CARDIAC OUTPUT

Cardiac output = heart rate x stroke volume. The ejection fraction = stroke volume/left ventricular end- diastolic volume (LVEDV). Therefore, stroke volume ejection fraction x L VEDV, or 0.50 x 100 ml = 50 nit Cardiac output = 50 ml x 70 beats/mm = 3500 mI/minute, or 3.5 liters/mm.

Ans. is. A. Decreases by increase in heart rate

[REF: Ganong’s 22′ e p. 570-571]

Stroke volume = cardiac output/heart rate (amount of blood pumped by heart per beat), hence stroke volume is indirectly proportional to heart rate, hence increases. Heart rate decreases stroke volume.

After load is determined by peripheral resistance, hence nothing to do with stroke volume determination.

Stroke volume depends upon end diastolic volume.

Ans. B. End diastolic volume 

“For cardiac contraction, the preload is usually considered to be the end-diastolic pressure when the ventricle has become filled.”

Quantitatively, preload can be calculated as

Where LVEDP = Left ventricular end-diastolic pressure, LVEDR = Left ventricular end-diastolic radius (at the ventricle’s midpoint), and h = thickness of the ventricle. This calculation is based on the Law of Laplace.

Preload is the degree to which the myocardium is stretched before it contracts. Increasing the preload therefore increases the length of muscle fiber. 

• The force of contraction of cardiac muscle depends on its preload and afterload. According to Frank Starling’s law: Energy of contraction is proportional to the initial length of cardiac muscle fiber.
• When cardiac output is regulated by changes in cardiac muscle fiber length, this is referred to as heterometric regulation. 
• Regulation of cardiac output due to changes in contractility independent of the length is sometimes called homometric regulation.

Preload is the initial stretching of the cardiac myocytes prior to contraction; therefore, it is related to the sarcomere length at the end of diastole. Sarcomere length cannot be determined in the intact heart so indirect indices of preload, such as ventricular end-diastolic volume or pressure, must be used.

Ref: Cardiovascular Physiology Concepts By Richard E. Klabunde, 2005, Page 69; Guyton’s physiology 22nd edition, Page 111.

Stroke volume = cardiac output/heart rate, i.e it is inversely proportional to heart rate. As a result when heart rate increases the stroke volume decreases. This reduction in stroke volume at high heart rates is due to a decrease in the length of time the heart spends in diastole and thus a reduction in time available to the heart for filling.

Stroke volume refers to quantity of blood ejected with each heart stroke. According to Starling’s law of heart, stroke volume is determined primarily by the preload. As the preload increases, stroke volume also increases until it reaches a plateau. Stroke volume can also be increased by sympathetic stimulation of the heart.

Ref: Physiology Secrets By Hershel Raff, 2nd edn, page 74

EFFECT OF VARIOUS CONDITIONS ON CARDIAC OUTPUT

Ref: Ganong’s Review of physiology, 23rd Ed, Page 514

Cardiac output = heart rate X stroke volume: is the correct answer.

Starling’s law of the heart describes the relationship between end diastolic volume or preload and cardiac contractility. It states that cardiac contractility is maximized at a particular preload. It also states that cardiac contractility declines as the preload is increased or decreased from this optimum. The basis for this principle is that at a particular preload, the myocardium is “stretched” to a point that maximizes the number of actin and myosin units that may interact in a given contraction. 2nd choice is incorrect. Heart rate x stroke volume = cardiac output. 3rd choice is incorrect. Preload is related to end diastolic volume and passive wall tension exerted on the diastolic ventricle. 4th choice is incorrect. End diastolic volume – end systolic volume = stroke volume.

Cardiac output is the product of the heart rate and stroke volume (CO = HR x SV). 

Therefore, cardiac output decreases by bradycardia.

Ref: Mohrman D.E., Heller L.J. (2010). Chapter 3. The Heart Pump. In D.E. Mohrman, L.J. Heller (Eds), Cardiovascular Physiology, 7e.

The kidneys receive 20–25% of the cardiac output. They receive the highest blood flow per gram of organ weight in the body i.e, 400 mL/min/ 100 gm. This is several times greater per unit weight of organ than the blood flow through most other organs.

Ref: Radiological Imaging of the Kidney edited by Emilio Quaia, 2011, Page 24.

In severe anemia, diminished transport of oxygen in the blood leads to hypoxia in the tissues. The hypoxia causes small arteries and arterioles to dilate, which allows greater-than-normal amounts of blood to return to the heart. In severe anemia, the viscosity of blood may decrease by 50% or more because blood viscosity depends largely on the concentration of red blood cells. This decrease in viscosity lowers the resistance to blood flow in the peripheral tissues (decreases peripheral vascular resistance) allowing even greater amounts of blood to return to the heart.

Blood is often shunted away from the splanchnic vascular bed in anemia, which can cause gastrointestinal problems.

Ref: Mohrman D.E., Heller L.J. (2010). Answers to Study Questions. In D.E. Mohrman, L.J. Heller (Eds), Cardiovascular Physiology, 7e.

The cardiac output (CO) is equal to the volume of blood ejected from the heart during each systole (i.e., the stroke volume; SV) multiplied by the number of times the heart beats each minute (heart rate; HR). In other words, CO = SV x HR. Therefore, SV = CO/HR, and since CO = 5000 mL/min, and HR = 50/min, SV = 5000/50 = 100 mL.

Ref: Mohrman D.E., Heller L.J. (2010). Chapter 1. Overview of the Cardiovascular System. In D.E. Mohrman, L.J. Heller (Eds), Cardiovascular Physiology, 7e.

The paired renal arteries take 20% of cardiac output to supply organs that represent less than one-hundredth of total body weight.

Ref: Gray’s anatomy 40th edition, Chapter 91.

A i.e. 3 liters / min/m²

Ans. B i.e. 5 litre

• The output of the heart per unit of time is the cardiac output.
• In a resting, supine man, it averages about 5.0 L/min (70 mL × 72 beats/min).

B i.e. COP per unit body surface area

B i.e. V/Q ratio

D i.e. Standing from lying position

B i.e. Setwart-Hamilton Principle

A i.e End diastolic volume of ventricles

According to frank-starling law, the length of muscle fibers (extent of the pre-load) is proportionate to the end diastolic volumeQ

A i.e. Rise in central venous pressure

On assumption of erect posture, the force of gravity opposes the return of blood   incentral venous pressure)Q

A i.e. Increase in the number of open capillaries

B i.e. The kidneys receive 5% of the cardiac output

–  Kidney receives 25% of cardiac output at restQ

–  Glucose is freely filtered across glomerular capillary membrane and therefore glucose concentration of glomerular filtrate is same as that of plasmaQ.

–  Glomerular (capillary) oncotic pressure (d/t plasma protein content) is higher than that of filtrate oncotic pressure in Bowman’s capsule (with almost 0 protein content).

–   Constriction of afferent arteriole decreases glomerular hydrostatic pressure (& GFR)Q, whereas afferent arteriole dilation & efferent arteriole constriction increase it.

D i.e. Electrical impedance cardiograph technology

– PA catheter & thermodilution technique are invasive procedure.

– Echo is noninvasive old technique to measure cardiac output

– Recent noninvasive advance to measure C.O. is electrical impedance Cardiographs technology.

D i.e. Decreased cardiac out put relative to total body mass

Obesity related changes

Ans. B (Mean Stroke Volume)

Mean stroke volume is the amount of blood pumped out of each ventricle per beat. It is calculated as the cardiac output in L/min divided by the heart rate.

Mean Stroke Volume =         Cardiac Output

                                            Heart Rate

Ans. B: Body surface area

Cardiac Output (CO) = Stroke Volume x Heart Rate

Normal SV is 70 mL and hence in a supine, resting man CO is 5.0 L/ min. (70 mLX 72 beats/min.) Cardiac Index (CI) = CO/ Body Surface Area (BSA) = SV x HR/BSA CI averages 3.2L

Ans. B: Rest

Preload

• It is the end volumetric pressure that stretches the right or left ventricle of the heart to its greatest geometric dimensions under variable physiologic demand.
• Preload is theoretically most accurately described as the initial stretching of a single cardiomyocyte prior to contraction.
• The term end-diastolic volume is better suited to the clinic, although not exactly equivalent to the strict definition of preload.
• Atrial pressure is a surrogate for preload.
• Quantitatively, preload can be calculated as LVEDP. LVEDR/ 2h
• Where LVEDP = Left ventricular end-diastolic pressure, LVEDR = Left ventricular end-diastolic radius (at the ventricle’s midpoint), and h = thickness of the ventricle.
• This calculation is based on the Law of Laplace.
• Preload is affected by venous blood pressure and the rate of venous return.
• These are affected by venous tone and volume of circulating blood.
• Preload is related to the ventricular end-diastolic volume; a higher end-diastolic volume implies a higher preload.
• Preload increases with exercise (slightly), increasing blood volume (over transfusion, polycythemia) and neuroendocrine excitement (sympathetic tone).
• An arteriovenous fistula can increase preload Afterload
• It is the tension or stress developed in the wall of the left ventricle during ejection.
• Following Laplace’s law, the tension upon the muscle fibers in the heart wall is the product of the pressure within the ventricle, multiplied by the volume within the ventricle, divided by the wall thickness.
• Therefore, a dilated left ventricle has a higher afterload.
• Conversely, a hypertrophied left ventricle has a lower afterload.
• When contractility becomes impaired and the ventricle dilates, the afterload rises and limits output.
• This may start a vicious circle, in which cardiac output is reduced as oxygen requirements are increased.
• Afterload can also be described as the pressure that the chambers of the heart must generate in order to eject blood out of the heart and thus is a consequence of the aortic pressure (for the left ventricle) and pulmonic pressure or pulmonary artery pressure (for the right ventricle).
• The pressure in the ventricles must be greater than the systemic and pulmonary pressure to open the aortic and pulmonic valves, respectively.
• As afterload increases, cardiac output decreases. Preload best describes the maximum viscous blood volume of end-diastole while afterload better describes the maximum tension of the myocardial muscle mass in end-systole.

Ans. D: 40%

The cardiac output starts to increase from 5^t1 week of pregnancy and reaches its peak 40-50% at about 30-34 weeks. Cardiac output increase further during labour (+50%) and immediately following delivery (+70%)

Ans. is ‘c’ i.e., Cardiac output is increased in anemia

Cardiac output is increased in conditions which cause decrease in peripheral vascular resistance :-

Exercise

1. AV fistula or shunt
2. Severe anemia
3. Thyrotoxicosis
4. Wet beri-beri
5. About other options

Blood viscosity is low in anemia and high in polycythemia.

Ans. is ‘c’ i.e., Increased cardiac contractility

Cardiac output is the product of stroke volume and heart rate. Hence any factor which affects either the stroke volume or the heart rate or both affects the cardiac output.

A) Factors affecting stroke volume

Stroke volume, which is the amount of blood pumped by the heart during one stroke, depends mainly on three factors : ‑

Preload (Degree of ventricular filling during diastole) : – Cardiac preload is represented by volume of venous blood that distends the ventricle, i.e., venous return determines the preload. An increase in preload, i.e., increase in venous return results in a higher end-diastolic volume (Preload). This results in stretching of myocardial fiber and this increase in length of myofibril increases the strength of cardiac contraction in accordance with the Frank-Starling law or Starling’s law of the heart. Accord­ing to Starling’s law, greater the initial length of muscle fiber, greater is the force of contraction. The initial length of muscle fiber (length of fiber at the initiation of contraction/systole) refers to length of the fiber at the end of the diastole, i.e., end-diastolic fiber length. Thus, the factors which improve venous return increase the cardiac output by increasing end-diastolic ventricular volume and length, i.e., preload. Opposite is true for factors which decrease venous return.

Ans. is ‘a’ i.e., CO x TPR

• Arterial blood pressure is the product of the cardiac output and the total peripheral vascular resistance (TPR). Mean blood pressure is the major determinant of adequate blood flow through the tissues.

Mean BP = Cardiac output x Total peripheral resistance

• If cardiac output is expressed as a product of stroke volume and heart rate, the formula blood pressure can be expressed as the product of three variables (the triple product) : –

Mean BP = Stroke volume x Heart rate x TPR

• Blood pressure is therefore affected by conditions that affect any of these factors. Changes in cardiac output (or stroke volume) affect mainly the systolic pressure while changes in peripheral resistance affect mainly the diastolic pressure.

Ans. b. Stewart-Hamilton equation

Stewart Hamilton equation

• The thermodilution technique has become the de-facto clinical standard for measuring cardiac output because of its ease of implementation and the long clinical experience using it in various settings.
• It is a variant of the indicator dilution method, in which a known amount of a substance is injected into a peripheral vein and its concentration change measured over time in serial arterial samples.
• As its name implies, the thermodilution method uses a thermal indicator, whereas other indicator dilution methods use various substances, such as indocyanine green dye.
• The fundamental physical basis for the indicator dilution method is given by the Stewart-Hamilton equation, named after the two investigators who were instrumental in the development of this technique