What affects one side of the heart eventually will effect both sides as the heart and lungs are interconnected systems. Left side failure occurs when left ventricular output is less than the volume of blood received from the right side of the heart via the pulmonary circulation. Congestion in the pulmonary circuit ensues and the systemic blood pressure falls. Myocardial infarction is the most common cause of left heart failure but it can also be caused by hypertension, aortic insufficiency or cardiomyopathy.
Right heart failure, similarly, occurs when the right ventricle cannot pump the volume of blood returned to it. The resulting congestion of the systemic venous system and decreased output to the lungs causes venous distention, swelling of distensible organs to produce hepatomegaly, splenomegaly and peripheral edema. In addition, many of the effects of left heart failure are seen because of the inadequate return from the lungs and output of the left ventricle. The causes of right heart failure are left heart failure, obstructive lung disease, and congenital heart defects.
Treatments are generally aimed at increasing the pumping ability of the heart, reducing the volume of blood that must be pumped, reducing fluid retention and management of vascular tone.
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Treatments are generally aimed at increasing the pumping ability of the heart, reducing the volume of blood that must be pumped, reducing fluid retention and management of vascular tone.
Cardiogenic shock
Any factor that depresses myocardial function can precipitate cardiogenic shock. The most common cause is myocardial infarction. The prognosis once shock ensues is not good and the mortality rate following myocardial infarction is 60-80%. When the pumping ability of the heart is diminished, systolic blood pressure drops, and the sympathetic nervous system is activated causing peripheral vasoconstriction and increased heart rate (tachycardia). The net effect increases the load on the heart in an effort to maintain coronary and cerebral blood flow. These mechanisms may compensate and maintain arterial pressure or they might be inadequate and irreversible shock is the end. Peripheral tissues are functioning under anaerobic conditions and it is the lactic acid produced that eventually cause cellular death.
Cardiomyopathy
Conditions that affect the ventricular muscle and decrease the pumping ability of the heart are classified as cardiomyopathies. Inflammation of the myocardium due to infection or damage caused by radiation or chemicals is called myocarditis. Many types of myocarditis will resolve with bed rest, drug therapy, and fluid restriction.
Congestive cardiomyopathy is a feature of beriberi, alcoholism, diabetes, drug toxicity and some neuromuscular disorders. Enlargement of the heart that is seen is a result of dialation and enlargement of the heart that can no longer pump efficiently. The symptoms are then characteristic of double sided congestive heart failure.
Hypertrophic cardiomyopathy is an asymmetric increase in ventricular muscle mass. The ventricular septum is especially enlarged causing the left ventricle to be misshapen and obstructing the blood flow from the ventricle. Symptoms are basically those of left congestive heart failure.
Congestive cardiomyopathy is a feature of beriberi, alcoholism, diabetes, drug toxicity and some neuromuscular disorders. Enlargement of the heart that is seen is a result of dialation and enlargement of the heart that can no longer pump efficiently. The symptoms are then characteristic of double sided congestive heart failure.
Hypertrophic cardiomyopathy is an asymmetric increase in ventricular muscle mass. The ventricular septum is especially enlarged causing the left ventricle to be misshapen and obstructing the blood flow from the ventricle. Symptoms are basically those of left congestive heart failure.
Coronary artery disease
Coronary artery disease occurs when the interior of the vessels supplying the heart become blocked and restrict blood flow to the heart. It occurs when fatty plaques are formed inside the lumen of the arteries. The levels of low density lipoproteins (LDL), specifically oxidized LDL, in the blood correlate with the severity of atherosclerosis. Blood clots can form at the plaque and cut off the flow of blood.
Treatments for coronary artery disease include bypass surgery, balloon angioplasty, and laser angioplasty. Bypass surgery consists of taking a vessel from somewhere else in the body (usually the leg) and grafting it into the coronary circulation to reroute blood flow around the blockage. Coronary bypass surgery is very effective in treating angina. Balloon angioplasty has become a very common procedure where a catheter is introduced into an artery in the leg or arm and is guided to the blockage. A small balloon is inflated that flattens the plaque against the artery so that the vessel is opened and blood flow is restored. Laser angioplasty operates in a similar fashion except the catheter delivers an optical fiber to the blocked area. The plaque is destroyed by irradiation with laser light and blood flow is restored.
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Ischemic heart disease
Angina pectoris, or chest pain, is caused by decreased oxygen delivery to the myocardium usually due to blockage of the coronary arteries. The severe pain usually radiates to the left shoulder and down the left arm but may also radiate to the abdomen, back or jaw. The steady severe pain and feeling of pressure in the chest may last from a few seconds to several minutes. Inhalation of amyl nitrate or sublingual nitroglycerin can help to dilate the coronary vessels temporarily.
Angina may be treated surgically by bypassing problem areas, opening the blood vessels (angioplasty) or by transmyocardial revascularization. This latter procedure involves the use of a laser to drill small holes in the myocardium that allow blood to enter and muscular access to oxygen. Laser transmyocardial revascularization is used in patients that have angina that isn't eliminated by opening up the coronary arteries. An alternative procedure, percutaneous transluminal myocardial revascularization, uses a catheter inserted into an artery in the thigh or arm that is then placed into the left ventricle where 15-30 holes are laser drilled into the myocardium before the catheter is withdrawn. This procedure is less invasive than direct transmyocardial revascularization as it does not require opening the chest. Sometimes transmyocardial revascularization is used in addition to bypass for patients with severe angina.
Angina may be treated surgically by bypassing problem areas, opening the blood vessels (angioplasty) or by transmyocardial revascularization. This latter procedure involves the use of a laser to drill small holes in the myocardium that allow blood to enter and muscular access to oxygen. Laser transmyocardial revascularization is used in patients that have angina that isn't eliminated by opening up the coronary arteries. An alternative procedure, percutaneous transluminal myocardial revascularization, uses a catheter inserted into an artery in the thigh or arm that is then placed into the left ventricle where 15-30 holes are laser drilled into the myocardium before the catheter is withdrawn. This procedure is less invasive than direct transmyocardial revascularization as it does not require opening the chest. Sometimes transmyocardial revascularization is used in addition to bypass for patients with severe angina.
Arrhythmia
The normal heat beat is initiated at the pacemaking sinoatrial node. An irregular heart beat is known as an arrhythmia including alterations in rate and atrioventricular conduction. Physiological, pathological and pharmacological causes can effect the conduction or discharge of impulses within the heart. An arrhythmia can be a tachycardia or increased heart rate, usually over 100 beats/minute, or a slower heart rate called bradycardia which is usually under 60 beats/minute. Physiological causes of tachycardia include emotion, exercise, fever, or stress. Bradycardia is normally seen during sleep. Arrhythmias are common in patients with acute myocardial infarction (80%), during anesthesia (50%), and in about 25% of patients on digitalis.
The arrhythmia may represent a lack of normal communication between the atrial conduction system and the ventricles. Because the atria are electrically isolated from the ventricles except for the conductive fibers, the atria can enter tachycardia without the ventricles being effected. An ectopic focus is usually involved in this case. An ectopic focus is an area of myocardial tissue that takes over pacemaker functions because it spontaneously discharges more rapidly than the sinoatrial node, usually because of injury. Ectopic foci can occur in the ventricles too and frequently do following a myocardial infarct. Some drugs, such as digitalis, sympatholytics, or cholinergics can alter heart rate due to direct effects on cardiac muscle or the nervous regulation of the heart.
Therapy for arrhythmias is aimed at decreasing pacemaker activity and modifying impaired conduction. The mechanisms involve the use of sodium channel blockers, calcium channel blockers and/or beta blockers in an effort to decrease the automaticity, conduction, and excitability of the heart or increase the refractory period of cardiac muscle. the effect is more pronounced in depolarized or injured tissue than in normal cardiac muscle. Drug-induced arrhythmias can result from toxic effects on cardiac conduction systems with increased dosages.
Atrial fibrillation is where the atria beat rapidly and incompletely in a disorderly and irregular manner. This is due multiple waves of excitation passing over the atria. Ventricular fibrillation, similarly, is when the ventricular muscle contracts in an uncoordinated fashion due to the rapid discharge of multiple ventricular ectopic foci. Fibrillating atria or ventricles cannot efficiently pump blood and in the case of ventricular fibrillation that lasts more than a few minutes it is fatal if the patient is not treated. Electronic defibrillators can stop ventricular fibrillation by initiating an electric shock that resets and restores normal rhythm to the heart.
The arrhythmia may represent a lack of normal communication between the atrial conduction system and the ventricles. Because the atria are electrically isolated from the ventricles except for the conductive fibers, the atria can enter tachycardia without the ventricles being effected. An ectopic focus is usually involved in this case. An ectopic focus is an area of myocardial tissue that takes over pacemaker functions because it spontaneously discharges more rapidly than the sinoatrial node, usually because of injury. Ectopic foci can occur in the ventricles too and frequently do following a myocardial infarct. Some drugs, such as digitalis, sympatholytics, or cholinergics can alter heart rate due to direct effects on cardiac muscle or the nervous regulation of the heart.
Therapy for arrhythmias is aimed at decreasing pacemaker activity and modifying impaired conduction. The mechanisms involve the use of sodium channel blockers, calcium channel blockers and/or beta blockers in an effort to decrease the automaticity, conduction, and excitability of the heart or increase the refractory period of cardiac muscle. the effect is more pronounced in depolarized or injured tissue than in normal cardiac muscle. Drug-induced arrhythmias can result from toxic effects on cardiac conduction systems with increased dosages.
Atrial fibrillation is where the atria beat rapidly and incompletely in a disorderly and irregular manner. This is due multiple waves of excitation passing over the atria. Ventricular fibrillation, similarly, is when the ventricular muscle contracts in an uncoordinated fashion due to the rapid discharge of multiple ventricular ectopic foci. Fibrillating atria or ventricles cannot efficiently pump blood and in the case of ventricular fibrillation that lasts more than a few minutes it is fatal if the patient is not treated. Electronic defibrillators can stop ventricular fibrillation by initiating an electric shock that resets and restores normal rhythm to the heart.
Myocardial infarction
Ischemic necrosis of the myocardium results from inadequate blood flow and therefore oxygen delivery to the myocardium that causes irreversible cell damage and cellular death. Symptoms are pain similar to angina pectoralis, shock, arrhythmias, cardiac failure, and possibly sudden death. Some 10-25% of myocardial infarcts occur without chest pain so angina is not a perfect indicator.
The electrocardiogram (ECG) is the most useful direct test available for diagnosis of a heart attack. Laboratory tests are often inconclusive but several parameters give abnormal results in most patients and can therefore be used as indicative of an infarct. Cellular death releases myocardial enzymes that can be used to diagnose the severity of the infarct. Enzymes such as lactate dehydrogenase, creatine phosphokinase, and serum aspartate aminotransferase levels are elevated at certain times after an infarct has occurred and may also give some indication of the severity of the damage.
The time between the onset of ischemia and muscle cell death is about 15 to 20 minutes in most cases. Almost always the infarction occurs in the left ventricle and left ventricular function may be significantly diminished. The larger the affected area of the myocardium the greater the loss of contractility. All myocardial infarctions have a central area of necrosis that is surrounded by an area of injury. Myocardial tissue does not regenerate after injury so the necrotic tissue is replaced by scar tissue that may inhibit contractility. If a large area of tissue is involved the heart as a pump may be compromised and the symptoms of congestive heart failure or cardiogenic shock will be seen.
Complications of myocardial infarction include various disturbances in the normal heart rhythm, congestive heart failure, cardiogenic shock, thromboembolisms, pericarditis, and myocardial rupture. Ninety percent of patients will have some disturbance of rhythm following myocardial infarction. This is a result of local changes that effect automaticity and conduction of the heart muscle.
Ten percent of those that die from a myocardial infarction have emboli to the brain, kidney, spleen or mesentery. Emboli almost always originate in the peripheral venous system due to bed rest and heart failure. With modern day management including anticoagulation therapy and early mobilization, pulmonary embolisms have become rare complications of heart attacks. Rupture of the myocardial wall can occur in cases of severe myocardial damage and results in almost immediate death.
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| Congestive Heart Failure |
The electrocardiogram (ECG) is the most useful direct test available for diagnosis of a heart attack. Laboratory tests are often inconclusive but several parameters give abnormal results in most patients and can therefore be used as indicative of an infarct. Cellular death releases myocardial enzymes that can be used to diagnose the severity of the infarct. Enzymes such as lactate dehydrogenase, creatine phosphokinase, and serum aspartate aminotransferase levels are elevated at certain times after an infarct has occurred and may also give some indication of the severity of the damage.
The time between the onset of ischemia and muscle cell death is about 15 to 20 minutes in most cases. Almost always the infarction occurs in the left ventricle and left ventricular function may be significantly diminished. The larger the affected area of the myocardium the greater the loss of contractility. All myocardial infarctions have a central area of necrosis that is surrounded by an area of injury. Myocardial tissue does not regenerate after injury so the necrotic tissue is replaced by scar tissue that may inhibit contractility. If a large area of tissue is involved the heart as a pump may be compromised and the symptoms of congestive heart failure or cardiogenic shock will be seen.
Complications of myocardial infarction include various disturbances in the normal heart rhythm, congestive heart failure, cardiogenic shock, thromboembolisms, pericarditis, and myocardial rupture. Ninety percent of patients will have some disturbance of rhythm following myocardial infarction. This is a result of local changes that effect automaticity and conduction of the heart muscle.
Ten percent of those that die from a myocardial infarction have emboli to the brain, kidney, spleen or mesentery. Emboli almost always originate in the peripheral venous system due to bed rest and heart failure. With modern day management including anticoagulation therapy and early mobilization, pulmonary embolisms have become rare complications of heart attacks. Rupture of the myocardial wall can occur in cases of severe myocardial damage and results in almost immediate death.
Infections
Infections of the pericardium or endocardium of the heart may be caused by a variety of organisms including bacteria, fungi, rickettsiae, and sometimes viruses or parasites. The infective organism is usually of low virulence and therefore slow growing causing the infection to develop gradually over weeks and months. Sometimes however, a more virulent organisms can cause rapid development of an infection.
In endocarditis, the infection invades the cardiac valves and leaflets thus preventing normal alignment of the cusps. This can lead to incomplete closure of the valves or regurgitation leading to cardiac murmurs. Symptoms include fever, blood in the urine, enlarged spleen, nodules on the pads of the fingers, petechiae (small pinpoint hemorrhages in the skin), and anemia. Treatment involves determining the causative agent and directing antibiotic therapy at the microorganism. Without treatment recovery is rare and death usually results.
When the pericardial sac is inflamed due to open heart surgery, myocardial infarction, viral or bacterial infections, tumors, or trauma it may become thickened and fibrotic. The change in compliance of the pericardial membrane restricts ventricular filling. In acute pericarditis, chest pain and electrocardiographic changes are seen but the most important sign is that of an audible pericardial friction rub that sounds like sandpaper rubbing together. When fluid accumulates between the layers of the pericardium cardiac compression and tamponade can result. As fluid accumulates in the pericardium, the pressure rises. When it equals or exceeds that of the heart during diastole, structures such as the right atrium and ventricle become compressed and blood is not returned to the heart. This is life-threatening and death may occur from circulatory collapse.
In endocarditis, the infection invades the cardiac valves and leaflets thus preventing normal alignment of the cusps. This can lead to incomplete closure of the valves or regurgitation leading to cardiac murmurs. Symptoms include fever, blood in the urine, enlarged spleen, nodules on the pads of the fingers, petechiae (small pinpoint hemorrhages in the skin), and anemia. Treatment involves determining the causative agent and directing antibiotic therapy at the microorganism. Without treatment recovery is rare and death usually results.
When the pericardial sac is inflamed due to open heart surgery, myocardial infarction, viral or bacterial infections, tumors, or trauma it may become thickened and fibrotic. The change in compliance of the pericardial membrane restricts ventricular filling. In acute pericarditis, chest pain and electrocardiographic changes are seen but the most important sign is that of an audible pericardial friction rub that sounds like sandpaper rubbing together. When fluid accumulates between the layers of the pericardium cardiac compression and tamponade can result. As fluid accumulates in the pericardium, the pressure rises. When it equals or exceeds that of the heart during diastole, structures such as the right atrium and ventricle become compressed and blood is not returned to the heart. This is life-threatening and death may occur from circulatory collapse.
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