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Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is atherosclerosis and what causes it

A
  • fatty deposits in arterial walls
  • hardening or stiffening of blood vessel walls

cause: chronic inflammation and activation of immune system in the artery wall - leading to deposition of lipids which form atheromatous plaques

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2
Q

RF for atherosclerosis (10)

A

non modifiable: age, FH, male sex

modifiable: HTN, diabetes, high cholesterol, obesity, inactivity, smoking, alcohol.

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3
Q

modifiable RF for CVD

A

diet, exercise and weight loss (Mediterranean diet)
stop smoking
stop drinking
optimize treatment of comorbidities

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4
Q

What is QRISK

A

percentage probability of having stroke / MI in the next 10 years.

If QRISK > 10 then initiate statin. Atorvastatin 20mg OD at night

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5
Q

Angina

A

Constricting chest pain (+- radiation to l arm / jaw) due to narrowing of coronary vessels leading to reduced blood supply to myocardium during times of high oxygen demand.

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6
Q

stable vs unstable angina

A

stable angina is relieved by rest / GTN spray symptoms come on during increased oxygen demand

unstable angina is when symptoms come on randomly whilst at rest

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7
Q

Investigations for angina (8)

A

Gold standard: CT coronary angiography
Cardiac exam
FBC - anaemia
LFTs - statin initiation
Lipid profile
UEs - baseline needed prior to starting meds such as ACEi
HbA1c
Thyroid function

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8
Q

Angina Management (4) RAMP

A

Refer to cardiology (urgently if unstable)

Advise about diagnosis, lifestyle changes, GTN use and when to call ambulance ( GTN 5mins, GTN if symptoms, GTN and 999)

Medical: 1. short term symptomatic relief GTN
2. long term symptomatic relief: BB bisoprolol 5mg, CCB amlodipine 5mg (coronary vasodilatation)
3. secondary prevention 4As

Procedural: PCI percutaneous coronary intervention with angioplasty. CABG

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9
Q

Acute coronary syndrome

A

ACS is usually caused by a thrombus from an atherosclerotic plaque
- unstable angina
- STEMI
- NSTEMI

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10
Q

Diagnosing ACS

A

perform ECG, if not STEMI then troponins

STEMI - ST elevation / LBBB

NSTEMI - raised troponins + ECG changes: ST depression, pathological q waves, T wave inversion

Unstable angina: normal ECG and troponins

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11
Q

ACS symptoms (6)

A

Constricting central chest pain
Jaw / arm radiation
sweating and clamminess
SOB
palpitations
feeling of impeding doom

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12
Q

Acute STEMI treatment

A

pre hospital - 300mg aspirin

Primary PCI - if available within 2 hours
Thrombolysis - fibrinolytic agent to dissolve clot. Increased risk of bleeding

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13
Q

Acute NSTEMI treatment BATMAN

A

Betablocker - bisoprolol
Aspirin - 300mg
Ticagrelor 180mg or 300mg clopidogrel
Morphine - pain relief
Anticoagulant - LMW heprain
Nitrites - GTN to relief coronary spasm

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14
Q

Grace score ?

A

probability of death / future MI within 6 months

< 5% low
5-10% medium
> 10% high risk

medium-high risk PCI within 4 days

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15
Q

Complications of MI? DREAD

A

Death
Rupture of atrial septum / papillary muscles
Edema = heart failure
Arrhythmia or Aneurysm

Dressler’s syndrome: pericarditis 2-3 weeks after MI.
pleuritic chest pain, pericardial rub, pericardial effusion.
ECG: ST elevation + T wave inversion, echo, raised ESR, CRP
treatment: high dose Aspirin

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16
Q

Triggers of acute left ventricular failure (4)

A

Iatrogenic - ie fluid overload in elderly
sepsis
MI
Arrhythmias

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17
Q

Presentation of acute left ventricular failure LVF (symptoms + OE)

A

Symptoms: SOB (exacerbated by lying flat) cough (white/pink frothy sputum), unwell

OE: increased RR, low sats, tachycardia, 3rd HS, crackles on auscultation.

+- symptoms related to underlying cause e.g MI, fever, arrhythmia

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18
Q

acute LVF work up (7)

A

history
cardiac exam
ECG - arrhythmias / MI cause
Echo - ejection fraction >50% normal
CXR - cardiomegally > 50% lung diameter, pulmonary oedema
ABG - T1 resp failure
Routine bloods: FBC, ESR, CRP, UEs, BNP, troponins

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19
Q

Chronic heart failure and presentation (5)

A

inability of LV to pump effectively due to either impaired contraction or relaxation leading to build up fluid due to chronic back-pressure

increased SOB particularly on exertion
cough - white/pink frothy sputum
orthopnoea
paroxysmal nocturnal dyspnoea (PND)
peripheral oedema

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20
Q

Causes of chronic heart failure (4)

A

Ischaemic heart disease
HTN
valvular heart disease - aortic stenosis
arrhythmias

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21
Q

Management overview of chronic heart failure

A

referral to specialist
explanation of condition
medical management - ABAL

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22
Q

Management overview of chronic heart failure

A

referral to specialist
explanation of condition
medical management - ABAL
surgical management - in severe aortic stenosis or mitral regurgitation

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23
Q

Medical management of chronic heart failure (ABAL)

A

ACEi - titrated up to 10mg
Betablocker - bisoprolol - titrated up to 10mg
Aldosterone antagonist aka potassium sparing diuretics

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24
Q

Cor Pulmonale and causes (5)

A

Cor Pulmonale is R sided HF which is caused by resp disease causing pulmonary HTN leading to increased back pressure in the venous system

causes: COPD, PE, CF, interstitial lung disease, primary pulmonary HTN

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25
Q

Cor Pulmonale symptoms

A

early stage often asymptomatic

hypoxia
cyanosis
Raised JVP
peripheral oedema
hepatomegally due to back pressure in hepatic vein
third heart sound
murmurs - pan systolic tricuspid regurgitation?

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26
Q

Cor Pulmonale management

A

treating symptoms and underlying cause
oxygen
poor prognosis

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27
Q

Causes of HTN (5) ROPE

A

Primary HTN - essential HTN no identifiable cause ~95%

Secondary ~5% :
Renal
Obesity
Pregnancy - pre-eclampsia
Endocrine - Conns syndrome (hyper aldosteronism)

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28
Q

Complications of HTN (5)

A

Ischaemic heart disease
cerebrovascular accident - stroke or haemorrhage
hypertensive retinopathy
hypertensive nephropathy
heart failure

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29
Q

HTN diagnosis

A

clinical and ambulatory/home readings
Stage 1 >140/90 >135/85
Stage 2 >160/100 >150/95

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30
Q

HTN management

A

Investigate end organ damage
Advice on lifestyle changes: regular exercise, less salt, smoking cessation

Medical:
Step 1: u 55 and non black ACEi - ramipril 10mg
o 55 or black CCB - amlodipine 10mg
Step 2: non-black ACEi + CCB
black CCB + ARB
Step 3: ACEi + CCB + Thiazide like diuretic

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31
Q

what is the third HS

A

S3 whihc follow 0.1s after S2
LUB DE DUB
rapid ventricular filling causing chordae tendineae to pull
normal in young people
sign of heart failure in older patients

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32
Q

assessing a murmur (script)

A

Site - where is it heard the loudest
Character - soft, blowing, crescendo, decrescendo
Radiation - radiation to axilla (MR) / carotids (AS)
Intensity - grade 1-6 (usually 2/3)
Pitch - high/low = velocity
Timing - systolic / diastolic

33
Q

causes of mitral stenosis (2)

A

Rheumatic fever

Infective endocarditis

34
Q

mitral stenosis - description, presentation, causes

A

narrowed mitral valve which causes:
** mid-diastolic ow pitched rumbling murmur. LUB durr

loud S1 due to increased force required to close stenotic valve.
Tapping apex beat due to loud S1 - palpable HS

-Malar flush caused by back pressure of blood in pulmonary system causing increased CO2 and vasodilation
- AF caused by strain on LA by MS

causes: rheumatic fever, infective endocarditis

35
Q

mitral regurgitation - description

A

incompetent mitral valve which allows a back-flow of blood during systole causes:
**pan systolic high-pitched whistling murmur. BURRR

The murmur radiates to the L axilla.
It results in congestive cardiac failure due to leaky valve causing reduced ejection fraction.
S3 may be present

36
Q

causes of mitral regurgitation (5)

A

Idiopathic - old age
infective endocarditis
rheumatic heart disease
ischaemic heart disease
connective tissue disorders: Marfan syndrome

37
Q

Aortic stenosis - description, signs, causes (2)

A

a narrowed aortic valve causes:
** ejection systolic high pitched crescendo-decrescendo murmur Burr dub.

murmur radiates to carotids
slow rising pulse
narrow pulse pressure (pp is 1/4 of systolic)
** +- exertional syncope

Causes: idiopathic calcification with increased age
rheumatic heart disease

38
Q

Complications of valve replacement

A

Thrombus - stagnant blood
Infective endocarditis - staph coccus, strep coccus, enterococcus.
Haemolysis - causing anaemia

Bioprosthetic valve - 10 years
Mechanical valve 20 years + daily warfarin - INR 2.5-3.5 - clicking

39
Q

Treatment for Aortic Stenosis

A

TAVI - transcatheter aortic valve implantation

Xray guided catheter through femoral artery implantation.

in younger patients open surgery

40
Q

what happens in AF

A

Disorganised electrical activity in the atria leads to uncoordinated atrial contraction. Normal SA node conduction is overridden resulting in abnormal conduction of the ventricles resulting in:
- irregularly irregular ventricular contraction
- tachycardia
- incomplete ventricular filling leading to HF
- stagnant blood increasing risk of emboli

41
Q

presentation of AF (6)

A

often incidental finding

  • irregularly irregular rhythm
  • tachycardia
  • palpitations
  • breathlessness
  • dizziness / syncope
  • symptoms of associated conditions ie sepsis, thyrotoxicosis, stroke, MI
42
Q

Two causes of irregularly irregular rhythm + how to differentiate

A

AF : ventricular rate 110-160

Ventricular ectopic: ectopics disappear above a certain HR, therefore normal rhythm during exercise is ectopics.

43
Q

AF on ECG (3)

A

absent P waves
narrow QRS tachycardia
irregularly irregular rhythm

44
Q

valvular vs non-valvular AF

A

In valvular AF pathology in the valve has caused AF. This only applies to mitral stenosis and mechanical valves.

Pathology in other valves or AF of other cause is non-valvular AF.

45
Q

Most common causes of AF - AF affects mrs SMITH

A

Sepsis
Mitral pathology (rheumatic HD)
Ischaemic heart disease
Thyrotoxicosis
HTN

Others: PE, DM, electrolyte depletion, excessive caffeine

46
Q

Rate control in AF

A

only applicable where there is established AF +
no reversible cause of AF
AF not causing HF

aim to reduce HR <100 to aid filling of ventricles

BB: atenolol 50-100mg
CCB: diltiazem

47
Q

Rhythm control in AF

A

aim to restore heart to sinus rhythm

Pharmacological: flecanide, amiodarone (in structural HD)

Electrical: rapidly shock heart back to sinus. sedation/GA then controlled defib shock

Long-term: BetaBlocker, donedarone, amiodarone.

48
Q

Immediate vs Delayed cardioversion

A

Immediate: if AF present < 48 hours / haemodynamically unstable

Delayed: if AF > 48 hours + stable. This involves 3 weeks anticoagulation to reduce risk of atrial clot > embolus > stroke

49
Q

CHADSVASc

A

tool to assess whether person with AF requires anticogulation. Higher the score = higher risk of stroke

1 - consider anticoag
> 1 - start anticoag

C - congestive HF
H - HTN
A - age > 75 = 2
D - diabetes
S - stroke / TIA = 2
V - vascular disease
A - age 65-74
S - sex (female)

50
Q

Tools (2) used to assess patient’s risk of major bleeding whilst on anticoagulants

A

ORBIT tool
HAS-BLED

useful to compare risk of stroke vs risk of bleeding

51
Q

Cardiac Arrest Rhythms (4)

A

Shockable:
Ventricular Tachycardia (VT)
Ventricular Fibrilation (VF)

Non-shockable:
Pulseless electrical activity
Asystole

52
Q

Ventricular Tachycardia, symptoms (4), causes (4), treatment

A

VT: broad complex tachycardia originating from ventricles

Short lasting VT may be asymptomatic or present with: dizziness, palpitations, chest pain.

VT may turn into VF and lead to cardiac arrest.

Causes: ischaemic HD, cardiomyopathy, aortic stenosis, electrolyte imbalance

Treatment:
Amiodarone in stable patient
Cardioversion in VT with pulse
Defibrillation in pulseless VT

53
Q

Ventricular Tachycardia, ECG changes (4)

A

Monomorphic VT ECG:

wide-complex QRS tachycardia
uniform QRS complexes
Josephson’s sign: notching at S wave nadir
Northwest axis deviation

54
Q

Ventricular Fibrilation

A

Abnormal electrical activity of the heart where ventricles quiver up to 500bpm.

VF leads to cardiac arrest with LoC and no pulse.

Causes: ischaemic HD, cardiomyopathy, valvular disease.

ECG: chaotic irregular deflections of varying amplitude, no P, QRS, T waves.

55
Q

Narrow complex QRS causes (3) and treatment

A

Unstable:
up to 3 synchronized shocks
amiodarone infusion

Stable patient:
- Atrial Fibrilation: BB / CBB
- Atrial flutter: BB
- Supraventricular tachycardia: vagal manouvre, carotid massage, adenosine

56
Q

Atrial Flutter, pathophysiolgy and causes (4)

A

Atrial flutter is a form of supraventricular tachycardia

caused by re-entry circuit within the atria resulting in a self perpetuating electrical loop leading to atrial contraction ~ 300bpm.
Due to refractory period of the AV node there is a block on signal propagation to the ventricles ~150bpm

causes:
ischaemic HD, cardiomyopathy, thyrotoxicosis, HTN.

57
Q

Atrial Flutter treatment (4)

A

Rate/rhythm control: BB / cardioversion

Treat underlying reversible cause: HTN, thyrotoxicosis

Radiofrequency ablation of re-entry circuit

Anticoagulation: CHADSVASc

58
Q

What is first degree heart block, causes (4) and ECG changes

A

Delayed conduction through AV node, however it still leads to QRS
(Every P = QRS)

ECG: PR interval >220ms

Causes : ischaemic HD, rheumatic carditis, digoxin toxicity, electrolyte disturbance

59
Q

Second degree heart block, Mobitz T1, ECG changes

A

Second degree = not all p waves lead to QRS due to block in AV node

Mobitz T1: progressively weaker P wave signals (longer PR) eventually doesn’t lead to QRS then followed by normal PR and pattern repeats.

ECG:
progressively longer PR intervals
One non-conducted P wave followed by normal PR and QRS

60
Q

Second degree heart block: Mobitz 2 and ECG changes

A

Interruption of AV conduction leads to regular pattern of non-conducted P waves which could be 2:1, 3:1. PR interval remains normal.
Risk of asystole!

ECG:
PR interval is normal and constant
Non conducted P waves in 2:1, 3:1 block

61
Q

Third degree heart block, ECG

A

Third degree is complete heart block with no observable relationship between P waves QRS.
Ventricles occasionally contract due to slow ‘slow escape’ mechanism.

Significant risk of asystole!

ECG:
No relationship between P waves and QRS
QRS infrequent
QRS odd shape

62
Q

Treatment of bradycardias / heart block

A

Stable: observe

Unstable: Atropine 500mcg IV

Cardiac pacemaker

63
Q

RBBB + ECG

A

problem preventing conduction via the RBB. Septum is depolarized from the L as usual but RV is depolarized after the LV which creates a second R wave in V1.

ECG:
RSR wave in V1
wide QRS complex

64
Q

LBBB + ECG

A

problem preventing conduction via the LBB. Septum is depolarized from R to L.

ECG:
notched top “M” in lateral leads, particularly in V6
wide QRS complex
T wave inversion in lateral leads (I, VL, V5-6)
possible “W” in lead V1.

65
Q

Wolf Parkinson White, ECG, concerns

A

An accessory electrical pathway (bundle of Kent) connects the atria to ventricles which bypasses the AV node. - a depolarization wave reaches ventricles early resulting in pre-excitation - short PR interval.

ECG:
short PR interval
wide complex QRS
“slurred” Delta wave on upstroke of QRS

Concerns:
if patient has AF / atrial flutter this chaotic electrical activity may pass via accessory pathway and cause Ventricular Tachycardia.
BB, CBB, adenosine contraindicated due to suppression of AV node activity

66
Q

Localization of ischaemic area ST elevation
V1-V4

A

anterior / Septal - Proximal, LAD

67
Q

Localization of ischaemic area ST elevation
V5-V6, I, aVL

A

Lateral- distal LAD, L circumflex

68
Q

Localization of ischaemic area ST elevation
II, aVF, III

A

Inferior - RCA 90%, LCx 10%

69
Q

Infective Endocarditis, pathophys, RF (7), presentation

A

Infection of the Endocardium, disproportionally affecting those with structural heart disease. It can be classified as (mostly) L vs R sided and native valve vs prosthetic valve.
Pathophysiology triad of: bacteraemia, damage to valvular tissue + vegetation formation (platelet-fibrin matrix)
High mortality.

RF: valvular disease, prosthetic valve, structural HD, prev IE, cardiomyopathy, dental infection, IVDU, invasive vascular procedure.

Presentation: systemic features of infection, anaemia.
heart murmur, splinter haemorrhages, osler’s nodes, janeway lesions, clubbing.

70
Q

Pericarditis, causes (6), features (2)

A

Infection of the pericardium. Common in younger males.
Causes: idiopathic, infections, MI, Dressler’s syndrome, Ca, autoimmune.

Features: CP retrosternal radiating to trapezius ridge, pleuritic, exacerbated lying flat, relieved sitting forward. SOB, fever.

71
Q

Causes of long QT interval (3) + definition

A

increased myocardial repolarization
>440ms in men, >460ms in women
can lead to Torsades de pointes

  • Long QT syndrome
  • Medications: antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolides)
  • Electrolyte imbalance: hypokalaemia, hypomagnesemia, hypocalcimia)
72
Q

Pericarditis: examination (3), investigations, ECG (2)

A

Examination: pericardial rub, +- pericardial effusion (more distant heart sounds)
+- cardiac tamponade = hypotension, muffled heart sounds, raised JVP.

Investigations: troponin (sometimes raised), CRP raised. UEs, FBC, LFT, CXR, ECG

ECG: PR depression, concave/saddle shaped ST elevation

73
Q

Pericarditis management

A

1st line NSAID:
750-1000mg Aspirin PO TDS 1-2 weeks OR
600mg Ibuprofen PO TDS 1-2 weeks

+ PPI + Colchicine

74
Q

Why corticosteroids / NSAIDs are contraindicated in MI treatment

A

Avoided in initial management due to high frequency of impaired ventricular myocardial layer healing leading to increased rate of ventricular rupture.

(steroids / NSAIDs reduce inflammation and therefore healing process)

75
Q

Torsades de pointes

A

Torsades de pointes is a polymorphic ventricular tachycardia.
It occurs when a prolonged QT interval leads to spontaneous depolarizations prior to repolarizations which results in the ventricles continuing to stimulate continuous contractions without normal repolarization.

Torsades de pointes will either terminate spontaneously to sinus rhythm or progress to VT

76
Q

Torsades de pointes ECG findings (3)

A
  • polymorphic ventricular tachycardia = QRSs progressively get smaller then larger then smaller again.
  • prolonged QT interval
  • twisting QRS complexes around the baseline
77
Q

Torsades de pointes management (5)

A
  • correct the cause (electrolyte disturbance / medication)
  • magnesium infusion (smooth muscle relaxant)
  • defibrillation if VT occurs
  • betablockers (except sotalol)
  • pacemaker
78
Q

Cardiovascular Symptoms (6)

A
  • Chest pain
  • Palpitations - tap out rhythm
  • Dyspnoea - exertional / orthopnea / PND
  • Syncope - reduced CV perfusion (postural, exertional = A stenosis, random = arrhythmia)
  • Oedema - inadequate arterial supply = PVD
  • Claudication
79
Q

Cardiovascular Signs (5)

A
  • Cyanosis - poor circulation (peripheral vasoconstriction secondary to hypovolaemia) or inadequate oxygenation
  • SOB - underlying cardiovascular / resp disease
  • Pallor - anaemia / poor perfusion (congestive HF)
  • Malar flush - mitral stenosis
  • Oedema

Medicine (10 decks)

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