Mastering Heart Failure Pathophysiology

Systolic dysfunction refers to impaired cardiac contractility leading to a decreased ejection fraction. Diastolic dysfunction refers to impaired ventricular relaxation leading to decreased filling and increased ventricular pressure.

The main components of afterload are vascular resistance and ventricular wall tension.

Excessive afterload may impair ventricular ejection and increase wall tension.

Cardiac output = heart rate x stroke volume.

Pre-load is determined by venous return and end-diastolic volume (EDV).

Increased contractility increases cardiac output independent of preload and afterload.

Myocardial contractility is influenced by Ca2+ levels, L-type channels opening facilitated by cAMP, and Na+/Ca2+ exchange inhibited indirectly by cardiac glycosides.

The NYHA classification of heart failure categorizes patients based on their symptoms and limitations in physical activity.

Class II heart failure is characterized by slight limitation of physical activity. Patients are comfortable at rest, but ordinary physical activity results in fatigue, palpitation, and shortness of breath.

Systolic dysfunction is characterized by a decreased ejection fraction, indicating impaired cardiac contractility. Diastolic dysfunction is characterized by a preserved ejection fraction, but impaired ventricular relaxation and increased ventricular pressure.

The capillary wall is generally a barrier to proteins, but is permeable to water and most solutes. It is not a perfect filter, with the permeability for albumin being 1/1000th that of water.

Oncotic pressure is generated by plasma proteins, predominantly by albumin and to a lesser extent by globulins. It is approximately 28mmHg and draws fluid into the capillaries.

Capillary hydrostatic pressure forces fluid out of the capillaries and into the interstitium. It decreases from the arterial end to the venous end, with a pressure of approximately 30-40mmHg at the arterial end and 10-15mmHg at the venous end.

The lymphatic system drains excess fluid from the capillaries, helping to control the volume of interstitial fluid. It also plays a role in controlling the concentration of proteins in interstitial fluids and is involved in the immune response.

Venous return to the heart is influenced by factors such as sympathetic innervation, muscle pumps, and postural changes in hydrostatic pressure. It is a major determinant of cardiac output, which is important for overall circulation.

Decreased alveolar O2 reduces local alveolar blood flow in the lungs. The opposite effect observed in systemic vessels is increased blood flow. The mediator responsible for this effect is unknown.

The major routes across capillary membranes for fluids, solutes, and larger molecules/proteins are diffusion and bulk flow. Starling's forces, including hydrostatic and oncotic pressures, contribute to fluid homeostasis by balancing the movement of water between the capillaries and interstitial space. These forces determine the net transcapillary movement of water across capillary beds.

The factors that affect venous return and consequently determine cardiac output and blood pressure include blood volume, venous tone, skeletal muscle pump, and respiratory pump.

The lymphatic system plays a crucial role in fluid homeostasis by collecting excess interstitial fluid and returning it to the bloodstream. It helps maintain the balance of fluid between the capillaries and interstitial space, preventing edema and contributing to the movement of water across capillary beds.

Capillary diffusion is the net movement of nutrients, oxygen, and metabolic end products across capillary membranes. It is essential for the exchange of gases and nutrients between the blood and surrounding tissues. Through diffusion, these substances move from an area of higher concentration to an area of lower concentration, ensuring adequate supply to the tissues and removal of waste products.