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FCPS Preperation > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Pulse
* Character determined by?
* Best assessed in?
* Causes of bounding and slow rising pulse

A

★Character of the pulse Determined by
1. Stroke volume
2. Arterial compliance

★ Pulse is best assessed in
Major arteries such as brachial and Carotid artery

★ Bounding pulse
+AR
+Anaemina
+Sepsis

★ Slow rising pulse
+AS

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2
Q

JVP

  1. Determined by
  2. “a” wave type, cause
  3. V wave, Giant V wave
  4. X& Y descent
  5. Causes of Paradoxical JVP
A

★ Height of the JVP is determined by right atrial pressure
+ elevated in rt heart failure
+ reduced in hypovolemia

★ a wave - atrial systole
* Absent: AF
* Giant:
√TS
√PS
√ Pulmonary hypertension
√ Right heart failure
* Irregular canon ‘a’ wave:
3° heart block
* regular canon ‘a’ wave:
√ VT

★ v waves- ventricular systole
+ Giant v wave : TR , Constrictive Pericarditis

★ x descent - atrial relaxation & apical displacement of tricuspid valve ring

★ y descent - atrial emptying early in diastole
+Prominent & deep y descent: constrictive pericarditis
+Absent or slow Y descent: Cardiac tamponade

★Paradoxical JVP
+ Constrictive pericarditis
+ Cardiac tamponade
+ Pericardial effusion

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3
Q

Annulus Fibrosus

A

★ Separate atria and ventricles
★ Forms the skeleton for AV valves
★ Electrically insulate atria and ventricle / Forms a conduction barrier between atria and ventricle
★ Prevent conduction of transmission except av node

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4
Q

Cardiac Silhouette

A

On left is formed by
★ aortic arch
★ pulmonary trunk
★ left atrial appendage
★ LV

On right
★ RA
★ RV
★ Superior and inferior vena cava

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5
Q

𝗖𝗼𝗿𝗼𝗻𝗮𝗿𝘆 𝗰𝗶𝗿𝗰𝘂𝗹𝗮𝘁𝗶𝗼𝗻

A

𝗖𝗼𝗿𝗼𝗻𝗮𝗿𝘆 𝗰𝗶𝗿𝗰𝘂𝗹𝗮𝘁𝗶𝗼𝗻
Lt main coronary artery
+ LAD :
✓ 𝗔𝗻𝘁𝗲𝗿𝗶𝗼𝗿 𝗶𝗻𝘁𝗲𝗿𝘃𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝗴𝗿𝗼𝗼𝘃𝗲
✓ 𝗦𝘂𝗽𝗽𝗹𝗶𝗲𝘀 𝗮𝗻𝘁𝗲𝗿𝗶𝗼𝗿 𝗽𝗮𝗿𝘁 𝗼𝗳 𝘀𝗲𝗽𝘁𝘂𝗺 & 𝗮𝗻𝘁𝗲𝗿𝗶𝗼𝗿, 𝗹𝗮𝘁𝗲𝗿𝗮𝗹 & 𝗮𝗽𝗶𝗰𝗮𝗹 𝘄𝗮𝗹𝗹𝘀 𝗼𝗳 𝗟𝗩
+ Lt circumflex artery :
✓ 𝗣𝗼𝘀𝘁𝗲𝗿𝗶𝗼𝗿𝗹𝘆 𝗶𝗻 𝗔𝗩 𝗴𝗿𝗼𝗼𝘃𝗲
✓ 𝗦𝘂𝗽𝗽𝗹𝗶𝗲𝘀 𝗹𝗮𝘁𝗲𝗿𝗮𝗹, 𝗽𝗼𝘀𝘁𝗲𝗿𝗶𝗼𝗿 & 𝗶𝗻𝗳𝗲𝗿𝗶𝗼𝗿 𝘀𝗲𝗴𝗺𝗲𝗻𝘁𝘀 𝗼𝗳 𝗟𝗩
*** 𝙊𝙘𝙘𝙡𝙪𝙨𝙞𝙤𝙣 𝙤𝙛 𝙡𝙚𝙛𝙩 𝙢𝙖𝙞𝙣 𝙘𝙤𝙧𝙤𝙣𝙖𝙧𝙮 𝙖𝙧𝙩𝙚𝙧𝙮 𝙞𝙨 𝙪𝙨𝙪𝙖𝙡𝙡𝙮 𝙛𝙖𝙩𝙖𝙡
Right coronary artery
+ 𝗥𝘂𝗻𝘀 𝗶𝗻 𝗿𝗶𝗴𝗵𝘁 𝗔𝗩 𝗴𝗿𝗼𝗼𝘃𝗲
+ 𝗦𝘂𝗽𝗽𝗹𝗶𝗲𝘀 𝗥𝗔, 𝗥𝗩 & 𝗶𝗻𝗳𝗲𝗿𝗼𝗽𝗼𝘀𝘁𝗲𝗿𝗶𝗼𝗿 𝗮𝘀𝗽𝗲𝗰𝘁𝘀 𝗼𝗳 𝗟𝗩, 𝗦𝗔 𝗻𝗼𝗱𝗲 (𝟲𝟬%) & 𝗔𝗩 ( 𝟵𝟬%)
+ 𝙋𝙧𝙤𝙭𝙞𝙢𝙖𝙡 𝙤𝙘𝙘𝙡𝙪𝙨𝙞𝙤𝙣 𝙤𝙛 𝙍𝘾𝘼 𝙩𝙝𝙚𝙧𝙚𝙛𝙤𝙧𝙚 𝙤𝙛𝙩𝙚𝙣 𝙧𝙚𝙨𝙪𝙡𝙩𝙨 𝙞𝙣 𝙨𝙞𝙣𝙪𝙨 𝙗𝙧𝙖𝙙𝙮𝙘𝙖𝙧𝙙𝙞𝙖 & 𝘼𝙑 𝙣𝙤𝙙𝙖𝙡 𝙗𝙡𝙤𝙘𝙠.

*** Posterior descending artery
+ 𝗥𝘂𝗻𝘀 𝗶𝗻 𝗽𝗼𝘀𝘁𝗲𝗿𝗶𝗼𝗿 𝗶𝗻𝘁𝗲𝗿𝘃𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝗴𝗿𝗼𝗼𝘃𝗲
+ 𝗦𝘂𝗽𝗽𝗹𝗶𝗲𝘀 𝗶𝗻𝗳𝗲𝗿𝗶𝗼𝗿 𝗽𝗮𝗿𝘁 𝗼𝗳 𝗶𝗻𝘁𝗲𝗿𝘃𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝘀𝗲𝗽𝘁𝘂𝗺
+ 𝗧𝗵𝗶𝘀 𝗶𝘀 𝗮 𝗯𝗿𝗮𝗻𝗰𝗵 𝗼𝗳 𝗥𝗖𝗔 𝗶𝗻 𝗮𝗽𝗽𝗿𝗼𝘅𝗶𝗺𝗮𝘁𝗲𝗹𝘆 𝟵𝟬% 𝗼𝗳 𝗽𝗲𝗼𝗽𝗹𝗲 (dominant right system) & is
supplied by CX in the remainder (dominant left system).

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6
Q

Depolarization starts in?

A

SA node
- Situated at the junction of SVC and RA
- Rate is Influenced by ANS

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7
Q

Nerve Supply of heart

A
  • Effects of sympathetic activity
    + β𝟭-𝗮𝗱𝗿𝗲𝗻𝗼𝗰𝗲𝗽𝘁𝗼𝗿𝘀 𝗶𝗻 𝗵𝗲𝗮𝗿𝘁 𝗿𝗲𝘀𝘂𝗹𝘁𝘀: 𝗣𝗼𝘀𝗶𝘁𝗶𝘃𝗲 𝗶𝗻𝗼𝘁𝗿𝗼𝗽𝗶𝗰 & 𝗰𝗵𝗿𝗼𝗻𝗼𝘁𝗿𝗼𝗽𝗶𝗰 𝗲𝗳𝗳𝗲𝗰𝘁𝘀,
    + β𝟮-𝗮𝗱𝗿𝗲𝗻𝗼𝗰𝗲𝗽𝘁𝗼𝗿𝘀 𝗶𝗻 𝘃𝗮𝘀𝗰𝘂𝗹𝗮𝗿 𝘀𝗺𝗼𝗼𝘁𝗵 𝗺𝘂𝘀𝗰𝗹𝗲 : 𝗩𝗮𝘀𝗼𝗱𝗶𝗹𝗮𝘁𝗮𝘁𝗶𝗼𝗻
  • Parasympathetic
    + Pre- Preganglionic & sensory fibers reach the heart through vagus nerves
    + Cholinergic nerves supply AV & SA nodes via muscarinic (M2) receptors
    + Under resting conditions, vagal inhibitory activity predominates & heart rate is slow
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8
Q

The basic unit of contraction

A

Sarcomere

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9
Q

Cardiac peptide

A

***ANP
+ 𝗩𝗮𝘀𝗼𝗱𝗶𝗹𝗮𝘁𝗼𝗿𝘀: 𝗥𝗲𝗱𝘂𝗰𝗲 𝗯𝗹𝗼𝗼𝗱 𝗽𝗿𝗲𝘀𝘀𝘂𝗿𝗲 (𝗕𝗣)
+ 𝗗𝗶𝘂𝗿𝗲𝘁𝗶𝗰: 𝗥𝗲𝗻𝗮𝗹 𝗲𝘅𝗰𝗿𝗲𝘁𝗶𝗼𝗻 𝗼𝗳 𝘄𝗮𝘁𝗲𝗿 & 𝗡𝗮
+ 𝗥𝗲𝗹𝗲𝗮𝘀𝗲𝗱 𝗯𝘆 𝗔𝘁𝗿𝗶𝗮𝗹 𝗺𝘆𝗼𝗰𝘆𝘁𝗲𝘀 in response to stretch

*** BNP
+ Produced by 𝘃𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝗰𝗮𝗿𝗱𝗶𝗼𝗺𝘆𝗼𝗰𝘆𝘁𝗲𝘀 in response to stretch (Ex - heart failure)
+ 𝗛𝗮𝘀 𝗱𝗶𝘂𝗿𝗲𝘁𝗶𝗰 𝗽𝗿𝗼𝗽𝗲𝗿𝘁𝗶𝗲𝘀.

*** Neprilysin
+ 𝗘𝗻𝘇𝘆𝗺𝗲 𝗽𝗿𝗼𝗱𝘂𝗰𝗲𝗱 𝗯𝘆 𝗸𝗶𝗱𝗻𝗲𝘆 & 𝗼𝘁𝗵𝗲𝗿 𝘁𝗶𝘀𝘀𝘂𝗲𝘀
+ 𝗕𝗿𝗲𝗮𝗸𝘀 𝗱𝗼𝘄𝗻 𝗔𝗡𝗣, 𝗕𝗡𝗣 & 𝗼𝘁𝗵𝗲𝗿 𝗽𝗿𝗼𝘁𝗲𝗶𝗻𝘀
+ 𝗔𝗰𝘁𝘀 𝗮𝘀 𝗮 𝘃𝗮𝘀𝗼𝗰𝗼𝗻𝘀𝘁𝗿𝗶𝗰𝘁𝗼𝗿
+ 𝗧𝗵𝗲𝗿𝗮𝗽𝗲𝘂𝘁𝗶𝗰 𝘁𝗮𝗿𝗴𝗲𝘁 𝗶𝗻 𝗽𝗮𝘁𝗶𝗲𝗻𝘁𝘀 𝘄𝗶𝘁𝗵 𝗛𝗙

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10
Q

importance of Windkessel effect of the central artery

A

𝗣𝗿𝗲𝘃𝗲𝗻𝘁𝘀 𝗲𝘅𝗰𝗲𝘀𝘀𝗶𝘃𝗲 𝗿𝗶𝘀𝗲𝘀 𝗶𝗻 𝘀𝘆𝘀𝘁𝗼𝗹𝗶𝗰 𝗕𝗣 𝘄𝗵𝗶𝗹𝗲 𝘀𝘂𝘀𝘁𝗮𝗶𝗻𝗶𝗻𝗴 𝗱𝗶𝗮𝘀𝘁𝗼𝗹𝗶𝗰 𝗕𝗣 there by 𝗥𝗲𝗱𝘂𝗰𝗲𝘀 𝗰𝗮𝗿𝗱𝗶𝗮𝗰 𝗮𝗳𝘁𝗲𝗿𝗹𝗼𝗮𝗱 & 𝗺𝗮𝗶𝗻𝘁𝗮𝗶𝗻𝘀 𝗰𝗼𝗿𝗼𝗻𝗮𝗿𝘆 𝗽𝗲𝗿𝗳𝘂𝘀𝗶𝗼𝗻

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11
Q

Substances released from endothelium

A

** Substances released from endothelium
Vasodilators
+ Nitric Oxide
+ Prostacyclin
+ Endothelium-derived hyperpolarising factor
Vasoconstrictors
+ Endothelin-1
+ Angiotensin II
Von Willebrand factor (glycoprotein) : Promotes thrombus formation
Tissue plasminogen activator : Induce fibrinolysis & thrombus dissolution

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12
Q

Pulsus paradoxus

A

*** Pulsus paradoxus (exaggerated / > 10 mmHg ↓ BP during inspiration)
+ 𝗦𝗲𝘃𝗲𝗿𝗲 𝗮𝘀𝘁𝗵𝗺𝗮 𝗼𝗿 𝗖𝗢𝗣𝗗
+ 𝗖𝗵𝗮𝗿𝗮𝗰𝘁𝗲𝗿𝗶𝘀𝘁𝗶𝗰 𝗼𝗳 𝗰𝗮𝗿𝗱𝗶𝗮𝗰 𝘁𝗮𝗺𝗽𝗼𝗻𝗮𝗱𝗲

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13
Q

P wave

A

P wave
+ 𝗔𝘁𝗿𝗶𝗮𝗹 𝗱𝗲𝗽𝗼𝗹𝗮𝗿𝗶𝘀𝗮𝘁𝗶𝗼𝗻
+ 𝗔𝗯𝘀𝗲𝗻𝘁 : 𝗔𝘁𝗿𝗶𝗮𝗹 𝗳𝗶𝗯𝗿𝗶𝗹𝗹𝗮𝘁𝗶𝗼𝗻 (𝗦𝗕𝗔)
+ 𝗧𝗮𝗹𝗹 𝗣 : 𝗥𝘁 𝗮𝘁𝗿𝗶𝗮𝗹 𝗲𝗻𝗹𝗮𝗿𝗴𝗲𝗺𝗲𝗻𝘁 (𝗣 𝗽𝘂𝗹𝗺𝗼𝗻𝗮𝗹𝗲)
+ 𝗡𝗼𝘁𝗰𝗵𝗲𝗱 𝗣 : 𝗟𝘁 𝗮𝘁𝗿𝗶𝗮𝗹 𝗲𝗻𝗹𝗮𝗿𝗴𝗲𝗺𝗲𝗻𝘁
(𝗣 𝗺𝗶𝘁𝗿𝗮𝗹𝗲)

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14
Q

PR interval

A

PR interval
+ 𝗥𝗲𝗳𝗹𝗲𝗰𝘁𝘀 𝗱𝘂𝗿𝗮𝘁𝗶𝗼𝗻 𝗼𝗳 𝗔𝗩 𝗻𝗼𝗱𝗮𝗹 𝗰𝗼𝗻𝗱𝘂𝗰𝘁𝗶𝗼𝗻
+ 𝗣𝗿𝗼𝗹𝗼𝗻𝗴𝗲𝗱 : 𝗜𝗺𝗽𝗮𝗶𝗿𝗲𝗱 𝗔𝗩 𝗻𝗼𝗱𝗮𝗹 𝗰𝗼𝗻𝗱𝘂𝗰𝘁𝗶𝗼𝗻
+ 𝗦𝗵𝗼𝗿𝘁 : 𝗪𝗣𝗪 𝘀𝘆𝗻𝗱𝗿𝗼𝗺𝗲 (𝗦𝗕𝗔)
+ 𝗗𝗲𝗽𝗿𝗲𝘀𝘀𝗶𝗼𝗻 : 𝗦𝗽𝗲𝗰𝗶𝗳𝗶𝗰 𝗼𝗳 𝗮𝗰𝘂𝘁𝗲 𝗽𝗲𝗿𝗶𝗰𝗮𝗿𝗱𝗶𝘁𝗶𝘀 (𝗦𝗕𝗔)

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15
Q

QRS complex

A

duration Increased : RBBB / LBBB
Increased QRS amplitude: Left ventricular hypertrophy

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16
Q

T wave

A

T wave
+ 𝗩𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝗿𝗲𝗽𝗼𝗹𝗮𝗿𝗶𝘀𝗮𝘁𝗶𝗼𝗻
+ 𝗧𝗮𝗹𝗹, 𝗽𝗲𝗮𝗸𝗲𝗱 𝗧 : 𝗛𝘆𝗽𝗲𝗿𝗸𝗮𝗹𝗲𝗺𝗶𝗮
+ T inversion: Ishchemia, Hypokalemia

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17
Q

ST segment

A

ST segment
+ 𝗪𝗶𝗱𝗲𝘀𝗽𝗿𝗲𝗮𝗱 𝘀𝗮𝗱𝗱𝗹𝗲 𝘀𝗮𝗵𝗽𝗲𝗱 𝗲𝗹𝗲𝘃𝗮𝘁𝗶𝗼𝗻 : 𝗔𝗰𝘂𝘁𝗲 𝗽𝗲𝗿𝗶𝗰𝗮𝗿𝗱𝗶𝘁𝗶𝘀
+ 𝗣𝗲𝗿𝘀𝗶𝘀𝘁𝗲𝗻𝘁 𝗦𝗧 𝗲𝗹𝗲𝘃𝗮𝘁𝗶𝗼𝗻 : 𝗟𝘁 𝘃𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝗮𝗻𝗲𝘂𝗿𝘆𝘀𝗺 (𝗦𝗕𝗔)
+ Elevation: Ischemia
+ Depression: Ischemia or Infarction

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18
Q

𝙇𝙚𝙖𝙙𝙨 of ECG

A

𝙇𝙚𝙖𝙙𝙨
𝙑1 & 𝙑2&raquo_space;> 𝙍𝙑
𝙑3 & 𝙑4&raquo_space;> 𝙞𝙣𝙩𝙚𝙧𝙫𝙚𝙣𝙩𝙧𝙞𝙘𝙪𝙡𝙖𝙧 𝙨𝙚𝙥𝙩𝙪𝙢
𝙑5 & 𝙑6 𝙤𝙫𝙚𝙧 &raquo_space;> 𝙇𝙑

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19
Q

Normal Cardiac axis

A

Between -30 and +90 Degree

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20
Q

Exercise ECG (positive, Contraindication)

A

considered positive if
+ Angina occurs
+ BP falls or fails to increase or
+ ST segment shifts > 1 mm

𝙎𝙩𝙧𝙚𝙨𝙨 𝙩𝙚𝙨𝙩𝙞𝙣𝙜 𝙞𝙨 𝙘𝙤𝙣𝙩𝙧𝙖𝙞𝙣𝙙𝙞𝙘𝙖𝙩𝙚𝙙 𝙞𝙣
+ 𝙖𝙘𝙪𝙩𝙚 𝙘𝙤𝙧𝙤𝙣𝙖𝙧𝙮 𝙨𝙮𝙣𝙙𝙧𝙤𝙢𝙚
+ 𝙙𝙚𝙘𝙤𝙢𝙥𝙚𝙣𝙨𝙖𝙩𝙚𝙙 𝙝𝙚𝙖𝙧𝙩 𝙛𝙖𝙞𝙡𝙪𝙧𝙚
+ 𝙨𝙚𝙫𝙚𝙧𝙚 𝙝𝙮𝙥𝙚𝙧𝙩𝙚𝙣𝙨𝙞𝙤𝙣

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21
Q

NT-proBNP

A

NT-proBNP
+ Measured in preference to BNP since it is more stable
+ Indications
✓ 𝗗𝗶𝗮𝗴𝗻𝗼𝘀𝗶𝘀 𝗼𝗳 𝗟𝗩 𝗱𝘆𝘀𝗳𝘂𝗻𝗰𝘁𝗶𝗼𝗻
✓ 𝗔𝘀𝘀𝗲𝘀𝘀 𝗽𝗿𝗼𝗴𝗻𝗼𝘀𝗶𝘀 & 𝗿𝗲𝘀𝗽𝗼𝗻𝘀𝗲 𝘁𝗼 𝘁𝗵𝗲𝗿𝗮𝗽𝘆 𝗶𝗻 𝗽𝗮𝘁𝗶𝗲𝗻𝘁𝘀 𝘄𝗶𝘁𝗵 𝗵𝗲𝗮𝗿𝘁 𝗳𝗮𝗶𝗹𝘂𝗿𝗲

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22
Q

What is the cornerstone of Dx of MI?

A

TROPONIN I
increased in
CARDIAC
* MI, Myocarditis
* Pulmonary embolism
* Pulmonary edema
* Cardiac surgery, trauma
* Tachyarrhythmia
* Aortic dissection

NON CARDIAC
* Septic shock, Stroke,SAH
* Prolonged hypotension
* ESRD
* Burn

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23
Q

What are the baseline investigation for a patient with chest pain on exertion

A
  1. CBC / FBC
  2. FBS
  3. Lipid profile
  4. TFT
  5. ECG
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24
Q

What is the first line test of choice to diagnose angina due to coronary artery disease

A

CT Coronary angiography

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25
Q

Causes of sudden arrhythmic death

A

Coronary artery disease

  1. Myocardial Ischaemia
  2. AMI
  3. Prior myocardial infarction with myocardial scarring

Structural heart disease

  1. AS
  2. CHD
  3. Cardiomyopathy (hypertrophic, dilated, arrhythmogenic right ventricular)

Non structural heart disease

  1. Long QT Syndrome
  2. Brugada syndrome
  3. Wolff- Parkinson- White syndrome
  4. ADR (torsades de pointes)
  5. Severe electrolyte abnormality
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26
Q

Features of benign innocent heart murmur

A

Soft
Mid diastolic
Heard at left sternal border
No radiation
No other cardiac abnormality

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27
Q

First Heart Sound

A

Timing: Onset of systole
Cause: Due to the closure of Mitral and tricuspid valve
Nature: Usually single or narrowly splitting
Loud HS: Hyperdynamic circulation (anemia, Thyrotoxicosis, Pregnancy), MS
Soft HS: HF, MR

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28
Q

Second Heart Sound

A

Timing: End of the systole
Cause: The closure of Aortic and Pulmonary valve
Nature: Split on inspiration, Single on expiration
Features:
Fixed wide splitting- ASD
Wide but variable splitting- RBBB
Reversed Splitting- LBBB
Loud HS: HTN, ASD without P. HTN, Hyperdynamic state
Soft HS: AS

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29
Q

Third Heart Sound

A

Timing: Early in diastole Just after S2
Nature: Low pitched often heard as gallop (an early sign of LVF)
Origin: From ventricular wall
Causes: Physiological: Young People, Pregnancy
Pathological Cause: HF, MR

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30
Q

Fourth Heart Sound

A

End of diastole Just before S1
Ventricular Origin
Low Pitch
Absent In AF
Feature of severe LVF

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31
Q

Systolic Click

A

Early or Mid Systole
Brief High-intensity Sound
AS, PS, Floppy mitral valve
Prosthetic Heart

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32
Q

Opening Snap

A

Early in Diastole
Severe MS

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33
Q

Causes of Ejection Systolic Murmur

A

Aortic Stenosis
Pulmonary Stenosis
ASD
Aortic Or Pulmonary Flow Murmur
Benign Murmur

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34
Q

Pan Systolic Murmur

A

Mitral Regurgitation
Tricuspid Regurgitation
VSD

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35
Q

Late Systolic Murmur

A

Mitral Valve Prolapse

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36
Q

Early Diastolic Murmur

A

Aortic regurgitation
Pulmonary Regurgitation

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37
Q

Mid Diastolic murmur

A

MS
TS
Austin flint Murmur
Mitral Or tricuspid Flow murmur

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38
Q

Continuous murmur

A

PDA

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39
Q

Most common causes of right heart failure

A

Chronic lung disease
Pulmonary embolism
Pulmonary valvular stenosis

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40
Q

Biventricular heart failure occurs in

A

Dilated cardiomyopathy
Coronary heart disease affecting both ventricle

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41
Q

Cardiac Output is determined by

A

Preload
afterload
Myocardial contractility

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42
Q

Obstructive Cause of HF

A

Ventricular Outflow obstruction:
HTN, AS - LHF
P. HTN , PS - RHF

Ventricular Inflow Obstruction:
MS, TS

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43
Q

HF Due to Volume Overload

A
  1. Left ventricular volume overload: Aortic and Mitral regurgitation
  2. VSD
  3. Right ventricular volume Overload: ASD
  4. Increased Metabolic demand
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44
Q

Arrhythmitic Cause of HF

A

AF
Tachycardia
CHB

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45
Q

HF Due to Diastolic dysfunction

A

Constrictive Pericarditis
Restrictive Cardiomyopathy
Cardiac Tamponade
LVH and Fibrosis

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46
Q

HF Due Reduced Ventricular Contractility

A

MI
Myocarditis/ Cardiomyopathy

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47
Q

Causes of High Output failure

A

Large AV shunt
Beri-beri
Anemia
Thyrotoxicosis

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48
Q

Effect of prolonged sympathetic stimulation

A

Cardiac myocyte apoptosis
Cardiac Hypertrophy
Focal cardiac necrosis

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49
Q

Clinical Presentation Of ALHF

A

𝗔𝗰𝘂𝘁𝗲 𝗹𝗲𝗳𝘁 𝗵𝗲𝗮𝗿𝘁 𝗳𝗮𝗶𝗹𝘂𝗿𝗲:
- 𝗣𝗿𝗲𝘀𝗲𝗻𝘁𝘀 𝘄𝗶𝘁𝗵 𝘀𝘂𝗱𝗱𝗲𝗻 𝗼𝗻𝘀𝗲𝘁 𝗼𝗳 𝗱𝘆𝘀𝗽𝗻𝗼𝗲𝗮 𝗮𝘁 𝗿𝗲𝘀𝘁 𝘁𝗵𝗮𝘁 𝗿𝗮𝗽𝗶𝗱𝗹𝘆 𝗽𝗿𝗼𝗴𝗿𝗲𝘀𝘀𝗲𝘀 𝘁𝗼 𝗮𝗰𝘂𝘁𝗲
𝗿𝗲𝘀𝗽𝗶𝗿𝗮𝘁𝗼𝗿𝘆 𝗱𝗶𝘀𝘁𝗿𝗲𝘀𝘀, 𝗼𝗿𝘁𝗵𝗼𝗽𝗻𝗼𝗲𝗮 & ultimately respiratory failure
- The patient appears agitated, pale & clammy
- Cool peripheries & rapid pulse
- BP: usually high because of SNS activation, but may be normal or low
- Gallop rhythm with 𝗔 𝘁𝗵𝗶𝗿𝗱 𝗵𝗲𝗮𝗿𝘁 𝘀𝗼𝘂𝗻𝗱 𝗵𝗲𝗮𝗿𝗱 𝗾𝘂𝗶𝘁𝗲 𝗲𝗮𝗿𝗹𝘆 𝗶𝗻 𝘁𝗵𝗲 𝗱𝗲𝘃𝗲𝗹𝗼𝗽𝗺𝗲𝗻𝘁 𝗼𝗳 𝗮𝗰𝘂𝘁𝗲 𝗹𝗲𝗳𝘁- 𝘀𝗶𝗱𝗲𝗱 𝗵𝗲𝗮𝗿𝘁 𝗳𝗮𝗶𝗹𝘂𝗿𝗲

  • 𝗔 𝗻𝗲𝘄 𝘀𝘆𝘀𝘁𝗼𝗹𝗶𝗰 𝗺𝘂𝗿𝗺𝘂𝗿 𝗺𝗮𝘆 𝘀𝗶𝗴𝗻𝗶𝗳𝘆
    + 𝗔𝗰𝘂𝘁𝗲 𝗺𝗶𝘁𝗿𝗮𝗹 𝗿𝗲𝗴𝘂𝗿𝗴𝗶𝘁𝗮𝘁𝗶𝗼𝗻 𝗼𝗿
    + 𝗩𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝘀𝗲𝗽𝘁𝗮𝗹 𝗿𝘂𝗽𝘁𝘂𝗿𝗲

-Chest examination may reveal
+ Crepitations at lung bases if there is pulmonary edema or
+ Crepitation throughout the lung field if severe

50
Q

Factors that may aggravate HF in Pre-existing Heart Disease

A
  1. MI
  2. Intercurrent Illness
  3. Arrhythmia
  4. Administration of a negative inotropic drug (B-blocker) or Fluid-retaining properties (NSAIDs, Glucocorticoid)
  5. Pulmonary embolism
  6. Increased metabolic Demand
  7. IV fluid overload
51
Q

C/F of Chronic heart Failure

A

𝗖𝗵𝗿𝗼𝗻𝗶𝗰 𝗵𝗲𝗮𝗿𝘁 𝗳𝗮𝗶𝗹𝘂𝗿𝗲
Clinical features
+ Fatigue & poor effort intolerance
+ Oliguria & uremia
+ Lt heart failure > Pulmonary edema > Dyspnoea & inspiratory crepitation over lung bases
+ Rt heart failure: High JVP with hepatic congestion & dependent peripheral edema

52
Q

C/F of LHF and RHF

A

LHF:
Raised JVP (++)
Pulmonary Oedema
Pleural Effusion
Cardiomegaly
Peripheral Oedema

RHF:
Raised JVP (++++)
Tender Hepatomegaly
Ascites
Peripheral Pitting Oedema (+++)

53
Q

Complication Of Heart Failure

A

Complications
#𝗥𝗲𝗻𝗮𝗹 𝗳𝗮𝗶𝗹𝘂𝗿𝗲
#𝗛𝘆𝗽𝗼𝗸𝗮𝗹𝗮𝗲𝗺𝗶𝗮 due to
+ K losing diuretics
+ Hyperaldosteronism due to
✓ Activation of RAAS
✓ Impaired aldosterone metabolism from hepatic congestion
#𝗛𝘆𝗽𝗲𝗿𝗸𝗮𝗹𝗲𝗺𝗶𝗮 due to
+ ACEi, ARB & Mineralocorticoid receptor antagonist
#𝗛𝘆𝗽𝗼𝗻𝗮𝘁𝗿𝗮𝗲𝗺𝗶𝗮
+ 𝗙𝗲𝗮𝘁𝘂𝗿𝗲 𝗼𝗳 𝘀𝗲𝘃𝗲𝗿𝗲 𝗵𝗲𝗮𝗿𝘁 𝗳𝗮𝗶𝗹𝘂𝗿𝗲 & 𝗣𝗼𝗼𝗿 𝗽𝗿𝗼𝗴𝗻𝗼𝘀𝘁𝗶𝗰 𝘀𝗶𝗴𝗻 (𝗦𝗕𝗔)
#𝗜𝗺𝗽𝗮𝗶𝗿𝗲𝗱 𝗹𝗶𝘃𝗲𝗿 𝗳𝘂𝗻𝗰𝘁𝗶𝗼𝗻
#𝗧𝗵𝗿𝗼𝗺𝗯𝗼𝗲𝗺𝗯𝗼𝗹𝗶𝘀𝗺
#𝗔𝘁𝗿𝗶𝗮𝗹 & 𝘃𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝗮𝗿𝗿𝗵𝘆𝘁𝗵𝗺𝗶𝗮
#𝗦𝘂𝗱𝗱𝗲𝗻 𝗱𝗲𝗮𝘁𝗵
+ 𝗠𝗼𝘀𝘁 𝗼𝗳𝘁𝗲𝗻 𝗱𝘂𝗲 𝘁𝗼 𝘃𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝗳𝗶𝗯𝗿𝗶𝗹𝗹𝗮𝘁𝗶𝗼𝗻 (𝗦𝗕𝗔)***

54
Q

CXR findings In HF

A

CXR should be performed in all cases
+ 𝗔𝗯𝗻𝗼𝗿𝗺𝗮𝗹 𝗱𝗶𝘀𝘁𝗲𝗻𝘁𝗶𝗼𝗻 𝗼𝗳 𝘂𝗽𝗽𝗲𝗿 𝗹𝗼𝗯𝗲 𝗽𝘂𝗹𝗺𝗼𝗻𝗮𝗿𝘆 𝘃𝗲𝗶𝗻𝘀
+ 𝗠𝗼𝗿𝗲 𝗽𝗿𝗼𝗺𝗶𝗻𝗲𝗻𝘁 𝘃𝗮𝘀𝗰𝘂𝗹𝗮𝗿𝗶𝘁𝘆 𝗼𝗳 𝗹𝘂𝗻𝗴 𝗳𝗶𝗲𝗹𝗱
+ 𝗗𝗶𝗹𝗮𝘁𝗮𝘁𝗶𝗼𝗻 𝗼𝗳 𝗽𝘂𝗹𝗺𝗼𝗻𝗮𝗿𝘆 𝗮𝗿𝘁𝗲𝗿𝗶𝗲𝘀
+ 𝗞𝗲𝗿𝗹𝗲𝘆 𝗕 𝗹𝗶𝗻𝗲 : 𝗛𝗼𝗿𝗶𝘇𝗼𝗻𝘁𝗮𝗹 𝗹𝗶𝗻𝗲𝘀 𝗶𝗻 𝗰𝗼𝘀𝘁𝗼𝗽𝗵𝗿𝗲𝗻𝗶𝗰 𝗮𝗻𝗴𝗹𝗲𝘀
(Due to interstitial oedema > thickened interlobular septa & dilated lymphatics)
+ Pleural effusion in severe cases

55
Q

In the Mx of Pulmonary Oedema which steps are use to reduce pre-load

A
  1. Sit the patient UP
  2. CPAP by tight-fitting mask ( also reduce Pulmonary capillary Hydraulic gradient)
  3. Administration of nitrate ( also reduce afterload )

To correct Hypoxia - Give High Flow Oxygen
To Combat Fluid Overload - Diuretics

56
Q

What are the drugs Improve mortality in CHF?

A

IMPROVE MORTALITY IN CHF
* ACEi
* ARB
* Spironolactone
* B blocker
* SGLT2i
* Sacubitril
* Cardiac resynchronization therapy device

57
Q

Which Vaccination Is considered in HF patient ?

A

Influenza and Pneumococcal Vaccination

58
Q

ACE - I

A

EFFECT:

+ ↓ Peripheral vasoconstriction
+ ↓ Activation of sympathetic nervous system & RAAS
+ ↓ Salt & water retention

A/E :
✓ Hypotension
✓ Hyperkalemia
✓ Renal impairment
✓ Dry cough
✓ Teratogenicity
+ Renal function & serum potassium must be monitored & should be checked 1–2 weeks after starting therapy

59
Q

Effect Of diuretics on HF

A
  1. Reduce pre-load
  2. Improve pulmonary and venous congestion
  3. Reduce after-load and Ventricular volume
60
Q

Which drug reduces the risk of arrhythmia and Sudden death In HF

A

Beta Blocker

It is more effective than ACE i at reducing Mortality rate

61
Q

Which drug is used to control heart rate in HF not controlled by B Blocker

A

Ivabradin

62
Q

Cardiac Transplantation

A

Most common indications:
+ Coronary artery disease
+ Dilated cardiomyopathy

Contraindicated in:
+ Pulmonary vascular disease due to long-standing left heart failure
+ Complex congenital heart disease (Eisenmenger’s syndrome)
+ Primary pulmonary hypertension

Complications:
+Rejection
+Accelerated Atherosclerosis
+Infection: CMV, Aspergillus

Heart-lung transplantation in Eisenmenger’s syndrome

Lung transplantation for primary pulmonary hypertension

63
Q

Which condition HR does not change with breathing/ Posture change?

A

Absence of heart rate variation with breathing or changes in posture due to
+ Diabetic neuropathy
+ Autonomic neuropathy or
+ Increased sympathetic drive

64
Q

Causes of Sinus Bradycardia

A

Myocardial Infarction
Sinus node disease ( sick sinus syndrome)
Hypothermia
Hypothyroidism
Cholestatic jaundice
Raised ICP
Drugs ( B blocker, verapamil, Digoxin)

65
Q

Causes of sinus tachycardia

A

Anxiety
Fever
Anaemia
HF
Thyrotoxicosis
Phaeochromocytoma
Drugs ( B agonist)

66
Q

Common features of sinoatrial Disease

A

Sinus bradycardia
AV Block
Sinoatrial Block
Paroxysmal Atrial Fibrillation
Paroxysmal Atrial Tachycardia

67
Q

First Degree AV Block

A

𝗙𝗶𝗿𝘀𝘁 𝗱𝗲𝗴𝗿𝗲𝗲 𝗔𝗩 𝗯𝗹𝗼𝗰𝗸

𝗔𝗩 𝗰𝗼𝗻𝗱𝘂𝗰𝘁𝗶𝗼𝗻 𝗶𝘀 𝗱𝗲𝗹𝗮𝘆𝗲𝗱
𝗣𝗥 𝗶𝗻𝘁𝗲𝗿𝘃𝗮𝗹 𝗶𝘀 𝗽𝗿𝗼𝗹𝗼𝗻𝗴𝗲𝗱 (> 𝟬.𝟮𝟬 𝘀𝗲𝗰)
𝗡𝗼 𝗱𝗿𝗼𝗽𝗽𝗲𝗱 𝗯𝗲𝗮𝘁
Rarely causes symptoms
Does not usually require treatment

68
Q

Third degree AV block

A

𝗧𝗛𝗜𝗥𝗗-𝗗𝗘𝗚𝗥𝗘𝗘 𝗔𝗩 𝗕𝗟𝗢𝗖𝗞
Conduction fails completely. Atria & ventricles beat independently - known as AV dissociation

Escape rhythm arising in
+ 𝗔𝗩 𝗻𝗼𝗱𝗲 𝗼𝗿 𝗕𝘂𝗻𝗱𝗹𝗲 𝗼𝗳 𝗛𝗶𝘀 (𝗻𝗮𝗿𝗿𝗼𝘄 𝗤𝗥𝗦 ) 𝗼𝗿
+ 𝗗𝗶𝘀𝘁𝗮𝗹 𝗣𝘂𝗿𝗸𝗶𝗻𝗷𝗲 𝘁𝗶𝘀𝘀𝘂𝗲𝘀 (𝗯𝗿𝗼𝗮𝗱 𝗤𝗥𝗦)

𝗦𝗹𝗼𝘄 (𝟮𝟱–𝟱𝟬/𝗺𝗶𝗻), 𝗿𝗲𝗴𝘂𝗹𝗮𝗿 𝗽𝘂𝗹𝘀𝗲 𝘁𝗵𝗮𝘁 𝗱𝗼𝗲𝘀 𝗻𝗼𝘁 𝘃𝗮𝗿𝘆 𝘄𝗶𝘁𝗵 𝗲𝘅𝗲𝗿𝗰𝗶𝘀𝗲 (except congenital complete AV block)
𝗜𝗻𝗰𝗿𝗲𝗮𝘀𝗲𝗱 𝘀𝘁𝗿𝗼𝗸𝗲 𝘃𝗼𝗹𝘂𝗺𝗲
𝗟𝗮𝗿𝗴𝗲-𝘃𝗼𝗹𝘂𝗺𝗲 𝗽𝘂𝗹𝘀𝗲
𝗖𝗮𝗻𝗻𝗼𝗻 𝗮 𝘄𝗮𝘃𝗲𝘀
𝗩𝗮𝗿𝗶𝗮𝗯𝗹𝗲 𝗜𝗻𝘁𝗲𝗻𝘀𝗶𝘁𝘆 𝗼𝗳 𝘁𝗵𝗲 𝟭𝘀𝘁 𝗵𝗲𝗮𝗿𝘁 𝘀𝗼𝘂𝗻𝗱 due to loss of AV synchrony. (𝗦𝗕𝗔 𝗝𝗨𝗟 𝟮𝟮,JUL 23)

𝗧𝘆𝗽𝗶𝗰𝗮𝗹 𝗽𝗿𝗲𝘀𝗲𝗻𝘁𝗮𝘁𝗶𝗼𝗻 -
𝗥𝗲𝗰𝘂𝗿𝗿𝗲𝗻𝘁 𝘀𝘆𝗻𝗰𝗼𝗽𝗲 𝗼𝗿 ‘𝗦𝘁𝗼𝗸𝗲𝘀 𝗔𝗱𝗮𝗺𝘀’ 𝗮𝘁𝘁𝗮𝗰𝗸𝘀
+ Sudden loss of consciousness that occurs without warning & results in collapse
+ A brief anoxic seizure (due to cerebral ischemia)
𝗣𝗮𝗹𝗹𝗼𝗿 & 𝗮 𝗱𝗲𝗮𝘁𝗵-𝗹𝗶𝗸𝗲 𝗮𝗽𝗽𝗲𝗮𝗿𝗮𝗻𝗰𝗲 𝗱𝘂𝗿𝗶𝗻𝗴 𝗮𝘁𝘁𝗮𝗰𝗸 & 𝗰𝗵𝗮𝗿𝗮𝗰𝘁𝗲𝗿𝗶𝘀𝘁𝗶𝗰 𝗳𝗹𝘂𝘀𝗵 𝘄𝗵𝗲𝗻 𝗵𝗲𝗮𝗿𝘁 𝘀𝘁𝗮𝗿𝘁𝘀 𝗯𝗲𝗮𝘁𝗶𝗻𝗴 𝗮𝗴𝗮𝗶𝗻

*** Indication of permanent pacemaker :
𝗦𝘆𝗺𝗽𝘁𝗼𝗺𝗮𝘁𝗶𝗰 𝗯𝗿𝗮𝗱𝘆𝗮𝗿𝗿𝗵𝘆𝘁𝗵𝗺𝗶𝗮
𝗠𝗼𝗯𝗶𝘁𝘇 𝘁𝘆𝗽𝗲 𝗜𝗜 𝗼𝗿
𝗧𝗵𝗶𝗿𝗱-𝗱𝗲𝗴𝗿𝗲𝗲 𝗔𝗩 𝗵𝗲𝗮𝗿𝘁 𝗯𝗹𝗼𝗰𝗸

69
Q

Causes of AV Block

A

Idiopathic Fibrosis
MI
Inflammation:
Infective Endocarditis
Sarcoidosis
Chaga’s Disease
Trauma
Drugs:
B blocker
Digoxin
Calcium Antagonist

70
Q

Atrial Flutter

A

𝗔𝗧𝗥𝗜𝗔𝗟 𝗙𝗟𝗨𝗧𝗧𝗘𝗥
Characterized by a 𝗹𝗮𝗿𝗴𝗲 (𝗺𝗮𝗰𝗿𝗼) 𝗿𝗲-𝗲𝗻𝘁𝗿𝘆 𝗰𝗶𝗿𝗰𝘂𝗶𝘁, 𝘂𝘀𝘂𝗮𝗹𝗹𝘆 𝘄𝗶𝘁𝗵𝗶𝗻 𝗿𝗶𝗴𝗵𝘁 𝗮𝘁𝗿𝗶𝘂𝗺 𝗲𝗻𝗰𝗶𝗿𝗰𝗹𝗶𝗻𝗴 𝘁𝗿𝗶𝗰𝘂𝘀𝗽𝗶𝗱 𝗮𝗻𝗻𝘂𝗹𝘂𝘀

The atrial rate is approximately 300/min and is usually associated with 2: 1, 3: 1, or 4: 1 AV block.

𝗔𝘁𝗿𝗶𝗮𝗹 𝗳𝗹𝘂𝘁𝘁𝗲𝗿 𝘀𝗵𝗼𝘂𝗹𝗱 𝗯𝗲 𝘀𝘂𝘀𝗽𝗲𝗰𝘁𝗲𝗱 𝘄𝗵𝗲𝗻 𝘁𝗵𝗲𝗿𝗲 𝗶𝘀 𝗮 𝗻𝗮𝗿𝗿𝗼𝘄-𝗰𝗼𝗺𝗽𝗹𝗲𝘅 𝘁𝗮𝗰𝗵𝘆𝗰𝗮𝗿𝗱𝗶𝗮 𝗼𝗳 𝟭𝟱𝟬/𝗺𝗶𝗻

𝗖𝗮𝗿𝗼𝘁𝗶𝗱 𝘀𝗶𝗻𝘂𝘀 𝗽𝗿𝗲𝘀𝘀𝘂𝗿𝗲 𝗼𝗿 𝗜𝗩 𝗮𝗱𝗲𝗻𝗼𝘀𝗶𝗻𝗲 𝗺𝗮𝘆 𝗵𝗲𝗹𝗽 𝘁𝗼 𝗲𝘀𝘁𝗮𝗯𝗹𝗶𝘀𝗵 𝗱𝘅 by temporarily ↑ degree of AV block & revealing flutter waves

ECG shows saw-tooth flutter waves

Management

Rate control : Digoxin, β-blockers or verapamil or
Rhythm control: DC cardioversion or catheter ablation
𝗖𝗹𝗮𝘀𝘀 𝗜𝗰 𝗮𝗻𝘁𝗶-𝗮𝗿𝗿𝗵𝘆𝘁𝗵𝗺𝗶𝗰 𝗱𝗿𝘂𝗴𝘀 𝘀𝘂𝗰𝗵 𝗮𝘀 𝗳𝗹𝗲𝗰𝗮𝗶𝗻𝗶𝗱𝗲 𝗮𝗿𝗲 𝗰𝗼𝗻𝘁𝗿𝗮𝗶𝗻𝗱𝗶𝗰𝗮𝘁𝗲𝗱

*** Catheter ablation :
+ > 𝟵𝟬% 𝗰𝗵𝗮𝗻𝗰𝗲 𝗼𝗳 𝗽𝗲𝗿𝗺𝗮𝗻𝗲𝗻𝘁 𝗰𝘂𝗿𝗲
+ 𝗧𝗿𝗲𝗮𝘁𝗺𝗲𝗻𝘁 𝗼𝗳 𝗰𝗵𝗼𝗶𝗰𝗲 𝗳𝗼𝗿 𝗽𝗮𝘁𝗶𝗲𝗻𝘁𝘀 𝘄𝗶𝘁𝗵 𝗽𝗲𝗿𝘀𝗶𝘀𝘁𝗲𝗻𝘁 𝘀𝘆𝗺𝗽𝘁𝗼𝗺𝘀

71
Q

What is the most common sustained Cardiac arrhythmia ?

A

𝗔𝗧𝗥𝗜𝗔𝗟 𝗙𝗜𝗕𝗥𝗜𝗟𝗟𝗔𝗧𝗜𝗢𝗡

*** 𝗔𝘁𝗿𝗶𝗮𝗹 𝗳𝗶𝗯𝗿𝗶𝗹𝗹𝗮𝘁𝗶𝗼𝗻 (𝗔𝗙) - 𝗺𝗼𝘀𝘁 𝗰𝗼𝗺𝗺𝗼𝗻 𝘀𝘂𝘀𝘁𝗮𝗶𝗻𝗲𝗱 𝗰𝗮𝗿𝗱𝗶𝗮𝗰 𝗮𝗿𝗿𝗵𝘆𝘁𝗵𝗺𝗶𝗮 (𝗦𝗕𝗔)

Complex arrhythmia characterized by both - 𝗮𝗯𝗻𝗼𝗿𝗺𝗮𝗹 𝗮𝘂𝘁𝗼𝗺𝗮𝘁𝗶𝗰 𝗳𝗶𝗿𝗶𝗻𝗴
- 𝗽𝗿𝗲𝘀𝗲𝗻𝗰𝗲 𝗼𝗳 𝗺𝘂𝗹𝘁𝗶𝗽𝗹𝗲 𝗶𝗻𝘁𝗲𝗿𝗮𝗰𝘁𝗶𝗻𝗴 𝗿𝗲-𝗲𝗻𝘁𝗿𝘆 𝗰𝗶𝗿𝗰𝘂𝗶𝘁𝘀 𝘄𝗶𝘁𝗵𝗶𝗻 𝗮𝘁𝗿𝗶𝗮

Ectopic beats arising 𝗳𝗿𝗼𝗺
- 𝗰𝗼𝗻𝗱𝘂𝗰𝘁𝗶𝗻𝗴 𝘁𝗶𝘀𝘀𝘂𝗲 𝗶𝗻 𝗽𝘂𝗹𝗺𝗼𝗻𝗮𝗿𝘆 𝘃𝗲𝗶𝗻𝘀
- 𝗱𝗶𝘀𝗲𝗮𝘀𝗲𝗱 𝗮𝘁𝗿𝗶𝗮𝗹 𝘁𝗶𝘀𝘀𝘂𝗲

𝗔𝘁𝗿𝗶𝗮 𝗯𝗲𝗮𝘁 𝗿𝗮𝗽𝗶𝗱𝗹𝘆 𝗯𝘂𝘁 𝗶𝗻 𝗮𝗻 𝘂𝗻𝗰𝗼𝗼𝗿𝗱𝗶𝗻𝗮𝘁𝗲𝗱 & 𝗶𝗻𝗲𝗳𝗳𝗲𝗰𝘁𝗶𝘃𝗲 𝗺𝗮𝗻𝗻𝗲𝗿
Ventricles are activated irregularly at a rate determined by conduction through the AV node
This produces 𝗰𝗵𝗮𝗿𝗮𝗰𝘁𝗲𝗿𝗶𝘀𝘁𝗶𝗰 ‘𝗶𝗿𝗿𝗲𝗴𝘂𝗹𝗮𝗿𝗹𝘆 𝗶𝗿𝗿𝗲𝗴𝘂𝗹𝗮𝗿’ 𝗽𝘂𝗹𝘀𝗲

72
Q

ECG Findings OF AF

A

ECG shows
+ 𝗡𝗼𝗿𝗺𝗮𝗹 𝗯𝘂𝘁 𝗶𝗿𝗿𝗲𝗴𝘂𝗹𝗮𝗿 𝗤𝗥𝗦 𝗰𝗼𝗺𝗽𝗹𝗲𝘅𝗲𝘀
+ 𝗡𝗼 𝗣 𝘄𝗮𝘃𝗲𝘀
+ 𝗕𝗮𝘀𝗲𝗹𝗶𝗻𝗲 𝗺𝗮𝘆 𝘀𝗵𝗼𝘄 𝗶𝗿𝗿𝗲𝗴𝘂𝗹𝗮𝗿 𝗳𝗶𝗯𝗿𝗶𝗹𝗹𝗮𝘁𝗶𝗼𝗻 𝘄𝗮𝘃𝗲𝘀

73
Q

Mx of Atrial fibrillation

A

Management

𝗣𝗮𝗿𝗼𝘅𝘆𝘀𝗺𝗮𝗹 𝗔𝗙
Occasional attacks of AF that are well tolerated do not necessarily require treatment.
𝗕𝗲𝘁𝗮-𝗯𝗹𝗼𝗰𝗸𝗲𝗿𝘀 - 𝗙𝗶𝗿𝘀𝘁-𝗹𝗶𝗻𝗲 𝘁𝗵𝗲𝗿𝗮𝗽𝘆 (𝗦𝗕𝗔)
The most effective agent for prevention is amiodarone (Side effects restrict its use)

𝗣𝗲𝗿𝘀𝗶𝘀𝘁𝗲𝗻𝘁 𝗔𝗙
Principle of Rx
+ Rate or rhythm control
+ Prophylaxis against thromboembolism

Rhythm control
Indication
+ Troublesome symptoms
+ Treatable underlying cause
+ No structural heart disease
+ Young patient
+ Duration < 3 months

Option :
+ Electrical cardioversion
+ Pharmacological cardioversion

If present < 48 hours: Immediate cardioversion

+ 𝗦𝘁𝗮𝗯𝗹𝗲 & 𝗻𝗼 𝗵/𝗼 𝗼𝗳 𝘀𝘁𝗿𝘂𝗰𝘁𝘂𝗿𝗮𝗹 𝗵𝗲𝗮𝗿𝘁 𝗱𝗶𝘀𝗲𝗮𝘀𝗲 : 𝗜𝗩 𝗙𝗹𝗲𝗰𝗮𝗶𝗻𝗶𝗱𝗲
+ 𝗦𝘁𝗿𝘂𝗰𝘁𝘂𝗿𝗮𝗹 𝗼𝗿 𝗜𝗛𝗗: 𝗔𝗺𝗶𝗼𝗱𝗮𝗿𝗼𝗻𝗲
+ DC cardioversion can be used

Rate control
Option
+ 𝟭𝘀𝘁 𝗰𝗵𝗼𝗶𝗰𝗲 : β-𝗯𝗹𝗼𝗰𝗸𝗲𝗿 (𝗦𝗕𝗔)
+ 𝗔𝗹𝘁𝗲𝗿𝗻𝗮𝘁𝗶𝘃𝗲 : 𝗥𝗮𝘁𝗲-𝗹𝗶𝗺𝗶𝘁𝗶𝗻𝗴 𝗖𝗖𝗕 (𝘃𝗲𝗿𝗮𝗽𝗮𝗺𝗶𝗹 / 𝗱𝗶𝗹𝘁𝗶𝗮𝘇𝗲𝗺)
+ 𝗜𝗳 𝗵𝘆𝗽𝗼𝘁𝗲𝗻𝘀𝗶𝗼𝗻 𝗼𝗿 𝗛𝗙 𝗽𝗿𝗲𝘀𝗲𝗻𝘁: 𝗗𝗶𝗴𝗼𝘅𝗶𝗻
𝗖𝗮𝗹𝗰𝗶𝘂𝗺 𝗰𝗵𝗮𝗻𝗻𝗲𝗹 𝗮𝗻𝘁𝗮𝗴𝗼𝗻𝗶𝘀𝘁𝘀 𝘀𝗵𝗼𝘂𝗹𝗱 𝗻𝗼𝘁 𝗯𝗲 𝘂𝘀𝗲𝗱 𝘄𝗶𝘁𝗵 β-𝗯𝗹𝗼𝗰𝗸𝗲𝗿𝘀 𝗯𝗲𝗰𝗮𝘂𝘀𝗲 𝗼𝗳 𝗿𝗶𝘀𝗸 𝗼𝗳 𝗯𝗿𝗮𝗱𝘆𝗰𝗮𝗿𝗱𝗶𝗮

Thromboprophylaxis
𝗔𝗙 𝘀𝗲𝗰𝗼𝗻𝗱𝗮𝗿𝘆 𝘁𝗼 𝗠𝗶𝘁𝗿𝗮𝗹 𝘃𝗮𝗹𝘃𝗲 𝗱𝗶𝘀𝗲𝗮𝘀𝗲 : 𝗚𝗶𝘃𝗲 𝗮𝗻𝘁𝗶𝗰𝗼𝗮𝗴𝘂𝗹𝗮𝗻𝘁
𝗔𝗙 𝘄𝗶𝘁𝗵𝗼𝘂𝘁 𝗺𝗶𝘁𝗿𝗮 𝘃𝗮𝗹𝘃𝗲 𝗱𝗶𝘀𝗲𝗮𝘀𝗲 : 𝗗𝗼 𝗖𝗛𝗔𝟮 𝗗𝗦𝟮-𝗩𝗔𝗦𝗰 𝘀𝘁𝗿𝗼𝗸𝗲 𝗿𝗶𝘀𝗸 𝘀𝗰𝗼𝗿𝗶𝗻𝗴
𝗗𝗶𝗿𝗲𝗰𝘁-𝗮𝗰𝘁𝗶𝗻𝗴 𝗼𝗿𝗮𝗹 𝗮𝗻𝘁𝗶𝗰𝗼𝗮𝗴𝘂𝗹𝗮𝗻𝘁𝘀 (𝗗𝗢𝗔𝗖𝘀)
𝗵𝗮𝘃𝗲 𝗹𝗮𝗿𝗴𝗲𝗹𝘆 𝗿𝗲𝗽𝗹𝗮𝗰𝗲𝗱 𝘄𝗮𝗿𝗳𝗮𝗿𝗶𝗻 𝗳𝗼𝗿 𝘀𝘁𝗿𝗼𝗸𝗲 𝗽𝗿𝗲𝘃𝗲𝗻𝘁𝗶𝗼𝗻 𝗶𝗻 𝗔𝗙

74
Q

What are the DOACs and What are their advantage ?

A

DOACs include
+ Factor Xa inhibitors (Rivaroxaban, apixaban & edoxaban)
+ Direct thrombin inhibitor (Dabigatran)

Advantage
+ 𝗘𝗳𝗳𝗲𝗰𝘁𝗶𝘃𝗲 𝗮𝘁 𝗽𝗿𝗲𝘃𝗲𝗻𝘁𝗶𝗻𝗴 𝘁𝗵𝗿𝗼𝗺𝗯𝗼𝘁𝗶𝗰 𝘀𝘁𝗿𝗼𝗸𝗲
+ 𝗚𝗲𝗻𝗲𝗿𝗮𝗹𝗹𝘆 𝗮𝘀𝘀𝗼𝗰𝗶𝗮𝘁𝗲𝗱 𝘄𝗶𝘁𝗵 𝗮 𝗹𝗼𝘄𝗲𝗿 𝗿𝗶𝘀𝗸 𝗼𝗳 𝗶𝗻𝘁𝗿𝗮𝗰𝗿𝗮𝗻𝗶𝗮𝗹 𝗵𝗮𝗲𝗺𝗼𝗿𝗿𝗵𝗮𝗴𝗲
+ 𝗟𝗮𝗰𝗸 𝗼𝗳 𝗿𝗲𝗾𝘂𝗶𝗿𝗲𝗺𝗲𝗻𝘁 𝗳𝗼𝗿 𝗺𝗼𝗻𝗶𝘁𝗼𝗿𝗶𝗻𝗴
+ 𝗙𝗲𝘄𝗲𝗿 𝗱𝗿𝘂𝗴 & 𝗳𝗼𝗼𝗱 𝗶𝗻𝘁𝗲𝗿𝗮𝗰𝘁𝗶𝗼𝗻𝘀

75
Q

Which agent revers the effect of DOACs

A

Agents that reverse effects of DOACs include
+ 𝗜𝗱𝗮𝗿𝘂𝗰𝗶𝘇𝘂𝗺𝗮𝗯 : 𝗕𝗶𝗻𝗱𝘀 𝘁𝗼 𝗱𝗮𝗯𝗶𝗴𝗮𝘁𝗿𝗮𝗻
+ 𝗔𝗻𝗱𝗲𝘅𝗮𝗻𝗲𝘁 𝗮𝗹𝗳𝗮 : 𝗕𝗶𝗻𝗱𝘀 𝘁𝗼 𝗮𝗽𝗶𝘅𝗮𝗯𝗮𝗻 & 𝗿𝗶𝘃𝗮𝗿𝗼𝘅𝗮𝗯𝗮𝗻.

76
Q

What are the SVT

A

AVNRT
AVRT
AT

77
Q

AVNRT

A

HR: 120-240
Duration: A few Seconds to many Hours
Usually Occurs in the absence of Structural Heart Disease
ECG: Tachycardia with normal QRS Complex
MX: Acute Episode: Carotid sinus Pressure or Valsalva manoeuvre
To restore Sinus rhythm: IV Adenosine / Verapamil
If severe Hemodynamic compromise: DC Cardioversion
Recurrent SVT: Catheter ablation is the most effective therapy

78
Q

AVRT

A

ECG: Shortened PR Interval
Delta Wave ( slurred Initial deflection of QRS Complex)

Catheter ablation is the first line and most effective and curative treatment

Prophylactic: Flecainide and Propafenone

79
Q

What are the pathognomonic features of VT

A

AV dissociation
Capture / Fusion Beats

80
Q

Where VT Occur most commonly?

A

Acute MI
Chronic CAD
Cardiomyopathy

VT is associated with
Extensive Ventricular disease
Impaired Left ventricular function
Ventricular aneurysm

81
Q

Which conditions it become difficult to distinguish between VT and SVT on ECG

A

It may be difficult to distinguish VT from SVT with
+ Bundle branch block
+ Pre-excitation (WPW syndrome)on ECG

Features In favor of VT are
H/O MI
AV Dissociation
Capture/ Fusion beats
Extreme Left axis deviation
Very Broad QRS Complex (140ms)
Irresponsive to carotid sinus massage Or IV adenosine

82
Q

Idioventricular Rhythm

A

Occurs to the patient recovering from MI

Rate: Slightly above the preceding sinus node and below 120 bpm
Self-limiting
Asymptomatic
Reflect reperfusion of Infarct territory and may be a good sign

do not require Treatment

83
Q

VT with Systolic BP less than 90 mmHg what is mx?

A

Synchronized DC Cardioversion

If the arrhythmia is well tolerated then IV amiodarone

84
Q

Treatment of Choice for VT in Normal heart ?

A

Catheter ablation

85
Q

Torsades de pointes

A

𝗧𝗢𝗥𝗦𝗔𝗗𝗘𝗦 𝗗𝗘 𝗣𝗢𝗜𝗡𝗧𝗘𝗦
This form of 𝗽𝗼𝗹𝘆𝗺𝗼𝗿𝗽𝗵𝗶𝗰 𝗩𝗧 𝗶𝘀 𝗮 𝗰𝗼𝗺𝗽𝗹𝗶𝗰𝗮𝘁𝗶𝗼𝗻 𝗼𝗳 𝗽𝗿𝗼𝗹𝗼𝗻𝗴𝗲𝗱 𝘃𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝗿𝗲𝗽𝗼𝗹𝗮𝗿𝗶𝘀𝗮𝘁𝗶𝗼𝗻 (𝗽𝗿𝗼𝗹𝗼𝗻𝗴𝗲𝗱 𝗤𝗧 𝗶𝗻𝘁𝗲𝗿𝘃𝗮𝗹)

ECG: 𝗥𝗮𝗽𝗶𝗱 𝗶𝗿𝗿𝗲𝗴𝘂𝗹𝗮𝗿 𝗰𝗼𝗺𝗽𝗹𝗲𝘅𝗲𝘀 that seem to twist around baseline as 𝗺𝗲𝗮𝗻 𝗤𝗥𝗦 𝗮𝘅𝗶𝘀 𝗰𝗵𝗮𝗻𝗴𝗲𝘀

MX: IV Mg should be given in all cases (8mmol over 15min then 72 mmol over 24 hours )

86
Q

Congenital Long QT syndrome

A

Congenital long QT: Mutations in genes that code for 𝗰𝗮𝗿𝗱𝗶𝗮𝗰 𝗞 𝗼𝗿 𝗡𝗮 𝗰𝗵𝗮𝗻𝗻𝗲𝗹𝘀

Triggers
+ Long QT1 : Vigorous exercise
+ Long QT2 : Sudden noise
+ Long QT3 : Sleep

𝗖𝗼𝗻𝗴𝗲𝗻𝗶𝘁𝗮𝗹 𝗹𝗼𝗻𝗴 𝗤𝗧: 𝗕𝗲𝘁𝗮 𝗯𝗹𝗼𝗰𝗸𝗲𝗿𝘀 (𝗦𝗕𝗔)
𝗥𝗲𝘀𝗶𝘀𝘁𝗮𝗻𝘁 𝗮𝗿𝗿𝗵𝘆𝘁𝗵𝗺𝗶𝗮: 𝗟𝗲𝗳𝘁 𝘀𝘁𝗲𝗹𝗹𝗮𝘁𝗲 𝗴𝗮𝗻𝗴𝗹𝗶𝗼𝗻 𝗯𝗹𝗼𝗰𝗸

87
Q

Brugada Syndrome

A

Genetic Disorder Present with Polymorphic VT and Sudden death
Commonly Caused By Mutation In the SCN5A Gene Which encodes Na Channels
ECG: RBBB, ST elevation In The V1 and V2 without prolongation of the QT interval

Mx: Implantable Defibrillator

88
Q

Classification Of Anti-Arrhythmic Drug According TO M/A

A

Class 1: Membrane stabilizing agents ( Na channel blockers)
1(a) Prolong AP: Disopyramide, Quinidine
1(b) Shorten AP: Lidocaine , Mexiletine
1(c) No effect on AP: Flecainide, Propafenone

Class 2: B Blocker
Atenolol, Bisoprolol, metoprolol

Class 3: Drugs Whose Main Effect to Prolong AP
Amiodarone, Dronedarone, Sotalol

Class 4: Slow Calcium Channel blocker:
Diltiazem, Verapamil

89
Q

Classification of Anti-Arrhythmic drug acc to site of Action

A

SA Node:
Atropine
B blocker
Verapamil
Diltiazem

AV node:
Adenosine
B blocker
Digoxin
Diltiazem
Verapamil

Ventricles:
Lidocaine
Mexiletine
B blocker

Atria, Ventricle accessory Conducting tissue
Class 1(a)+ 1(C) + amiodarone

90
Q

Digoxin Toxicity

A

Extra cardiac:
Anorexia, Nausea , Vomiting, Diarrhoea, Altered Color vision (xanthopsia)

Cardiac:
Bradycardia
Multiple Ventricular ectopic
Ventricular bigeminy
Atrial Tachycardia
Ventricular Tachycardia
Ventricular fibrillation

91
Q

Permanent Pace maker Indication and Complication

A

Indication:
Single Chamber :
Atrial pacing: Sinoatrial Disease without AV block
Ventricular Pacing: Continuous AF and bradycardia

Dual Chamber:
2nd and 3rd Degree heart block

Complication:
Early :
Pneumothorax
Cardiac Tamponade
Infection
Lead displacement

Late:
Infection
Erosion of the lead
Lead fracture
Chronic pain

92
Q

What is the most powerful independent risk factor for atherosclerosis

A

AGE

93
Q

What is the imp modifiable risk factor for CAD?

A

Smoking

94
Q

What are the six stages of atherosclerosis

A

Initial lesion
Fatty streak
Intermediate lesion
atheroma
Fibroatheroma
Complicated

95
Q

Coronary blood flow usually occurs in-

A

Diastole

96
Q

Factors Influencing Myocardial Oxygen supply and Coronary Blood Flow

A

Myocardial Oxygen Supply:
HR
BP
Myocardial Contractility
LVH
Valve disease

Coronary Blood Flow:
Duration of Diastole
Coronary perfusion pressure
Coronary Vasomotor tone
Oxygenation:
Hb
O2 Saturation

97
Q

What is prinzmetal’s angina

A

Coronary artery Spasm+ Transient ST elevation

98
Q

Three Characteristics features of angina

A
  1. Constricting Discomfort in the center of the chest, Or in the neck, Shoulder, Jaw and arms
  2. Precipitate by Physical Exertion
  3. Relieved By rest (GTN) within 5 minutes
99
Q

What is the most common cause of angina pectoris

A

Coronary Atherosclerosis

100
Q

Syndrome X

A

+ 𝗧𝘆𝗽𝗶𝗰𝗮𝗹 𝗮𝗻𝗴𝗶𝗻𝗮 𝗼𝗻 𝗲𝗳𝗳𝗼𝗿𝘁
+ 𝗡𝗼𝗿𝗺𝗮𝗹 𝗰𝗼𝗿𝗼𝗻𝗮𝗿𝘆 𝗮𝗿𝘁𝗲𝗿𝗶𝗲𝘀 𝗼𝗻 𝗮𝗻𝗴𝗶𝗼𝗴𝗿𝗮𝗽𝗵𝘆
+ 𝗢𝗯𝗷𝗲𝗰𝘁𝗶𝘃𝗲 𝗲𝘃𝗶𝗱𝗲𝗻𝗰𝗲 𝗼𝗳 𝗺𝘆𝗼𝗰𝗮𝗿𝗱𝗶𝗮𝗹 𝗶𝘀𝗰𝗵𝗮𝗲𝗺𝗶𝗮 𝗼𝗻 𝘀𝘁𝗿𝗲𝘀𝘀 𝘁𝗲𝘀𝘁𝗶𝗻𝗴
+ 𝗠𝗼𝗿𝗲 𝗰𝗼𝗺𝗺𝗼𝗻 𝗶𝗻 𝘄𝗼𝗺𝗲𝗻
+ 𝗚𝗼𝗼𝗱 𝗽𝗿𝗼𝗴𝗻𝗼𝘀𝗶𝘀
+ 𝗥𝗲𝘀𝗽𝗼𝗻𝗱 𝘃𝗮𝗿𝗶𝗮𝗯𝗹𝘆 𝘁𝗼 𝗮𝗻𝘁𝗶 𝗮𝗻𝗴𝗶𝗻𝗮𝗹 𝘁𝗵𝗲𝗿𝗮𝗽𝘆

101
Q

False Positive result on ECG can be found in

A

Digoxin toxicity
LVH
BBB
WPW Syndrome

102
Q

Nitrates

A

Lowered Preload and afterload which reduce myocardial Oxygen Demand.
Coronary Vasodilation which increases Oxygen Supply

A/E:
Headache
Hypotension
Syncope rarely

103
Q

Which anti-anginal drug is safe In HF

A

Ivabradine (If Channel antagonist)

104
Q

Which arteries are used for Bypass grafting

A

Internal mammary artery
Radial Artery
Saphenous vain

105
Q

Characteristics of Unstable angina

A

Unstable angina
+ New-onset or rapidly worsening angina (crescendo angina)
+ Angina on minimal exertion
+ Angina at rest in the absence of myocardial damage

106
Q

Dx criteria of AMI

A

Fall/ Rise Troponin level with at least one value above the 99th centile upper reference limit with one of the following:
- Symptoms of AMI
- New Ischaemic ECG Change
- Pathological Q on ECG
- New loss of viable myocardium and regional wall abnormality on imaging
- Identification of Coronary thrombus on angiography or autopsy

107
Q

Common Arrhythmia in ACS

A

VF
VT
Ventricular Ectopic
AF
AV Block
Idioventricular Rhythm
Sinus Bradycardia

108
Q

Patient H/O ACS having recurrent angina with dynamic ECG change Should be treated with

A

Glycoprotein IIb/IIIa receptor antagonist
Tirofiban
Abciximab

109
Q

Pericarditis

A

Occurs on 2nd and 3rd day
Different pain develops on the same side and may worse sometime, sometimes it may only present during INSPIRATION
A Pericardial rub may be present

RX: Opiate based analgesic

110
Q

Persistent Fever, Pericarditis, Pleurisy

A

Dressler syndrome

Due to autoimmunity
Usually occurs a few days or a few months after MI

Rx with: High Dose aspirin
(NSAIDs, Glucocorticoid steroid may be required)

111
Q

Pan systolic murmur + Pulmonary Oedema with 3rd heart sound after MI

A

Papillary Muscle rupture confirmed by Echocardiography

112
Q

Pan systolic murmur + RHF + Haemodynamic deterioration

A

Ventricular septal rupture

Confirmed by Echocardiography and cardiac catheterization

113
Q

Which drug should be given to prevent ventricular remodeling and HF

A
  1. ACE Inhibitors
  2. Beta blocker
  3. Mineralocorticoid Antagonist
114
Q

Ventricular Aneurysm

A

♦️ Complications of aneurysm

+ Heart failure

+ Ventricular arrhythmias

+ Mural thrombus & systemic embolism

♦️ Other features

+ Paradoxical impulse on chest wall,

+ 𝗣𝗲𝗿𝘀𝗶𝘀𝘁𝗲𝗻𝘁 𝗦𝗧 𝗲𝗹𝗲𝘃𝗮𝘁𝗶𝗼𝗻 𝗼𝗻 𝗘𝗖𝗚 (𝗦𝗕𝗔)

+ Sometimes an unusual bulge from cardiac silhouette on chest X-ray

♦️ 𝗘𝗰𝗵𝗼𝗰𝗮𝗿𝗱𝗶𝗼𝗴𝗿𝗮𝗽𝗵𝘆 𝗶𝘀 𝗱𝗶𝗮𝗴𝗻𝗼𝘀𝘁𝗶𝗰

115
Q

What is the earliest change in the ECG in MI

A

𝗘𝗮𝗿𝗹𝗶𝗲𝘀𝘁 𝗘𝗖𝗚 𝗰𝗵𝗮𝗻𝗴𝗲 : 𝗦𝗧-𝘀𝗲𝗴𝗺𝗲𝗻𝘁 𝗱𝗲𝘃𝗶𝗮𝘁𝗶𝗼𝗻 (𝗦𝗕𝗔)

116
Q

ECG change According to vessel occlusion

A

Proximal occlusion of a major coronary artery :

🔹ST elevation (or new bundle branch block) >

🔹Diminution in size of R & in transmural infarction, development of Q

>

🔹T wave invertion (Persists after ST segment has returned to normal)

*** Partial occlusion of a major vessel or complete occlusion of a minor vessel

🔹 Causing unstable angina or partial thickness (subendocardial) MI

🔹 ST depression & T wave change

🔹 Some loss of R wave

🔹 Absence of Q wave

🔹 No ST elevation

117
Q

ECG changes in Lead V1- V4 indicate

A

Anteroseptal infarction

118
Q

ECG changes in lead V4 - V6, avL and Lead I indicate

A

Anterolateral infarction

119
Q

ECG changes in Lead II,III and aVF indicate

A

Inferior infarction

120
Q

Which lead change will occur in posterior LV infarction

A

𝗣𝗼𝘀𝘁𝗲𝗿𝗶𝗼𝗿 𝘄𝗮𝗹𝗹 𝗼𝗳 𝗟𝗩 : 𝗥𝗲𝗰𝗶𝗽𝗿𝗼𝗰𝗮𝗹 𝗦𝗧 𝗱𝗲𝗽𝗿𝗲𝘀𝘀𝗶𝗼𝗻 & 𝘁𝗮𝗹𝗹 𝗥 𝗶𝗻 𝗩𝟭 - 𝗩𝟰

121
Q

Cardiac Biomarkers and Blood investigation

A

𝗖𝗮𝗿𝗱𝗶𝗮𝗰 𝗯𝗶𝗼𝗺𝗮𝗿𝗸𝗲𝗿

🔹 Unstable angina : No detectable ↑ in troponin

🔹 MI : ↑ In troponin T,I & other cardiac enzymes

*** Troponins T & I

+ 𝗜𝗻𝗰𝗿𝗲𝗮𝘀𝗲 𝘄𝗶𝘁𝗵𝗶𝗻 𝟯–𝟲 𝗵𝗼𝘂𝗿𝘀

+ 𝗣𝗲𝗮𝗸 𝗮𝘁 𝗮𝗯𝗼𝘂𝘁 𝟯𝟲 𝗵𝗼𝘂𝗿𝘀

+ 𝗥𝗲𝗺𝗮𝗶𝗻 𝗲𝗹𝗲𝘃𝗮𝘁𝗲𝗱 𝗳𝗼𝗿 𝘂𝗽 𝘁𝗼 𝟮 𝘄𝗲𝗲𝗸𝘀.

♦️ ↑ WBC,CRP & ESR

♦️ Lipids should be measured within 24 hr as there is often a transient fall in cholesterol in the 3 months following infarction

122
Q

𝗖𝗼𝗿𝗼𝗻𝗮𝗿𝘆 𝗮𝗿𝘁𝗲𝗿𝗶𝗼𝗴𝗿𝗮𝗽𝗵𝘆 / Angiography Indication

A

+ 𝗮𝗹𝗹 𝗽𝗮𝘁𝗶𝗲𝗻𝘁𝘀 𝗮𝘁 𝗺𝗼𝗱𝗲𝗿𝗮𝘁𝗲 𝗼𝗿 𝗵𝗶𝗴𝗵 𝗿𝗶𝘀𝗸 𝗼𝗳 𝗮 𝗳𝘂𝗿𝘁𝗵𝗲𝗿 𝗲𝘃𝗲𝗻𝘁

+ 𝗪𝗵𝗼 𝗳𝗮𝗶𝗹 𝘁𝗼 𝘀𝗲𝘁𝘁𝗹𝗲 𝗼𝗻 𝗺𝗲𝗱𝗶𝗰𝗮𝗹 𝘁𝗵𝗲𝗿𝗮𝗽𝘆

+ 𝗪𝗶𝘁𝗵 𝗲𝘅𝘁𝗲𝗻𝘀𝗶𝘃𝗲 𝗘𝗖𝗚 𝗰𝗵𝗮𝗻𝗴𝗲𝘀

+ 𝗪𝗶𝘁𝗵 𝗮𝗻 𝗲𝗹𝗲𝘃𝗮𝘁𝗲𝗱 𝗰𝗮𝗿𝗱𝗶𝗮𝗰 𝘁𝗿𝗼𝗽𝗼𝗻𝗶𝗻

+ 𝗪𝗶𝘁𝗵 𝘀𝗲𝘃𝗲𝗿𝗲 𝗽𝗿𝗲-𝗲𝘅𝗶𝘀𝘁𝗶𝗻𝗴 𝘀𝘁𝗮𝗯𝗹𝗲 𝗮𝗻𝗴𝗶𝗻𝗮

FCPS Preperation (5 decks)

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