Complications

The complications after a heart attack are manifold and are almost always related to how quickly the affected person is treated after the attack. As a result of a heart attack, the heart often becomes pumping weak (insufficiency). If a particularly severe heart attack is present, the affected person may remain in a coma for a long time.

Many drugs are administered and the person is also ventilated. This leads to complications such as infections, which can even lead to pneumonia. In addition, a long rehabilitation period must be expected.

Furthermore, complications such as reduced performance, reduced resilience, fatigue, etc. can occur. The complications are divided into early and late complications.

Among the first are all events that occur in the first 48 hours. This is the most dangerous period, 40% do not survive the first day after a heart attack. Early complications include left heart failure, in which up to 20% of the left ventricle is affected by the infarct and dies.

If more than 40% are affected, this usually results in a cardiogenic (heart-related) shock, which is 90% fatal. This results in a drop in blood pressure and pump failure of the heart. Another complication is cardiac arrhythmia.

These include additional contractions of the ventricle, which increase the risk of ventricular fibrillation. Ventricular fibrillation often occurs within four hours after myocardial infarction and leads to death in 80% of patients. Late complications include

Arterial embolisms
Pericarditis
Cardiac wall aneurysm (bulging of the heart wall)
Heart Failure
Arrythmias

Since a heart attack happens differently to each person, the exact duration cannot be predicted.

Signs such as nausea and vomiting, which are very unspecific symptoms, can appear weeks or days before a heart attack. However, this does not allow us to determine the time at which the heart attack will occur. If symptoms such as chest pain and tightness in the chest persist for more than 5 minutes, the heart attack is a probable diagnosis, so an emergency doctor should be called immediately if such signs occur.

It is quite possible that the symptoms will last for more than 30 minutes if the person is not receiving proper care in the meantime. Laboratory During blood sampling, the inflammation values are always determined, which show an elevated reactive protein C and possibly elevated white blood cells. In addition, the blood sedimentation rate is increased.

However, these inflammation values are very unspecific and do not necessarily indicate a myocardial infarction. Another non-specific marker is LDH, an enzyme called lactate dehydrogenase, which is used for late diagnosis. It only returns to normal after one to two weeks.

More specific markers of a HI are troponin T and I. They are heart muscle specific markers, which increase about three hours after the infarction, reach their maximum after 20 hours and normalize only after one to two weeks. They are considered very safe if they are measured over a period of 10 hours and 5 days.

On the fourth day, troponin T correlates with the size of the infarct. Unfortunately, positive troponin values can also occur in cases of pulmonary embolism, myocarditis, acute and chronic heart muscle weakness, renal insufficiency or stroke. Furthermore, the enzyme creatine kinase can be determined.

It is the lead enzyme, which increases in case of muscular or cardiac damage. Again, the level of creatine kinase and the size of the myocardial infarction correlate with each other. There are four subgroups of this enzyme.

Creatine kinase MB stands for the myocardial type and is important for the diagnosis of a heart attack. If this increases by between 6-20% in relation to the total creatine kinase, this indicates a release from the heart muscle. The cause may be an infarction, but it can also be caused by myocarditis or heart surgery.

There is a rapid test for a protein called “heart fatty acid binding protein”. This is positive just 30 minutes after a heart attack has occurred. ECG The electrocardiogram is an important diagnostic tool to better visualize a myocardial infarction.

It shows the sum of the electrical activity of all myocardial fibers.It can often be negative in the first 24 hours after the infarction-like symptoms. A second ECG must therefore be performed after 24 hours to confirm or rule out a myocardial infarction if necessary. Only if the ECG is negative twice and there are no troponin T and troponin I or creatine kinase-MB abnormalities can an infarction be ruled out.

The ECG can be used to describe the extent and location of the infarction and to determine the age of the myocardial infarction. The typical sign of an infarction is the so-called ST elevation. There are several waves on the ECG.

The area between S and T is the distance in which the excitation of the chamber is reduced and the heart muscle relaxes again. Elevation in this area increases oxygen deprivation, is indicative of an infarction and is also known as STEMI (ST-segment elevation myocardial infarction). There are three stages, each with their own typical ECG changes that indicate the age of the infarction.

In addition to STEMI, there is NSTEMI, a non-ST elevation myocardial infarction. It is more likely to be a ST segment depression. Here the typical laboratory with troponin T/I and the enzyme increase of creatine kinase-MB is proving.

With the ECG, several recordings are made along the heart. This enables the doctor to tell where the infarct is located, because exactly these derivations look suspicious. Imaging techniques Echocardiography can be used to visualize the heart and its structures in a similar way to ultrasound.

Thus the valves, vessels and size are clearly visible to the trained examiner. The complete heart function can be assessed, from the atrium and ventricular filling to the pumping function. A lack of thickness increase in the infarct zone and a regional wall movement disorder can be detected.

In a very fresh infarction, such wall movement disorders occur very early, even before the ECG changes and enzyme increases. If no wall movement disorders occur, a myocardial infarction can be ruled out to 95%. A magnetic resonance tomography can also show structural changes in the heart.

However, the gold standard of imaging procedures is left heart catheterization. The examination takes place under sterile conditions. The patient lies on the examination table and receives a local anesthetic at the puncture site.

This is either in the groin at the femoral artery or at the wrist at the radial artery. A catheter (a wire) is then advanced to the heart. The catheter is used to fill contrast medium into the left ventricle.

At the same time, X-rays are taken, which are transmitted to a monitor. Possible narrowing or occlusion of the coronary arteries can thus be well visualized. In order to make a correct diagnosis of a heart attack, the patient’s medical history, i.e. the questioning of the patient, first plays an important role.

If the suspicion of a myocardial infarction is confirmed, blood tests in particular are used. This involves testing various substances in the blood that are normally found within the heart muscle cells. This is because in the event of a heart attack, the cells break down and release their substances into the blood, where they can be detected.

One substance that generally indicates the destruction of cells is LDH. LDH is found in almost all cells and is involved in their metabolism. The typical marker for the presence of a heart attack is troponin T. Troponin T is an enzyme that is only present in heart muscle cells.

So if there is too much of it in the blood, this clearly indicates damage to the heart. In addition to the blood tests, an ECG is also recommended. This uses electrodes to measure the electrical activity in the heart.

These are recorded as waves and spikes. If these deviate from the typical pattern, a heart attack is suspected. The most frequent change is that the distance between the S-wave and the T-wave is higher.

This is why it is also called an ST elevation infarction. According to the guidelines, the treatment of a heart attack should be in the following order: The emergency physicians are usually the first to see a heart attack patient. They immediately give oxygen and a nitro preparation (a drug to stimulate the blood circulation of the heart) is sprayed under the tongue.

Anticoagulants and acetylsalicylic acid are administered via a venous access. In one study it was shown that early administration of acetylsalicylic acid (Aspirin) reduces the risk of killing by 20%.In addition, patients are given beta-blockers unless they have contraindications such as low heart rhythm, asthma, heart failure, age >70 years or cardiac conduction disorders. These lower the resting heart rate and blood pressure.

This reduces the risk of developing ventricular fibrillation. As soon as the patient arrives at the hospital, the circulation is closely monitored. Nitrates or morphine (a powerful opiate) can be administered if the pain is severe.

The acetylsalicylic acid medication (ASA) is continued and additional anticoagulants are administered. The beta-blockers will also be retained as a drug if there is no contraindication. In reperfusion therapy, two procedures come into question.

In the conservative method, so-called fibrinolytics are administered, which break up the blood clot that is blocking the coronary artery and thus dissolve it. These drugs include: They may only be used if the heart attack was not more than 6 hours ago, there are no contraindications and a confirmed ECG change has been determined. Contraindications against lysis therapy (dissolution of the thrombus using special drugs) are The second procedure is a surgical approach.

During the left heart catheter examination a “percutaneous transluminal coronary angioplasty” can be performed simultaneously. This is the gold standard of heart attack therapy. In this procedure, a guiding catheter (small tube) is inserted through either the inguinal artery (Arteria Femoralis) or the forearm artery (Arteria Radialis) and advanced to the aortic valve and coronary arteries.

A balloon catheter is inserted through this. An attempt is made to reopen the narrowed or occluded vessel at the heart by means of the balloon, which can be expanded manually. A stent, a small net-like, cylinder-shaped vessel, can be inserted as an additional support.

As a long-term therapy, anticoagulants and beta-blockers are nowadays prescribed on a permanent basis. Blood clotting inhibitors include those that directly inhibit platelet aggregation (acetylsalicylic acid or clopidogrel) and coumarins, which indirectly prevent blood clotting via vitamin K. Additionally the patient should take Cholesterinsenker, since they lower the second infarct rate and the mortality rate clearly.

General measures (securing life)
Reperfusion therapy (reopening of closed coronary vessels)
Prophylaxis of coronary re-thrombosis
Therapy of complications
Streptokinase
Alteplase (r-t-PA) or
Reteplase (r-PA)
Stomach and intestinal ulcer (ulcera)
Ocular fundus bleeding
Headaches
Blood coagulation disorders in the history
Pregnancy
A stroke less than 6 months ago (apoplexy)
Aneurysms (abnormal bulging of the vessels)
An operation or accident less than 1-2 weeks before the operation
Main artery (aorta)
Ventricle
Coronary arteries
Atrium (Atrium)
Vena cava (vena cava)
Carotid artery (carotid artery)

There are two goals in the care of a heart attack which the first aider should pursue: first of all, the heart should be relieved.

In addition, the patient’s symptoms should of course be alleviated as successfully as possible. Since the circulation often breaks down during a heart attack, fainting spells can occur. Therefore the patient should lie down.

Ideally, the upper part of the body should be elevated a little. As a result, less blood flows back to the heart, so that the heart can save a little strength. People who have been known to have heart problems for some time often have a nitro spray.

This contains a substance that can dilate the blood vessels. Since the narrowing of the coronary arteries is in most cases the cause of a heart attack, the drug is ideally suited to dilate the vessels again in an emergency. Of course, if a heart attack is suspected, the emergency doctor should be called immediately.

The paramedics can then provide further assistance. They provide the person with oxygen, for example. They can also administer painkillers and thus alleviate the acute symptoms.

In most cases, a heart attack occurs when one or more of the coronary arteries are blocked.As a result, not enough blood can flow into the tissue behind the constriction. This results in a reduced supply of oxygen and other nutrients. As a result, the heart cells die, which can lead to irregularities in the pumping action of the heart.

In order to restore the supply to the heart muscle cells, the constriction or blockage must be overcome. This is often achieved with a stent. A stent can be thought of as a round wire mesh.

In most cases, the stent is inserted into the coronary vessel with a catheter. A long wire is pushed from the artery on the thigh or forearm to the heart, from where the catheter enters the coronary arteries. The stent is placed in the coronary vessel in such a way that it lies all around the vessel wall and from then on keeps the vessel open.

To prevent the clogging material from re-accumulating, the stent is often additionally coated with certain substances. In this way, the affected coronary vessel can be kept open permanently, thus preventing renewed heart attacks. Often a blockage or narrowing of the coronary vessels is the cause of a heart attack.

The fact that the vessel has a constriction means that the tissue behind it is no longer sufficiently supplied with blood. The obvious therapy is therefore to restore the blood supply to the cells. One possibility for this is bypass surgery.

In most cases, a vessel from another part of the body is used to bridge the constriction. This vessel is connected to the aorta and behind the constriction is connected to the coronary vessel. This allows the blood to flow past the constriction and supply the heart muscle cells again.

People who suffer a very severe heart attack are often put into an artificial coma. As a result, the body uses less energy so that the heart can recover better. They are given artificial respiration and various accesses (usually to the veins) through which drugs can be administered.

Among other things, these drugs are intended to support the heart and circulation as long as the heart is not able to do this on its own. The artificial coma also has disadvantages, however. The bodily functions are “on the back burner” for a while, so after waking up the person has to get used to everyday stress.

Unfortunately, many people (almost 40%) still die on the first day after a heart attack. Without a revascularization in hospital, another 15% die. Thus the risk of dying of a heart attack within the first month increases to about 50%.

In the first two years after discharge, 5-10% of all patients suffer sudden cardiac death. The long-term prognosis depends on several factors. On the one hand, the size of the infarct area and the ischemic signs (chest tightness and ECG signs) and, on the other hand, the cardiac arrhythmia and the number of affected vessels.

The persistence of risk factors is also an important factor. If it is possible, the above risk factors must be brought under control in order to improve the prognosis a little.

LDL cholesterol increase
High blood pressure
Smoking
Diabetes mellitus
Age (over 45 years for men and over 55 years for women)

A heart attack occurs when heart muscle cells are not sufficiently supplied with blood and other nutrients.

This is often the case when the coronary arteries are clogged. The reduced supply causes the death of heart muscle cells. The signal that stimulates the heart muscle cells to contract is passed from cell to cell and through fine nerve bundles.

Cell death can cause interruptions in this transmission of stimuli. This leads to the heart no longer beating in a coordinated manner. The rhythm gets confused.

These cardiac arrhythmias can continue even after the acute situation of an infarction. However, they can be treated with medication. About half of the people who suffer a heart attack die in the acute situation.

This is usually due to the cardiac arrhythmias that are triggered by the infarction and cannot be remedied quickly enough. For long-term survival after a heart attack, the first 2 hours after the infarction are particularly crucial. The faster the affected person is treated and the faster the constriction in the coronary arteries expands again, the better the prognosis.In addition, survival naturally depends on the size of the affected area and thus on the complications that follow. About 5 to 10% die of sudden cardiac death in the first 2 years after a heart attack. The rate of new heart attacks is also high.