Lecture 5

Cardiac output

Amount of blood pumped by the heart per minute (based on left ventricle)

Heart rate

Number of times the heart beats per minute and firing rate of the SA node (100 times per minute)

Stroke volume

Volume of blood ejected with each heartbeat

SV equation

SV = EDV - ESV

Cardiac output equation

CO = HR x SV

Cardiac reserve

Represents the difference between cardiac output at rest and maximal cardiac output achieved during intense exercise

Maximal cardiac output

Achieved during high-intensity exercise and reflects the body’s max demand for oxygen and nutrients. (athletes have higher maximal cardiac output than untrained)

Intrinsic regulation

Heart normal function and does not depend on neural or hormonal regulation

Extrinsic regulation

Outside sources controlling the heart (nervous system and hormones)

3 main factors regulating stroke volume (PAC)

Preload, afterload, contractility

Preload

Degree of stretch in the ventricular walls before contraction, which determines the initial length of cardiac muscle fibres

Greater the preload

Greater the force of contraction

What influences the force generation during contraction?

Myosin and actin overlap

What controls the optimal overlap?

Preload

Frank starling law of the heart

As EDV increases, there is an increase in stroke volume which contributes to more efficient cardiac output

What is the mechanical advantage by stretching cardiac muscle cells?

Stretching the cells enhance the length of the sarcomeres where the actin and myosin myofilaments are positioned which increases the overlap and improves force-generating capacity

Does the stretch optimize or increase the overlap?

Optimize

Steps for Preload

Increased EDV, is increased stretch on the walls is increased overlap of actin and myosin, increased force of contraction then increased stroke volume

What is a pivotal factor to determine EDV?

Venous return

Venous return

Volume of blood returning to the heart from the systemic circulation

At rest, venous return is influenced by?

Pressure differences within the vasculature

Boost venous return

Muscle pump mechanism

What forms the foundation of the muscle

Deep veins in the limbs that are surrounded by skeletal muscle since skeletal muscles contract and can exert pressure on the veins to actively push blood towards the heart

Degree of muscle pump activity

is correlated with the intensity of muscle contractions

Greater muscle pump activity

Accelerates venous return, contributes to higher cardiac output by increasing EDV

Afterload

Pressure that contracting ventricles must generate to overcome the pressure in the aorta and open the semilunar valves to facilitate blood ejection

Normal afterload pressure?

80 mmHg

Elevated blood pressure

Hypertension, increases afterload to demand stronger, more forceful ventricular contractions to overcome higher pressure

Higher afterload impacts?

Stroke volume since heart works harder during each contraction to meet the increased pressure requirements

Contractility

Forcefulness of ventricular contractions

What does contractility influence?

Stroke volume by determining the strength of each contraction

What kind of regulation does contractility involve and what agents?

Extrinsic regulation with inotropic agents

Positive inotropic agents

Increase contractility by opening calcium channels in cardiac muscle cells

Two positive inotropic agents?

Cardiac accelerator nerves and adrenal medulla

Cardiac accelerator nerves

Release norepinephrine which accelerates the opening of calcium channels and enhances contraction force

Adrenal medulla

Releases epinephrine and norepinephrine during the sympathetic nervous system responses to stimulate calcium channel opening and support increased force of contraction

Negative inotropic agents

Decrease contractility in different ways depending on meds

Types of negative inotropic agents?

Calcium channel blockers, beta blockers

Calcium channel blockers

Block calcium channels to reduce myocardial contraction force

Beta blockers

Block beta-adrenergic receptors to inhibit the effects of the sympathetic nervous system neurotransmitters (epinephrine and norepinephrine) and prevent an crease in the force of contraction

Why are negative inotropic agents prescribed and to who?

For individuals with heart conditions to manage contractions, decrease the heart oxygen demand

Regulation of heart rate

Gender, age, ions, physical fitness, autonomic nervous system, temperature, hormones

Gender: Female resting heart rate

Usually higher than males

Age

Gradual reduction in the maximum heart rate a person can achieve during physical acitvity (220-age) = decrease of one bpm with each year

Ions

Changes in extracellular ion concentrations (postassium, sodium and calcium) can affect the generation of action potentials

Excess or reduced potassium

Decreases heart rate

Physical fitness

higher levels of physical fitness have lower rest heart rates

What is maximal heart rate predicted by and what does not affect it?

Age, and there is no difference between trained and untrained individuals

Autonomic nervous system

Heart rate is controlled by sympathetic and parasympathetic nervous system

Temperature

heart rate is sensitive to changes in temp

Increase in temperature

Elevate heart rate (dissipate excess heat through skin)

Decrease in temperature

Reduction in heart rate (hibernation)

Hormones

Influence heart rate by affecting the ANS

Does intrinsic or extrinsic regulate heart rate

Extrinsic

PNS what does it do to heart rate?

It lowers the heart rate (100) to resting rate of (70-75) via the vagus nerve

How does the vagus nerve decrease heart rate

It innervates the SA node and releases acetylcholine to cause hyperpolarization with a lot of potassium channels opening to delay threshold which decreases heart rate

Sympathetic nervous system

Will increase heart rate beyond 100 bpm since it overrides PNS

What does SNS use

Cardiac accelerator nerves that release norepinephrine and adrenal medulla that release epinephrine and norepinephrine

Releasing norenephrine

Increases heart rate by opening calcium channels which speeds up threshold

How long does hormonal control take vs neural control?

Longer because it must be released into the bloodstream and travel to the heart (backup)

How is blood pressured measured?

Using baroreceptors which are located in the walls of blood vessels (internal carotid arteries and aorta)

Baroreceptors

Detect stretch in blood vessel walls to send info to medulla oblongata and the brain stem

Changes in blood pressure triggers?

Sympathetic and parasympathetic responses to adjust heart rate and maintain homeostasis

Changes in blood pH, CO2 and oxygen are measured/monitored using?

Chemoreceptors

Chemoreceptors found?

In brainstem where they measure the changes in the CSF (carotid artery and aorta body)

PNS response via vagus nerve

Targets SA node to decrease heart rate, if SA node is not working it will target AV node for acetylcholine to release and hyperpolarize the heart

Sympathetic nervous system response via cardiac accelerator nerves

Target the SA and AV nodes and the myocardium to increase heart rate and force contraction in ventricles to increase stroke volume (norenephrine = opening calcium channels)

Sympathetic nervous system response hormones via adrenal gland

Target the myocardium/ventricles and the SA node to increase contractile forces and possibly heart rate (release epinephrine and norepinephrine)