Women and Heart Attacks

How Do I Know If I Am Having a Heart Attack? By Tony Neaverson

Most patients have symptoms prior to an actual heart attack – generally a “tightness” behind the breastbone, which generally is caused by an increase in heart rate. The coronary arteries fill in between heart beats therefore anything which increases your heart rate will reduce the time your coronary arteries have to provide blood flow to the heart muscle- the myocardium. Once the heart muscle is deprived of oxygen it becomes irritable leading to palpitations and, if not relieved, death of the muscle.

Most patients have symptoms prior to an actual heart attack – generally a “tightness” behind the breastbone, which generally is caused by an increase in heart rate. The coronary arteries fill in between heart beats therefore anything which increases your heart rate will reduce the time your coronary arteries have to provide blood flow to the heart muscle- the myocardium. Once the heart muscle is deprived of oxygen it becomes irritable leading to palpitations and, if not relieved, death of the muscle. Surrounding the dead muscle is a variable sized area of heart muscle at risk of dying because of inadequate oxygen supply – this condition is known as myocardial ischaemia. The heart rate is under the control of the autonomic nervous systems, which, in the case of the heart, is driven by adrenaline the so-called “flight or fight” hormone. Adrenaline acts at various sites of the body - On the sinus node in the heart which controls rate to increase heart rate - On the bronchial tubes in the lung to cause them to dilate allowing greater flow of air into the lungs - On the small arteries in the skin and gut to constrict (narrow) reducing blood flow to these areas and making more blood available to the muscles- to fight or fly - Increases the blood sugar by increasing breakdown of glycogen to glucose, important food for the muscles to contract better. Whilst increased adrenaline production is common with exercise it also occurs in states of shock, fear, or anger producing gooseflesh and sweating (remember the first time you saw the shower scene in the Hitchcock Movie Psycho). As well as increasing the heart rate adrenaline may cause cardiac irregularity, increased blood pressure, or palpitations. It is this irregularity which may lead the heart to chaotic beats and finally fibrillation and death. This is the first symptom of a heart attack in about 20% of people – sudden death – the victim just collapses to the ground. Whilst he may gasp a few breaths he has no cardiac output- no blood is leaving his heart- he is pulseless. This terminal condition (ventricular fibrillation) is very easily treated by first aid measures and cardiac shock- termed defibrillation. Nowadays many areas which have high populations (or as in aeroplanes, confined areas) have people friendly defibrillators available which only shock patients who have rhythms which are treatable by shock. These machines have easy instructions and any bystander who can read can apply the electrodes and save the patient’s life. Often people wrongly refer to this cause of death as a massive heart attack- it takes some time (often up to an hour) to die from a massive heart attack. In this case the heart attack causes such significant damage to the main ventricle of the heart as to reduce blood pressure to critically low levels and death results. Cause of Heart Attacks The pathological cause of heart attacks is a clot of blood, which forms over an area on the lining of a coronary artery which, is “ready” for a clot to form – this area is termed a vulnerable plaque. It was previously thought that clots developed on the lining of arterial walls that had become calcified and thickened - it is now known that rarely are these areas the sites of clots. Calcification and deposition of cholesterol within the arterial wall reduces the lumen size and therefore flow of blood through this section of the artery is likewise reduced. This reduced flow may be sufficient to provide enough oxygen to the heart muscle during rest or light work. However once the heart is required to work harder the blood flow is insufficient to provide enough oxygen to the heart muscle and symptoms follow. Angina- Pectoris and Decubitus When the heart muscle receives insufficient oxygen it produces lactic and pyruvic acids and these produces the tightness in the chest known as angina the type of angina which occurs during exercise is termed Angina Pectoris. The obvious treatment is to reduce the heart work by ceasing whatever activity has caused the heart rate to rise. Whilst typically angina pectoris occurs as tightness in the chest it may move up into the throat or down one or both arms. Occasionally it may only occur in the teeth or in the back between the shoulder blades. Patients may describe it as a “weight on my chest” or “constriction”. Occasionally the only symptom may be acute breathlessness. The cardinal feature is the relation to increased heart work and its relief by stopping activity. In addition one should use a trintrin preparation. If pain is present use another dose after five minutes or so and repeat twice. The treatment of angina is beyond the scope of this article however drugs which reduce the work the heart has to do (like putting a governor on your heart) are most effective and as they block the action of adrenaline are termed betablockers. Drugs, which dilate the coronary arteries (trintrins), are also helpful. These come as patches, tablets for sucking, sprays for inhalation or as solutions for intravenous use in hospital. These should be used only when the tightness is present and not when you feel giddy or weak as they will reduce blood pressure and may cause you to faint. These also dilate all arteries and therefore may cause headache. Trintrins are particularly dangerous when used in conjunction with some of the newer drugs for erectile dysfunction eg viagra and these must not be used within 24 hours of each other Spasm of the coronary arteries may also cause reduction in blood flow to the heart. Everyone has some degree of spasm within their bodies and angina is generally due to mixture of both atheroma and spasm. However angina, which occurs at rest particularly at night around 2.0am waking the patient, is due to vasospasm and is termed angina decubitus. The symptoms are similar to angina pectoris but in this case it is spasm of the artery and the treatment is not betablockade therapy but a group of drugs called calcium antagonists. These drugs relieve the spasm of the artery. Unstable Angina Should the pain be prolonged and not relieved by rest and trintrin therapy the term unstable angina is used. In this case the pain is more severe and often associated with an increase in sympathetic overactivity. Symptoms such as sweating, nausea, vomiting, palpitations, faintness or a feeling of wanting to faint (presyncope), or even syncope are common. This is a medical emergency and an ambulance should be called without delay, as it is impossible to differentiate unstable angina from a heart attack without electrocardiograph and blood studies. If you believe that you may have this syndrome whilst waiting for the ambulance chew a whole aspirin tablet. This condition is generally associated with a clot being formed within one of the main coronary arteries and hospitalisation is necessary so that a definitive diagnosis may be made and urgent treatment to protect the heart from damage instituted. Differential Diagnosis Angina is often confused with indigestion and many patients rationalise that whilst they may consider the pain could be angina it “simply cannot happen to me’ and it is probably only indigestion or just wind. One eminent Professor of Cardiology writing in one of the journals described how he waited for eighteen hours before going to Hospital as he thought it “ was simply bad indigestion”. He finished up with bypass surgery! Indigestion is generally in the pit of the stomach burning in nature, often relieved by belching or by drinking a glass of milk or alkali. It has no relation to exercise, rarely referred to the arms or back, and may come up into throat as a burning sensation. Trintrins have no effect. Hiatus hernia or oesophageal reflux may mimic vasospastic angina as they both occur at night when the patient is prone. Silent Ischaemia Some patients, generally those with high pain thresholds, may have myocardial ischaemia which is entirely asymptomatic. Rarely patients may be found with classical electrocardiographic changes of a heart attack without remembering anything remotely like the symptoms, which are noted above. On a treadmill exercise test these patients may develop changes on their cardiograph, which are diagnostic of myocardial ischaemia. They may develop high blood pressure or more dangerous, a fall in blood pressure during exercise without any actual pain. These patients are very difficult to treat, as, unlike most of us, they do not get chest tightness of pressure before they develop dangerous cardiac abnormalities. These people require invasive or nuclear studies to ascertain the workload that causes trouble. They can then be warned to control their work level. Heart Failure and Cardiac Irregularities Patients in their senior years may develop heart failure without any pain or tightness. The Electrocardiographic changes of a previous heart attack are found on routine examination. Atrial fibrillation, a not uncommon rhythm disturbance, often has myocardial ischaemia as its underlying cause, particularly in the elderly. This irregularity results in a reduction in the output from the left ventricle (stroke volume). As blood continues to fill the ventricle from above the lower output results in the heart becoming distended with blood. Heart muscle like all other muscles when stretched contracts with greater strength thereby increasing the output. The patient is unaware of anything the matter with his heart until an xray is taken showing an enlarged heart . (Compensated Heart Failure) However if the reason for the reduction in stroke volume remains then eventually (when the heart cannot enlarge further) pressure within the ventricle rises and is passed backwards through the atrium and on into the pulmonary arterioles causing fluid to move into the air sacs of the lungs and the patients notices increasing shortness of breath breathlessness. (Decompensated Heart Failure)

Article Provided by Neocardia