Cardiovascular Physiology Quiz 17

The initial phase of the pacemaker potential where the cell membrane gradually depolarizes due to the influx of sodium ions and efflux of potassium ions.

The phase where the cell membrane reaches its threshold potential, triggering the opening of voltage-gated calcium channels. Calcium ions flow into the cell, causing a rapid and full depolarization.

The phase where the cell membrane repolarizes back to its resting potential. This occurs due to the closure of calcium channels after some time and the opening of voltage-gated potassium channels, allowing potassium ions to flow out.

The final phase of the pacemaker potential where the cell membrane reaches its minimum potential (a hyperpolarized state) before repeating the cycle. The opening of nonspecific cation channels initiates the next cycle.

A specialized group of cells in the upper right atrium of the heart that initiates the electrical impulse for each heartbeat.

The inherent ability of the SA node to depolarize at a specific rate, typically around 60 or more times per minute.

The influence of the sympathetic and parasympathetic nervous systems on the rate of the SA node.

The system of specialized cardiac tissues in the heart that conducts electrical impulses, ensuring coordinated contraction of the heart chambers.

The amount of blood ejected from the left ventricle with each heartbeat.

The total volume of blood pumped by the heart per minute.

The amount of blood remaining in the ventricle after contraction.

The amount of blood in the ventricle before contraction.

The percentage of blood ejected from the ventricle with each beat, calculated by dividing stroke volume by end-diastolic volume.

The pressure in the ventricles exceeds the pressure in the pulmonary trunk and aorta, causing the semilunar valves to open and blood to rapidly flow out.

The brief period when the ventricles relax and the pressure within falls, but the AV valves are still closed.

The sound of the semilunar valves snapping shut during the isovolumetric relaxation phase.

The amount of blood pumped by the heart into the pulmonary and systemic circuits in one minute.

The number of heartbeats per minute, typically 60-80.

The amount of blood pushed out of the ventricle during each heartbeat.

The heart rate and stroke volume together determine cardiac output.

The phase of the cardiac cycle during which blood flows from the atria into the ventricles.

The pressure inside the ventricles is lower than the pressure in the atria, pulmonary trunk, and aorta during this phase. This pressure difference forces blood to flow from the atria into the ventricles.

The semilunar valves, located at the exits of the ventricles, are closed during this phase. This prevents blood from flowing back into the ventricles from the aorta and pulmonary trunk.

The atrioventricular valves, located between the atria and ventricles, are open during this phase. This allows blood to flow from the atria into the ventricles.

This phase is called 'isovolumetric' because the volume of blood in the ventricles remains constant despite the contraction of the ventricles.

The 'S1' heart sound, a 'lubb' sound, is produced during this phase when the AV valves close.

A condition where the heart's electrical activity becomes chaotic, causing parts of the heart to contract while others are resting, leading to an ineffective heartbeat.

A type of fibrillation that occurs in the atria, the upper chambers of the heart. It doesn't usually cause a significant threat because atrial contraction isn't crucial for ventricular filling, but it manifests on an ECG as an irregular rhythm without identifiable P waves.

A life-threatening type of fibrillation where the ventricles, the lower heart chambers, fail to pump blood effectively, leading to a rapid decrease in blood flow and potential cardiac arrest.

A medical procedure used to treat ventricular fibrillation. It involves delivering a controlled electric shock to the heart, which resets the electrical activity, allowing the heart to regain normal rhythm.

A condition where the heart doesn't show any electrical activity on an ECG, effectively meaning it's not beating. Defibrillation is not effective in this scenario as there's no electrical activity to reset.

A blockage in the conduction pathway between the atria and ventricles, preventing proper electrical signals from reaching the ventricles and leading to a slowed heart rate.

A heart block that often occurs in the right or left bundle branches, resulting in a wider QRS complex on an ECG because the depolarization takes longer to spread through the ventricles.

A condition where the heart's electrical activity is not coordinated, leading to an irregular heart rhythm, but typically not a life-threatening condition as atrial contraction is not essential for ventricular filling.

The parasympathetic nervous system primarily affects the heart's SA node, decreasing the rate of action potential generation, leading to a slower heart rate.

Epinephrine and norepinephrine, released by the adrenal medulla in response to sympathetic nervous system activation, have positive inotropic and chronotropic effects on the heart, similar to sympathetic nerve stimulation but with a longer duration.

Aldosterone and antidiuretic hormone promote water retention, increasing blood volume and preload, which in turn strengthens heart contractions and increases cardiac output.

Atrial natriuretic peptide (ANP) reduces blood volume and preload by promoting sodium and water excretion, thereby decreasing cardiac output.

Changes in electrolyte concentrations in the extracellular fluid can significantly alter the duration and magnitude of the heart's action potential, impacting cardiac output.

Body temperature influences heart rate by affecting the firing rate of the SA node. Increased temperature accelerates the firing rate, while decreased temperature slows it down.

Cardiac output is the volume of blood pumped by the heart per minute. It is determined by factors like heart rate, stroke volume, and preload.

The strength of heart contractions is influenced by preload, the amount of stretch on the heart muscle prior to contraction. This stretch is dependent on venous return, the volume of blood returning to the heart.