বিসমিল্লাহির রহমানির রহীম 

#DAVIDSON_REVIEW 
#CARDIOLOGY 1

Cardiology থেকে প্রায় ১৫ টা প্রশ্ন থাকে।5/6 ta Anatomy & Physiology related. Cardiology basic একটা পোস্ট
দেওয়া আছে।কিছুটা কভার হবে। 

N.B. 
Davodson Anatomy & physiology ভাল করে বুঝে পড়বেন।তাহলে অনেকপ্রশ্ন কমননা থাকলেওবুঝে উওরদিতে
পারবেন।মুখস্থ করে গেলে পরিক্ষায় না পারার সম্ভাবনা অনেক বেশি।😥😥

### Page 442 -460 ( 387- 401)

Anatomy & Physiology ********

Box 16.1 *****
Box 16.2 ***** (𝗠𝗖𝗤 𝗝𝗔𝗡 𝟮𝟬)
Box 16.3 ***
Box 16.4 ***
Fig 16.9 **
Fig 16.17 (16.18) **
Box 16.7 *****
Fig 16.20 (23rd) ***** (𝐒𝐁𝐀 𝐉𝐀𝐍 𝟐𝟐)
Box 16.8 ********** 𝗦𝗕𝗔 𝗝𝗨𝗟 𝟮𝟮
Box 16.9 ***** (𝗠𝗖𝗤 𝗝𝗔𝗡 𝟮𝟬)
Box 16.11 ***
Fig 16.23 **

Page 443 (387)

Box 5 

♦️Height of jugular venous pulse is determined by right atrial pressure 

   + Elevated in right heart failure  
   + Reduced in hypovolaemia

   ♦️a wave - Atrial systole  

+ 𝗔𝗯𝘀𝗲𝗻𝘁 : 𝗔𝘁𝗿𝗶𝗮𝗹𝗳𝗶𝗯𝗿𝗶𝗹𝗹𝗮𝘁𝗶𝗼𝗻 (𝗦𝗕𝗔)
+ Giant :
   ✓ Tricuspid stenosis
   ✓ pulmonary stenosis 
   ✓ Pulmonary hypertension
   ✓ Right heart failure
+ 𝗜𝗿𝗿𝗲𝗴𝘂𝗹𝗮𝗿 𝗰𝗮𝗻𝗻𝗼𝗻 𝗮 𝘄𝗮𝘃𝗲 : 𝟯° 𝗵𝗲𝗮𝗿𝘁 𝗯𝗹𝗼𝗰𝗸 (𝗦𝗕𝗔)
+ Regular cannon a wave
   ✓ Ventricular tachycardia
   ✓ Atrioventricular re entry tachycardia 

   ♦️v waves - Ventricular systole 

+ 𝗚𝗶𝗮𝗻𝘁 𝘃 (𝗰-𝘃) 𝘄𝗮𝘃𝗲 : 𝗧𝗿𝗶𝗰𝘂𝘀𝗽𝗶𝗱 𝗿𝗲𝗴𝘂𝗿𝗴𝗶𝘁𝗮𝘁𝗶𝗼𝗻 (𝗦𝗕𝗔)  

   ♦️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  

   ♦️Parodoxical JVP (Kussmaul's sign)

+ 𝗖𝗼𝗻𝘀𝘁𝗿𝗶𝗰𝘁𝗶𝘃𝗲 𝗽𝗲𝗿𝗶𝗰𝗮𝗿𝗱𝗶𝘁𝗶𝘀 (𝗠𝗼𝗿𝗲 𝗰𝗼𝗺𝗺𝗼𝗻)
+ 𝗖𝗮𝗿𝗱𝗶𝗮𝗰 𝘁𝗮𝗺𝗽𝗼𝗻𝗮𝗱𝗲 (𝗥𝗮𝗿𝗲)
+ 𝗣𝗲𝗿𝗶𝗰𝗮𝗿𝗱𝗶𝗮𝗹 𝗲𝗳𝗳𝘂𝘀𝗶𝗼𝗻
 
(Ref - Notes & wiki)

   *** Distinguishing venous/arterial pulsation in the neck 

♦️Venous pulse : Two peaks in each cardiac cycle. Arterial pulse : One peak
♦️Height of venous pulse varies with respiration (falls on inspiration) & position
♦️Abdominal compression causes venous pulse to rise
♦️Venous pulse is not easily palpable & can be occluded with light pressure

   *** Box 7
🔹𝗩𝗼𝗹𝘂𝗺𝗲 𝗼𝘃𝗲𝗿𝗹𝗼𝗮𝗱 (𝗠𝗥 / 𝗔𝗥) : 𝗗𝗶𝘀𝗽𝗹𝗮𝗰𝗲𝗱, 𝘁𝗵𝗿𝘂𝘀𝘁𝗶𝗻𝗴 
🔹𝗣𝗿𝗲𝘀𝘀𝘂𝗿𝗲 𝗼𝘃𝗲𝗿𝗹𝗼𝗮𝗱 (𝗔𝗦 / 𝗛𝗧𝗡) : 𝗗𝗶𝘀𝗰𝗿𝗲𝘁𝗲, 𝗵𝗲𝗮𝘃𝗶𝗻𝗴 
🔹Dyskinetic (Left ventricular aneurysm): Displaced, incoordinate 
🔹 𝗣𝗮𝗹𝗽𝗮𝗯𝗹𝗲 𝗦𝟭 / 𝗧𝗮𝗽𝗽𝗶𝗻𝗴 𝗮𝗽𝗲𝘅 𝗯𝗲𝗮𝘁 : 𝗠𝗶𝘁𝗿𝗮𝗹 𝘀𝘁𝗲𝗻𝗼𝘀𝗶𝘀
🔹 𝗣𝗮𝗹𝗽𝗮𝗯𝗹𝗲 𝗣𝟮 : 𝗦𝗲𝘃𝗲𝗿𝗲 𝗽𝘂𝗹𝗺𝗼𝗻𝗮𝗿𝘆 𝗛𝗧𝗡 
🔹 𝗟𝗲𝗳𝘁 𝗽𝗮𝗿𝗮𝘀𝘁𝗲𝗿𝗻𝗮𝗹 𝗵𝗲𝗮𝘃𝗲 𝗼𝗿 ‘𝗹𝗶𝗳𝘁’ : 𝗥𝗶𝗴𝗵𝘁 𝘃𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝗵𝘆𝗽𝗲𝗿𝘁𝗿𝗼𝗽𝗵𝘆
🔹Palpable thrill : Aortic stenosis

𝗔𝗻𝗮𝘁𝗼𝗺𝘆  

🔹Left atrium (LA) sits anterior to esophagus & descending aorta.

🔹Right atrium (RA) receives blood from superior & inferior venae cavae & coronary sinus
🔹LA receives blood from four pulmonary veins, two from each of left & right lungs. 

   *** Annulus fibrosus

+ 𝗦𝗲𝗽𝗮𝗿𝗮𝘁𝗲𝘀 𝗮𝘁𝗿𝗶𝗮 & 𝘃𝗲𝗻𝘁𝗿𝗶𝗰𝗹𝗲𝘀
+ 𝗙𝗼𝗿𝗺𝘀 𝘁𝗵𝗲 𝘀𝗸𝗲𝗹𝗲𝘁𝗼𝗻 𝗳𝗼𝗿 𝗔𝗩 𝘃𝗮𝗹𝘃𝗲𝘀 
+ 𝗘𝗹𝗲𝗰𝘁𝗿𝗶𝗰𝗮𝗹𝗹𝘆 𝗶𝗻𝘀𝘂𝗹𝗮𝘁𝗲𝘀 𝗮𝘁𝗿𝗶𝗮 𝗳𝗿𝗼𝗺 𝘃𝗲𝗻𝘁𝗿𝗶𝗰𝗹𝗲𝘀
(𝗦𝗕𝗔) / 𝙛𝙤𝙧𝙢𝙨 𝙖 𝙘𝙤𝙣𝙙𝙪𝙘𝙩𝙞𝙤𝙣 𝙗𝙖𝙧𝙧𝙞𝙚𝙧 𝙗𝙚𝙩𝙬𝙚𝙚𝙣 𝙖𝙩𝙧𝙞𝙖 & 𝙫𝙚𝙣𝙩𝙧𝙞𝙘𝙡𝙚𝙨
+ 𝗣𝗿𝗲𝘃𝗲𝗻𝘁𝘀 𝘁𝗿𝗮𝗻𝘀𝗺𝗶𝘀𝘀𝗶𝗼𝗻 𝗼𝗳 𝗰𝗼𝗻𝗱𝘂𝗰𝘁𝗶𝗼𝗻 𝗲𝘅𝗰𝗲𝗽𝘁 𝗔𝗩 𝗻𝗼𝗱𝗲 
*** 𝙊𝙣 𝙡𝙚𝙛𝙩, 𝙘𝙖𝙧𝙙𝙞𝙖𝙘 𝙨𝙞𝙡𝙝𝙤𝙪𝙚𝙩𝙩𝙚 𝙞𝙨 𝙛𝙤𝙧𝙢𝙚𝙙 𝙗𝙮      
  + 𝙖𝙤𝙧𝙩𝙞𝙘 𝙖𝙧𝙘𝙝 
  + 𝙥𝙪𝙡𝙢𝙤𝙣𝙖𝙧𝙮 𝙩𝙧𝙪𝙣𝙠
  + 𝙡𝙚𝙛𝙩 𝙖𝙩𝙧𝙞𝙖𝙡 𝙖𝙥𝙥𝙚𝙣𝙙𝙖𝙜𝙚  
  + 𝙇𝙑. 

*** 𝙊𝙣 𝙧𝙞𝙜𝙝𝙩,𝙨𝙞𝙡𝙝𝙤𝙪𝙚𝙩𝙩𝙚 𝙞𝙨 𝙛𝙤𝙧𝙢𝙚𝙙 𝙗𝙮 

  + 𝙍𝘼 
  + 𝗦𝙪𝙥𝙚𝙧𝙞𝙤𝙧 & 𝙞𝙣𝙛𝙚𝙧𝙞𝙤𝙧 𝙫𝙚𝙣𝙖𝙚 𝙘𝙖𝙫𝙖𝙚 
  + 𝙍𝙑
.

*** 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%)
+ 

   *** 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 remainder (dominant left system).
+ 𝙋𝙧𝙤𝙭𝙞𝙢𝙖𝙡𝙤𝙘𝙘𝙡𝙪𝙨𝙞𝙤𝙣𝙤𝙛 𝙍𝘾𝘼 𝙩𝙝𝙚𝙧𝙚𝙛𝙤𝙧𝙚𝙤𝙛𝙩𝙚𝙣𝙧𝙚𝙨𝙪𝙡𝙩𝙨𝙞𝙣 𝙨𝙞𝙣𝙪𝙨 𝙗𝙧𝙖𝙙𝙮𝙘𝙖𝙧𝙙𝙞𝙖 & 𝘼𝙑𝙣𝙤𝙙𝙖𝙡𝙗𝙡𝙤𝙘𝙠.
(𝐒𝐁𝐀 𝐉𝐀𝐍 𝟐𝟐)

🔷 Venous system follows coronary arteries but in AV𝗱𝗿𝗮𝗶𝗻𝘀 𝗶𝗻𝘁𝗼 𝗰𝗼𝗿𝗼𝗻𝗮𝗿𝘆 𝘀𝗶𝗻𝘂𝘀
groove & then to RA
  
   *** Effects of sympathetic activity
♦️β𝟭-𝗮𝗱𝗿𝗲𝗻𝗼𝗰𝗲𝗽𝘁𝗼𝗿𝘀 𝗶𝗻 𝗵𝗲𝗮𝗿𝘁 𝗿𝗲𝘀𝘂𝗹𝘁𝘀 
   + 𝗣𝗼𝘀𝗶𝘁𝗶𝘃𝗲 𝗶𝗻𝗼𝘁𝗿𝗼𝗽𝗶𝗰 & 𝗰𝗵𝗿𝗼𝗻𝗼𝘁𝗿𝗼𝗽𝗶𝗰 𝗲𝗳𝗳𝗲𝗰𝘁𝘀, 
♦️β𝟮-𝗮𝗱𝗿𝗲𝗻𝗼𝗰𝗲𝗽𝘁𝗼𝗿𝘀 𝗶𝗻 𝘃𝗮𝘀𝗰𝘂𝗹𝗮𝗿 𝘀𝗺𝗼𝗼𝘁𝗵 𝗺𝘂𝘀𝗰𝗹𝗲 : 𝗩𝗮𝘀𝗼𝗱𝗶𝗹𝗮𝘁𝗮𝘁𝗶𝗼𝗻

   *** Parasympathetic 
♦️Pre- ganglionic & sensory fibres reach vagus nerves
♦️Cholinergic nerves supply AV & SA nodes via muscarinic (M2) receptors
♦️Under resting conditions, vagal inhibitory activity predominates & heart rate is slow
.

𝗣𝗵𝘆𝘀𝗶𝗼𝗹𝗼𝗴𝘆 

🔹 Electrical conduction : By Intercalated disc via gap junctions & Mechanical conduction :
via fascia adherens
🔹Basic unit of contraction : Sarcomere 
🔹Enlargement of heart seen in heart failure is due to slippage of myofibrils & adjacent cells
rather than lengthening of sarcomere. 

   *** 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 

   *** Central arteries (ex- aorta)

+ 𝗣𝗿𝗲𝗱𝗼𝗺𝗶𝗻𝗮𝗻𝘁𝗹𝘆 𝗰𝗼𝗺𝗽𝗼𝘀𝗲𝗱 𝗼𝗳 𝗲𝗹𝗮𝘀𝘁𝗶𝗰 𝘁𝗶𝘀𝘀𝘂𝗲 𝘄𝗶𝘁𝗵 𝗹𝗶𝘁𝘁𝗹𝗲 𝗼𝗿 𝗻𝗼 𝘃𝗮𝘀𝗰𝘂𝗹𝗮𝗿
𝘀𝗺𝗼𝗼𝘁𝗵 𝗺𝘂𝘀𝗰𝗹𝗲 𝗰𝗲𝗹𝗹𝘀.
+ 𝗣𝗿𝗲𝘃𝗲𝗻𝘁𝘀 𝗲𝘅𝗰𝗲𝘀𝘀𝗶𝘃𝗲 𝗿𝗶𝘀𝗲𝘀 𝗶𝗻 𝘀𝘆𝘀𝘁𝗼𝗹𝗶𝗰 𝗕𝗣 𝘄𝗵𝗶𝗹𝗲 𝘀𝘂𝘀𝘁𝗮𝗶𝗻𝗶𝗻𝗴 𝗱𝗶𝗮𝘀𝘁𝗼𝗹𝗶𝗰 𝗕𝗣
+ 𝗥𝗲𝗱𝘂𝗰𝗲𝘀 𝗰𝗮𝗿𝗱𝗶𝗮𝗰 𝗮𝗳𝘁𝗲𝗿𝗹𝗼𝗮𝗱 & 𝗺𝗮𝗶𝗻𝘁𝗮𝗶𝗻𝘀 𝗰𝗼𝗿𝗼𝗻𝗮𝗿𝘆 𝗽𝗲𝗿𝗳𝘂𝘀𝗶𝗼𝗻
+ These benefits are lost with progressive arterial stiffening (With ageing & advanced renal
disease)

   *** 
♦️Vasoconstriction : α-adrenoceptors 
♦️Vasodilatation : Muscarinic & β2 adrenoceptors
♦️Predominant effect of sympathetic stimulation in coronary arteries : Vasodilatation
♦️Parasympathetic stimulation : Modest dilatation of normal coronary arteries

   *** Vasoconstrictors : 
+ 𝗡𝗼𝗿𝗮𝗱𝗿𝗲𝗻𝗮𝗹𝗶𝗻𝗲 (𝗻𝗼𝗿𝗲𝗽𝗶𝗻𝗲𝗽𝗵𝗿𝗶𝗻𝗲)
+ 𝗔𝗻𝗴𝗶𝗼𝘁𝗲𝗻𝘀𝗶𝗻 𝗜𝗜 
+ 𝗘𝗻𝗱𝗼𝘁𝗵𝗲𝗹𝗶𝗻-𝟭

   *** Vasodilators
+ 𝗔𝗱𝗲𝗻𝗼𝘀𝗶𝗻𝗲
+ 𝗕𝗿𝗮𝗱𝘆𝗸𝗶𝗻𝗶𝗻
+ 𝗣𝗿𝗼𝘀𝘁𝗮𝗴𝗹𝗮𝗻𝗱𝗶𝗻𝘀 
+ 𝗡𝗶𝘁𝗿𝗶𝗰 𝗼𝘅𝗶𝗱𝗲  

*** Narrowing or stenosis in a coronary artery does not limit flow, even during exercise, until
cross-sectional area of vessel is 𝗿𝗲𝗱𝘂𝗰𝗲𝗱 𝗯𝘆 𝗮𝘁 𝗹𝗲𝗮𝘀𝘁 𝟳𝟬%. 

   *** 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

Box 16.1 
   + Inspiration & expiration e change আলাদা করে পড়তে হবে 
   + বক্সের নিচে ২ টা লাইন ***

   *** During inspiration

🔹↓ Intrathoracic pressure > ↑ Return of venous blood into chest & rt side of heart > ↑ CO
from RV
🔹Blood is sequestered in lungs due to ↑ Capacitance of pulmonary vascular bed > ↓ in
blood flow to LV > ↓ BP

   *** During expiration 

🔹 ↓ Venous return to right heart > ↓ RV output 
🔹 ↑ Venous return to left side of heart > ↑ LV output > ↑ BP

   *** Pulsus parasdoxus (exaggerated / > 10 mmHg ↓ BP during inspiration) 

   + 𝗦𝗲𝘃𝗲𝗿𝗲 𝗮𝘀𝘁𝗵𝗺𝗮 𝗼𝗿 𝗖𝗢𝗣𝗗
   + 𝗖𝗵𝗮𝗿𝗮𝗰𝘁𝗲𝗿𝗶𝘀𝘁𝗶𝗰 𝗼𝗳 𝗰𝗮𝗿𝗱𝗶𝗮𝗰 𝘁𝗮𝗺𝗽𝗼𝗻𝗮𝗱𝗲
.

                     𝗜𝗡𝗩𝗘𝗦𝗧𝗜𝗚𝗔𝗧𝗜𝗢𝗡 

𝗘𝗖𝗚 & Box 16.2

🔹ECG : Main test used in diagnosis of myocardial ischaemia & infarction

🔹Repolarisation is slower & spreads from epicardium to endocardium

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

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

   ♦️Widened QRS duration 

+ Increased : RBBB / LBBB

   ♦️Increased QRS amplitude

+ Left ventricular hypertrophy

   ♦️Q wave
+ Previous myocardial infarction

   ♦️T wave
+ 𝗩𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝗿𝗲𝗽𝗼𝗹𝗮𝗿𝗶𝘀𝗮𝘁𝗶𝗼𝗻
+ 𝗧𝗮𝗹𝗹, 𝗽𝗲𝗮𝗸𝗲𝗱 𝗧 : 𝗛𝘆𝗽𝗲𝗿𝗸𝗮𝗹𝗲𝗺𝗶𝗮 (𝗦𝗕𝗔)

   ♦️ST segment
+ 𝗪𝗶𝗱𝗲𝘀𝗽𝗿𝗲𝗮𝗱 𝘀𝗮𝗱𝗱𝗹𝗲 𝘀𝗮𝗵𝗽𝗲𝗱 𝗲𝗹𝗲𝘃𝗮𝘁𝗶𝗼𝗻 : 𝗔𝗰𝘂𝘁𝗲 𝗽𝗲𝗿𝗶𝗰𝗮𝗿𝗱𝗶𝘁𝗶𝘀
+ 𝗣𝗲𝗿𝘀𝗶𝘀𝘁𝗲𝗻𝘁 𝗦𝗧 𝗲𝗹𝗲𝘃𝗮𝘁𝗶𝗼𝗻 : 𝗟𝘁 𝘃𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝗮𝗻𝗲𝘂𝗿𝘆𝘀𝗺 (𝗦𝗕𝗔)

   ♦️QT interval 
+ Represents total duration of ventricular depolarisation & repolarisation
+ Prolonged : Box 16.28
  

   *** 𝙉𝙤𝙧𝙢𝙖𝙡 𝙘𝙖𝙧𝙙𝙞𝙖𝙘 𝙖𝙭𝙞𝙨 𝙡𝙞𝙚𝙨 𝙗𝙚𝙩𝙬𝙚𝙚𝙣 −30° 𝙖𝙣𝙙 +90°. 

   *** 𝙇𝙚𝙖𝙙𝙨 
🔹𝙑1 & 𝙑2 >>> 𝙍𝙑
🔹𝙑3 & 𝙑4 >>> 𝙞𝙣𝙩𝙚𝙧𝙫𝙚𝙣𝙩𝙧𝙞𝙘𝙪𝙡𝙖𝙧𝙨𝙚𝙥𝙩𝙪𝙢
🔹𝙑5 & 𝙑6 𝙤𝙫𝙚𝙧 >>> 𝙇𝙑

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

   ***** TROPONIN I increased in

❤️CARDIAC
   • MI, Myocarditis
   • Pulmonary embolism
   • Pulmonary oedema
   • Cardiac surgery, trauma
   • Tachyarrhythmia
   • Aortic dissection

❤️NON CARDIAC
   • Septic shock,Stroke,SAH
   • Prolonged hypotension
   • ESRD
   • Burn
.
  
Chest X-ray 

   *** Lt atrial dilatation

+ Prominence of lt atrial appendage
+ Straight lt heart border
+ A double cardiac shadow to rt of sternum
+ Widening of angle of carina (bifurcation of the trachea)

   *** Transoesophagial echocardiography

♦️Useful for -
   + Lt atrial appendage
   + Pulmonary veins
   + Thoracic aorta 
   + Interatrial septum
especially if the patient is overweight or has obstructive airway disease

   *** 𝙏𝙊𝙀 𝙥𝙖𝙧𝙩𝙞𝙘𝙪𝙡𝙖𝙧𝙡𝙮 𝙫𝙖𝙡𝙪𝙖𝙗𝙡𝙚 𝙛𝙤𝙧

+ 𝙥𝙧𝙤𝙨𝙩𝙝𝙚𝙩𝙞𝙘 (𝙚𝙨𝙥𝙚𝙘𝙞𝙖𝙡𝙡𝙮 𝙢𝙞𝙩𝙧𝙖𝙡) 𝙫𝙖𝙡𝙫𝙚 𝙙𝙮𝙨𝙛𝙪𝙣𝙘𝙩𝙞𝙤𝙣    
+ 𝘼𝙎𝘿
+ 𝙖𝙤𝙧𝙩𝙞𝙘 𝙙𝙞𝙨𝙨𝙚𝙘𝙩𝙞𝙤𝙣
+ 𝙞𝙣𝙛𝙚𝙘𝙩𝙞𝙫𝙚 𝙚𝙣𝙙𝙤𝙘𝙖𝙧𝙙𝙞𝙩𝙞𝙨 (𝙫𝙚𝙜𝙚𝙩𝙖𝙩𝙞𝙤𝙣𝙨 𝙩𝙤𝙤 𝙨𝙢𝙖𝙡𝙡 𝙛𝙤𝙧 𝙏𝙏𝙀) 
+ 𝙨𝙮𝙨𝙩𝙚𝙢𝙞𝙘 𝙚𝙢𝙗𝙤𝙡𝙞𝙨𝙢 (𝙞𝙣𝙩𝙧𝙖𝙘𝙖𝙧𝙙𝙞𝙖𝙘 𝙩𝙝𝙧𝙤𝙢𝙗𝙪𝙨 𝙤𝙧 𝙢𝙖𝙨𝙨𝙚𝙨)

🔹Contrast CT are very useful for 

   + Aortic dissection
   + Pulmonary embolism
🔹Electrophysiological study (EPS)
   + Most commonly to evaluate patients for catheter ablation 
   + Risk stratification of suspected ventricular arrhythmia 
.

Chest pain on exertion

   *** 𝗖𝗧 𝗰𝗼𝗿𝗼𝗻𝗮𝗿𝘆 𝗮𝗻𝗴𝗶𝗼𝗴𝗿𝗮𝗽𝗵𝘆 : 𝗙𝗶𝗿𝘀𝘁-𝗹𝗶𝗻𝗲 𝘁𝗲𝘀𝘁 𝗼𝗳 𝗰𝗵𝗼𝗶𝗰𝗲 𝘁𝗼 𝗱𝗶𝗮𝗴𝗻𝗼𝘀𝗲 𝗮𝗻𝗴𝗶𝗻𝗮

𝗱𝘂𝗲 𝘁𝗼 𝗰𝗼𝗿𝗼𝗻𝗮𝗿𝘆 𝗮𝗿𝘁𝗲𝗿𝘆 𝗱𝗶𝘀𝗲𝗮𝘀𝗲
.

Palpitations

💗 Recurrent, short-lived & irregular   

   + Usually due to atrial or ventricular extrasystoles (ectopic beats)
💗 Episodes of a pounding, forceful & relatively fast (90–120/ min) heart beat 
   + Common manifestation of anxiety
   + Hyperdynamic circulation : Anaemia, pregnancy & thyrotoxicosis
   + Aortic regurgitation
💗 Discrete bouts, very rapid (> 120/min) 
   + Paroxysmal SVT or VT
💗 In contrast, AF typically present with irregular & usually rapid palpitation. 

🔹Palpitation associated with pre-syncope or syncope may reflect more serious structural or
electrical disease & should be investigated without delay 
.

Box 16.7
   + MCQ
   + Structural / Non structural seperately পড়তে হবে 
.

Fig 16.20 (23rd)

+ 𝙍𝙚𝙫𝙚𝙧𝙨𝙞𝙗𝙡𝙚 𝙘𝙖𝙪𝙨𝙚 *** (4H 4 T) (𝐒𝐁𝐀 𝐉𝐀𝐍 𝟐𝟐)
.

Box 16.8 
   + Both SBA & MCQ
   + সব পড়তে হবে।

   𝗤 : 𝗧𝗶𝗺𝗶𝗻𝗴 𝗼𝗳 𝟮𝗻𝗱 𝗵𝗲𝗮𝗿𝘁 𝘀𝗼𝘂𝗻𝗱? 𝗦𝗕𝗔 𝗝𝗨𝗟 𝟮𝟮

.

❤️Benign murmurs do not occur in diastole ❤️Systolic murmurs that radiate or are
associated with a thrill are almost always pathological
.
Box 16.11
   + MCQ
   + সব পড়তে হবে।
.

𝗠𝗨𝗥𝗠𝗨𝗥 

   *** Ejection/Mid systolic

+ 𝗔𝗼𝗿𝘁𝗶𝗰 𝘀𝘁𝗲𝗻𝗼𝘀𝗶𝘀
+ 𝗣𝘂𝗹𝗺𝗼𝗻𝗮𝗿𝘆 𝘀𝘁𝗲𝗻𝗼𝘀𝗶𝘀
+ 𝗕𝗲𝗻𝗶𝗴𝗻 𝗺𝘂𝗿𝗺𝘂𝗿
+ 𝗔𝗦𝗗
+ 𝗔𝗼𝗿𝘁𝗶𝗰/𝗣𝘂𝗹𝗺𝗼𝗻𝗮𝗿𝘆 𝗳𝗹𝗼𝘄 𝗺𝘂𝗿𝗺𝘂𝗿

   *** Pansystolic
+ 𝗠𝗶𝘁𝗿𝗮𝗹 𝗿𝗲𝗴𝘂𝗿𝗴𝗶𝘁𝗮𝘁𝗶𝗼𝗻
+ 𝗔𝗼𝗿𝘁𝗶𝗰 𝗿𝗲𝗴𝘂𝗿𝗴𝗶𝘁𝗮𝘁𝗶𝗼𝗻
+ 𝗩𝗲𝗻𝘁𝗿𝗶𝗰𝘂𝗹𝗮𝗿 𝘀𝗲𝗽𝘁𝗮𝗹 𝗱𝗲𝗳𝗲𝗰𝘁

   *** Late systolic 

+ 𝗠𝗶𝘁𝗿𝗮𝗹 𝘃𝗮𝗹𝘃𝗲 𝗽𝗿𝗼𝗹𝗮𝗽𝘀𝗲 

   *** Early diastolic

+ 𝗔𝗼𝗿𝘁𝗶𝗰 𝗿𝗲𝗴𝘂𝗿𝗴𝗶𝘁𝗮𝘁𝗶𝗼𝗻
+ 𝗣𝘂𝗹𝗺𝗼𝗻𝗮𝗿𝘆 𝗿𝗲𝗴𝘂𝗿𝗴𝗶𝘁𝗮𝘁𝗶𝗼𝗻

   *** Mid diastolic

+ 𝗠𝗶𝘁𝗿𝗮𝗹 𝘀𝘁𝗲𝗻𝗼𝘀𝗶𝘀
+ 𝗧𝗿𝗶𝗰𝘂𝘀𝗽𝗶𝗱 𝘀𝘁𝗲𝗻𝗼𝘀𝗶𝘀
+ 𝗔𝘂𝘀𝘁𝗶𝗻 𝗳𝗹𝗶𝗻𝘁 𝗺𝘂𝗿𝗺𝘂𝗿 (𝗦𝗲𝘃𝗲𝗿𝗲 𝗔𝗥)
+ 𝗠𝗶𝘁𝗿𝗮𝗹/𝗧𝗿𝗶𝗰𝘂𝘀𝗽𝗶𝗱 𝗳𝗹𝗼𝘄 𝗺𝘂𝗿𝗺𝘂𝗿
 
   *** Continuous murmur 
• 𝗣𝗗𝗔 (𝗠𝗮𝗰𝗵𝗶𝗻𝗲𝗿𝘆) (𝗦𝗕𝗔)
• 𝗕𝗿𝘂𝗶𝘁 𝗳𝗿𝗼𝗺 𝗮𝗿𝘁𝗲𝗿𝗶𝗮𝗹 𝘀𝗵𝘂𝗻𝘁,𝘃𝗲𝗻𝗼𝘂𝘀 𝗵𝘂𝗺𝗽
• 𝗣𝗲𝗿𝗶𝗰𝗮𝗿𝗱𝗶𝗮𝗹 𝗳𝗿𝗶𝗰𝘁𝗶𝗼𝗻 𝗿𝘂𝗯

TO BE CONTINUED