2.3 - Heart Physiology Part II

Cardiac output (CO)

The amount of blood pumped by each ventricle in one minute; calculated as CO = HR x SV

Stroke volume (SV) measurement method

Normally measured using an echocardiogram to record EDV and ESV and calculating the difference (SV = EDV - ESV); can also be measured with a specialized catheter, which is more precise but more invasive and dangerous

Variables impacting stroke volume

Size of the heart, physical condition of the individual, sex, contractility, duration of contraction, EDV, and afterload/resistance

Normal stroke volume range (adult)

55-100 mL

Average resting heart rate

Approximately 75 bpm, ranging from 60-100 bpm in some individuals

Average resting cardiac output range

4.0-8.0 L/min (per ventricle, not the total for the heart; right and left ventricle output is assumed equal because the circulatory system is a closed loop)

Ejection fraction

A measurement of blood pumped or ejected from the heart with each contraction, calculated as SV divided by EDV and expressed as a percentage; normal range is approximately 50-70%

Ejection fraction clinical relevance

Important for diagnosing and managing cardiac conditions such as heart failure and valve diseases, and for guiding treatment decisions

Cardiac output during exercise (young healthy individual)

HR may increase to 150 bpm and SV may increase from 70 mL to approximately 130 mL, raising CO to approximately 19.5 L/min (4-5 times resting rate)

Top athlete maximum cardiac output

May increase resting CO by 7-8 times at peak performance

Cardiac reserve

The difference between maximum and resting cardiac output; measures the residual capacity of the heart to pump blood

Effect of exercise training on the heart

Enhances heart efficiency, enabling greater stroke volume and increased cardiac output during activity, partly because the myocardium becomes stronger and more efficient

Newborn resting heart rate

Approximately 120 bpm; HR gradually decreases until young adulthood

Maximum heart rate calculation

220 minus the individual's age (e.g., a 40-year-old has an expected max HR of about 180 bpm)

HR and SV relationship as HR rises

As HR increases, all phases of the cardiac cycle shorten, particularly diastole; SV initially stays high but eventually decreases due to decreased ventricular filling time

CO response across rising HR (young healthy individual)

CO rises as HR increases from resting to about 120 bpm; CO remains stable from 120-160 bpm as SV decreases to offset rising HR; CO decreases above 160 bpm as SV falls faster than HR rises

Target heart rate (target zone)

About 60-90% of maximum heart rate, generally between 120 and 160 bpm; the range in which the heart and lungs receive maximum benefit from aerobic exercise while maintaining CO

Conditioned athlete heart rate and cardiac output

Athletes can have a decreased HR but normal CO because a stronger heart muscle pumps more blood per beat (increased SV due to decreased ESV)

Cardioaccelerator centers

Paired centers of the medulla oblongata that stimulate heart activity via sympathetic stimulation of the cardioaccelerator nerves

Cardioinhibitory centers

Paired centers of the medulla oblongata that decrease heart activity via parasympathetic stimulation through the vagus nerve (cranial nerve X)

Autonomic tone (cardiac)

The slight stimulation both cardiovascular centers provide to the heart at rest

Vagal tone

The dominant parasympathetic signal to the heart at rest

Cardiac plexus

A paired complex network of nerve fibers near the base of the heart through which sympathetic and parasympathetic stimulation flow

Cardiac nerves

Fibers from the cardioaccelerator center that travel via sympathetic ganglia (cervical ganglia plus superior thoracic ganglia T1-T4) to the SA and AV nodes, atria, and ventricles

Sympathetic vs parasympathetic innervation of ventricles

The ventricles are more richly innervated by sympathetic fibers than parasympathetic fibers

Norepinephrine (NE) effect on the heart

Released by sympathetic stimulation at the neuromuscular junction of the cardiac nerves; binds beta-1 receptors, shortens the repolarization period, and speeds depolarization and contraction, increasing heart rate

Beta blockers (mechanism)

Cardiac medications that block receptors binding NE, slowing heart rate; used to treat hypertension, though overprescription may cause bradycardia or heart stoppage

Acetylcholine (ACh) effect on the heart

Released by parasympathetic stimulation via the vagus nerve at the neuromuscular junction; binds muscarinic receptors and opens ligand-gated potassium ion channels, slowing HR

ACh mechanism of hyperpolarization

Potassium ions flow down their concentration gradient out of the cell, making the inside more negative (hyperpolarized), which slows spontaneous depolarization and extends repolarization

Intrinsic SA node rate without nervous stimulation

Approximately 100 bpm; parasympathetic stimulation normally slows this to resting rates, and decreasing parasympathetic stimulation allows HR to rise to about 100 bpm, with further increases requiring sympathetic stimulation

Cardiac reflexes

The process by which cardiovascular centers use input from proprioceptors, baroreceptors, chemoreceptors, and the limbic system to precisely regulate heart function

Proprioceptors (cardiac regulation)

Receptors in muscles, joint capsules, and tendons that detect position and movement; increased firing during physical activity causes the cardiac centers to suppress parasympathetic and increase sympathetic stimulation

Baroreceptors

Stretch receptors located in the aortic sinus, carotid bodies, venae cavae, and other locations that signal blood pressure, activity level, and blood distribution

Baroreceptor reflex

The mechanism by which increased baroreceptor firing (from increased pressure/stretch) causes decreased sympathetic and increased parasympathetic stimulation to slow HR, and decreased firing causes the opposite to raise HR and maintain blood pressure

Atrial reflex (Bainbridge reflex)

A reflex triggered by stretch receptors in the atria detecting increased blood volume/venous return, which increases sympathetic impulses to raise HR and CO, maintaining homeostasis

Chemoreceptors (cardiac regulation)

Innervated by the glossopharyngeal and vagus nerves; detect metabolic byproducts (CO2, H+, lactic acid) and falling oxygen levels, providing feedback about the need for increased or decreased blood flow

Limbic system effect on heart rate

Can significantly impact HR related to emotional state; stress can cause higher than normal HR, often with a surge in cortisol; meditation and slow breathing can lower HR and ease anxiety

Effect of fever on heart rate

Increases cardiac output

Effect of hypothermia on heart rate

Decreases cardiac output

Effect of aging on heart rate

Elderly individuals usually have a heart rate less than 70 bpm

Effect of excessive thyroid hormone on heart rate

Increases heart rate

Preload

Another way of expressing EDV; the stretch on the ventricles prior to contraction; the greater the EDV, the greater the preload

Filling time (FT)

The duration of ventricular diastole during which filling occurs; more rapid heart contraction shortens filling time, lowering EDV and preload

Venous return (VR)

The process of blood flowing back into the heart (ventricles); increased venous return raises EDV/preload and stretches cardiac muscle to a greater degree

Frank-Starling mechanism (Starling's Law of the Heart)

States that, within physiological limits, the force of heart contraction is directly proportional to the initial length of the muscle fiber; greater ventricular stretch (within limits) produces a more powerful contraction and increased SV

Atrial kick

The contraction of the atria that provides the last 20-30 percent of ventricular filling

Contractility

The force of contraction of the heart muscle; greater contractility decreases ESV and increases SV, while lesser contractility increases ESV and decreases SV

Positive inotropic factors

Factors that increase contractility, such as sympathetic stimulation, epinephrine, norepinephrine, thyroid hormones, glucagon, and hypercalcemia

Negative inotropic factors

Factors that decrease contractility, such as parasympathetic stimulation, hyperkalemia, beta blockers, and calcium channel blockers

Sympathetic stimulation effect on contractility

Releases NE at the neuromuscular junction and stimulates the adrenal cortex to secrete epinephrine and NE; these bind alpha and beta receptors to increase metabolic rate and force of contraction, increasing SV and decreasing ESV

Parasympathetic stimulation effect on contractility

Releases ACh at the neuromuscular junction from the vagus nerve, hyperpolarizing the membrane and inhibiting contraction; primarily acts in the atria, decreasing atrial kick, EDV, and preload, and directly decreasing ventricular contraction force

Hypercalcemia (cardiac effect)

Excess calcium acts as a positive inotropic agent because higher intracellular calcium increases the strength of contraction

Hyperkalemia (cardiac effect)

Excess potassium acts as a negative inotropic agent, decreasing contractility

Angina pectoris

Chest pain historically treated with early beta-blocker drugs, which revolutionized cardiac patient care

Beta blocker therapeutic effects

Block beta-adrenergic receptors of the sympathetic "fight-or-flight" response, reducing heart rate, blood pressure, and strength of heart contractions; used for hypertension, heart rhythm disorders, and angina pectoris

Afterload

The tension the ventricles must develop to pump blood effectively against resistance in the vascular system; represents the pressure/resistance overcome by the ventricles after contraction has begun

Afterload (left ventricle)

Reflects the resistance in the aorta and systemic arteries that the left ventricle must overcome to pump blood out during systole

Afterload (right ventricle)

Determined by the pressure in the pulmonary arteries that must be overcome to pump blood into the lungs

Valve stenosis effect on afterload

Damage to valves that makes them harder to open increases afterload

Vasoconstriction effect on afterload

Increases afterload by narrowing blood vessels and raising resistance to blood flow, requiring the heart to pump harder

Vasodilation effect on afterload

Decreases afterload by widening blood vessels and reducing resistance to blood flow, easing the heart's workload

Decreased venous return causes

Decreased blood volume from bleeding or dehydration, decreased peripheral blood flow, or decreased heart rate; results in decreased EDV, SV, and CO

Increased venous return causes

Muscular contraction from exercise or increased peripheral blood flow; results in increased EDV, SV, and CO

Decreased filling time effect

Caused by increased HR (less time between beats); decreases EDV, SV, and CO

Increased filling time effect

Caused by decreased HR (more time between beats); increases EDV, SV, and CO

Baroreceptor response to decreased stretch

Decreased parasympathetic and increased sympathetic nerve impulses, resulting in increased HR, SV, and CO

Baroreceptor response to increased stretch

Increased parasympathetic and decreased sympathetic nerve impulses, resulting in decreased HR, SV, and CO

Chemoreceptor response to increased O2/decreased CO2, H+, lactic acid

Decreased sympathetic system activity, resulting in decreased HR, SV, and CO

Chemoreceptor response to decreased O2/increased CO2, H+, lactic acid

Increased sympathetic impulses, resulting in increased HR, SV, and CO