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6th Year Cardio MJ > dpd > Flashcards

dpd Flashcards

1
Q

Ix for chest pain

A
  1. ECG - STEMI, vs NSTEMI
  2. Troponin - +=coronary agiography, PCI, - = ETT
  3. Echo -regional wall motion abnormality
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2
Q

Ddx of chest pain x4 broad categories

A

cardiac
resp
GI
MSK

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3
Q

CARDIAC causes of CP

A
  1. IHD: Angina pectoris; ACS (MI) - tight chest pain w/ nausea + sweating. Rx: Diabetes, smoking, HTN
  2. AD: sudden onset chest pain radiating to back. Rx: HTN. O/E: Difference in BP between 2 arms + early diastolic murmur (aortic regurgitation)
  3. Pericarditis : pleuritic chest pain - sharp + worse on inspiration. Better when leaning forward. Preceding flu-like illness
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4
Q

RESP causes of CP

A
  1. PE: Acute onset SOB, swollen leg, pleuritic, haemoptysis. Rx: Immobility, Malignancy, FHx, recent fracture
  2. Pneumonia: Cough, Fever, Sputum
  3. Pneumothorax: Pleuritic chest pain, acute onset
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5
Q

GI causes of CP

A

Oesophageal spasm
Oesophagitis
Gastritis
GORD

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6
Q

MSK causes of CP

A

Costochondritis (Tietze’s syndrome: more localized over sternum) - musculoskeletal tenderness

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7
Q

What coronary artery is affected in an anterior MI + which ECG leads are affected?

A

Left Anterior Descending

V1-V4

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8
Q

What coronary artery is affected in an inferior MI + which ECG leads are affected?

A

Right coronary artery

II, III, aVF

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9
Q

What coronary artery is affected in a lateral MI + which ECG leads are affected?

A

Left circumflex artery

V5, V6, I, aVL

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10
Q

What coronary artery is affected in a posterior MI + which ECG leads are affected?

A 
POSTERIOR DESCENDING (usually a branch of RCA)
Tall R wave + ST depression in V1 - V3
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11
Q

Which cardiac enzyme is most sensitive for MI?

How long does it stay high for?

A

Troponin
Measured at 3 hr & observe increments - measure serial troponin

Stays elevated for up to 2-3 days afterwards

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12
Q

30 y/o man comes in w/ collapse. Before: no warning. During: no tongue biting. After: Not confused. FHx: Brother died at a young age. O/E: HS: S1+S2+0; no difference in lying and standing BP, Vesicular breath sounds, Abdo SNT, CNI - XII NAD, Normal I, T, P, R, C, S, Gait. What is the most likely cause of his collapse?

  1. Aortic stenosis
  2. Pulmonary embolism
  3. Postural hypotension
  4. Seizure
  5. Tachyarrhythmia
A

Tacharrythmia e.g. VT due to FHx which indicates cardiac arrhythmia.
Not PE because there is no outflow obstruction on right side + no risk factors

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13
Q

Causes of collapse

A

1.CARDIAC (VAOP)
Vasovagal - incr vagal discharge (pale, sweaty before collapse, no confusion)
Arrhythmia
Outflow obstruction - left: aortic stenosis, HOCM or right: PE
Postural hypotension
2.NEURO: seizure
3.HYPOS: check CBG

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14
Q

what is long QT syndrome and what does it predispose to

A
  • abnormal ventricular REPOLARISATION

- predisposes to VT

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15
Q

Causes of long QT

A

Congenital: Long QT snydrome eg mutations in K+ channel + FHx
Acquired: Hypokalaemia/ hypomagnaesemia
Drugs eg clarithromycin

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16
Q

Ddx of systolic murmurs

A
  1. AS
  2. Mitral regurgitation
  3. Tricuspid regurgitation
  4. VSD
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17
Q

45Y man - f+malaise - IVDU

O/E: T38, JVP raised to earlobes. HS: S1+2+PSM (louder on inspiration)

A

TRICUSPID REGURG

  • IVDU prone to IE which affects right heart and cause TR
  • JVP incr to earlobes also suggests TR
  • PSM indicates TR or MR or VSD but right sided murmurs louder on insp (tricuspid or pulmonary)
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18
Q

Right and left sided murmurs louder on what (RILE)

A

Right - inspiration (tricuspid or pulmonary)

Left - expiration (aortic or mitral)

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19
Q

Ddx of increased JVP

A
  1. RHF - secondary to LHF (CHF) or pulmonary HTN (PE, COPD)
  2. TR - damage to valve leaflets (IE, IVDU) or RV dilatation of the valve ring (valve root enlarges) so leaks through valve
  3. CONSTRICTIVE PERICARDITIS - thickening/calcification of pericarditis: caused by inf (TB), inflammation (CT disease eg lupus, sarcoid), malignancy
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20
Q

how does COPD –> RHF

A

chronic hypoxia –> chronic VC –> pulmonary HTN

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21
Q

what are the clin feats of AS

A

loudest in aortic area
ESM
radiates to carotids
assoc with slow rising pulse, narrow pulse pressure

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22
Q

what are clin feats of MR

A 
loudes in mitral area
PSM - high pitches 'whistling'
radiates to axilla
assoc with displaced apex beat
loudest on expiration
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23
Q

what are clin feats of TR

A

louder in tricuspid area: left lower sternal edge (assoc with high JVP)
louder on inspiration
hepatomegaly

24
Q

clin feats of VSD

A

loudest at left sternal border accompanied by parasternal thrill

25
Q

what does an ECG tell you

A

Ischaemic changes: ST elevation, depression
Electrical abnormalities : prolonged QT interval, tachy
Structural abnormalities: Deep S in V1, deep R in V6 =
LVH = HTN

26
Q

what are characteristics and causes of sinus tachy

A

characteristics: incr HR, all components present (PQRST)
causes: sepsis, hypovolaemia, endocrine (thyrotoxicosis, phaeochromocytoma)

27
Q

what are characteristics and causes and tx of SVT

A

characteristics: fast, regular, narrow complex (<3 small squares), no P wave before QRS
cause: re-entry circuit
TX: is pt haemodynamically stable? Y - vagal manouvres, N - DC Cardioversion. Next is IV adenosine 6mg (slow conduction through AV node) –> IV adenosine 12mg –> IV adenosine 12mg –> IV beta blocker, IV amiodarone

28
Q

what are the two types of SVT

A
  1. AVNRT - re=entry circuit at AV node. No p wave as depolarisation from AVN not SAN. Normal ECG after resolved
  2. AVRT - re-entry circuit via bundle of kent –> short PR interval (P wave present) + delta wave (slurred upstroke) when not tachy. Tx: RFA to destroy accessory pathway
29
Q

what are characteristics + causes of AF

A

irregularly irregular narrow complex tachy (>120bpm); no p waves

causes: thyrotoxicosis, alcohol, heart (muscle - IHD, HTN; valve (Rheumatic HD); pericardium (pericarditis); lung (pneumonia, PE, cancer, other lung pathology)
- pathogenesis: believed that AF originates in RA near pulmonary vasculature: changes in O2, CO2, or pressure on these cells leads to AF

30
Q

what are characteristics of atrial flutter on ECG

A

chaotic atrial activity, no p waves, narrow QRS, saw-tooth baseline

31
Q

what are characteristics + causes of VT

A

BROAD COMPLEX TACHYCARDIA = VT until proven otherwise; fast; regular
causes: ischaemia, electrolyte abnormality (K+, Mg2+), long QT (look at old ECGs)

32
Q

mx of acute fast AF if pt is haemodynamically stable

A
  1. Anticoagulation to reduce stroke
  2. Rate control with IV beta blockers or digoxin (if pt acutely unwell with pneumonia digoxin is used less)
  3. Rhythm control - if <48h since onset, either DC cardioversion or flecainide (CI in IHD)
    - if >48h anticoagulate for 3-4wks before DC cardioversion (to reduce risk of throwing off a clot from atrium)
33
Q

mx of acute fast AF or SVT if pt haemodyn UNSTABLE

A

3x shocks DC cardioversion

34
Q

mx of pulseless VT

A

shockable rhythm –> defribillate

35
Q

mx of VT w/ NO haemodynamic compromise

A

IV amiodarone
treat underlying cause eg decr K+ or Mg 2+
IF recurrent, consider ICD

36
Q

mx of SVT in pt haemodynamically stable

A
  1. Vagal manouvres (blow into syringe, immerse face in cold water, carotid massage)
  2. IV adenosine (CI in asthmatics –> verapamil)
  3. Cardiac (rhythm) strip - mark when adenosine given
37
Q

ECG findings of LVH

A

Sokolov-Lyon criteria: Deep S wave in V1/2 + tallest R wave height in V5-6 >35mm (>7 large squares)
-indicates HTN or aortic stenosis

38
Q

Ix for LVH

A

Echo (gold std)

ECG (SiR)

39
Q

Characteristic ECG finding in 1st degree heart block

A

prolonged PR interval

-can be physiologically normal in athletes

40
Q

Characteristic ECG finding in:
A.2nd degree heart bock general
B.2nd degree T1
C.2nd degree T2

A

A.P waves not followed by QRS
B.PR interval gets longer and longer till 1 failed transmission - must monitor regularly to ensure it doesn’t become T2
(usu due to functional suppression eg drugs, irreversible ischaemia)
C. intermittent non-conducted P waves without prolongation of PR interval ie regularly, irregular pulse
(due to structural damage eg infarction, necrosis, fibrosis ‘all or nothing phenomenon, fixed ratio block, 2:1, 3:1)

41
Q

characteristic ECG finding in 3rd degree heart block

A

Complete dissocation between P and QRS complexes

Broad QRS complex due to generation from ventricles (for HR, count QRS complex as this is what pumps blood around)

42
Q

how to treat 3rd degree heart block

A

ACUTE: atropine - block VAGUS to increase HR
CHRONIC: pacemaker

43
Q

A 78 y/o man is brought in by ambulance and is unconscious and not breathing. Carotid pulse is absent + temp is 29. ECG shows irregular unformed QRS complexes with no p waves. What is the most likely diagnosis?

  1. Asystole
  2. AF
  3. VF
  4. VT
  5. SVT
44
Q

A 78 y/o man is brought in by ambulance and is unconscious and not breathing. Carotid pulse is absent + temp is 29. ECG shows irregular unformed QRS complexes with no p waves. A diagnosis of VF is made. What is the management in this case?

A

Normally you would shock VF but in this case, hypothermia affects the metabolism of drugs (cardiotoxic) and shock will not work so only do CPR

45
Q

mx of VF/ pulseless VT

A
  1. shock
  2. CPR 2 mins
  3. assess rhythm
  4. adrenaline every 3-5 mins (after 3rd shock)
  5. amiodarone 300mg after 3 shocks
  6. correct reversible causes (4Hs + 4Ts)
46
Q

causes of VF x8 (4Hs 4Ts)

A 
Hypoxia
Hypothermia
Hypovolaemia
Hypo/hyperkalaemia
Tension pneumothorax
Toxins
Tamponade
Thromboembolism
47
Q

mx of asystole/PEA

A
  1. CPR (2 mins)
  2. Adrenaline every 3-5mins
  3. Correct reversible causes
48
Q

A 30 y/o woman presents with URTI, pleuritc chest pain which is better when leaning forward. ECG: diffuse STEMI in all leads (global ST elevation). O/E: Temp 36.5; raised JVP; S1 + S2+ S3; Fine crackles in the chest + peripheral oedema. What is the most likely diagnosis?

A

Pericarditis
Global ST elevation (can’t have all coronaries blocked otherwise would be dead), infection + better when leaning forward all indicates pericarditis

49
Q

mx of pericarditis

A

analgesia + reassurance

pericarditis is self limiting

50
Q

Ddx of pleuritic chest pain (5x Ps)

A 
pericarditis 
pleural pathology (sub-diaphragmatic pathology eg hepatic abscess)
pneumonia 
pneumothorax
PE
51
Q

A 65 y/o woman presents w/ breathlessness over a few hours + orthopnoea. PMHx: 2 x MIs. DH: Aspirin, simvastatin, ramipril, bisprolol. O/E: S1 + S2 + S3, What is the most likely diagnosis?

A

Heart failure - SOB, orthopnoea, fine crepitations, rasied JVP, peripheral oedema + S3

52
Q

mx of acute HF with pulmonary oedema

A
  1. Sit pt up
  2. 60-100% O2
  3. GTN infusion (venodilator so decreases preload)
  4. Diamorphine (venodilator so decreases preload)
  5. IV Furosemide - not oral because if they have gut oedema with pulmonary oedema they will not absorb the drug orally. Daily weights needed.
    Treat underlying cause e.g. MI
53
Q

mx of chronic HF

A

5Conservative: stop smoking, alcohol and lose weight
Medical: (ABD - ACEi, BB, Diuretic e.g. spinronolactone)

  1. ACEi + BB
  2. ARB + spironolactone
  3. Digoxin + CRT (cardiac resynchronization therapy)
54
Q

5Ps of pleuritic CP

A 
PE
Pneumothorax
Pericarditis
Pleurisy
Pneumonia
\+ subphrenic pathology eg abscess
\+rib fractures
\+costochondritis
55
Q

what happens in subclavian steal syndrome

A
  • stenosis of the subclavian artery proximal to the origin of the vertebral artery results in blood being ‘stolen’ from the brain by retrograde blood flow down the vertebral artery + into the arm –> less blood flows to brain –> COLLAPSE
  • occurs when there is an incr demand for blood in the arm ie. due to writing on whiteboard
  • causes: CERVICAL RIB, ATHEROSLCEROSIS, TAKYASU’S ARTERITIS

6th Year Cardio MJ (4 decks)

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