229 Development of the Heart
Aging and the Heart
As a person ages, the walls of the heart thicken, the heart becomes heavier, valves stiffen and leak, and the aorta becomes larger.
Learning Objectives
Describe the effects of aging on the heart
Key Takeaways
Key Points
- The heart muscle becomes less efficient with age, with a decrease in both maximum cardiac output and heart rate.
- As a person ages, heart valves may become thickened by fibrosis or calcification, leading to heart murmurs and less efficient pumping.
- The health of the myocardium depends on its blood supply, and with age there is greater likelihood that atherosclerosis will narrow the coronary arteries.
- Atherosclerosis is the deposition of cholesterol on and in the walls of the arteries, which decreases blood flow and forms rough surfaces that may cause intravascular clot formation.
Key Terms
- arrhythmia: An irregular heartbeat.
- cardiac output: The volume of blood pumped by the heart each minute calculated as heart rate (HR) X (times) stroke volume (SV).
- atherosclerosis: The clogging or hardening of arteries or blood vessels caused by plaques (accumulations of fatty deposits, usually cholesterol).
After age 30, changes in the blood vessels that serve the brain tissue that reduce nourishment to the brain, resulting in the malfunction and death of brain cells. By age 80, cerebral blood flow is 20% less and renal blood flow 50% less than at age 30. As a person ages, the walls of the heart thicken and the heart becomes heavier, heart valves stiffen and are more likely to calcify, and the aorta, the major vessel carrying blood out of the heart, becomes larger.
The heart muscle becomes less efficient with age with a decrease in both maximum cardiac output and heart rate, although resting levels may be more than adequate. The health of the myocardium depends on its blood supply, and with age there is greater likelihood that arthrosclerosis will narrow the coronary arteries. Atherosclerosis is the deposition of cholesterol on and in the walls of the arteries, which decreases blood flow and forms rough surfaces that may cause intravascular clot formation. High blood pressure (hypertension) causes the left ventricle to work harder. It may enlarge and outgrow its blood supply, thus becoming weaker. A weak ventricle is not an efficient pump, so this issue may progress to congestive heart failure. This process may be slow or rapid. The heart valves may become thickened by fibrosis or calcification, leading to heart murmurs and less efficient pumping. Arrhythmias are also more common with age, as the cells of the conduction pathway become less efficient.
Development of the Heart
Vasculogenesis is the development of new blood vessels.
Learning Objectives
Describe the development of the heart
Key Takeaways
Key Points
- The development of the circulatory system occurs by the process of vasculogenesis during weeks four through eight of human development.
- Vasculogenesis, in contrast to angiogenesis, is when endothelial precursor cells (angioblasts) migrate and differentiate in response to local cues (such as growth factors and extracellular matrix) to form new blood vessels.
- The human arterial system originates from the aortic arches and the dorsal aortae starting from week four of human development. The dorsal aortae are initially bilateral and then fuse to form the definitive dorsal aorta.
- Vasculogenesis occurs when endothelial precursor cells migrate and differentiate in response to local cues (such as growth factors and extracellular matrix) to form new vessels. These vascular trees are then pruned and extended through angiogenesis to create the appropriate vessel organization.
Key Terms
- aortic arches: Also known as pharyngeal arch arteries, this series of six paired, embryological vascular structures gives rise to several major arteries. They are ventral to the dorsal aorta.
- angiogenesis: The formation and development of new blood vessels.
- vasculogenesis: The formation and development of the vascular system, including the formation of blood vessels from endothelial cells.
The development of the circulatory system occurs by the process of vasculogenesis followed by angiogenesis, the sprouting of new vessels from pre-existing ones. The human arterial and venous systems develop from different embryonic areas. While the arterial system develops mainly from the aortic arches, the venous system arises from three bilateral veins during weeks four through eight of human development.
Arterial Development
The human arterial system originates from the aortic arches and from the dorsal aortae starting from week four of human development. Aortic arch 1 almost completely regresses except to form the maxillary arteries. Aortic arch 2 also completely regresses except to form the stapedial arteries. The definitive formation of the arterial system arise from aortic arches 3, 4 and 6, while aortic arch 5 completely regresses.
The dorsal aortae are initially bilateral and then fuse to form the definitive dorsal aorta. Approximately 30 posterolateral branches arise from the aorta to form the intercostal arteries, upper and lower extremity arteries, lumbar arteries, and lateral sacral arteries. The lateral branches of the aorta form the definitive renal, suprarenal, and gonadal arteries. The ventral branches of the aorta consist of the vitelline arteries and umbilical arteries. The vitelline arteries form the celiac, superior, and inferior mesenteric arteries of the gastrointestinal tract. After birth, the umbilical arteries form the internal iliac arteries.
Venous Development
The human venous system develops mainly from the vitelline veins, the umbilical veins, and the cardinal veins, all of which empty into the sinus venosus. Vasculogenesis is the process of blood vessel formation by new production of endothelial cells, in contrast with angiogenesis in which new blood vessels are formed from pre-existing vessels. For example, if a monolayer of endothelial cells begins sprouting to form capillaries, angiogenesis is occurring. Vasculogenesis occurs when endothelial precursor cells (angioblasts) migrate and differentiate in response to local cues (such as growth factors and extracellular matrix) to form new blood vessels. These vascular trees are then pruned and extended through angiogenesis.
Heart Failure
Heart failure is defined as the inability of the heart to supply blood to the organs of the body.
Learning Objectives
Describe heart failure and its treatments
Key Takeaways
Key Points
- Common causes of heart failure include myocardial infarction and other forms of ischemic heart disease, hypertension, valvular heart disease, and cardiomyopathy.
- Heart failure can cause a number of symptoms including shortness of breath, leg swelling, and exercise intolerance.
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Management of heart failure requires a multimodal approach.
Treatment commonly consists of lifestyle changes and/or medications, but can also include implanted devices (pacemakers or ventricular assist devices) and in severe cases, heart transplant. - It involves a combination of lifestyle modifications, medications, and possibly the use of devices or surgery.
Key Terms
- electrocardiogram: The visual output that an electrocardiograph produces.
- congestive heart failure: A syndrome marked by weakness, edema, and shortness of breath, caused by the inability of the heart to circulate the blood adequately to the lungs and other tissues.
- myocardial infarction: Necrosis of heart muscle caused by an interruption to the heart’s blood supply, often as a result of coronary thrombosis or artery occlusion.
Heart failure (HF), often called congestive heart failure (CHF), is generally defined as the inability of the heart to supply sufficient blood flow to meet the needs of the body. Heart failure can cause symptoms including shortness of breath, leg swelling, and exercise intolerance. The condition is diagnosed with echocardiography and blood tests. Treatment commonly consists of lifestyle measures (such as smoking cessation, light exercise including breathing protocols, decreased salt intake, and other dietary changes) and medications. Sometimes it is treated with implanted devices (pacemakers or ventricular assist devices) and occasionally a heart transplant.
Causes of Heart Failure
Common causes of heart failure include myocardial infarction and other forms of ischemic heart disease, hypertension, valvular heart disease, and cardiomyopathy. The term heart failure is sometimes incorrectly used to describe other cardiac-related illnesses, such as myocardial infarction (heart attack) or cardiac arrest. However, these conditions can lead to heart failure, a disease that is common, costly, disabling, and potentially deadly. In developed countries, around 2% of adults suffer from heart failure, but in those over the age of 65, this increases to 6 to 10%.
Heart failure may also occur when the body’s requirements for oxygen and nutrients are increased and the demand outstrips what the heart can provide, (termed high-output cardiac failure). This can occur from severe anemia, Gram negative septicaemia, beriberi (vitamin B1/thiamine deficiency), thyrotoxicosis, Paget’s disease (a bone disease that puts strain upon the heart), arteriovenous fistulae, or arteriovenous malformations.
Symptoms of Heart Failure
Common respiratory signs include tachypnea (increased rate of breathing) and increased work of breathing (non-specific signs of respiratory distress). Rales or crackles, heard initially in the lung bases and later throughout the lung fields suggest the development of pulmonary edema (fluid in the alveoli). Cyanosis, which suggests severe hypoxemia, is a late sign of extremely severe pulmonary edema.
Additional signs indicating left ventricular failure include a laterally displaced apex beat (which occurs if the heart is enlarged) and a gallop rhythm (additional heart sounds) may be heard as a marker of increased blood flow, or increased intra-cardiac pressure. Heart murmurs may indicate the presence of valvular heart disease, either as a cause (aortic stenosis) or result (mitral regurgitation) of heart failure.
Diagnosis and Treatment of Heart Failure
Echocardiography is commonly used to support a clinical diagnosis of heart failure. This modality uses ultrasound to determine the stroke volume (SV, the amount of blood in the heart that exits the ventricles with each beat), the end-diastolic volume (EDV, the total amount of blood at the end of diastole), and the SV in proportion to the EDV, a value known as the ejection fraction (EF). Echocardiography may also aid in deciding what treatments will help the patient, such as medication, insertion of an implantable cardioverter-defibrillator, or cardiac resynchronization therapy.
Chest X-rays are frequently used to aid in the diagnosis of CHF. In some patients, this may show visible enlargement of the heart. An electrocardiogram (ECG/EKG) may be used to identify arrhythmias, ischemic heart disease, right and left ventricular hypertrophy, and presence of conduction delay or abnormalities (e.g. left bundle branch block).
Treatment focuses on improving the symptoms and preventing the progression of the disease. Reversible causes of the heart failure also need to be addressed: (e.g. infection, alcohol ingestion, anemia, thyrotoxicosis, arrhythmia, hypertension). Treatments include lifestyle and pharmacological modalities.