Cardiac Output and Regulation

Cardiac Output

• Cardiac output refers to the volume of blood each ventricle pumps per minute.
• Cardiac output (ml/minute) is calculated by multiplying stroke volume (ml/beat) by heart rate (beats/min).
• On average, heart rate is 70 bpm.
• Average stroke volume is 70−80 ml/beat.
• Average cardiac output is 5,500 ml/minute.
• Stroke volume is the blood pumped per beat by each ventricular contraction, normally 70-80ml/beat.
• Cardiac Rate (HR) equals the beats/contractions per minute.
• If SV is 70ml and HR is 70bpm, then CO is 4900ml/min.
• Total blood volume is about 5.0L.
• The sinoatrial (SA) node without neuronal influences drives the heart at its spontaneous activity rate (about 70 bpm).
• Sympathetic and parasympathetic activity influences heart rate and has a chronotropic effect.

Regulation of Cardiac Rate

• The cardiac control center of the medulla coordinates autonomic innervation activity with the heart.
• Cardiac rate is affected by higher brain areas and sensory feedback from pressure receptors (baroreceptors).
• Autonomic innervation of the SA node is the main controller of HR.
• Parasympathetic activity decreases HR via a negative chronotropic effect by hyperpolarizing SA node cardiocytes.
• Sympathetic activity increases HR via a positive chronotropic effect by depolarizing SA node cardiocytes.
• Sympathetic endings in the atria and ventricles can stimulate increased strength of contraction (=inotropic effect).
• Sympathetic endings in the atria and ventricles can increase cardiac rate (=chronotropic effect).

Regulation of Stroke Volume

• Stroke volume is regulated by three variables: end diastolic volume, total peripheral resistance, and contractility.
• End diastolic volume (EDV) is the volume of blood in the ventricles at the end of diastole and is sometimes called preload.
• Stroke volume increases with increased EDV, normally about 110-130ml.
• Stroke volume is directly proportional to EDV.
• About 60% of blood is ejected at rest (ejection fraction), and about 90% during exercise.
• Total peripheral resistance refers to the frictional resistance in the arteries.
• Total peripheral resistance is inversely related to stroke volume.
• Contractility is the strength of ventricular contraction.
• Stroke volume increases with contractility.

Total Peripheral Resistance

• Total peripheral resistance affects stroke volume and is the sum of all vascular resistances within systemic circulation.
• Changes in resistance in these circuits determine relative blood flow.
• Total peripheral resistance (TPR) is the impedance to ejection of blood from the ventricle.
• Stroke volume is inversely proportional to TPR.
• A vessel with half the diameter has 16 times the resistance.
• As resistance increases, stroke volume decreases (inversely proportional).

Contractility

• Contractility is the strength of ventricular contraction.
• Intrinsic contractility involves the stretch of the myocardium.
• Extrinsic contractility involves sympathetic stimulation.
• Stroke volume is directly proportional to contractility.
• Strength of ventricular contraction varies directly with EDV, which is an intrinsic property of the myocardium.
• As EDV increases, the myocardium stretches, leading to stronger contraction and increased stroke volume.
• Regarding actin and myosin: increasing interaction of actin and myosin generates more force.
• At any given EDV, contraction depends upon the level of sympathoadrenal activity.
• Norepinephrine and epinephrine promote an increased force of myocardial contraction (positive inotropic effect) due to increased Ca2+ in sarcomeres.

Venous Return

• Venous return, the return of blood to the heart via the veins, affects EDV, SV, and CO.
• Venous return is dependent upon blood volume, venous pressure, venoconstriction caused by sympathetic nervous system, the skeletal muscle pump, and pressure drop in the thorax during inhalation.

Total Blood Volume

• Veins hold most of the blood in the body (~70%) and are called capacitance vessels.
• Capacitance vessels have thin walls that stretch easily to accommodate more blood without increased pressure (=higher compliance).
• Capacitance vessels have only 0-10 mm Hg pressure.
• Total blood volume affects venous pressure and therefore venous return.
• Total blood volume constitutes a small fraction of total body fluid.
• 2/3 of body H2O is inside cells (intracellular compartment).
• 1/3 of total body H2O is outside cells (extracellular compartment), 80% of which is interstitial fluid and 20% is blood plasma.
• Extracellular fluid distribution between blood and interstitial compartments is in a state of dynamic equilibrium.
• Movement out of capillaries is driven by hydrostatic pressure (plasma water pressure) exerted against the capillary wall.
• Hydrostatic pressure promotes the formation of tissue fluid.
• Net filtration pressure refers to hydrostatic pressure in the capillary outward.
• Movement is also affected by colloid osmotic pressure, or osmotic pressure exerted by proteins in the fluid.
• A difference between osmotic pressures inside and outside of capillaries affects fluid movement.
• Plasma osmotic pressure = 25 mm Hg; interstitial osmotic pressure = 0 mm Hg.
• Edema, the excessive accumulation of ECF, may result from high blood pressure, venous obstruction, leakage of plasma proteins into ECF, low plasma protein levels resulting from liver disease or malnutrition, or obstruction of lymphatic drainage.

Kidney Regulation of Total Blood Volume

• Antidiuretic hormone (ADH) is released by the posterior pituitary when osmoreceptors detect high osmolality (concentrated body fluids).
• ADH is released from excess salt intake or dehydration.
• ADH release is inhibited by low osmolality (dilute body fluids).
• ADH stimulates thirst, H2O reabsorption (retention) in kidneys, and arterial vasoconstriction.
• Aldosterone, a steroid hormone secreted by the adrenal cortex, helps maintain blood volume and pressure through reabsorption and retention of salt in the kidneys.
• Water reabsorption follows salt reabsorption.
• Aldosterone release is stimulated by salt deprivation, low blood volume, and low blood pressure.

Renin-Angiotensin-Aldosterone System (RAAS)

• Angiotensin II is generated when there is a body salt deficit, low blood volume, or low blood pressure.
• Angiotensin II causes vasoconstriction, aldosterone secretion, and thirst to increase blood pressure.
• ACE inhibitors are medications that treat high blood pressure by inhibiting the ACE enzyme.
• If ACE is inhibited, no angiotensin II is produced, aldosterone secretion is inhibited, and vasoconstriction is reduced.

Atrial Natriuretic Peptide (ANP)

• ANP works antagonistically to aldosterone and ADH.
• Expanded blood volume is detected by stretch receptors in the left atrium of the heart and causes the release of ANP.
• ANP inhibits aldosterone secretion, promoting salt and water excretion, which reduces blood volume and blood pressure.
• ANP also promotes vasodilation, which lowers BP.

Total Peripheral Resistance Regulation

• Sympathoadrenal activation increases CO and vascular resistance in the skin and viscera.
• Sympathoadrenal activation of the factors above increase blood flow to skeletal muscles.
• Blood is shunted away from viscera and skin and into muscles.
• Skeletal muscle arterioles dilate in response to epinephrine, and sympathetic fibers release ACh, which also dilates their arterioles.
• Autoregulation maintains a fairly constant blood flow despite variations in BP.
• Myogenic control mechanisms (vessel wall smooth muscle automatically contracts when stretched and relaxes when not stretched).
• Metabolic control mechanisms matches blood flow to local tissue needs.
• Low O2, low pH, and high CO2 or adenosine from high metabolism cause vasodilation to maintain homeostasis.
• When BP increases, cerebral arterioles constrict; when BP decreases, arterioles dilate (= myogenic regulation).
• Arterioles dilate and constrict in response to changes in CO2 levels (= metabolic regulation).
• Exercise initiates increases in: Cardiac output, Blood flow to skeletal muscles, Cardiac rate, and Stroke volume.
• Exercise improves: Sympathoadrenal system, Venous return, Metabolic vasodilation in muscles, Sympathetic vasoconstriction in viscera, Skeletal muscle activity and Deeper breathing.