Cardio Flashcards

1
Q

What happens in atherogenesis?

A

Damage to endothelial cells → endothelium secretes chemoattractants → leukocytes migrate and accumulate in intima → foam cells/macrophages/T-lymphocytes form fatty streaks → foam cells rupture, releasing lipids + SMC migrate from media to intima → dense, fibrous cap w necrotic core formed
This plaque can partially occlude the lumen → blood flood is restricted → ischemia
Plaque can rupture → thrombus formed →lumen is fully occluded → infarction

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2
Q

Which arteries does atherogenesis affect most commonly?

A

LAD, circumflex, RCA

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3
Q

What are the risk factors for IHD?

A

age
smoking
obesity, high serum cholesterol
diabetes
hypertension
family history
M>F

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4
Q

What is IHD?

A

cardiac myocyte damage (and eventual death) due to insufficient oxygen-rich blood
in ascending order of severity: stable angina> unstable angina > NSTEMI > STEMI
can be due to increased myocardial workload + coronary artery occlusion OR due to insufficient oxygen-rich blood supply
main causes: atheroma, valvular disease (aortic stenosis), anaemia (demand & supply)

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5
Q

What is angina?

A

Angina is the result of myocardial ischaemia, where blood supply < metabolic demand

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6
Q

What is stable angina?

A

chest pain precipitated by exposure to cold/exercise

lasts 1-5 minutes

relieved by rest/GTN spray
radiation of pain
induced by exertion
relieved by rest/GTN spray

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7
Q

What is unstable angina/stemi/nstemi?

A

chest pain at rest

prolonged, >20 minutes

no relief by rest/GTN spray
NSTEMI, STEMI: increase in troponin, myoglobin, CK levels

STEMI: ST-elevations on ECG

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8
Q

What is prinzmetal’s angina?

A

caused by coronary artery spasms; occur at rest/night

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9
Q

What are the symptoms of IHD?

A

chest pain: discomfort, heaviness, squeezing, burning
radiation: left arm, shoulder, neck, jaw
NSFW: nausea, sweating, fatigue, weak breathing
Some patients will have atypical presentations!
no pain
low-grade fever
pale, cool, clammy skin
hyper/hypotension

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10
Q

How is IHD diagnosed?

A

history taking, physical examination
investigations
resting ECG
exercise ECG (to induce ischaemia)
Blood tests: HBA1C, FBC, cholesterol profile
CT coronary angiography*
biological markers: troponin, myoglobin, CK

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11
Q

How is IHD treated?

A

BANS
statin: simvastatin
nitrate: GTN spray (to abort attacks)
dual antiplatelet: aspirin + clopidogrel
Acute (UA/NSTEMI): BMOAN
b-blocker, morphine, oxygen, aspirin, nitrate
Acute STEMI
(if available within 120 min of medical contact) PCI
if not, fibrinolysis (alteplase, streptokinase)
surgical interventions
PCI
CABG (preferred in patients with diabetes, >65 years)

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12
Q

What areas of the heart are represented by the ECG leads?

A
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13
Q

What is heart failure?

A

Inability of the heart to deliver blood and thus oxygen at a rate that is commensurate with the requirements of the body

can result from structural/functional cardiac disorder that impairs the heart’s ability to function

when heart begins to fail, other systems try to compensate to maintain CO and perfusion

[sympathetic system activation] BP falls → detected by baroreceptors → sympathetic activation → positively inotropic/chronotropic → CO increases

RAAS system

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14
Q

What causes heart failure?

A

Ischemic heart disease*

cardiomyopathy (heart walls become thickened, stiff or stretched)

valvular heart disease (AS/MR)

hypertension

alcohol excess

cor pulmonale (disease of lung/pulmonary vessels → pulmonary hypertension → RV hypertrophy → RHF with venous overload, peripheral oedema, hepatic congestion)

anemia, arrhythmias, hyperthyroidism

congestive HF = both sided HF

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15
Q

What are the different types of heart failure?

A

systolic HF: inability of ventricle to contract properly

diastolic HF: inability of ventricle to relax and fill

acute/chronic

HF reserved ejection fraction

systolic, EF <40%

HF preserved ejection fraction

diastolic, EF > 40%

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16
Q

What are the risk factors for heart failure?

A

>65, male, obese, people who have previously had an MI, African descent

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17
Q

What are the signs and symptoms of heart failure?

A

SOFA PC

shortness of breath

orthopnea

fatigue

ankle swelling

pulmonary oedema (due to backflow from decreased CO; produced cough with pink frothy sputum)

cold peripheries

Raised JVP

End respiratory crackles

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18
Q

How is heart failure diagnosed?

A

Blood test

brain natriuretic peptide (BNP)*

ECG

Transthoracic ECG

wall motion abnormalities

valvular disease

cardiomyopathies

Chest X-Ray

Alveolar oedema

B-lines

Cardiomegaly

Dilated upper lobe vessels

Effusion (pleural)

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19
Q

How is heart failure treated?

A

Acute HF: OMFG

oxygen, morphine, furosemide, GTN spray

Chronic HF

lifestyle

stop smoking!

eat less salt, optimise weight and nutrition

avoid NSAIDs/verapamil

medical: AABCDD

1st line: ACE-I + B-blocker

2nd line: ARB + nitrate

3rd line: cardiac resynchronization or digoxin

diuretics: furosemide (symptom relief)

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20
Q

What is stage 1 hypertension?

A

>140/90 mmHg or ABPM >135/85

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21
Q

How does hypertension present?

A

Usually asymptomatic

Malignant: look for damage in brain, eye, heart, kidney

H(ead)-EYE-PE(cs, heart)R(enal)

Head: cerebral oedema, haemorrhage → stroke symptoms, headache

Eye: papilloedema, cotton-wool spots

Pecs/heart: AHF, aortic dissection → chest pain, dyspnoea

Renal: AKI → haematuria, proteinuria

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22
Q

How is hypertension diagnosed?

A

If patient comes in with clinic BP > 140/90

recheck BP on 2-3 occasions over next few weeks/months

if persistently high, offer ABPM

if stage 1 diagnosed → do QRISK to decide treatment

if stage 2 diagnosed → start antihypertensive treatment

If patient has malignant hypertension AND signs of papilloedema and/or signs of renal haemorrhage

same day admission

start antihypertensive drug treatment immediately

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23
Q

How is hypertension treated?

A

First line: ACE-I

Second line: ACE-I + CCB, or ACE-I + Diuretic

Third line: ACE-I + CCB + Diuretic

for diabetics, ACE-I is ALWAYS first line

for black patients, start with CCB as they are not responsive to ACE-I

give CCB before D, unless evidence of oedema/intolerance

ACE-I are CI in pregnancy/if patient is on general anestheia

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24
Q

What is pericarditis?

A

Inflammation of the pericardium with/ without effusion

Common in young adults (tend to have prior viral infection)

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25
Q

What causes pericarditis?

A

Causes:

Infectious

Viral (common)

Coxsackievirus

Bacterial

Mycobacterium tuberculosis

Non-infectious

Trauma (common)

Uraemia, MI

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26
Q

How does pericarditis present?

A

Chest pain

Relieved by sitting forward/ leaning forward

Worsened by inspiration

Fever/ shortness of breath → sign of infection

Pericardial friction rub (high pitched scratchy sound heard loudest on the midline during inspiration)

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27
Q

How is pericarditis investigated?

A

ECG (diagnostic)

Saddle- shaped ST elevation

PR depression

Do a echo/ chest X-ray if suspect effusion

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28
Q

How is pericarditis managed?

A

NSAIDs (ibuprofen) + Colchicine

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29
Q

What are the complications of pericarditis?

A

Cardiac tamponade

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30
Q

What is cardiac tamponade?

A

Life threatening condition whereby there is an accumulation of fluid in the pericardial space → compression of the heart chambers → decrease in venous return → decrease in filling in the heart → reducing cardiac output

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31
Q

How does cardiac tamponade present?

A

Beck’s triad

falling BP

rising JVP

muffled heart sound

Pulsus paradoxus (large decrease in stroke volume → systolic blood pressure drops by > 10mmHg on inspiration

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32
Q

How is cardiac tamponade investigated?

A

Echocardiogram

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33
Q

How is cardiac tamponade managed?

A

pericardiocentesis (removal of the fluids from the pericardial space)

34
Q

What is infective endocarditis?

A

Infection of the inner lining of the heart/ valves (endocardium)

35
Q

What causes infective endocarditis?

A

Stahpylococcus aureus (most common → IVDU)

Streptococcus viridans (mouth/ oral sugery, most common→ non-IVDU)

Staphylococcus epidermis (prosthetic valves)

36
Q

How does infective endocarditis present?

A

signs of infection (fever, fatigue, loss of appetite)

Splinter haemorrhages

Osler nodes (tender nodules in finger)

Janeway lesions (nodules on palms)

Roth spots (haemorrhage with clear centre on fundoscopy)

*If someone comes in with fever and a new murmur, suspect IE

37
Q

How is infective endocarditis diagnosed?

A

Modified Duke’s Criteria

Echo (gold standard)

38
Q

What is the modified Duke’s criteria?

A
39
Q

How is infective endocarditis treated?

A

Antibiotics (4-6 weeks)

If staphylococcus

(Flucloxacillin + rifampicin + gentamicin)

*MRSA → vancomycin + rifampicin + gentamicin

Not staphylococcus

Benzylpenicillin + gentamicin

Not sure which organism (first line)

FAG (flucloxacillin + ampilicin + gentamicin)

40
Q

Valvular disease

A
41
Q

What is tachycardia?

A

Fast heart rate >100 bpm

42
Q

What is atrial tachycardia?

A

Abnormal P waves

Normal QRS

>150bpm

43
Q

What is AV nodal re-entrant tachycardia?

A

Absent P wave

Normal QRS

44
Q

What is ventricular tachycardia?

A

No P waves

Regular wide QRS

No T waves

45
Q

What is bradycardia?

A

Slow heart rate <60bpm

PR interval between 0.12 and 0.20 seconds

QRS complex <0.12

46
Q

What is atrial fibrillation?

A

Chaotic irregular rhythm with an irregular ventricular rate

No P waves

Irregularly irregular QRS

●Stroke risk increase due to static blood in the atria – it pools and it remains still, causing it to clot and embolise

47
Q

What causes atrial fibrillation?

A
  • Idiopathic
  • Hypertension
  • Heart failure
  • Coronary artery disease
  • Valvular heart disease
  • Cardiac surgery
  • Cardiomyopathy
  • Rheumatic heart disease
48
Q

What are the risk factors for atrial fibrillation?

A
  • 60+
  • Diabetes
  • High BP
  • Coronary artery disease
  • Past MI
  • Structural heart disease
49
Q

How does atrial fibrillation present?

A
  • Asymptomatic
  • Palpitations
  • Dyspnoea
  • Chest pains
  • Fatigue
  • NO P WAVES ON ECG
  • Rapid/irregular QRS
  • Apical pulse>radial
50
Q

What is the pathophysiology of atrial fibrillation?

A

continuous rapid activation of the atria with no organised mechanical action at 300-600bpm.

51
Q

How is atrial fibrillation treated?

A

Cardioversion

  • Give a LMWH
  • Shock with defibrillator

●LMWH = low molecular weight heparin e.g. dalteparin to prevent thromboembolism

52
Q

What is atrial flutter?

A

organised atrial rhythm at a rate of 250-350bpm

Sawtooth pattern on ECG (F-waves) - definitive diagnosis

53
Q

What causes atrial flutter?

A
  • Idiopathic
  • Coronary heart disease
  • Obesity
  • Hypertension
  • Heart failure
  • COPD

Pericarditis

54
Q

What are the risk factors for atrial flutter?

A

Atrial fibrillation

55
Q

How does atrial flutter present?

A
  • Palpitations
  • Breathlessness
  • Chest pain
  • Dizziness
  • Syncope
  • Fatigue
56
Q

How is atrial flutter treated?

A

Cardioversion

  • Give a LMWH
  • Shock with defibrillator
  • Catheter ablation – creates a conduction block
  • IV Amiodarone – restore sinus rhythm
57
Q

What is the pathophysiology of atrial flutter?

A

the P wave produces a sawtooth patten with regular conduction to the ventricles

  • Wave of contraction around the atria causing the repolarisation of the AV node
58
Q

What is bundle branch block?

A

a block in the conduction of one of the bundle branches, so the ventricles don’t receive impulses at the same time

59
Q

What is right bundle branch block?

A

Right Bundle Branch Block

MaRRoW

Wide QRS

60
Q

What causes right bundle branch block?

A
  • Pulmonary embolism
  • IHD
  • Atrial Ventricular Septal Defect
61
Q

What is the pathophysiology of right bundle branch block?

A
  • Right bundle doesn’t conduct
  • Impulse spreads from left ventricle to right
  • Late activation of RV
62
Q

How is right bundle branch block diagnosed?

A

ECG

63
Q

How does right bundle branch block present?

A
  • Asymptomatic
  • Syncope/Presyncope
64
Q

How is right bundle branch block treated?

A
  • Pacemaker
  • CRT – cardiac resynchronisation therapy
  • Reduce blood pressure
65
Q

What is left bundle branch block?

A

WiLLiaM

Wide QRS + notched top

T wave inversion in lateral leads

66
Q

What causes left bundle branch block?

A
  • IHD
  • Aortic valve disease
67
Q

What is the pathophysiology of left bundle branch block?

A
  • Left bundle doesn’t conduct
  • Impulse spreads from right ventricle to left

Late activation of LV

68
Q

How is LBBB diagnosed?

A

ECG

69
Q

How does LBBB present?

A
  • Asymptomatic
  • Syncope/Presyncope
70
Q

How is LBBB treated?

A
  • Pacemaker
  • CRT – cardiac resynchronisation therapy
  • Reduce blood pressure
71
Q

What is heart block?

A

a block at any level of the conduction system in which conduction seizes

72
Q

What is 1st degree heart block?

A

PR interval >200ms

Asymptomatic

73
Q

What is 2nd degree heart block: Mobitz I?

A

Progressive lengthening of PR interval

One non-conducted P wave

Next PR interval is shorter

Light headedness

Dizziness

Syncope

74
Q

What is 2nd degree heart block: Mobitz II?

A

Constant PR

Occasional non-conducted P-waves

Wide QRS

75
Q

What is 2nd degree hear block: 2:1?

A

Two waves per QRS

Normal consistent PR intervals

SOB

Postural hypotension

Chest pain

76
Q

What is 3rd degree heart block?

A

P waves and QRS at different rates

Dissociation

Abnormally shaped QRS

Dizziness

Blackouts

Permanent pacemaker

IV atropine

77
Q

What causes heart block?

A
  • Athletes
  • Sick sinus syndrome
  • IHD – esp MI
  • Acute myocarditis
  • Drugs
  • Congenital
  • Aortic valve calcification
  • Cardiac surgery/trauma
78
Q

How do you investigate heart block?

A

ECG

79
Q

How do you treat heart block?

A

Cardioversion

  • Give a LMWH
  • Shock with defibrillator
  • Catheter ablation – creates a conduction block
  • IV Amiodarone – restore sinus rhythm
80
Q

What is stage 2 hypertension?

A

>160/100 or ABPM 150/95

81
Q

What is malignant hypertension?

A

>180/110

82
Q

What causes hypertension?

A

Primary: unknown

Secondary: renal disease/pregnancy/endocrine diseases/coarctation/drugs and toxins