Heart rate

Vertebrate Closed Circulatory Systems
• Closed circulatory systems
• Cardiac anatomy & its O2 supply
• The myogenic heart & the cardiac cycle
• Blood pressure
• Anatomical variations
• Other ‘hearts’
Cardiac cycle – pumping action of the heart
Two phases
• Systole – contraction
• Blood is forced out into the circulation
• Diastole – relaxation
• Blood enters the heart
Closed vertebrate circulatory system
• Multi-chambered heart
• Capillaries connect arterial & venous systems
• Respiratory pigments present in red blood cells
Lower BP,
thinner walled
Tunica media = vascular smooth
muscle + elastin fibres
Anatomy of the chambered heart
All vertebrates
• Similar developmental pathway
• Myogenic contractions
• Similar intrinsic properties
Fish: The simplest/earliest design
• Four cardiac chambers
bulbus/conus arteriosus
• All contain muscle (cardiac & smooth)
• Surrounded by a pericardial sac
• Atrium & ventricle propel blood
• Venous BP  atrial contraction  ventricular contraction
• Hagfishes: incomplete pericardial sac
• Sharks & Rays: pericardial sac is stiff; conus arteriosus has cardiac muscle
• Primitive Fishes: conus is reduced & bulbus also present
• Teleosts: bulbus arteriosus (VSM & elastin fibres)
Closed vertebrate circulatory system
• Blood pressure can be regulated, even venous blood pressure
• High blood pressure, high flow rate & faster circulation time
• Exquisite control of blood flow distribution at arterioles (VSM)
• High capillary density reduces blood velocity & the diffusion
distance to cells
• High resistance to flow b/c of small diameter arterioles (R = r4)
• High resistance  high blood pressure  thicker-walled
hearts & higher cardiac O2 needs
Myocardial cells
• Striated cells
• Electrically connected (desmosomes)
• ‘Unstable’ membrane potential
Adult mammalian cardiomyocyte
Adult fish cardiomyocyte
Fish cardiac myocytes also have a reduced sarcoplasmic reticulum (SR),
& lack an extensive t-tubular system
Consequence: Ca2+ handling during excitation-contraction varies
Two types
• Compact – tightly packed cells arranged in a regular pattern
• Spongy – meshwork of loosely connected cells
Relative proportions vary among species
• Mammals: mostly compact
• Fish and amphibians: mostly spongy
• Arranged into trabeculae that extend into the heart chambers
Cardiac muscle O2 supply
• A working muscle requires ATP
• ATP requirement proportional to cardiac power output
• Venous blood supply
• Simplest, but intricate design
• Last organ supplied with O2
• Coronary blood supply
• Compact design
• First organ supplied with O2
Phylogeny & Ontogeny
• Hagfishes & Lampreys: spongy
• Sharks & Rays: spongy plus variable compact (athletic ability)
• Teleosts: most spongy; some have variable compact (athletic/hypoxia)
• Amphibians & reptiles: spongy; some have compact (athletic/hypoxia)
• Neonatal birds & mammals: spongy
• Adult birds & mammals: 99% compact
Cardiac muscle blood & O2 supply
Most fish = Trabeculae = venous
Mammals = compact = coronary
Variable compact/spongy
Octopus coronaries
Initiation of cardiac contraction
Neurogenic pacemakers:
rhythm generated in neurons
(some invertebrates)
Myogenic pacemakers:
rhythm generated in myocytes
(vertebrates and some invertebrates)
Artificial pacemakers:
rhythm generated by device
Control of Contraction
• Vertebrate hearts are myogenic – cardiomyocytes
produce spontaneous rhythmic depolarizations
• Cardiomyocytes are electrically coupled via gap
junctions to insure coordinated contractions
• Pacemaker – cells with the fastest intrinsic rhythm
• Fish: located in the sinus venosus
• Other vertebrates: sinoatrial (SA) node in the right
Myogenic contractions
All cardiomyocytes can contract without an external stimulus
Resting membrane potential is ‘unstable’ = Pacemaker potential
Specialised cells (pacemaker) set intrinsic heart rate
Relative timing & speeds of opening of specific ion channels
Increasing heart rate
• Norepinephrine is released from
sympathetic neurons and
epinephrine is released from the
adrenal medulla
• More Na+ and Ca2+ channels open
• Rate of depolarization and action
potentials increase
Decreasing heart rate
• Acetylcholine is released from
parasympathetic neurons
• More K+ channels open
• Pacemaker cells hyperpolarize
• Time for depolarization takes longer
Increasing Heart Rate
Decreasing Heart Rate
Modulation of heart rate
Depolarization travels through heart in two ways
1. Directly between cardiomyocytes
• Cardiomyocytes are
connected via gap
• Electrical signals
can pass directly
from cell to cell
2. Specialized conducting pathways
• Modified cardiomyocytes
that lack contractile
• Specialized for electrical
impulse conduction
Syncitial & sequential cardiac contractions
All cardiomyocytes of a chamber contract together
Electrically coupled cells (desmosomes)
Specialized conduction fibres
Cardiac chambers contract sequentially, after blood has moved
Delays in electrical conduction between chambers
• Sums all the electrical activity of
syncytial contractions & relaxations
• P wave: atrial depolarization
• QRS complex: ventricular depolarization
• T wave: ventricular repolarization
Impulse conduction – step 1
Impulse conduction – step 2a
Impulse conduction – step 2b
Impulse conduction – step 3
Impulse conduction – step 4
Conducting Pathways
Myogenic contractions
• All cardiomyocytes can contract without an external stimulus
• Different myocardial cells activate different ion channels
• Plateau phase – extended depolarization that corresponds to the
refractory period and last as long as the muscle contraction
• Prevents tetanus
Absence of funny channels
Fast Na+ channel
Slow L-type Ca2+ channel
Excitation-contraction coupling
Cardiac action potentials
Cardiac pumping cycle
ATP  muscle contraction  blood pressure  blood flow
Isometric contraction  blood pressure (wall tension) until valves open
Isotonic contraction  blood flow (cardiac output) after valves open
Muscle thickness determines pressure
Vertebrate Hearts
Vertebrate hearts have 3 main layers
• Pericardium
• Myocardium
• Endocardium
Vertebrate Hearts
Have complex walls with four main parts
• Pericardium – sac of connective that surround the heart
• Two layers: parietal (outer) and visceral (inner) pericardium
• Filled with a lubricating fluid
• Epicardium – outer layer of heart made of connective tissue
• Continuous with visceral pericardium
• Contain nerves that regulate the heart
• Contain coronary arteries
• Myocardium – the middle layer of heart muscle
• Endocardium – innermost layer of connective tissue covered by
epithelial cells (called endothelium)
Vertebrate hearts - Myocardium
• Muscle layer
• Composed of cardiomyocytes
• Specialized type of muscle cell
Oxygen supply to heart
• Myocardium extremely oxidative; has high O2 demand
• Coronary arteries supply oxygen to compact myocardium
• Spongy myocardium obtains oxygen from blood flowing through the heart
Mammalian cardiac anatomy
Two atria
Two ventricles
Mammalian cardiac cycle
Step 1: Late diastole, chambers relaxed, passive filling
Step 2: Atrial systole, EDV
Step 3: Isovolumic ventricular contraction
Step 4: Ventricular Ejection
Step 5: Early diastole, semilunar valves close
Electrical and Mechanical Events in the Cardiac Cycle
• Heart sounds: opening and
closing of valves
Figure 9.26
Heart Pressures
• The two ventricles contract simultaneously, but the left ventricle contracts
more forcefully and develops higher pressure
• Resistance in the pulmonary circuit is low due to high capillary density in
• Less pressure is needed to pump blood through this circuit
• The low pressure also protects the delicate blood vessels of the lungs
Heart Pressures
Heart Pressures
Cardiac Output
• Cardiac output (CO) – amount of blood the heart pumps
per unit time
• Stroke volume (SV) – amount of blood the heart pumps
with each beat
• Heart rate (HR): rate of contraction
• CO = HR X SV
• Bradycardia – decrease in HR
• Tachycardia – increase in HR
Modulating cardiac output
• By changing heart rate
• By changing stroke volume
Concept check: How would you modulate heart rate?
Slow heart rate = bradycardia
Fast heart rate = tachycardia
Stroke volume is regulated in two ways:
1) Extrinsically (by nervous system and hormones)
2) Intrinsically (via local mechanisms)
Modulation of cardiac output
Control of cardiac output: Intrinsic control mechanisms
• The importance of cardiac output (Q)
• Heart rate
Pacemaker rate: temperature; body size
• Cardiac stroke volume
Species variability
Effects of filling (venous) pressure
The importance of cardiac output (Q)
Flow (output) of blood per unit time from the heart (ml/min/kg)
Cardiac power output (= ATP need = O2 need)
Power output = Q x [blood pressure developed]
Right vs left
Atrium vs ventricle
The importance of cardiac output (Q)
Respiratory function:
O2 uptake = Q x (A-V O2 difference)
(Cao2-Cvo2); tissue O2 extraction
Q10 effect: O2 uptake doubles for +10oC
Species variability in routine & maximum Q values
@ 37oC
70-300 ml/min/kg
@ 10oC
10-30 ml/min/kg
@ 10oC
15-50 ml/min/kg
@ 28oC
100-200 ml/min/kg
@ 0oC
100 ml/min/kg
[Hb] is a primary determinant of Cao2
Q10 effect
~ x8
~ x8
~ x2
~ x16
Contribution of Q during exercise
O2 uptake = Q x (A-V O2 difference)
Q = [heart rate] x [cardiac stroke volume]
Human exercising
= 3-fold increase
= 2.5-fold increase
= 20% increase
= 3-fold increase
Volume = O2 delivery to tissues
10-fold increase
Regulation of Q during exercise
Q = [heart rate] x [cardiac stroke volume]
• Intrinsic pacemaker rate
Body mass
• Extrinsic modulation of pacemaker
• Intrinsic contractile properties
Cardiac stretch
• Extrinsic modulation of contractility
Acute temperature effect on heart rate
Ectotherms & Endotherms
Cooling by D10oC 
2x decrease
Q10 ~ 2
Temperature, oC
Temperature acclimation (resetting of pacemaker rate)
1. Compensation
eg, trout, Q10 = 1-2
2. Downregulation
eg, turtles, Q10 > 3
Temperature, oC
Acute Q10 ~ 2
Control of intrinsic pacemaker rate
Body mass & heart rate
HR = k . BM-0.25
hummingbird (1 g)
60 bpm
Body Mass
20 bpm
120 bpm is maximum
for many ectotherms
Intrinsic control of stroke volume
1. Automatic matching output of chambers
ventricular output must match atrial output – all vertebrates
right & left ventricular matching – crocodiles, birds & mammals
2. Varying stroke volume
Alter cardiac emptying (end-systolic volume) = D muscle contraction
Alter cardiac filling (end diastolic volume)
= D venous pressure
Many fishes (2-3x increase)
Small increases (<50%) other vertebrates
How? The Frank-Starling mechanism:
Control of Stroke Volume
Frank-Starling effect – an increase in
end-diastolic volume results in a more
forceful contraction of the ventricle
and an increase in SV
• Due to length-tension relationship
for muscle
• Allows heart to automatically
compensate for increases in the
amount of blood returning to the
heart (autoregulation)
Level of sympathetic activity shifts the
position of the cardiac muscle lengthtension relationship
Frank-Starling mechanism:
An intrinsic property of all vertebrate cardiomyocytes
Venous pressure  cardiac filling  myocyte stretch  stronger contraction
contractile unit
passive stretch
Venous filling pressure
Control of Stroke Volume
The nervous and endocrine system can cause the heart to contract more
forcefully and consequently pump more blood with each beat
Control of stroke volume
Control of cardiac output & flow distribution
Extrinsic control mechanisms
• Cardiac stroke volume
Change in contractility
- importance of calcium
•Heart rate
Sympathetic & parasympathetic neural controls
- mechanisms
- species diversity
• Blood flow distribution
Arteriolar controls
neural, humoral, paracrine, autocrine
Changing heart rate (vagal inhibition)
Pacemaker rate rarely equals measured HR
Inhibition & excitation
Vagus innervation of
pacemaker & atrium
All vertebrate hearts
Except hagfish &
Sympathetic innervation
of pacemaker, atrium &
Some advanced,
athletic teleost fishes,
Amphibians, reptiles,
birds & mammals
Cardiac stores: primitive fish
Innervated Chromaffin
tissue: other fishes
Adrenal medulla
Negative chronotropic effects (vagal inhibition)
0 mV
-60 mV
Positive chronotropic effects (adrenergic stimulation)
0 mV
-60 mV

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