Myocardial Infarction

Definition
ST Elevation 1mm in limb leads
ST elevation 2mm in chest leads
New LBBB
Posterior MI - Tall R waves in V1-V3 ST depression +/- T wave inversion
 plus CP within 10 hours

Features
Diaphoresis is the strongest predictor of AMI, as is nausea and vomiting, and radiating to both shoulders.
Severity of pain is not associated with the likelihood of MI.

ECG Diagnosis

 II, III, aVF = inferior leads
   V1-V2 = septal leads (not V3, V4 as seen in some texts (see Zipes et al, 2004))
   V1-V6 = anterior leads

   I, aVL, V6 = lateral leads


Treatment
Aspirin - inhibits platelet aggregation by inhibiting cyclo-oxygenase, and thus formation of thromboxane A2.

Clopidogrel - promotes formation of platelet c-AMP, lowering platelet calcium, and reducing platelet aggregation.

Ticagrelor - anti-platelet agent that is a useful alternative to clopidogrel.

Fondaparinux - factor Xa inhibitor that has less associated bleeding complications.

Right Ventricular Infarction
In 50% of patients with inferior myocardial infarction, the clinical triad of high central venous pressure, clear lung fields, and hypotension combined with right sided ECG changes is strongly suggestive of right ventricular infarction. Look for this carefully using a V4R which may confirm ST elevation, and do an echo.
This is treated by maintaining right ventricular preload, so drugs that reduce preload (nitrates and opiates) should be avoided. Fluid challenge is important, with careful monitoring.

Troponin
A protein, involved in muscle contraction. Very cardiospecific, with little crossover into skeletal muscle. In renal failure, troponin just isn't cleared as quickly, so can be falsely high. With a roche or abbot high sensitivity troponin - normal at arrival and three hours = rule out ischaemia.
Troponin peaks within 12 - 24 hours, and remains elevated for about two weeks.

Remember troponin is normal in unstable angina

Cocaine Associated
Cocaine causes a sympathomimetic response, with increase in heart rate and blood pressure. It can cause acute thrombosis of the coronary artery - this is probably due to more than an increase in platelet count and activation.
Make sure you rule out aortic dissection as well, and “crack lung,” -  hypoxemia, hemoptysis,
respiratory failure, and diffuse pulmonary infiltrates. Also, think about MI if patient presents with dyspnoea or diaphoresis.

Troponin is still very useful, and about two thirds of MI events occurred within 3 hours of cocaine ingestion. ECGs are abnormal in 56 - 84% of patients, although this may be early repolarisation mis-interpreted.

Treat as per normal ACS, but make sure you give early benzodiazepines. GTN might still help. Beta blockers are probably safe.

References
http://circ.ahajournals.org/content/117/14/1897
http://calgaryguide.ucalgary.ca/wp-content/uploads/image.php?img=2015/04/MI-Findings-on-Investigations.jpg
https://www.rcemlearning.co.uk/modules/chest-pain-syndromes/
https://www.aliem.com/2013/03/chest-pain-value-of-good-history/
https://www.rcemlearning.co.uk/modules/management-of-stemi-and-its-complications/ 
https://www.rcemlearning.co.uk/modules/unstable-angina-and-non-stemi-risk-assessment-and-management/ 
https://www.aliem.com/2010/11/paucis-verbis-sgarbossas-criteria-with-lbbb/
https://www.aliem.com/2013/05/pv-card-early-repolarization-vs-stemi-on-ekg/

Aortic Disection

Doctors.net 
EnlightenMe
Potential use of d-dimers
Hypertensive Emergency
Walking Problems
Chest X-ray
CEMPaedia
Collapse and Shock
Clot or Bleeding
 
BMJ Learning
Learning Module
Article

FOAM
http://emcrit.org/podcasts/aortic-dissection/
http://lifeinthefastlane.com/education/ccc/acute-aortic-dissection/
http://lifeinthefastlane.com/2010/03/cardiovascular-curveball-008/
http://lifeinthefastlane.com/2010/09/die-like-a-king/
http://lifeinthefastlane.com/2008/11/aortic-dissection-lecture-notes/
http://flippedemclassroom.wordpress.com/2013/06/07/aortic-dissection/
http://academiclifeinem.com/paucis-verbis-international-registry-on-aortic-dissection-irad/

Pathophysiology
Aortic disection is caused by a disruption of the media layer of the aorta. For this to start, this needs a tear of intima with the formation of a false lumen between layers. An important variation of ATAD is an acute intramural haematoma - bleeding within the wall without an intimal defect. The treatment is the same.

There are three possibilities as to how the blood gets into the media:
-    Atherosclerotic ulcer leading to intimal tear
-    Disruption of vasa vasorum causing intramural haematoma
-    De novo intimal tear

Most tears occur in the ascending aorta due to greater pressure on the aortic wall. Once the dissection process occurs blood tracks through the media to varying degrees and may dissect down from the aortic root to the bifurcation of the common iliac arteries in a matter of seconds.

                  Location of primary aortic tear     Incidence
                  Ascending aorta                           70%
                  Descending thoracic aorta            15-20%
                  Arch of the aorta                          10%
                  Abdominal aorta                           <5%




Risk Factors
Thrombus - 2/3 of patients
Embolism - 1/3 of patients

White (79%)
Men (68%)
over 40



Inherited disease (especially younger patients < 40 yrs)
 - Marfan’s syndrome (fibrillin gene mutations)
 - Ehlers-Danlos syndrome type IV (collagen defects)
 - Turner syndrome
 - annulo- aortic ectasia
 - familial aortic dissection.

    
Aortic wall stress 
- Hypertension (72%)
- Previous cardiovascular surgery
- Bicuspid or unicommisural aortic valve
- Aortic coarctation
- Iatrogenic
- Infection (syphilis)
- Arteritis such as Takayasu’s or giant cell, aortic dilatation / aneurysm, wall thinning
- ‘crack’ cocaine (abrupt catecholamine-induced hypertension).

Reduced resistance aortic wall 
- Increasing age
- pregnancy (debatable).

Clinical Symptoms

The clinical symptoms vary depending on which branch vessel is occluded:
Coronary vessel(s)                    ST elevation myocardial infarction
Common carotid(s)                   any type of stroke
Subclavian(s)                            an acutely ischaemic upper limb
Coeliac/mesenteric vessel(s)      ischaemic bowel
Renal vessel(s)                          frank haematuria
Spinal artery(ies)                       sudden onset painless paraplegia

Ascending aorta:                       haemopericardium (syncope and /or sudden death)
                                                right haemothorax (invariably sudden death)
Arch of aorta:                           mediastinal haematoma
                                                interatrial septal haematoma (cardiac conduction defects)
                                                compression of pulmonary trunk/ artery
Descending aorta:                     left haemothorax (sudden death)
                                                rarely into oesophagus (profuse haematemesis)
Abdominal aorta:                      retroperitoneal haemorrhage (back pain with shock)
                                                rarely intraperitoneal haemorrhage (shock and acute abdomen)
Aortic root:                              aortic regurgitation can occur when the dissection process extends into or around the aortic valvular support. The aortic root can dilate so much that the aortic leaflets cannot fully appose during diastole, allowing regurgitation of blood. 

Pain
Pain is the most common symptom. 
The pain is said to be severe or ‘worst ever’ (90%), abrupt (90%), sharp (64%) or tearing (50%) retrosternal or interscapular pain (50%), migrating (16%), down the back (46%), maximal at onset (not crescendo build up, as in an AMI).

The pain in aortic dissection occurs in the anterior chest 70-80% of the time in patients with a type A dissection and back pain occurs only in 50% of all patients. Abdominal pain was found to be the third commonest site of initial pain and other sites described were the throat, neck and extremities.

Patients may also describe the classic migration of pain from the chest, back or abdomen to one or more limbs or to the neck and this is thought to be due to peripheral extension of the dissection from the primary intimal tear.

In 5-15% of patients however, no pain occurs at all. This is typically the case in those patients presenting with syncope, stroke, congestive cardiac failure or the elderly. 

Cardiac Signs
- Aortic incompetence (32%)
- cardiac tamponade, 
- myocardial ischaemia (although only 2-5% of ECGs mimick AMI)
-  BP differences >20 mmHg in arms
- missing pulse (15%).
        
Other Signs
- Pleural rub or effusion, haemothorax
- Altered consciousness
- syncope (13 %), 
- hemiplegia (5%)
- paraplegia.
 - abdominal pain (43% descending, 22% ascending)
- intestinal ischaemia 
- oliguria
 
Diagnosis
Transthoracic Echocardiography -  78.3% sensitivity and 83.0% specificity for diagnosing proximal dissection. Cannot accurately visualise the descending aorta in most patients. Can diagnose aortic incompetence. 
May identify a free intimal flap within the aortic lumen - sensitivity is approximately 80% for type A dissections but only 50% for type B. 

CT - 83-100% sensitive
  Will reveal pericardial fluid which will suggest dissection diagnosis in the right clinical context. 
 
ECG - normal in 30% of cases
   STEMI patterns in 3% (Changes consistently with AMI do not rule out dissection)
   15% acute ischaemic changes
   41% had non-specific ST segment and T wave changes

Chest X-ray - normal in 12% of cases
   Mediastinal widening in 60% of cases 
   Abnormal aortic contour 50% of cases
   Soft tissue shadow behind a calcified aortic annulus (15%)
   Globular heart (haemopericardium) 
   Pleural effusion (haemothorax)  


 
Bloods - D-dimer has a sensitivity of below 95%

Treatment
The most important step in treatment is diagnosis - 40% cases are initially misdiagnosed. Mortality increases every hour from onset of disease.


Even if there are signs of tamponade, do not perform pericardiocentesis. 

There are two main types of disection: 
     Stanford A: De Bakey 1 and II: Proximal
     Stanford B: Proximal
     Stanford B: DeBakey IIIa and IIIb: Distal
     Stanford A dissections normally have surgical treatment, and type B has medical management.  
 
 
Medical Management
Analgesia
Blood Pressure Control:
 - Control blood pressure with labetalol (a mixed alpha and beta blockers)
  - Causes vasodilatation and reduces cardiac contractility
 - Doesn't cause reflex tachycardia that is seen with other vasodilators. 
Best to use a mixture of beta blockers and vasodilators - so metoprolol and GTN

  
Ten year survival rates of patients who are discharged from hospital range from 30% to 60%