What is the significance of LVH and the old posterolateral MI?

A posterolateral MI is caused by the occlusion of the circumflex artery, a branch of the left coronary artery. This artery supplies the posterolateral left ventricle and anterolateral papillary muscles. Thus, depending on the severity of occlusion, an old posterolateral MI could cause a loss of function of part of the left ventricle and its associated papillary muscles. Such damage would cause weakening of the left ventricle’s ability to sustain systemic blood pressure, both through damage to the ventricle and the mitral valve (through the damage to the papillary muscles). This weakening would result in hypertrophy of the remaining anteromedial muscle of the left ventricle, independent of any other causative factors.

What is an echocardiogram?
An echocardiogram is a type of ultrasound that uses sound waves to produce images of the heart. High-pitched sound waves are sent through a transducer and then bounce off the heart. The transducer receives the echoes of these sound waves and converts them to moving pictures of the heart that are seen on a video screen.

Echocardiograms provide a variety of information, including:
– Size of the heart
– Pumping strength of the heart
– The presence and extent of damage to myocardium
– Valvular disease
– Structural abnormalities

What are the different types of echocardiograms?
Transthoracic echocardiogram (TTE)
– Most common type
– Pictures are obtained by moving the transducer as required over the chest/abdominal wall
– This test is chosen to:
o look for causes of abnormal heart sounds, hypertrophy of the heart, unexplained chest pains, shortness of breath, or irregular heartbeats
o examine the thickness and movement of the walls of the heart
o examine the valves and their functionality
o measure the shape and size of the heart’s chambers
o examine the ability of the heart’s chambers to perform fully à ejection fraction may be measured
o detect disease that affects the myocardium and the heart’s function (eg cardiomyopathy)
o detect clots and tumours in the heart
o detect congenital heart defects
o examine the heart’s function following an infarction
o identify a specific cause of heart failure
o detect a pericardial effusion or a thickening of the pericardium

Transoesophageal echocardiogram (TOE or TEE)
– Pictures are obtained by passing a probe down the (sedated and anaesthetised) oesophageus
– Shows clearer pictures of the heart because the probe is physically located closer to the heart, and there is not interference from the lungs and sternum/ribs
– This test is chosen to:
o monitor heart function during surgery
o examine the function of an artificial heart valve
o detect masses and clots in the left atrium
o identify a cardiac shunt (abnormal blood flow through chambers)
o detect endocarditis
o guide procedures performed during cardiac catheterisation
o detect an aortic dissection

Stress echocardiogram
– Pictures are taken immediately before and immediately following exercise (walking on a treadmill/cycling on stationary bike) à if unable to physically exercise, a chemical (dobutamine) is injected into the bloodstream to stimulate the heart to beat faster and harder, as in exercise
– This test is chosen to:
o identify and monitor ischaemia/coronary heart disease

Doppler echocardiogram
– When sound waves bounce off blood cells moving through the heart and its vessels, they change pitch
– These characteristic changes (Doppler signals) can help measure the speed and direction of blood flow in the heart
– Doppler techniques are incorporated into most TTEs and TOEs and may be used in stress echocardiograms
– This test is chosen to:
o measure the speed at which blood travels through the heart
o measure the blood pressure and speed of blood flow through the heart valves

Sources
http://www.webmd.com/heart-disease/echocardiogram, accessed 16/2/08
http://www.webmd.com/heart-disease/echocardiogram, accessed 16/2/08

My first blog!

Heart + Coronary Artery Anatomy

The heart is slightly larger than a clenched fist and located in the chest (duhhh!). It consists of endocardium (endothelium), myocardium (muscle) and epicardium (mesothelium). There are two atria, two ventricles, separated by a fibrous skeleton, which keeps the valves patent, provides attachments for parts of the valves and the myocardium and electrically isolates the ventricles from the atria to facilitate proper contraction. It has four surfaces, sternocostal, diaphragmatic and right and left pulmonary surfaces. There are four valves (aortic, pulmonary, tricuspid and mitral) of which, the mitral and tricuspid are anchored by papillary muscles and chordae tendineae to prevent backflow into the atria. The upper border of the heart corresponds to a line connecting the inferior border of the second left costal cartilage to the superior border of the right third costal cartilage. The right border is a line connecting the third right costal cartilage to the sixth right costal cartilage. The inferior border is a line connecting the inferior of the right border to a point in the fifth intercostal space close the left MCL. The left border connects the inferior and superior. The apex should be in the fifth intercostal space MCL.

The heart is supplied by the coronary arteries, which can be varied in position and supply, thay are the first branch of the aorta and consist of left and right coronary arteries, which take separate routes around the pulmonary trunk. The right coronary artery originates at the right aortic sinus and passes right of the pulmonary trunk, giving a branch to the sino-atrial node (60% of the time). It than travles in the coronary groove, giving the right marginal branch to supply the right border of the heart. It then continues to the posterior aspect of the heart giving a branch to the AV node. In the majority (67%) the right will give the posterior interventricular branch making it the dominant artery. In conclusion, the RCA supplies the right atrium, most of right ventricle, part of the left ventricle, part of the IV septum, and the SA and AV nodes. The left coronary artery arises from the left aortic sinus, passing left of the pulmonary trunk and into the coronary groove. In 40% of people it will supply the SA node, while it also divides into the left descending and circumflex branches, with the former dividing again into the anterior Iv and lateral diagonal branches, while the circumflex gives a left marginal branch, and in one third of people will continue to form the posterior IV, making it the dominant artery. The LCE therefore, supplies the left atrium, most of the left ventricle, part of the right ventricle most of the IVS and occasionally the SA node. Hearts are 67% right dominant, 15% left dominant and 18% co-dominant.

Hope you are confused, because I most certainly am. Pictures help, this all came from Moore and Dalley which did a great job.

Angiography

This is done by inserting dye into the coronary arteries via a catheter inserted in femoral or brachial arteries. Radio-opaque dye is injected and radiographs are taken to determine the paths and any blockage or stenotic areas of the vessels. Pretty simple?

For video: http://ccal.stanford.edu/case/case16/movie16_3.html

IHD - Symptoms/Investigations/Complications/Prognosis

Symptoms of IHD:
Angina
Radiating pain
Nausea
Breathlessness
Weakness
Feeling faint

Signs of IHD:
Diskinetic cardiac apex (no apex beat)
Mitral regurgitation
Pulmonary Oedema
Cardiac enlargement
Arterial bruits
3rd and or 4th heart sounds – sometimes only if examined during an anginal attack due to transient left ventricular failure.
Apical systolic murmur (papillary muscle death)


There may be evidence of other atherosclerotic disease at other sights i.e.
o Abdominal aortic aneurism
o Carotid bruit
o Diminished peripheral pulses
o Increased light reflexes because of hypertension
o Anemia
o Thyroid disease

If the chest wall is tender or if pain can be reproduced by chest palpation then it is unlikely to be

Investigations

Cardiac Markers












Troponin and CK/CKMB are the cardiac markers that are currently investigated.
CK is released as in skeletal muscle breakdown (trauma, prolonged exercise, hypothermia) but CKMB is specific to cardiac muscle.

CK-CKMB ratio is usually less than 5% anything higher = bad

Troponin is great but it stays elevated (as one can see from the beautiful graph) for many days after an event making it less useful for repeat infarctions or after any cardiac surgery. Also it peaks after 12 to 24 hours so it can show the size of the infarct but not immediately. Last interesting thing is that Troponin levels are thought to rise before injury actually occurs thus it can be used for early detection.


Complications of MI

Heart failure

Myocardial rupture and aneurismal dilation – Rupture of the free wall of the ventricle is normally early and fatal. A sub acute rupture may allow for pericardiocentesis followed by the surgical repair of the rupture. Aneurysmal dilation of the infracted myocardium is a late complication that may require surgical repair.

Ventricular septal Defect VSD – Mortality is very high with a 12-month inoperative mortality of 92%.

Mitral Regurgitation

Cardiac Arrhythmias - including ventricular tachycardia, atrial fibrillation and bradyarrhythmias

Conduction Disturbances – Are very common following an MI. Heart Block can last for only a few minutes, but frequently continues for several days. Permanent pacing may need to be considered if heart block persists for over two weeks.


Prognosis of IHD:

Principal prognostic indicators:
o Age
o Functional state of the left ventricle
o Locations and severity of arterial narrowing
o And activity and severity of myocardial infarction
o Blood pressure
o Diabetes
o ST segment deviation
Using these factors, 90-day mortality ranged from as low as 0.4% in patients with no risk factors to 21.1% for those with more than 4 risk factors.

ECG continued

To complement Margot's stunning work, here's a little more on groupings.

ECG lead groupings

I assume we all know by now that ST elevation is grounds for diagnosis of acute myocardial infarction, Q waves are good reason to believe that there has been a past MI and that ST depression can mean ischaemia. What we may not know is that these changes are generally not present in all leads of an ECG. By looking at the basic principles of the ECG and where the electrodes are places, we are able to determine where an infarction has occurred, or which area of the heart is ischaemic. This is ultimately achieved through lead groupings.

Each lead of the ECG looks at a different part of the heart. Leads V1 through V6 measure conduction in a transverse plane, transecting the heart; the other leads focus on coronal plane, running along the anterior aspect of the heart.

The following pictures should help explain which leads do which!

Inferior (right coronary artery) – II, III, aVF
Right Ventricle

Anterior (left anterior descending) – V2, V3, V4
Septal and anterior parts of left ventricle

Septal – V1, V2
Intraventricular septum

Lateral – I, aVL, V5, V6
Lateral right ventricle

Any combinations of these can also happen.

Hence, ST elevation inV2, V3, I, aVL suggests an anterolateral MI.

Pix: http://medinfo.ufl.edu/~ekg/QRST%20changes.html
The rest taken lovingly, albeit sparingly, from ECG made easy.

ECG

The ECG in Chest Pain
An ECG should be performed on all patients presenting to the ED with chest pain à the baseline ECG is rarely normal but if it is, should be repeated every 15 minutes whilst the patient still has chest pain. NB: a normal ECG does not rule out the diagnosis of MI – this may be indicative of a ‘microinfarction’, a small MI causing myocardial necrosis[1].

The physician’s aim is to answer three questions[2], using the ECG:
1. Does the patient have acute ST segment elevation MI, non Q-wave MI, acute coronary syndrome, or unstable angina?
2. How much myocardium is at risk?
3. Which artery is the culprit?

ECG changes are usually confined to leads that ‘face’ the infarction. The ECG signs of AMI are as follows:
– T wave changes (ischaemia) à almost immediately after coronary artery occlusion, there are T wave changes (initially peaked T waves followed by T wave inversion) in the leads reflecting the involved surface
– ST segment displacement (injury) à the T waves changes are accompanied by a maximal elevation of the ST segment, which gradually evolves into inverted, symmetrical T waves as the pathologic condition progresses
– Abnormal Q waves (cellular death) à appear as early as two hours after the onset of chest pain and are usually fully developed within 12 to 24 hours
Successful reperfusion will dramatically alter this evolution of the ECG in patients with AMI. Early signs include rapid reduction in ST segment elevation and resolution of conduction abnormalities.

The ECG in a STEMI
Elevation of the ST segment is an indication of acute myocardial injury (as opposed to infarction), either due to:
– Recent infarction
– Pericarditis à not usually a localised affair, therefore causes ST elevation in most leads

The normal ST segment:
All layers of the myocardium are at the same electrical potential; this is the plateau of the action potential. Therefore there is no current flow between areas of the heart, resulting in an isoelectric ST segment. However, this is not the case when the myocardium is acutely injured.

The ST segment following acute injury:
New ST segment elevation of 1mm or more in the limb leads and 2mm or more in the precordial leads is a powerful diagnostic feature of AMI. This occurs due to severe ischaemia and lack of nutrients, which affects the tissue immediately surrounding the centre of the infarct:
o This is non-functional tissue
o But may receive blood supply from collateral circulation
o Collateral supply is sufficient to keep tissue alive
o But insufficient to maintain membrane integrity
o Therefore injured tissue has a less negative membrane potential from the healthy myocardium
This chain of events, and ultimately the less negative membrane potential, results in a current that flows from the healthy tissue to the injured tissue during the ST segment, causing ST segment elevation (or depression).

Typical ECG changes in myocardial infarction (STEMI) - THIS IS A PRETTY GOOD SUMMARY TABLE (kumar and clarke table 13.32) AND NOW LOOKS POXY BUT WILL BE ALL GOOD IN THE COMPILED VERSION
NB: these changes are usually confined to leads that ‘face’ the infarction

Infarct site
Leads showing ST elements
Anterior:

Small
V3-V4
Extensive
V2-V5
Anteroseptal
V1-V3
Anterolateral
V4-V6, I, AVL
Lateral
I, AVL
Inferior
II, III, AVF
Posterior
V1, V2 (reciprocal)
Subendocardial
Any lead
Right ventricle
VR4
Kumar and Clarke, 6th edition, Table 13.32, p. 813


Sources
Kumar and Clarke, 6th edition, pp. 812-13
The ECG made easy, 4th edition, pp.84-85
Conover MB. Understanding electrocardiography. 8th ed. Missouri: Mosby; 2003. pp. 332-39.


[1] Albert JS, Thyfesen K, Antman E, Bassand JP: Myocardial infaction redefined – a consensus document of the joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction, J Am Coll Cardiol 36:959-969, 2000.
[2] Wellens HJJ: Acute myocardial infarction and left bundle-branch block – can we lift the veil? N Engl J Med 334:528-529, 1996.

Acute Treatment of ST Elevation Myocardial Infarction (STEMI)

1. Aspirin
a. 150-300mg chewed
b. Then 75-100mg p.o. daily

2. Glyceryl trinitrate
a. 0.3-1.0mg sublingual. Repeat

3. O2
a. 2-4L/min nasal cannula
b. 35-50%

4. Hx and Ex (including risk factors)
a. Cardio history and exam.
b. Resp. History and exam.
c. CVD risk factors

5. Intravenous access and blood tests
a. 2 x 14 G i.v. catheters (orange)
b. FBE, lipids, glucose and biochemistry

6. 12 lead ECG

7. i.v. opiate and an antiemetic
a. Eg. Diamorphine 2.5-5mg (opiate, heroin)
b. Eg. Metoclopramide 10mg (antiemetic)

8. Beta-blocker for ongoing chest pain, hypertension, tachycardia
a. Eg. Atenolol 5mg i.v. repeated after 15mins then 25-50mg p.o. daily
b. Or metoprolol 5mg i.v. repeated to a max. Of 15mg then 25-50mg p.o. BD
c. Avoid in asthma, heart failure, hypotension, bradyarrythmias

9. MOST EFFECTIVE TREATMENT IS PCI (Percutaneous coronary intervention) otherwise give thrombolysis
a. Is preferred treatment within 90 minutes of event
b. Has been proven to be the most effective treatment for 12 or more hours from the onset of symptoms
c. The DANAMI 2 study showed a reduced mortality rate when compared to thrombolytic therapy (8.0% vs. 13.7%)


References
Kumar and Clark pp. 808-816
Rang and Dale’s pp. 597-598, 310-313, 392-393

DDx and Explanation of Cardiac Sx

Differential Diagnoses for Chest Pain

What - central/left/arm = AMI, retrosternal/interscapular = DAA
When - >30m = AMI, instantaneous = DAA
Qual - constricting, dull = AMI; sharp = pleuritic, tearing = DAA, tender = MS(local)/#Rib(resp+sternum)
Quan -
Associated Sx - dyspnoea = MI/PE/Anxiety, sweating/nausea = MI
Aggravating - exercise/cold/emotion = AMI, food/alcohol = GI, inspiration = pleuritis
Alleviating - GTN = angina (mins) oesophageal spasm (longer), leaning fwd = percarditis, Mylanta = curry
B - "doom" = AMI, "going to die" = bad prognostic marker. Page Craig.

Here are a few classical presentations of the common causes of chest pain:

AMI - tightness, central crushing squeeziness. radiating pain. dyspnoea.
Dissecting Aortic Aneurysm - Sudden onset of severe, sharp, stabbing pain. confirm by CT or Echo
Pericarditis - Sudden onset of pleuritic pain. Pericardial rub (L Sternal Border Squeakiness) and fever. Leaning Forward to reduce friction.
Pulmonary Embolus - Pleuritic, dyspnoea, tachypnoea, haemoptysis, syncope
Pneumothorax - Hx Trauma or thin young man. pleuritic pain in chest and back w dyspnoea. hyperresonance
Pleuritic Pain (exacerbated by inspiration)
Musculoskeletal pain - local tenderness
Rib Fracture - pain on respiration, sternal tenderness
Subdiaphragmatic - abdo symptoms
Herpes Zoster - neuropathic.

http://www.mdconsult.com.ezproxy.lib.monash.edu.au/das/article/body/87746543-2/jorg=journal&source=MI&sp=15273612&sid=0/N/457018/1.html?issn=0735-6757
ohcm - emergencies, Cardio
kumar+clarke - cardio

Etymology of Common Cardiac Symptoms.

ANGINA is a result of myocardial ischaemia - ?AMI, CAD
EXERTIONAL DYSPNOEA is due to an insufficiency of the heart to perfuse the body's tissues - ?CHF
PAROXYSMAL NOCTURNAL DYSPNOEA is due to an insufficiency of the heart to perfuse the body's tissues. ?CHF
ORTHOPNOEA is due to fluid in the lungs inhibiting perfusion of upper lobes of lungs - ?pleural effusion, CHF
PERIPHERAL OEDEMA is due to increased afterload to the heart causing a backlog, the fluid follows gravity - ?RHF
PALPITATIONS are any abnormal awareness of heartbeat - ?anxiety, ectopic beats, or AF or flutter.
INTERMITTENT CLAUDICATION is due to poor perfusion/ischaemia of peripheral tissues - ?PVD, CAD
SYNCOPE although can be neurological, can be due to poor cardiac output and therefore supply to the brain - ?Aortic Stenosis
FATIGUE can be due to poor perfusion - ?CHF, but also cancer, GI bleed, Resp disorder

Signs

CACHEXIA is a general sign of neoplasia. also cardiac due to congestive liver stuff.
TENDON XANTHOMATA are due to lipid deposits therefore indicate hyperlipidemia
XENTHALASMA are cholesterol deposits around the eyes therefore indicate hypercholesterolaemia
JVP a-wave corresponds to RA systole and S1, v corresponds to atrial filling. Indicates incr. atrial pressur, which can be due to RHF, CHF, Fluid Overload, Tricuspid stenosis, SVC Obstruction?
APEX BEAT absent = DOPES
Death, Obesity, Pericarditis, Emphysema, Situs inversus
deviated = cardiomegaly, skeletal defects (scoliosis, pectus excavatum)
abnormal: Double impulse - systole has 2 impulses. = hypertrophic cardiomyopathy.
uncoordinated, easily palpable. = MI.
"hyperdynamic" forceful, sustained apex beat = HTN.
"Hyperkinetic: palpated beat is distributed over greater area.= LV dilation.
"tapping": S1 is palpable
other visible pulsations may be PA in PHTN
HEAVES = disturbed blood flow in the heart
THRILL = often accompanies cardiac murmur ?used in grading (my ref is so bad i'm not including it)

HEART SOUNDS i reckon are easier to understand when you put them in the context of the cardiac cycle (Especially helpful when consultants use descriptive terms such as "mid-systolic" ... )

S1 = closing of mitral and tricuspid valves, the beginning of Vent. Systole
S2 = aortic and pulmonary closures, the end of systole
splitting of S2 is due to delay in RV Emptying, which can be normal due to decr. pressure in pulmonary trunk cf. aorta. Pathologies include RBBB, Pulm. stenosis, VSDs, mitral regurgitation
S3 = mid-diastolic, triple rythm. Ventricles are filling too fast, so Mitral (or tricuspid) filling too fast. indicates LVH, incr. Cardiac Output, aortic or mitral regurgitation

First Post!

G'day all,

This blog thing's worked pretty well in the past, but i'm well looking forward to margot and nish's compiling. If it's as good as their mousse and curry respectively, i'll be very satisfied, and not just in the tummy.

When you log in and go to "New Post" you can type your awesome, detailed but succinct, fruity but tangy, researched and referenced info into the text-box, and i think there's a button that lets you add photos/diagrams, because everyone loves them. i shall now test this function with a picture of a

kitten hugging a teddy bear.

cheers y'all!

- pat