WHAT TO EXPECT IN THE EMERGENCY ROOM

WHAT TO EXPECT IN THE EMERGENCY ROOM

The treatment of a heart attack has changed dramatically in the past 20 years.  Heart attack patients are no longer admitted to the hospital to be observed and kept at bedrest for two weeks.  Emergency rooms (ER) are now designed to place heart attack patients on a fast-tract to immediate, interventional, treatment.

A heart attack is caused a thrombotic (a blood clot) obstruction of one of the coronary arteries.  The chest pain associated with this obstruction is due to injury or damage to the heart muscle supplied by that artery.  The heart attack may be large or small, but all heart attacks are serious and are treated similarly.  There are no “mild” heart attacks.  Injured heart muscle can recover, but dead heart muscle cannot.  The aim is to reduce heart muscle damage by restoring blood flow in the affected artery.  Blood flow is restored by opening the artery and getting rid of the blood clot (thrombus) with a tiny balloon catheter in a Catheterization Laboratory (Cath Lab).  The longer the artery is obstructed the greater will be the heart muscle damage so we want to go to the cath lab as quickly as possible.  The aim, in ideal circumstances, is to open the artery within 90 minutes of the onset of the chest pain. 

Once the cardiologist arrives in the ER and the diagnosis is established, the ER becomes a flurry of activity.  Laboratory work, x-rays, ECG, I-V fluids, and oxygen must be obtained and started.  The procedure must be fully explained to the patient and the family to get the necessary permits signed.  This is a difficult time for the patient and family because there is some risk in the cath lab.   There is also risk in not doing anything.  My advice is to sign the permits and get to the cath lab as quickly as possible.  This approach to the heart attack patient has been approved by the hospital and the medical staff and the results are closely monitored.  The goal here is to stop further cardiac muscle injury.  This is modern day cardiology .  See blogs 12 and 13. 

Summary:  If you suspect a heart attack, call 911 and get to the hospital as quickly as possible.  I will devote a later blog to help you recognize the type of chest pain associated with a heart attack to assist you in deciding whether or not to call 911. 

THE SMOKERS PARADOX

THE SMOKERS PARADOX

I receive, by email, the contents of leading cardiology journals as a way to keep up with the changes in cardiology.  I can download an abstract, or, in some cases, the entire article, free of charge.  Recently an article looked at the prognosis of smokers (S) and non-smokers (NS) who were successfully resuscitated from sudden cardiac death.  The results showed it was the S who had a better survival than NS and the S were more apt to leave the hospital with brain function that was better than the NS.  This was called a S paradox because multiple studies, including my own, show that S die of heart disease approximately 10 years sooner than NS, but have less extensive and less severe atherosclerosis.    The real question, not answered by the authors, is how can these results be explained in view of the accelerated plaque development in S.  

This is my explanation, based on what I have seen under the microscope.  I am assuming that the majority of these patients received CPR (cardio pulmonary resuscitation) which involves compressing the heart between the sternum and the spine.  Please remember that the heart is a midline structure and only protrudes into the left chest.  This explains why coronary chest pain is in the middle, not the left chest and why compressing the sternum compresses the heart.  Sixteen years ago I published a paper (J Invas Cardiol 1997:9;578-585) showing that CPR was associated with direct injury to the heart in the form of cracks in the coronary arteries.  In compressing the heart between the sternum and the spine you naturally compress the coronary arteries as well.  The coronary arteries become steadily more calcified as we grow older, making them more brittle.  Thus the coronary arteries in the younger age S are less calcified and more pliable and more easily compressed without injury compared to the older NS patient with more extensive calcification.   If the artery is injured and cracked and is unable to dilate or contract this will affect coronary blood flow and overall cardiac function.  Figure 1 shows a calcified (blue color on right side of photo) coronary artery with fracture and wall rupture in a 61 year old man.  Figure 2 is a fracture of a large calcified plaque with leakage of red injection mass into the artery wall.

I conclude that S do better than the NS after resuscitation from cardiac arrest, because the heart and the coronary arteries in the S are not as severely injured as the NS and they recover heart function and cardiac output more rapidly, resulting in less brain damage.  Smoking has no redeeming features and no one should start smoking on the basis of this recent report.

HOW DO PLAQUES GROW?

In our first blog, using coronary calcification as an illustration, I showed arteriosclerosis (AS) is a dynamic, active, progressive disease process.  AS, in many ways, is similar to tuberculosis.  Shown here is a cross section of a coronary artery of a patient who died of heart disease containing a plaque that narrows the channel of the artery about 50%.  I would not consider this to be serious narrowing.  The red color is dye material I have injected into the artery to get it fully distended.  The plaque is the white material to the right of the red color, showing the plaque affects only 1 side of the artery wall, leaving the other side unaffected.  This is a typical plaque.  

We call plaque growth the “proliferation” of tissue.  Proliferation is the initial response or the first sign of arteriosclerosis.  The reason plaques begin to grow is believed to be started by a small focal injury (unknown injurious agent) to an area of the artery wall.  The body responds to this injury by growing scar tissue.  We call this the “proliferative phase” of arteriosclerosis.  It is easy to see that as the plaque continues to grow it could, in the fullness of time, completely obstruct the artery channel.

SUMMARY:  AS is a chronic progressive disease, initiated by focal injury to the artery wall, followed by progressive growth and proliferation scar tissue.  The proliferation of tissue should be viewed as a defensive response or an attempt to heal the injury.  However this tissue is fatally flawed and in the fullness of time will undergo degeneration and destruction, resulting in an “Atheroma.”

To Be Continued.