Heart Physiology

SL valves

• SL valves are strong/thick

  • Pulmonic and aortic

  • 3 cusps each

  • Open when pressure in the ventricle becomes greater than the pressure in the vessel beyond the valve

  • Close when pressure in the ventricle falls below the pressure in the vessel on the other side of the valve

AV valves

• AV valves- thinner

  • Tricuspid and Mitral

  • Attached to papillary muscles via chordae tendineae

  • During diastole the valves are open

    • Blood passively flows from incoming vessel (IVC/SVC, or pulmonary veins) into the ventricle

      • Papillary muscles relaxed

  • Atria contract to add last amount of blood to ventricle

    • Pressure atria > ventricle

  • Close when the pressure inside the ventricle > pressure in the atrium

    • During systole pressure in the ventricles is so high that without the papillary muscles contracting and holding on to the AV valve they would prolapse and blood would flow back into the atria during ventricular contraction

Microscopic anatomy of cardiac muscle (review)

• Cardiac muscle cells (cardiomyocytes)

  • Striated, branched

  • Contain many mitochondria

    • 25-25% of volume

    • Makes fibers highly resistant to fatigue

  • Involuntary control

• Contracts by sliding filament mechanism

• Each myocyte contains 1 (sometimes 2), centrally located nucleus

• Surrounded by a cell/plasma membrane known as the sarcolemma

  • Sarcolemma is surrounded by basement membrane and endomysium (loose connective tissue matrix)

Endomysium

• Endomysium lies between the muscle fibers or cells, surrounding and connecting them

  • Contains numerous capillaries

  • Connected to the fibrous skeleton

  • Acts as a tendon and an insertion

    • Giving cardiac muscle cells something to pull on or exert their force again

Anatomic differences between cardiac and skeletal muscles

• Skeletal muscle fibers are independent of one another

  • Structurally and functionally

• Cardiac muscle fibers interlock together at junctions called intercalated discs

  • Intercalated discs are held together by desmosomes and gap junctions

  • Desmosomes adhere two cells together, prevents cells from separating during contraction

  • Gap junctions provide communication between cells so ions can cross between cells to spread current faster across cardiomyocytes

• Cardiac muscle cells vary greatly in diameter and branch extensively

  • Less dramatic banding pattern than skeletal muscle

• Cardiac muscle fibers

  • Sarcoplasmic reticulum is simpler and lacks terminal cisterns

    • Do not have “triads” like skeletal muscle

  • T tubules are wider and fewer

    • Enter the cells once per sarcomere at Z discs

  • Sarcoplasmic reticulum (SR)- specialized form of the endoplasmic reticulum of muscle cells, dedicated to calcium ion (Ca2+) handling

  • T-Tubules- are invaginations of the sarcolemma

Physiologic Similarities between Cardiac and Skeletal Muscle

• Both contractile tissues

• Both require depolarization initiated by an AP

• Transmission of depolarization wave travels across sarcolemma and down the T tubules

• T tubule depolarization causes the opening of Ca2+ channels in the SR of the muscle cell

• Ca2+ spills into sarcoplasm and binds to troponin, changing the structure of the tropomyosin, uncovering the myosin bindings sites on actin

• Cross bridge cycling begins

Physiologic differences between Cardiac and Skeletal Muscle (overview)

• 1. Some cardiac muscle cells are self-excitable

• 2. Heart contracts as a unit

• 3. The mechanism of T tubules causing Ca2+ release from the SR

• 4. Tetanic contractions cannot occur in cardiac muscles

• 5. The heart relies almost exclusively on aerobic respiration

Some cardiac muscle cells are self-excitable

• The heart contains 2 kinds of myocytes

  • Contractile cells: responsible for contraction

    • The vast majority of cells are contractile (99%)

  • Pacemaker cells (nodal cells): noncontractile cells that spontaneously depolarize (1%)

    • Provides automaticity or autorhythmicity (intrinsic control)

      • Initiate depolarization of entire heart via gap junctions

      • No direct neural input needed

Heart contracts as a unit

• Gap junctions provide communications between all cardiac cells, linking them together to form one unit

  • This allows the wave of depolarization to travel from cell to cell across the heart

  • Contraction is all or none under normal circumstances

• Contraction of all cardiac myocytes ensures effective pumping action

• Skeletal muscles contract independently

  • AP comes from nerve at the NMJ

  • Impulses do not spread from cell to cel

The mechanism of T tubules causing Ca2+ release from the SR

• Cardiac muscles

  • Depolarization moved across sarcolemma and down T tubules

  • This depolarization wave causes opening of voltage gated slow Ca2+ channels

    • Both on sarcolemma and in the T tubules

  • These slow Ca2+ channels allow entry of 10-20% of the Ca2+ needed for contraction to enter from the extracellular fluid

  • Influx of Ca2+ from ECF triggers Ca2+ release from SR

    • Ca2+ release from SR provided the other 80-90% of calcium needed for contraction

• Skeletal muscles

  • As depol travels down T tubules, voltage sensitive membrane proteins cause SR to release Ca into sarcoplasm

  • Does not use extracellular Ca2

Tetanic contractions cannot occur in cardiac muscles

• Cardiac muscle fibers have longer absolute refractory period than skeletal muscle fibers

  • Absolute refractory period is almost as long as contraction period

  • Prevents summation of impulses

  • Allows heart the time it needs to relax and fill, to be an efficient pump

The heart relies almost exclusively on aerobic respiration

• Cardiac muscle has more mitochondria than skeletal muscle due to it’s dependence on oxygen

  • It cannot function without oxygen

• Skeletal muscle can use anaerobic respiration when oxygen not present

What sets the basic rhythm of the heart?

intrinsic conduction system

• The independent, coordinated activity of the heart is a function of:

  • Presence of gap junctions

  • Intrinsic cardiac conduction system

    • Network of noncontractile (autorhythmic) cells

    • Initiate and distribute impulses throughout heart

    • Resulting in depolarization and contraction occurring in an orderly, sequential manner

Cardiac pacemaker cells

• Have unstable resting membrane potentials that continuously depolarizes, drifting slowly toward the threshold

• Once threshold is hit AP occurs

• After repolarization the pacemaker cells spontaneously begin to slowly depolarize again

• The slow depolarizing period = pacemaker potential or prepotential 

  • This occurs slowly in comparison to the AP

• Pacemaker potential brings the resting membrane potential back to threshold initiating the next action 

Pacemaker action potential

• 1. Pacemaker potential:

  • Slow depolarization is due to : K+ channels are closed, but slow Na+ channels are open, letting in Na, causing interior to slowly become more positive (less negative)

  • Moves RMP from -60mV toward threshold of -40mV

• 2. Depolarization:

  • RMP reaches threshold and the AP begins

  • Ca2+ channels open (around 40 mV), allowing huge influx of Ca2+, leading to rising phase of action potential

• 3. Repolarization:

• Ca2+ channels close

• K+ channels open, allowing efflux of K+, and RMP becomes more negative 

Sequence of excitation

1. SA node

2. AV node

3. AV Bundle (bundle of HIS)

4. Right and left Bundles

5. Subendocardial conducting network (purkinje fibers)

SA Node

•  Located in the right atrium: just inferior to the entrance of the SVC

• Small crescent shaped collection of nodal tissue

• It is in charge because no other area of the conduction pathway fires as fast as the SA node

• Is the pacemaker of the heart, fires around 75 times per minute

• Creates the sinus rhythm

• 60-100 bpm

• Max ~150 bpm

AV node

• Smaller collection of nodal tissue

• Located in the inferior region of the interatrial septum, medial to the tricuspid valve

• When the impulse reaches the AV node it is delayed for about 0.1 second to allow atria to complete contraction

  • Delay due to smaller diameter of the fibers here, and fewer gap junctions

    • Like when road goes from 3 lanes to 1

  • It is the “rate limiting step”

  • Once past the AV node the signal moves fast

• Inherent rate of 40-60 bpm in absence of SA node input

AV Bundle (Bundle of His)

• Located superior part of IV septum

• It covers short distance

  • The only electrical connection between the atrium and the ventricles

  • There are no gap junctions between the atrium and the ventricles

  • Fibrous skeleton insulates the rest of the AV junction

Right and Left bundles AND subendocardial conducting network (purkinje fibers)

• Right and Left bundles

  • These branches proceed on each side of the muscular interventricular septum toward the heart's apex

• Subendocardial conducting network (Also referred to as Purkinje fibers)

  • Long strands of barrel-shaped cells with few myofibrils

  • These branches complete pathway through interventricular septum into apex and turn superiorly into the ventricular walls (limited superiorly by fibrous skeleton)

  • More branches to the left side due to it being larger

  • AV bundle and subendocardial conducting network depolarize 30 bpm in absence of AV and SA node input

  • Ventricular contraction immediately follows from apex toward atria

    • Ejects blood superiorly

  • Process from initiation at SA node to complete contraction takes ~0.22 seconds

Action potentials of contractile cardiac muscle cells (overview)

• Contractile muscle fibers make up bulk of heart and are responsible for pumping action

• Different from skeletal muscle contraction cardiac muscle action have plateau 

Contractile cardiac muscle cells AP

• Depolarization (Phase 0)

  • Opens fast voltage-gated Na+ channels; in the sarcolemma, allowing extracellular Na+ to enter cell

  • Influx of Na+ causes rising phase of AP (from 90 mV to +30 mV)

  • Depolarization caused by Na influx activates slow Ca2+ channels

    • Slow= opening is slightly delayed

  • Very brief Na channels quickly close (at 30mV)

• Early Repolarization (Phase 1)

  • Partial repolarization due to quick closure of Na channels and efflux of K+ and delay of Ca channels opening

• Plateau (Phase 2)

  • Voltage gated slow Ca2+ channels are open

  • Ca2+ enters from the extracellular fluid, prolonging the depolarization, creating the plateau, K+ efflux at similar rate keeps the line flat

  • As long as Ca2+ is entering the cells continue to contract

  • Muscle tension develops during the plateau, tension peaks just after plateau ends

• Repolarization (Phase 3)

  • After about 200 ms,

    • Slow Ca2+ channels are closed,

    • Voltage-gated K+ channels are open

    • The slope of the AP falls rapidly as K+ rushes out of the cell to restore the electrical conditions (RMP)

    • During repolarization, Ca2+ is pumped both back into SR and out of cell into extracellular space

• Resting (Phase 4)

  • When Na/K pumps restore ionic conditions

  • When this state is reached the absolute refractory period end

 Difference between contractile muscle fiber and skeletal muscle fiber contractions

• Skeletal muscle AP= 1–2 ms; Contraction= 15–100 ms

• Cardiac AP= 200+ ms; Contraction= 200+ ms

Benefit of longer plateau in cardiac muscle:

• Sustained contraction ensures efficient ejection of blood

• Longer refractory period prevents tetanic contractions

ECG definition + leads

• Electrocardiogram (ECG) is a graphic recording of electrical activity

• Composite of all electrical activity at given time; not a tracing of a single AP

• Electrodes are placed at various points on body to measure voltage differences

  • 12 lead ECG is most typical

  • 10 physical leads

  • 4 limb leads

  • 6 precordial leads

• 12 tracing

• ECG is a measure of voltage (mV)/ amplitude(mm) over time (s)

ECG features

• P wave: lasts about 0.08 seconds

  • Depolarization of SA node through the atria

  • Atrial contraction

• P-R interval: (0.16-0.2 seconds)

  • Is the time from the beginning of atrial excitation (beginning of P wave) to the beginning of ventricular excitation (beginning of the QRS)

  • Includes atrial depolarization, 

• QRS complex:

  • Result of ventricular depolarization

  • It precedes ventricular contraction

  • Atrial repolarization occurs during this time as well, this small amount of electrical activity is hidden in the large amplitude of the QRS

  • Average duration of the QRS complex is 0.08 s, normal is <0.1 s

• S-T segment:

  • Action potentials of the ventricular myocytes are in their plateau phases, the entire ventricular myocardium is depolarized, and contracting

• T wave:

  • Ventricular repolarization

  • Lasts about 0.16s

  • Repol is slow so it is wider (takes longer) than depol in QRS

• Q-T interval:

  • Lasts about 0.38 s

  • Includes ventricular depolarization(QRS) through ventricular repolarization (end of T wave)

Systole vs diastole

• Systole:

  • Phase of the heartbeat when the heart muscle contracts/pumps blood from the chambers into the next area (arteries)

• Diastole:

  • Phase of the heartbeat when the heart relaxes/allows the chambers to fill with blood

• Atrial systole and diastole are followed by ventricular systole and diastole

• When discussing cardiac cycle we are referring to ventricular systole and diastole

Cardiac cycle definition and overview

• Cardiac cycle: blood flow through heart during one complete heartbeat

  • Cycle represents series of pressure and blood volume changes that occur in one complete heartbeat

  • Mechanical events follow electrical events seen on ECG

• Four phases of the cardiac cycle

  • 1. Ventricular filing

  • 2. Isovolumetric contraction

  • 3. Ventricular ejection

  • 4. Isovolumetric relaxation

Two important points abt cardiac cycle

• 1. Blood flow through the heart is controlled entirely by pressure changes

• 2. Blood flows down a pressure gradient through and available opening

• The pressure changes

  • Reflect the alternating contraction and relaxation of the myocardium

  • Cause the heart valves to open/close

Ventricular filling

• Mid- late diastole

• Pressure in atria= high

• Pressure in ventricles= low

• AV valves open, SL valves closed

• 80% is passive filling of ventricles

• Atria depolarize and contraction (atrial systole)

• Remaining 20% fill ventricles

  • Depolarization spreads to ventricles

• Ventricles are full to max= end diastolic volume (EDV)

• P wave and beginning of QRS complex

Isovolumetric contraction

• Early systole

• Ventricular pressure > >atrial

• AV valves snap closed (S1)- starts the phase

• Atria relax/ repolarize

• Ventricles begin contracting

• Ventricles are closed chambers- all valves closed,

  • Building pressure, volume is constant (EDV)

• When ventricular pressure > aortic/pulmonic pressure the SL valves open and this phase is over

• Lasts a split second

• Most of QRS complex (depolarization occurs just before contraction)

Ventricular ejection

• Mid-late systole

• SL valves open, AV valves closed

• Blood is ejected from the ventricles into aorta and pulmonary trunk

• Ventricular pressures and vessel pressures increase initially

  • Normally peak at 120mmHg

  • When about half the volume in ventricle has been ejected the ventricular and aortic pressures start to drop

• Remaining volume at the end of this phase is end systolic volume –ESV

• At the end most of T wave occurs (electrical repol occurs before actual relaxation

Isovolumetric relaxation:

• Early diastole

• Pressure in the ventricles fall below pressure in the vessels, blood flows “backward”

• Blood rebounds off of closed valve

  • At the dicrotic notch

  • Causes small spike of pressure in aorta

• SL valves close (S2)- this starts the phase

• Ventricles are completely closed chambers, valves are closed

• Ventricles relax

  • Decreasing pressure, volume is constant (ESV)

• Atria are filling with blood, when atrial pressure exceeds ventricular pressure, the AV valves open which marks the end of this phase, and the cycle

• The cycle repeats…

Valves/Heart sounds

• AV valves

• Open = ventricular pressure drops below atrial pressure

  • End of Isovolumetric Relaxation

• Close = ventricular pressure exceeds atrial pressure

  • Beginning of Isovolumetric Contraction

  • Heart sound is S1

• SL valves

  • Open = ventricular pressure exceeds aortic/pulmonary trunk pressure

    • End of Isovolumetric Contraction

  • Close = ventricular pressure falls below aortic/ pulmonary trunk pressure

    • Beginning of Isovolumetric Relaxation

    • Heart sound S2

  • Systole occurs between heart sounds S1 and S2

  • Diastole occurs between heart sounds S2 and S

Length of cardiac cycle

• Cardiac cycle lasts about 0.8 seconds

  • Atrial systole lasts about 0.1 seconds

  • Ventricular systole lasts about 0.3 seconds

  • Quiescent period is total heart relaxation that lasts about 0.4 seconds

What modifies the basic rhythm of the heart

Modifying the basic rhythm: extrinsic innervation of the heart 

• Heart rate is modified by ANS via cardiac centers in medulla oblongata 

  • Cardioacceleratory center- sympathetic 

  • Cardioinhibitory center- parasympathetic

Cardioaccelerator center

• Cardioacceleratory center signals sympathetic neurons in the T1-T5 level of the thoracic spinal cord via interneurons

• The preganglionic neurons synapse with postganglionic neuron, in the ganglia of the sympathetic trunk (cervical and upper thoracic)

• The postganglionic fibers run through the cardiac plexus to the heart carrying a stimulatory impulse 

  • Innervate the SA and AV nodes, heart muscle and coronary arteries

Cardioinhibitory center

• The cardioinhibitory center (medulla) signals the parasympathetic system

• It signals the dorsal motor nucleus of the vagus in the medulla via interneurons

• The dorsal motor nucleus stimulates the vagal nerve to send inhibitory impulses down its branches → heart

  • Innervate the SA and AV node

Stroke volume

• Stroke volume: volume of blood pumped out of the ventricle with per beat

  • Correlates with force of ventricular contraction

  • Average is 70 mL/beat

• Mathematically: SV = EDV  ESV

  • Normal SV = 120 ml  50 ml = 70 ml/beat

  • Each ventricle pumps 70 ml/beat, about 60% of the original volume in 

Cardiac output

• Cardiac output (CO): amount of blood pumped out by each ventricle in 1 minute

  • CO= heart rate (HR) x stroke volume (SV)

  • At rest:

    • 75 beats/min x 70 ml/beat = 5.25L/min

• Normal adult blood volume is about 5L.

• Entire blood supply passes through each side of the heart in one minute

• CO changes based on changes in SV and/or HR 

  • increases when SV and/or HR increase

  • Decrease when SV and/or HR decrease

• CO is highly variable

  • Increases or decreases due to oxygen demand from the body

Cardiac reserve

• Cardiac reserve: difference between resting CO and maximal CO

  • CR= CO max - CO resting

  • Nonathletes cardiac reserve is 4-5 times resting CO

    • CR= 20-25L/min (CO max= 25-30 L/min)

    • 25 L/min- 5 L/min= 20 L/min

    • 30 L/min – 5 L/min= 25 L/min

  • CR in athletes could be 35 L/min

• CO is affected by factors that regulate HR and SV

End diastolic volume (EDV)

• End diastolic volume (EDV) – volume of blood that collects in a ventricle during diastole

  • Affected by length of ventricular diastole and venous pressure (preload)

  • Normal= 120 ml/beat

End systolic volume (ESV)

• End systolic volume (ESV) - volume of blood remaining in a ventricle after contraction

  • Affected by arterial blood pressure (afterload) and force of ventricular contraction (contractility)

  • Normal= 50 ml/beat

Regulation of stroke volume

• Three main factors that affect 

  • 1. Preload- direct relationship

    • Effects EDV

  • 2. Contractility- direct relationship

    • Effects ESV

  • 3. Afterload- indirect relationship

    • Effects ESV

Preload

• degree to which cardiac muscle cells are stretched just before they contract

  • Changes in preload cause changes in SV

    • In a normal heart the higher the preload the higher the SV, this relationship is called Frank-Starling law of the heart

      • The force or tension developed in a muscle fiber depends on the extent to which the fiber is stretched.

      • In a clinical situation, when increased quantities of blood flow into the heart (increasing preload), the walls of the heart stretch, and the SV increases

• Affects EDV- increased preload increases the EDV

  • Results in increased SV 

• Cardiac muscle exhibits a length-tension relationship

  • At rest, cardiac muscle cells are shorter than optimal length;

    • Stretching past this = dramatic increase in contractile force

• Most important factor in preload (stretching of cardiac muscle) is the amount of venous return

What increases EDV?

• Both exercise and increased filling time will increase EDV

• Exercise increases venous return (preload)

  • Increased sympathetic activity

  • Squeezing action of skeletal muscles

  • SV can double during exercise due to increased venous return

    • Exercise also increases HR which can decrease filling ime (smaller effect)

• Low venous return leads to decreased EDV

  • This decreases the stretch/ preload

  • Leads to decreased SV (and CO

Contractility

• EDV is the major intrinsic factor influencing SV, but extrinsic factors increase heart muscle contractility also enhancing SV.

• Contractility: the contractile strength achieved at given muscle length

  • Rises when more Ca 2+enters the sarcoplasm (from the extracellular fluid and the SR)

  • More contractility= more strength= more blood ejected from the heart (SV)

    • This reduces ESV

• Independent of muscle stretch and EDV

• Increased sympathetic activity (increased sympathetic nerve stimulation) increases contractility

• Sympathetic stimulation leads to release of neurotransmitters:

• norepinephrine (NE) or epinephrine (Epi)

• Epi and NE bind to Beta-1 receptors (G-protein coupled receptor)

• Through the second messenger system, cause an increase in Ca2+ entry

• Leading to more cross bridge formations enhancing ventricular contractility

  • Positive inotropic agents increase contractility

    • Thyroxine, glucagon, epinephrine, digitalis, high extracellular Ca2+

  • Negative inotropic agents decrease contractility

    • Acetylcholine/parasympathetic stimulation, Acidosis (excess H+), increased extracellular K+, calcium channel blockers

Afterload

• back pressure exerted by arterial blood

  • Afterload is pressure that ventricles must overcome (exceed) to eject blood

    • Back pressure from arterial blood pushing on SL valves is major pressure

      • Aortic pressure is around 80 mm Hg

      • Pulmonary trunk pressure is around 10 mm Hg

  • In healthy adults, afterload is not a major determinant of SV, it is constant

  • Think about how the left ventricle must work harder to eject blood into the aorta

  • The left ventricle is so much stronger it is overcoming 80mmHg at the same time the weaker right ventricle is overcoming 10mmHg

Regulation of HR

• In healthy heart SV is relatively constant

• Changes in HR may be needed to:

  • Counter a change in SV to maintain CO

    • SV has decreased due to volume loss, increased HR will keep CO constant

  • Increase the CO

• Heart rate can be regulated by:

  • 1. Autonomic nervous system- SNS and PSNS

  • 2. Chemicals

  • 3. Other factors

  • Positive chronotropic factors increase heart rate

  • Negative chronotropic factors decrease heart rate

Autonomic nervous system regulation of heart rate

• Most important extrinsic control affecting HR

• Sympathetic stimulation is a positive chronotrope (and inotrope)

• Parasympathetic stimulation is a negative chronotrope (and some inotrope)

Sympathetic nervous system (SNS) stimulation

• Can be stimulated by emotional or physical stressors

• Norepinephrine and/or epinephrine released

• Binds to β1-adrenergic receptors in the heart (SA, AV, ventricular muscle), causing:

• 1. Increasing heart rate (HR), due to pacemaker (SA) firing more rapidly, (chronotropic)

  • As a result, EDV decreased because of decreased fill time

• 2. Increased contractility (enhancing Ca 2+ into cells)= inc SV (inotropic)

  • ESV decreased (inc volume of ejected blood from ventricle)

  • Because both EDV and ESV decrease, SV can remain unchanged

• The decrease EDV (dec filling time) caused by increased HR, is offset by the decrease ESV (more blood ejected) caused by increased contractility

• Example: EDV – ESV = SV

  • Normal 120mL - 50mL= 70mL

  • Inc SNS 100mL - 30mL= 70mL

Parasympathetic nervous (PSNS) system stimulation

• Lowers HR when stressor(s) have passed

• Its neurotransmitter, Acetylcholine, binds to muscarinic receptors (G-protein coupled receptor)

• Opens K+ channels, hyperpolarizes pacemaker cells

• Making it harder to reach threshold potential which slows HR (neg chronotrope

• Has smaller effect on contractility due to the sparse innervation in the ventricles of the Vagus nerve (neg ____)

• Under resting conditions both the SNS and the PSNS are sending impulses to the SA node but the dominant influence is inhibitory

  • Lack of vagal nerve (vagal tone) would lead to an increase in HR to about 25bpm higher than normal(sympathetic would take over and increase rate)

• When sympathetic is activated, parasympathetic is inhibited, and vice-versa

  • Think about a teeter totter ( when activated it is just more of one at that time, and less of the other)

Atrial (Bainbridge) reflex

• Increase in atrial pressure results in increase in HR

• Sympathetic reflex initiated by baroreceptors in the atria 

  • Increase in stretch of atrial walls due to increased venous return= increased atrial filling

  • Stretch receptors signal the SNS to stimulate SA node to increase HR

  • This reflex prevents back up of blood in the

Chemical regulation of HR

• Hormones

  • Epinephrine

    • From acute stress response- fight or flight

    • Increases heart rate and contractility

  • Thyroxine

    • Increase metabolic rate /production of body heat

    • Works directly on the heart to increased heart rates

    • Enhances effects of norepinephrine and epinephrine

• Ions- Intra- and extracellular ion concentrations (Ca2+, K+, Na+, etc) must be maintained for normal heart function

  • Electrolyte imbalances are very dangerous to hear

Other Factors that Influence HR (10)

• Age

• Fastest as a fetus, 140-160 bpm, slows with age

• Gender

• Average faster in females (72-80) vs males (64-72) 

• Exercise

• Raises HR and BP

• Resting heart rate in athletes is lower, as low as 40 bpm

• Body temperature

• Increasing body temp = increased HR, example: fever

• Cold decreases HR