bio005 Ch14 Cardiac Output, Blood Flow, and Blood Pressure

Cardiac Output (CO)

• Cardiac output is volume of blood pumped/min by each ventricle

• Stroke volume (SV) = blood pumped/beat by each ventricle

• Heart rate (HR) = the number of beats/minute

• CO = SV x HR

• Total blood volume is about 5.5L

Cardiac Output (CO) equation

CO(mL/min)= SV(mL/beat) X HR(beat/min)

Regulation of Cardiac Rate

• Without neuronal influences, SA node will drive the heart at a rate of its spontaneous activity

• Autonomic innervation of SA node is the main controller/regulator of HR

  • The sympathetic nervous system increase heart rate.

  • The parasympathetic nervous system decrease heart rate.

• Cardiac control center of medulla oblongata coordinates activity of autonomic innervation

Regulation of Cardiac Rate: Sympathetic

• Norepinephrine and epinephrine (“adrenaline”) increase opening of pacemaker HCN (hyperpolarization- activated cyclic nucleotide) channels

  • This depolarizes SA node faster,increasing HR

Regulation of Cardiac Rate: Parasympathetic

• ACh promotes opening of K+ channels

  • Result: K+ outflow counters Na+ influx, slowing depolarization and decreasing HR

Effects of autonomic nerve activity on the heart

Stroke Volume

• Determined by 3 variables:

  • End diastolic volume (EDV) = volume of blood in ventricles at the end of diastole which is also called preload

  • Total peripheral resistance (TPR) = resistance to blood flow in arteries which is also called afterload

    • Afterload measures as the pressure required for ventricular ejection

• Contractility = strength of ventricular contraction

Regulation of Stroke Volume

• Preload/EDV is workload on the heart prior to contraction

  • Stroke volume is directly proportional to preload and contractility (as preload and contractility increase, so does stroke volume)

• Afterload/TPR impedes (make it harder for) ejection from ventricle

Ejection fraction

• Ejection fraction is stroke volume / preload

  • Normally, EF is 50-70%, average 60%; a useful clinical diagnostic tool.

    • Less than 40% = heart failure, more than 75% = heart hypertrophy

Frank-Starling Law of the Heart

• States that strength of

  ventricular contraction

  varies directly with

  preload/EDV

  • It’s an intrinsic property of the myocardium

  • As EDV increases,

    myocardium is stretched more, causing greater

    contraction and SV

Frank-Starling Law of the Heart

• (a) is state of myocardial

  sarcomeres just before filling

  • Actins overlap, actin-myosin interactions are reduced, and contraction would be weak

• In (b, c and d) there is increasing interaction of actin and myosin allowing more force to be developed

Extrinsic Control of Contractility

• At any given EDV, contraction depends upon level of sympathoadrenal activity

  • Norepinephrine and epinephrine produce an increase in HR and contraction (positive ionotropic effect)

    • Due to increased Ca2+ in sarcomeres

Variables that affect venous return and thus end-diastolic volume

venous return

• Venous return = return of blood to the heart via veins

• Controls EDV and thus SV and CO

• Dependent on:

  • Blood volume and venous pressure

  • Venoconstriction caused by sympathetic stimulation

  • Skeletal muscle pumps

Blood Pressure (BP)

• Blood pressure is controlled mainly by:

  • HR, SV, Peripheral resistance

    • an increase in any of these can result increased BP

• Sympathoadrenal activity raises BP via arteriole vasoconstriction and by increased CO

• Kidney plays role in BP by regulating blood volume

  and therefore stroke volume

Hypertension

• Blood pressure in excess of normal range for age and gender > 120/80 mmHg (2021 guidelines by ACA and AHA)

• Afflicts 47% of adults in the U.S.

• Most common type is primary/essential hypertension

  • Caused by complex and poorly understood

    processes but to do with sodium consumption

• Secondary hypertension is caused by known disease

  processes (examples next slide)

Hypertension (BP Chart)

Possible Causes of Secondary Hypertension

• Kidney disease – kidney disease; renal artery disease

• Endocrine disorder – excess catecholamines; excess aldosterone

• Nervous system disorder – including intracranial pressure; damage to vasomotor center

• Cardiovascular disorder – complete heart block; arteriosclerosis of aorta

Dangers of Hypertension

• Patients are often asymptomatic until substantial vascular damage occurs

  • Contributes to atherosclerosis

  • Increases workload of the heart leading to ventricular hypertrophy and congestive heart failure

  • Often damages cerebral blood vessels leading to stroke

  • silent killer

Treatment for hypertension

• Often includes lifestyle changes such as cessation of smoking, moderation in alcohol intake, consistent exercise, reduced Na+ intake (less than 5 g daily), eating fruits/vegetables etc

• Drug treatments include diuretics to reduce fluid volume, beta-blockers to decrease HR, calcium blockers