12 months post MI

  • double check
161
Q

dressers timeline post MI

A

4-6 weeks post infarct

double check

162
Q

Indication for CABG

A

chronic stable angina in the presence of optimal medical therapy (no prognostic benefit, only improves symptoms)

NSTEMI not responding to medical therapy -> either PCI or CABG (there is prognostic benefit in the acute setting)

163
Q

rate control in asthmatics

A

Verapamil

164
Q

TAVI vs AV replacement

A

in younger patients, you would go for a valve replacement because of longevity
-> still probably best definitive treatment

often TAVI is now used more (avoid bypass, similar outcomes)
historically it was only for older more frail patients.

165
Q

How do you rule out acute AD in a patient with an NSTEMI?

A

take a very careful history

CXR and urgent CT scan if you are worried

giving thrombolytic therapy or anticoagulant would be detrimental so if unsure -> imaging

166
Q

2 commonest causes of an absent left radial

A
  • AV fistula
  • radial artery harvested for bypass / CABG
167
Q

What are the causes of atrial stenosis?

A
  • age (calcification0
  • congenital bicuspid aortic valve
  • rheumatic heart disease
  • supravalvular stenosis
168
Q

what are ECG variants in athletes?

A
  • sinus bradycardia
  • junctional rhythm
  • first degree heart block
  • Mobitz type 1 (Wenckebach phenomenon)
169
Q

What is the normal duration of PR interval?

A

<200 ms

170
Q

What is classed as severe hypertension?

A

> 180/120 mmHg

171
Q

should you do a CXR in a patient with ?PE?

A

yes

it would not diagnose a PE

HOWEVER
it will help exclude differential diagnoses like a pneumothorax or a pleural effusion

172
Q

Kussmaul’s sign

A

JVP rises on inspiration

seen in constrictive pericarditis

173
Q

Digoxin or verapamil in angina?

A

verapamil

digoxin is more for arrythmia

174
Q

HTN not controlled on ACEi, CCB and thiazide like diuretic. What next?

A

K+ >4.5 -> alpha or beta blocker

If K+ < 4.5mmol/L or lower spironolactone would be the preferred 4th-line antihypertensive.

175
Q

NSTEMI antiplatelet choice

A

aspirin, plus either:
- ticagrelor, if not high bleeding risk
- clopidogrel, if high bleeding risk

176
Q

What are the 5 subtypes of pulm HTN?

A

1: pulomonary arterial hypertension (most idiopathic)

2: due to left heart disease

3: due to chronic lung disease

4: due to pulmonary artery occlusion (e.g. CTEPH)

5: mixed/unclear multifactorial mechanisms

177
Q

Causes of type 1 Pulmonary HTN

A
  • Idiopathic
  • Hereditary (e.g., BMPR2 loss-of-function mutation); Encodes a set of inhibitors of vascular smooth muscle cell proliferation -> Associated with a poor prognosis
  • Drug-induced: Methamphetamine, amiodarone (and possibly amphetamines and cocaine)
  • Associated conditions
    • Connective tissue diseases (e.g. systemic sclerosis, SLE)
    • Portopulmonary hypertension
    • Congenital heart disease (e.g., left-to-right shunt
    • HIV infection
    • Schistosomiasis
178
Q

Sx of pulmonary HTN

A
  • dyspnoea (on exertion)
  • CP or chest pressure
  • dizziness
  • syncope/fainting
  • tiredness
  • sx of underlying cause
179
Q

Common finding in pulmonary HTN

A

raised JVP

180
Q

Ix in pulm hypertension and the findings

A
  • Transthoracic Echo (1st line! to identify markers of pulm htn and estimate pressures. also looks at RV being affected)
  • cardiac catheterisation (R heart catheterisation is the confirmatory test)
  • ECG (may show R axis deviation)
  • CXR (R heart hypertrophy = prominent R heart border; enlarged central pulmonary arteries)
  • lung function tests can be used to assess for chronic lung disease e.g. COPD
181
Q

What are the causes of Type 1 pulmonary hypertension? (PAH)

A

Most idiopathic!

  1. Genetic
    (BMPR2 is the commonest mutation, in 75%)
  2. drugs/toxins
    (e.g. amiodarone, methamphetamines, possibly amphetamines and cocaine)
  3. underlying disease
    (e.g. connective tissue disease like SLE or systemic sclerosis; HIV; schistosomiasis; portopulmonary HTN; congenital heart disease.g L->R shunt)
182
Q

What pressure do you have in pulmonary HTN?

A

> 20 mmHg at rest

183
Q

Mx of pulmonary HTN

A

MDT approach

  1. manage the underlying cause

for primary consider:
- anticoagulants
- CCB (1st line pulmonary vasodilator)
- phosphodiesterase inhibitor SILDENAFIL (promotes pulmonary smooth muscle relaxation) reducing pulm HTN
- prostacyclin analogues (e.g. ILOPROST)
- endothelial receptor antagonist (bosentan) -> blocks vasoconstriction, teratogenic

184
Q

What is cor pulmonale?

A

Altered structure (i.e., hypertrophy, dilation) or impaired function of the right ventricle due to pulmonary hypertension resulting from a primary disorder of the respiratory or pulmonary artery system

185
Q

What are the complications of pulmonary hypertension?

A

right heart failure
arrhythmias (AF, VT, VF)
sudden death

186
Q

What group of people is affected by pulmonary HTN?

A

young females

187
Q

What is the pathophysiology of group 2 pulmonary hypertension?

A
  • LV failure
  • blood backs up in the lungs causing increased pressure in the lung circulation
  • you also get pulmonary oedema as fluid leaks into the alveoli
188
Q

Causes of group 5 (mixed/multifactorial) pulm HTN

A

Hematologic disorders
Systemic disorders
Metabolic disorders

189
Q

What is the pathophysiology of group 3 pulmonary hypertension?

A
  • in hypoxia, you get vasoconstriction of pulmonary vessels to shunt blood to better ventilated areas of the lungs.
  • This causes increased pulmonary pressures

in conditions like COPD there is also an inflammatory component to this.

190
Q

Define aortic regurgitation

A

reflux of blood from the aorta into the LV during diastole

191
Q

What causes aortic regurgitation?

A

Valve leaflet issues:
- bicuspid aortic valve
- rheumatic fever
- infective endocarditis
- trauma

aortic root/ascendign aorta dilation:
- systemic HTN
- aortic dissection
- aortitis (syphilis, Takayasu’s arteritis)
- Marfan’s syndrome
- arthritides (RA, sero -ve arthritidies)
- Ehler Danlos syndrome
- osteogenesis imperfecta
- pseudoxanthoma elasticum

192
Q

What are the complications of AR?

A

LV failure
pulmonary oedema

193
Q

name 2 causes of acute AR

A
  • aortic dissection
  • IE

acute AR is a surgical emergency!

194
Q

What happens to the end diastolic volume in AR?

A

increases because blood leaks from aorta into the LV during ventricular diastole

195
Q

Sx of acute and chronic AR

A

acute: severe dyspnoea, CP, hypotension (sudden cardiovascular collapse -> surgical emergency)

chronic AR: asymptomatic initially; then exertional dyspnoea, orthopnoea, fatigue, +/- angina

196
Q

Examination findings in AR

A
  • soft early diastolic murmur, 2nd ICS R sternal edge (best on expiration and leaning forwards)
  • Austin flint murmur (mid diastolic)
  • wide pulse pressure
  • collapsing water hammer pulse
197
Q

Eponymous signs of AR

A
  • Quincke’s sign: pulsation of nail bed
  • deMusset’s sign: head nodding in time with pulse
  • Corrigan’s sign: visible pulsations in the neck
  • Mueller sign: visible pulsation of the uvula
  • Traube sign: pistol shot (systolic and diastolic sounds) on auscultation of the femoral arteries.
  • Becker’s sign: visible pulsations of the pupils and retinal arteries
  • Duroziez sign: systolic and diastolic bruit heard on partial compression of the femoral artery with the stethoscope
  • Rosenbach sign: systolic pulsations of the liver
  • Gerhard sign: systolic pulsations of the spleen
  • Hill’s sign: popliteal cuff systolic pressure exceeding brachial pressure by >60 mmHg
198
Q

Mx of acute AR

A

surgical emergency

inotropes
vasodilators
urgent aortic valve replacement/repair

199
Q

Mx of chronic AR

A

surgical candidate:
aortic valve surgery (replacement/repar)

non-surgical candidate:
-> guideline directed medicatltherapy (e.g. vasodilators like nifedipine or ACEi)
OR
-> transcatheteric aortic valve implantation (TAVI)

200
Q

Ix in ?AR

A

CXR: enlarged LV, cardiomegaly, dilation of the ascending aorta (+/- pulmonary oedema with LHF)

Echo: diagnostic. Useful for assessing severity.

201
Q

Define AS

A

narrowing of the LV outflow at the level of the aortic valve

202
Q

Causes of AS

A
  • senile calcifications and degeneration
  • calcification of a congenital bicuspid aortic valve
  • rheumatic heart disease (commonest worldwide)
  • IE is also a cause
203
Q

What is the commonest cause of AS worldwide?

A

rheumatic heart disease

204
Q

Sx of aortic stenosis

A

initially asymptomatic

angina (increased O2 demand in the hypertrophied ventricles)
syncope or dizziness on exercise
HF sx (e.g. SOB)

205
Q

How does AS cause LHF?

A

narrowed opening of the AV in systole -> obstruction to BF from LV -> increased LV pressure -> LV concentric hypertrophy -> increased O2 demand + impaired ventricular filling during diastole -> LHF

206
Q

Clinical features of AS O/E

A
  • narrow pulse pressure
  • weak and delayed distal pulse (pulsus parvus et tardus)
  • harsh crescendo-decrescendo late systolic ejection murmur that radiates to the carotids and apex. louder on expiration.
  • soft or absent S2
  • S4 best heard at the apex
  • bicuspid valve may cause ejection click
207
Q

how to differentiate between AS and hypertrophic cardiomyopathy on auscultation?

A

valsalva and standing from squatting decreases or does not change intensity of murmur in contract to hypertrophic cardiomyopathy

both have a systolic murmur

208
Q

Signs of AS on ECG

A
  • signs of LV hypertrophy
  • LBBB
209
Q

Ix in AS

A

echo
CXR (to assess for pulm oedema)
ECG (may show LV hypertrophy or LBBB)
Cardiac angiography(to assess for other causes of angina)

210
Q

Mx of As

A

surgical mx unless contraindicated

-> AVR (aortic valve replacement) and repair
- surgical AVR
- transcatheter AVR
- percutaneous balloon valvuloplasty

medical: manage LVF (ACEi, vasodilators); abx prophylaxis against IE)

211
Q

complications of balloon valvoplasty in A S

A
  • MI
  • myocardial perforation
  • severe AR
212
Q

Difference AS and aortic sclerosis on auscultation and O/E

A

in sclerosis:

  • senile degeneration with no LV outflow tract obstruction
  • normal pulse character
  • no thrill palpable
  • ejection systolic murmur radiates only faintly
  • S2 normal
213
Q

Complications of AS

A
  • arrhythmias
  • stokes-Adams attacks
  • MI
  • LHF
  • sudden death
214
Q

RCA - which leads?

A

II, III, aVF

215
Q

What leads would you expect to see ST elevation in an MI with arrythmia and AV block?

A

II, III and aVF

this would be an inferior MI supplied by the RCA which also supplies the AV node

216
Q

In which condition do you see pulsus paradoxus?

A

cardiac tamponade

can also be seen in severe asthma

217
Q

what is pulsus paradoxus?

A

phenomenon where BP decreases by more than 10 mmHg during inspiration (-> faint or absent pulse on inspiration)

218
Q

What is Brugada syndrome?

A
  • inherited (AD) cardiovascular disease
  • channelopathy
  • pts present with sudden cardiac death
219
Q

Mx of Brugada syndrome

A

implantable cardiac defibrillator

Year 6 (37 decks)

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