5A & B Cardiac Output

It becomes more negative.

Cardiac output.

The distensibility of the ventricle.

The 'load' that the heart must eject blood against.

Vessel diameter and viscosity of blood.

It increases ventricular contractility.

The total quantity of blood available for providing adequate tissue perfusion.

The sum of all the local blood flows from individual segments of peripheral circulation.

The duration of ventricular diastole.

The number of times the heart beats per minute influences the amount of blood pumped out per minute.

Stroke Volume = End Diastolic Volume (EDV) - End Systolic Volume (ESV).

It measures cardiac output relative to body surface area.

The amount of blood pumped by the heart with each beat.

The volume of blood the heart pumps per minute.

Preload is the initial stretching of the cardiac myocytes prior to contraction, related to sarcomere length.

It increases venous return.

It contributes to the filling of the ventricles.

Cardiac Output = 5.6 L/min.

It decreases stroke volume.

Further stretching decreases the force of contraction.

CI = Cardiac output divided by body surface area in square meters.

Stroke Volume = 130 - 50 = 80.

Standing posture and gravity.

Responsible for the flow of blood from the veins of the limbs to the heart.

The number of times the heart beats per minute influences the amount of blood pumped out per minute.

Descent of the diaphragm.

It results in increased force generation, independent of preload and afterload.

More blood can be pumped out.

Mild hypoxia causes an increase in heart rate.

Enhanced venous return.

Venous return.

Cardiac output is expected to increase.

It causes changes in the amount of blood pumped out in one beat.

Aortic pressure.

Preload refers to the filling pressure of the ventricles, influenced by various factors.

Venous pressure influences the amount of blood returning to the heart.

It may increase the cardiac output.

The pressure gradually decreases.

The degree of stretch of the heart muscle before contraction.

Loss of myocardium negatively affects myocardial contractility.

Drugs can also influence heart rate.

To meet the requirements of the body.

Cardiac Output = Stroke Volume x Heart Rate.

Approximately 3 L/min/m².

Heart Rate = 70 beats per minute.

The resistance offered against ejection of blood from ventricles.

Filling pressure, ventricular distensibility, filling time, and atrial contraction.

Inotropy refers to the strength of myocardial contraction.

They act as positively inotropic agents, increasing myocardial contractility.

Moderate to severe hypoxia decreases cardiac output by directly suppressing myocardial contractility, while carbon dioxide depresses the myocardium.

It is reduced.

It shifts upward and to the left.

Due to increased venous return and decreased intrathoracic pressure.

It decreases due to reduced filling time.

The force of contraction increases when the initial length of the muscle increases.

By the volume of blood that fills the ventricle at the end of passive filling and atrial contraction, known as End Diastolic Volume (EDV).

It can decrease venous return when standing due to peripheral pooling of blood.

Positively inotropic factors.

Preload refers to the initial stretching of the cardiac muscle fibers before contraction, influencing stroke volume.

It increases peripheral resistance.

Stimulation of sympathetic nerves increases heart rate and myocardial contractility, which raises cardiac output.

It increases.

It is increased.

Acidosis depresses myocardial contractility due to increased H+ ion concentration.

It causes a reduction in ESV and an increase in SV.

Increasing inotropy leads to an increase in EF, while decreasing inotropy decreases EF.

The Frank-Starling curve shifts down and to the right.

Sympathetic stimulation increases heart rate and contractility, while parasympathetic stimulation decreases heart rate.

It decreases cardiac output.

An increase in heart rate typically increases cardiac output.

30%.

It refers to the variation of stroke volume at different ventricular muscle lengths.

An increase in preload (increase in EDV) causes an increase in the initial length of the muscle fibers.

Standing posture.

Negatively inotropic factors.

Increased myocardial contractility enhances the heart's ability to pump blood, increasing stroke volume.

It has less effect on myocardial contractility.

The valve proximal to the contracting muscle opens, while the distal valve closes.

Blood is propelled up towards the heart.

Oxygen supply is essential for the functioning myocardium, affecting cardiac output.

About 4.6 mm Hg.

It falls to zero.

The volume of blood remaining in the ventricles after contraction (systole).

It increases cardiac output.

The volume of blood the heart pumps per minute.

Causes moderate changes.

Decreases it by 20 – 30%.

Higher afterload results in higher ventricular work.

It increases peripheral resistance.

Deep veins present between the muscles are compressed.

Increased pressure in the compressed veins.

Aortic pressure and systemic arteriolar resistance.

Heart rate is influenced by the autonomic nervous system and circulating catecholamines.

The resistance the heart must overcome to eject blood.

The volume of blood in the ventricles at the end of filling (diastole).

EF = SV/EDV %.

By echocardiography.

Heart rate and stroke volume.

50 – 100%.

It decreases ventricular contractility.

The resistance the heart must overcome to eject blood during systole.

The amount of blood pumped by the heart with each beat.

The percentage of blood ejected from the heart during each contraction.

About 5.5 mm Hg.

End-systolic volume increases.

The degree of stretch of the ventricles at the end of diastole.

It is used as a clinical index for evaluating the inotropic state of the heart.

Heart rate and stroke volume.

The degree of stretch of the heart muscle before contraction, affecting stroke volume.

Increases it.

Increased viscosity decreases cardiac output.

Stimulation of sympathetic nerves increases heart rate, while stimulation of the vagus nerve decreases it.

They have a positive chronotropic effect, increasing heart rate.

Points where maximum contractility has been exceeded.

Digitalis increases myocardial contractility.

Higher venous blood pressure increases venous return, enhancing preload.

Gravity can hinder venous return from the lower body, affecting preload.

Approximately 70 mL per beat.

Stroke volume is the amount of blood ejected with each heartbeat, directly influencing cardiac output.

Up to 700%.

They can decrease it.

12 to 18 mm Hg.

The curve shifts downward and to the right.

Portions of the ventricular function curves where maximum contractility has been exceeded.

Thyroid hormones.

It acts as a driving force for venous return.

The relationship between stroke volume and end-diastolic volume.

Approximately 60-100 beats per minute.

The volume of blood the heart pumps per minute.

Increased contractility enhances stroke volume, thereby increasing cardiac output.

They can decrease it.

Stroke volume decreases.

It generally increases cardiac output, up to a certain point.

The stroke volume of the heart increases in response to an increase in the volume of blood filling the heart.

The respiratory pump facilitates venous return through pressure changes during breathing.

Preload, afterload, and myocardial contractility.

Increases it.

Cardiac output adjusted for body surface area, indicating the efficiency of the heart.

It increases cardiac output.

Approximately 4-8 liters per minute.

The resistance the heart must overcome to eject blood, impacting stroke volume.

Increased blood volume raises venous return, thus increasing preload.

The muscle pump aids venous return by compressing veins during muscle contraction.

Preload, afterload, myocardial contractility, and heart rate.

No change.

It increases cardiac output.