Welcome to Scribd, the world's digital library. Read, publish, and share books and documents. See more
Download
Standard view
Full view
of .
Look up keyword
Like this
22Activity
0 of .
Results for:
No results containing your search query
P. 1
Acute Coronary Syndrome

Acute Coronary Syndrome

Ratings:

5.0

(1)
|Views: 920|Likes:
Published by m3d1k
My notes on Acute Coronary Syndrome
My notes on Acute Coronary Syndrome

More info:

Published by: m3d1k on Mar 11, 2010
Copyright:Attribution Non-commercial

Availability:

Read on Scribd mobile: iPhone, iPad and Android.
download as PDF, TXT or read online from Scribd
See more
See less

04/02/2013

pdf

text

original

 
Acute Coronary Syndrome
 
Definition: a spectrum of clinical presentations:
o
 
Unstable angina: angina of recent onset (<2 months), worsening or angina at rest.
o
 
Non ST elevation myocardial infarction: incomplete occlusion of coronary vesselsleading to ischemia and mild necrosis of myocardium (Troponin-I raised only)
o
 
ST elevation myocardial infarction: complete occlusion of coronary vessels leading tonecrosis of the myocardium
 
Epidemiology: Leading cause of death in Ireland, 1,200,000 cases / year in the US, morecommon in males, age of onset 50-60.
 
Aetiology:
o
 
Atherosclerosis of the coronary vessels
 
Risk factors:
o
 
Non-modifiable: male, family history, age, ACE gene polymorphism
o
 
Modifiable: smoking, hypertension, hyperlipidemia, diabetes mellitus, obesity,sedentary lifestyle, high F-VII & fibrin, cocaine use, alcoholism, COX-2 inhibitors,hyperinsulinism, lipoprotein(A), OCP
 
Pathology
o
 
Formation of atheroma in the coronary vessels:
 
Following insult to the vascular endothelium platelets aggragate and lipids,scavenger cells (macrophages) move to the injured site and start ingestingthe lipid until they become foam cells.
 
There is also migration of muscle cells to the endothelium and hyperplasia
 
A fibrous cap is formed by fibroblasts at the endothelium
o
 
The major trigger for coronary thrombosis is considered to be plaque rupture causedby the dissolution of the fibrous cap due to the release of metalloproteinases(collagenases) from activated inflammatory cells. This event is followed by plateletactivation and aggregation, activation of the coagulation pathway, andvasoconstriction. This process culminates in coronary intraluminal thrombosis andvariable degrees of vascular occlusion
 
History & Exam
o
 
Central crushing chest pain, that may radiate to the arm, neck or jaw, brought on byexercise, cold weather, following a big meal, or stress.
o
 
The pain is associated with nausea +/- vomiting, diaphoresis, pallor, syncope or pre-syncope, palpitations and dyspnoea.
o
 
On examination:
 
Tachycardia, tachypnoea, hypo/hypertension, pallor, anxiety, signs of left orright heart failure, a 4
th
heart sound, pansystolic murmur.
 
Investigations: the diagnosis is clinical
o
 
Bloods:
 
FBC
haemoglobin (anaemia?), leucocytosis (infection?)
 
U&E
electrolyte disturbances establish a baseline for the patient andassess their renal function.
 
LFTs
deranged in case of right heart failure.
 
Coags
bleeding disorder, this patient may undergo thrombolysis.
 
Glucose
Diabetes mellitus, hypoglycaemia/hyperglycaemia
 
Fasting serum lipids
hyperlipidemia
 
BNP
heart failure??
 
Cardiac enzymes:
 
 
Troponin-I: highly sensitive and specific for myocardial muscleinjury, elevated in STEMI and non-STEMI. Rises 8 hours after the MIand peaks at 2-3 days, disappears from serum after 10 days.
 
CK-MB: cardiac creatine kinase, rises after 6 hours of MI, peaks after1-2 days.
 
LDH: rises after 2 days of MI, returns to normal after 10 days
 
AST: rises after 1 day of MI, peaks after 2 days of MI, and normalisesat the 3
rd
day.
 
 
Peak A is the early release of myoglobin or creatine kinase isoenzyme MB (CK-MB) after acute myocardial infarction (AMI). Peak B is the cardiac troponin level afterinfarction. Peak C is the CK-MB level after infarction. Peak D is the cardiac troponin level after unstable angina. Data are plotted on a relative scale, where 1.0 is set atthe myocardial-infarction cutoff concentration. Courtesy of Wu et al (1999). ROC = receiver operating characteristic
o
 
ECG:
 
Unstable angina: Normal, there may be ST Depression/T wave inversion
 
Non-STEMI: ST depression/T wave inversion
 
STEMI:
 
ST elevation for >1mm in 2 contiguous chest leads
 
New onset LBBB
o
 
Imaging:
 
CXR: Cardiomegaly?
 
ECHO: assessment of valves and EF? (heart failure)
 
Cardiac perfusion scintiography(assessment of a perfusion of themyocardium looking at areas that are under perfused
o
 
Invasive:
 
Angiogram: the gold standard to diagnose coronary artery disease, can betherapeutic as well.
 
Management
o
 
Advice patient regarding losing weight, stopping smoking, low fat diet, exercise (30minutes every day), good control of DM,
o
 
Acute management: (MONA BAH)
 
Oxygen (2-4L) as 70% of ACS patients is hypoxemic.
 
Morphine 2.5-5 mg IV + Metoclopramide 10mg IV (analgesia and antiemetic)
 
GTN spray sublingual 2 puffs (vasodilator)
 
Aspirin 300mg PO chewable (anti-platelet) + Clopidogrel 300mg PO (inhibitsplatelet aggregation)
 
Atenolol 5mg IV for 15 minutes (beta blocker)
 
Ramipril 2.5-10 mg PO (ACEI for thrombus remodelling)
 
Atorvastatin 80mg PO (HMG-CoA inhibitor for thrombus remodelling andhyperlipidemia)
o
 
If the patient has non-STEMI [Add] (since there is a thrombus that is incompletelyoccluding; want to prevent further formation of thrombus):
 
Enoxaparin (antithrombin; LMWH) 1mg/kg SC BD
 
Tirofiban (GP IIIa/IIb antagonist, prevents aggragation) 0.4mg/kg/min IV for30 mins then 0.1mg/kg/min IV for 48-108 hours
 
o
 
If the patient has STEMI [treatment as above +] thrombolyse the patient
 
Indicated in:
 
Symptoms of ischemia
 
Symptoms are within the last 12 hours
 
New LBBB
 
ST elevation in 2 contiguous chest leads >1mm
 
Contraindications
 
History of intracranial haemorrhage
 
Known structural cerebral vascular lesion (AV Malformation)
 
Intracranial malignancy
 
Ischemic stroke within the last 3 months (but not within 3 hours)
 
Suspected aortic dissection
 
Active bleeding or bleeding diathesis
 
Significant head trauma within the last 3 months.
 
Relative contraindications:
 
Poorly controlled chronic severe hypertension
 
Severely uncontrolled hypertension on presentation (>180 SBP,>110 DBP)
 
Recent internal bleeding (2-4 weeks)
 
Pregnancy
 
Active peptic ulcer
 
Use of anticoagulants (high INR
high risk of bleed)
 
Major surgery within the last 3 weeks or trauma
 
Ischemic stroke more than 3 months ago/ dementia
 
Noncompressible vascular punctures
 
Allergy (more than 5 days ago) to altepase/streptokinase.
 
Altepase (tissue-Plasminogen activator) 15mg IV stat, then 50mg IV for 30minutes, then 35mg IV for 1 hour
o
 
PCI or Fibrinolysis:
 
Fibrinolysis preferred if:
 
<3 hours from onset
 
PCI not available/delayed
 
door to balloon > 90min
 
door to balloon minus door to needle > 1hr
 
Door to needle goal <30min
 
No contraindications
 
PCI preferred if:
 
PCI available
 
Door to balloon < 90min
 
Door to balloon minus door to needle < 1hr
 
Fibrinolysis contraindications
 
Late Presentation > 3 hr
 
High risk STEMI
 
Killup 3 or higher
 
STEMI dx in doubt
o
 
Percutaneous intervention (PCI) (AKA cardiac catheterisation)
 
Indicated in:
 
Identification of the extent and severity of coronary artery disease
 
Assessment of valvular or cardiomyopathies
 
Confirming the diagnosis of ACS

Activity (22)

You've already reviewed this. Edit your review.
1 hundred reads
1 thousand reads
cindyzhong liked this
Agi Mary liked this
Agi Mary liked this
V Dani Widi liked this
Loz Hass liked this
Heri June liked this
regifer1517 liked this

You're Reading a Free Preview

Download
scribd
/*********** DO NOT ALTER ANYTHING BELOW THIS LINE ! ************/ var s_code=s.t();if(s_code)document.write(s_code)//-->