IHD Flashcards
Acute coronary syndrome consists of
-unstable angina, STEMI, STEMI, LBBB
Pathophysiology of stable angina
They have a stable plaque occluding. There are collaterals that are capable of supplying blood to the myocardium in stable resting stages.
Blood supply to the myocardium.
RCA divides into right marginal artery and posterior interventicular artery. LCA divides into left circumflex artery and left anterior descending artery (anterior interventicular artery)
Acute coronary syndrome pathophysiology
Due to the lack of collaterals and the sudden narrowing of the coronary artery due to the rupture of an immature plaque which has a thin capsule, exposes the highly thrombogenic lipid core. Inflammation at the shoulder of the plaque also cause a clot formation. There is a vascular spasm due to imbalance between vasoconstriction and vasodilators
Diagnosing 3 main categories for acute coronary syndrome
Pain, ECG changes, cardiac biomarkers.
Pain in acute coronary syndrome.
Acute chest pain, tightening type lasting more than 20 min retrosternal radiating to the jaw, shoulder left arm
ECG changes in acute coronary syndrome STEMI
- ST elevations of 2 Or more contiguous leads there should be a >= 1.0mm in limb leads or V4-6
- V2-3 > 2.5mm in <40y , >= 2.0mm in men >40y, >=1.5mm in women
- V7-9 >0.5mm
ECG changes in nstemi and unstable angina
- New ST depressions
- T inversions.
DDs for acute coronary syndrome.
- Aortic dissection
- acute pericarditis
- pulmonary embolism
- pneumothorax
- esophageal pain
- PUD
- acute pancreatitis
Mx of ACS
- Admit
- Acute side bed
- Check A, B, C and correct as necessary. Oxygen if SpO2 < 90%
- Connect to cardiac monitor
- Blood – FBC, SE, BU, S.Cr, Lipid profile, cardiac biomarkers, blood sugar
Troponin I – (highly specific and highly sensitive - may remain
elevated for upto 2 weeks) - Commence drug therapy
Aspirin 300 mg
Clopidogrel 300 mg
Atorvastatin 40-80 mg
IV morphine – 2.5 -5 mg as single dose/GTN – sublingual
IV metochlopromide 10 mg - Take 12 lead ECG & CXR if suspecting HF
ECG – ST elevation – STEMI
Non ST elevation but ST depression and T inversion – unstable angina or
NSTEMI
If the initial ECG is not diagnostic serial ECGs should be performed - Unstable angina and NSTEMI will be treated with Heparin
STEMI and LBBB wil be treated with streptokinase.
The best Mx would be PCI - Reperfusion
Percutaneous coronary intervention – limited
Thrombolytics- EgSK – 1.5 MU in 100 mL N/S over 1 hour(or fibrin specific
fibrinolytics)
ACS pain interms of ChLORIDE
Ch- Character –tightening type of pain
L – Location – Retrosternal
O – Onset – sudden onset
R – radiation – jaw, shoulder tip, left arm
I – Intensity – severe
D – duration - > 20-30 min
E – aggravating factors
ECG changes associated with STEMI
1.Hyperacute (10-20 min) -Tall peaking T waves and progressive ST
elevation
2.Acute (min to hrs)- ST elevation
3.Early (hours to days)- ST elevation disappear and Q waves appear
4.Intermediate (days to weeks)- Q waves and T inversions
Dosage of the thrombolytics
1.5 MU in 100 mL N/S over 1 hour(or fibrin specific fibrinolytics)
Indications of thrombolytics in ACS
Within 12 hours of onset of pain
STEMI
New onset LBBB
True posterior MI
Contraindications for thrombolysis (Absolute contraindications)
Past history of haemorrhagic stroke
PHx of ischaemic stroke within last 6 months
Intracranial tumour
Aortic dissection
Active internal bleeding within last 2 weeks
Assessing the response to thrombolysis
Relief of pain
Restoration of haemodynamic stability
Reduction of ST elevation by 50% in 60-90 min following administration
Time window for PCI as the first step
less than 120 minutes
PCI wire entry sites
Radial Artery
Femoral Artery
Q waves on the ECG means
- Indicates and old infarction
- Permanent on ECG
- Transmural infarction
Transmural infarction
whole thickness is involved
How to Dx a true posterior MI from anterior leads
If there is an ST depression in V1.
Most common reperfusion arrhythmia
Accelerated idioventricular arrhythmia
the cardiac biomarker that can be done within 1-2 hours
highly sensitive troponin I
Drug therapy in ACS stat Mx
Aspirin 300 mg
Clopidogrel 300 mg
Atorvastatin 40-80 mg
IV morphine – 2.5 -5 mg as single dose/GTN – sublingual
IV metochlopromide 10 mg
ECG changes with NSTEMI and unstable angina
Non ST elevation but ST depression and T inversion
Heparin is given for
- Unstable angina
- NSTEMI
Streptokinase is given for
- STEMI
- LBBB
ECG changes with STEMI within 10-20 min
- Tall peaking T waves
- progressive ST elevation
ECG changes with STEMI within mins to hours
ST elevation
ECG changes with STEMI within hours to days
ST elevation disappears and Q waves appear
ECG changes with STEMI within days to weeks
- Q waves
- T inversions
Inferior MI occurs due to a block in
Posterior interventricular artery
Why are heart blocks more common with inferior MI
conducting system is also supplied by RCA
Dressler Syndrome
Immune- mediated pericarditis
Ventricular ectopics after giving SK indicates
successful reperfusion
Assessing the response to thrombolysis
Relief of pain
Restoration of haemodynamic stability
Reduction of ST elevation by 50% in 60-90 min following administration
Beta Blockers are contraindicated in
- in patients with HR<60
- SBP<100
- conduction defects
strategies to limit infarct size
Β blockers
ACEI
Statin
Aspirin ( later maintenance dose)
Clopidogrel ( later maintenance dose)
(( other Gp2b/3a receptor inhibitors- abciximab, eptifibatide and tirofiban
Abciximab, eptifibatide, tirofiban mechanism
inhibit final common pathway for platelet adhesion and aggregation
Troponin I +ve - NSTEMI Mx
Enoxaparin 1mg/kg bdfor 72 hours
Troponin I –ve – Unstable angina Mx
Enoxaparin 1 mg/kgbd for 48-72 hours
Early complications for ACS
- Arrhythmia
- Heart Block
- HF and cardiogenic shock
- Post infarction angina
- Acute pericarditis
- Acute MR
Heart block is mostly seen in
Inferior MI
Mx of heart block due to ACS
Use atropine, consider
temporary cardiac pacing
Mx of cardiogenic shock in ACS
inotropes
Post infarction angina Mx
increase antianginal drugs,
consider coronary angiography
Rx of Acute pericarditis in ACS
No Rx needed
Acute MR Mx
Surgical referral
Intermediate and late complications of ACS
- VSD
- Dressler’s syndrome
principles of Mx prior to discharge
- Counsel regarding lifestyle modification
- Mx of stress
- Arrange for ECHO and coronary angiography
- Discharge with medications
Discharge medications
Clopidogrel
Aspirin
Atorvastatin
B Blockers
ACEI
Nitrates
Mechanism of Clopidogrel
inhibit P2Y 12receptors in platelets there by block ADP dependent activation of glycoprotein 2b/3a complex
Mechanism of aspirin
inhibit COX 1- reduce thromboxane A2 from platelet
Lifestyle modification post discharge
- Aerobic exercises ( 30 min brisk walking per day at least 5 days a week)
- Stop smoking, alcohol
- Reduce salt, fatty food, carbs
Pathophysiology of stable angina
most have stable plaque occluding 70-80%, calcified mature plaques which has thick capsule
P/C of stable angina
chest pain on exertion. Relieved by rest or GTN
Grading – Canadian Cardiovascular Society
o Grade 1 – ordinary [physical activity does not cause angina, angina at strenuous or
prolonged exercise
o Grade 2 – slight limitation of ordinary activity
o Grade 3 - marked limitation of ordinary activity
o Grade 4 – angina at any level of exertion
Ix done for stable angina to assess the severity
Exercise ECG
why is a normal ECG not done in stable angina
it can be normal in 50% of patients
Other Ix done for stable angina
- coronary angiography
- Angioplasty
- CABG
Mx of stable angina
o Lifestyle modification
o Medications – Aspirin( clopidogrel if aspirin is not tolerated) ,statin
Antianginal drugs
mechanism of nitrates
- Relaxation of vascular smooth muscle causing venodilation
- arteriolar dilation
- coronary artery dilation
Examples of nitrates
- GTN (sublingual)
- ISMN(iso sorbide mono
nitrate) ,ISDN (oral)
ADRS of nitrates
- Headache
- Flushing
- tolerance
- Postural hypotension
Beta blockers mechanism
- Reduction of heart rate
- myocardial contractility
Examples of Beta blockers
- Atenolol
- Bisoprolol
ADRS of beta blockers
- Conduction abnormalities
- Bronchoconstriction
- Worsening of PVD
- Impotence
- Depression
- Nightmares
- impaired glucose tolerance
- Bradycardia
Calcium channel blockers mechanism
- Vasodilation
- Conduction block
- Reduced myocardial
contractility
Two types of CCBs
- Dihydropyridine-**( not
preferred in IHD) **
Nifedipine - Non dihydropyridine-
Verapamil
Diltiazem
ADRS of dihydropyridine
- Oedema
- head ache
- flushing
- worsening heart failure
- Tachycardia
- gum hyperplasia
ADRS of non dihydropyridine
- Oedema
- Bradycardia
- heart block
- constipation
Beta blockers are not given together with
non- dihydropyridines - worsen bradycardia
why is dihydropyridines not recommended in IHD
tachycardia worsens IHD
K channel blocker
Nicorandil
SA node funny current channel blocker
Ivabradine
Inhibiting delayed Na channel
Ranolozine
Enoxaparin is given as (route of administration)
Subcutaneous
Cardiac troponin takes …… days to return to baseline
4-14 days sometimes
If a patient gets another chest pain episode 5 days after he got a STEMI. How to check if the second chest pain episode is also an MI?
Ask for a quantitative Troponin T. levels which should be reducing would suddenly increase.
Coronary artery vasospasm is
Prinzemetal angina
Prinzemetal angina is seen among
- common in females
- common among smokers
Inferior MI can present with….
- Epigastric pain
- AV block
If the BP reduce a little 30min after starting Streptokinase infusion. Next step?
Reduce the infusion rate and elevate the limbs
If the BP drops significantly 30 min after starting streptokinase infusion. Next step?
Stop SK and give IV NS bolus ( could be an allergy)
New risk factors for MI
- Hyperhomocystinemia
- Increased CRP
- Increased Fibrinogen
ECG leads V1- V4 look at the
anterior surface of the heart (septum)
aVL, V5, V6 look at the
lateral surface of the heart
II, III, aVF look at the
inferior surface of the heart
V7, V8, V9 look at the
back leads, Good to check for posterior MI
Can you have a STEMI in all leads in an ECG
Theoretically possible. but not possible to get acute blocks in all coronary arteries