Physiology Cardiac Physiology Chapter

The heart's right ventricle propels blood through the lungs, where it picks up oxygen and releases carbon dioxide. This is called pulmonary circulation.

The heart's left ventricle pumps blood throughout the body, delivering oxygen and nutrients while collecting waste products. This is called systemic circulation.

The arterial system branches out from the aorta and pulmonary artery, getting progressively smaller. These vessels are called arteries, arterioles, and capillaries.

The venous system collects blood from the capillaries and flows into the vena cava and pulmonary vein, becoming progressively larger. These vessels are called venules, veins, and the vena cava.

Capillary beds are the exchange system where oxygen and nutrients move from the blood to the tissues, and waste products move from the tissues to the blood.

The venous blood leaving the tissue would have less oxygen and more carbon dioxide, along with other waste products. This is because the blood couldn't deliver oxygen and nutrients properly.

The aorta is the largest artery in the body, branching out to carry oxygenated blood throughout the body.

The pulmonary artery carries deoxygenated blood from the heart to the lungs.

The phase of the cardiac cycle when the ventricles contract and eject blood into the aorta.

The pressure within the ventricle exceeds the pressure in the aorta, causing the aortic valve to open and blood to flow out.

The phase where the ventricles relax and blood flows back into the heart from the atrium.

The phase of the cardiac cycle where the ventricles relax and fill with blood from the atria.

Blood flow throughout the body is driven by pressure gradients. This pressure is influenced by the heart's contractions and gravity.

Baroreceptors are specialized mechanoreceptors located in the walls of the aortic arch and carotid sinus. They detect changes in blood vessel stretch or distention, which is caused by blood pressure.

Baroreceptors send signals to the central nervous system (CNS) about changes in blood pressure. The CNS then adjusts sympathetic and parasympathetic nervous system activity to regulate blood pressure.

When blood pressure rises, baroreceptors signal the CNS to decrease sympathetic activity, leading to a slower heart rate and vasodilation. Conversely, when blood pressure falls, the CNS increases sympathetic activity to raise heart rate and constrict blood vessels.

The baroreceptor reflex is a rapid mechanism (within a second) for regulating blood pressure. However, it primarily regulates short-term fluctuations in blood pressure and adapts to long-term changes, maintaining blood pressure around a new 'normal' level.

The baroreceptor reflex helps minimize drastic changes in blood pressure, preventing severe drops or increases. For example, in blood loss, the reflex helps limit the decrease in blood pressure, preventing a major drop.

This phase is characterized by a gradual decrease in membrane potential due to the outward flow of potassium ions and the inward influx of calcium ions balancing each other out. This phase extends the depolarization, allowing for a longer contraction in heart muscle cells compared to other excitable tissues.

The influx of calcium ions through voltage-gated channels is what primarily drives this plateau phase. These channels open more slowly than sodium and potassium channels, allowing for a sustained influx of calcium. The outflow of potassium ions through open channels counters this influx, achieving a balance that maintains the plateau.

The closing of voltage-gated calcium channels is the main event in this phase. This inactivation happens independently of voltage, unlike sodium channels, and occurs shortly after the calcium channels open. This decrease in calcium permeability allows for a rapid repolarization back to resting potential.

The potassium channels remain open during this phase, driving the potassium outflow and finally bringing the membrane potential back to its resting state. The leakage pathways for potassium also open wider, further enhancing this outward flow, contributing to the rapid decline in potential.

All voltage-gated channels for sodium, potassium, and calcium close during this phase. This is triggered as the membrane potential approaches the resting level. The resting membrane permeability and ion concentrations are restored.

The opening of voltage-gated sodium channels is the primary event in this initial depolarization phase. This rapid influx of sodium ions dramatically elevates the membrane potential, setting the stage for muscle contraction.

This phase refers to the brief period after depolarization, marked by the inactivation of sodium channels and the activation of potassium channels. The outward flow of potassium ions begins, leading to a slight decrease in membrane potential.

This phase is a crucial one, marked by a sustained depolarized state due to a balance between the outflow of potassium ions and the influx of calcium ions. This phase is essential for cardiac muscle contraction, as it allows for a prolonged action potential, resulting in a sustained contraction.

Sympathetic stimulation increases heart rate and contractility by activating beta1-adrenergic receptors on cardiac muscle cells. These receptors are coupled to Gs proteins, leading to increased cAMP production, which activates protein kinase A. This kinase phosphorylates key proteins in the heart, increasing contractility and heart rate.

Sympathetic stimulation leads to vasoconstriction in most blood vessels by activating alpha1-adrenergic receptors on vascular smooth muscle cells. These receptors are coupled to Gq proteins, triggering a cascade that leads to increased calcium levels in the smooth muscle cells, resulting in contraction and vasoconstriction.

Parasympathetic stimulation decreases heart rate by activating M2 muscarinic receptors on cardiac muscle cells. These receptors are coupled to Gi proteins, inhibiting adenylyl cyclase and reducing cAMP levels. This leads to decreased contractility and heart rate.

Parasympathetic stimulation can induce vasodilation in certain blood vessels by activating M3 muscarinic receptors on endothelial cells. These receptors are coupled to Gq proteins, triggering a signaling cascade that leads to the release of nitric oxide (NO). NO is a potent vasodilator.

The autonomic nervous system directly modulates heart rate and contraction strength, but it doesn't initiate the heart's contraction. The pacemaker cells in the heart, like the sinoatrial (SA) node, are responsible for generating the electrical impulses that drive heart contractions.

The baroreceptor-atrial volume receptor (AVR) reflex regulates blood volume by adjusting renin release and ultimately, the activity of the renin-angiotensin-aldosterone system (RAAS). When blood volume decreases, the AVR firing rate decreases, leading to increased renin release, RAAS activation, and reduced renal sodium and water excretion. Conversely, increased blood volume causes increased AVR firing, which suppresses renin release, dampens RAAS activity, and promotes sodium and water elimination from the kidneys.

The renin-angiotensin-aldosterone system (RAAS) plays a crucial role in regulating blood pressure. When blood pressure falls, the system activates, leading to vasoconstriction, increased blood volume, and ultimately, a rise in blood pressure. The RAAS also influences sodium reabsorption in the kidneys, further contributing to blood volume regulation.

An electrocardiogram (ECG) is a visual representation of electrical activity in the heart. It records the electrical potential changes as they move through the heart, offering insights into heart function.

Electrocardiograms (ECGs) typically consist of 12 leads, each representing a unique view of electrical activity in the heart. These leads are positioned strategically on the limbs and chest to capture different aspects of the electrical signals generated by the heart.

An electrocardiogram (ECG) provides a comprehensive view of the electrical activity in the heart, revealing rhythm abnormalities and potential underlying heart problems. It's a foundational diagnostic tool in cardiology, helping to detect and monitor heart conditions.