Human Physiology, An Integrated Approach

Eighth Edition

Chapter 14
Cardiovascular
Physiology
About This Chapter

14.1 Overview of the Cardiovascular System

14.2 Pressure, Volume, Flow, and Resistance
14.3 Cardiac Muscle and the Heart
14.4 The Heart as a Pump
14.1 Overview of the Cardiovascular System
• Cardiovascular system:
– Heart (pump)
– Blood (fluid)
– Blood vessels including
capillaries (tubes)
• The cardiovascular system
transports materials throughout
the body
– From external environment:
nutrients, water, and gases
– Materials between cells:
hormones, immune cells,
antibodies
• Waste eliminated by cells: CO2,
heat, and metabolic waste
The Cardiovascular System Consists of the Heart, Blood vessels, and Blood
• Blood vessels (vasculature)
– Arteries vs. veins
– Capillaries
– Portal system joins two capillary
beds in series
• Heart
– Septum divides heart into two
halves (left and right)
– Atrium receives blood returning to
heart
– Ventricle pumps blood out of heart

• Blood: cells and plasma

• Pulmonary vs. systemic circulation

– Pulmonary arteries vs. pulmonary
veins
– Aorta vs. inferior vena cava and
superior vena cava
14.2 Pressure, Volume, Flow, and Resistance
• Blood flows because liquids move from high to low pressure regions
• Pressure gradient = ΔP difference in pressure between two regions
• Blood flows out of the heart (highest pressure) into closed loop of
vessels (lower pressure)
• Fluid in motion has 2 components: dynamic (kinetic energy) and lateral
(hydrostatic pressure)
• The pressure of a fluid in motion decreases with distance
– Pressure is lost (due to friction) as blood moves through vessels
– Hydrostatic pressure: pressure exerted by a fluid not in motion
93@Aorta
▪ Exerted in all directions
Blood Flow

2-5
Pressure Changes in Liquids Without a Change in Volume
• Contraction of heart creates pressure without changing volume of blood
– Blood leaves heart to vessels, called driving pressure
• In vessels
– If blood vessels dilate, blood pressure decreases (fat straw)
– If blood vessels constrict, blood pressure increases (skinny straw)
• Volume changes affect blood pressure in cardiovascular system
• Blood flows from higher pressure to lower pressure
– Flow through a tube is directly proportional to the pressure gradient
• Flow is proportional to ΔP
▪ The higher the pressure gradient, the greater the fluid flow
Resistance Opposes Flow
• Flow through a tube is inversely proportional to resistance (Flow  1/R)
– Flow decreases as resistance increases
• Poiseuille’s Law (R =8Lη/πr 4 or R  Lη/r 4 )
– Resistance is proportional to length (L) of the tube (blood vessel)
▪ Resistance increases as length increases
– Resistance is proportional to viscosity (η) or thickness, of the fluid (blood)
▪ Resistance increases as viscosity increases
– Resistance is inversely proportional to tube radius to the fourth power
(R  1/r 4 )
▪ Resistance decreases as radius increases
– Vasoconstriction vs. vasodilation
• Flow P /R
– Flow increases as the pressure gradient increases (directly
proportional) or as resistance to flow decreases (inversely
proportional)
▪ More pressure = higher flow
▪ More resistance = lower flow
Figure 14.3e The Physics of Fluid Flow
As the radius of a tube decreases, the resistance to flow increases.

1
Resistance 
radius4
Tube A Tube B
1 1
R  R 
14 24
1
R 1 R 
16
1
Flow 
resistance Resistance increases as length increases
Tube A Tube B Resistance increases as viscosity increases
1 Flow 
1 Resistance decreases as radius increases
Flow  1
1
16
1 More pressure = higher flow
Flow  1 Flow 
16 More resistance = lower flow
Velocity Depends on the Flow Rate and the Cross-Sectional Area
• Flow usually means flow rate
– The volume of blood that passes a given point in the system per unit time

• Velocity of flow
– The distance a fixed volume of blood travels in a given period of time
– Formula v = Q A
▪ Q = flow rate
▪ A = cross-sectional area of the tube

• Mean arterial pressure (MAP)

– Primary driving force for blood force
– Pressure reserved in the arteries during heart relaxation
– MAP ∝ cardiac output (CO)  peripheral resistance (PR)
Flow rate (Q)
Velocity (v) =
Cross - sectional area (A)

At Point X At Point Y

12cm3 / min 12cm3 / min

v= v=
1cm2 12 cm2

v = 12cm / min v = 1 cm / min

14.3 Cardiac Muscle and The Heart
• The heart has four chambers
• The heart is made up mostly of myocardium
– Encased in pericardium
• Paired atria are thin-walled upper chambers
• Paired ventricles are thick-walled lower
chambers
• Blood vessels emerge from base of heart
– Aorta and pulmonary trunk carry blood
from heart
– Vena cava and pulmonary veins return
blood to heart
– Deoxygenated: vena cava → right
atrium → right ventricle → pulmonary
trunk
– Oxygenated: pulmonary veins → left
atrium → left ventricle → aorta
• Connective tissue rings serve as origin and
insertion for cardiac muscles
14.3 Cardiac Muscle and The Heart Capillary beds
of lungs where
gas exchange
occurs

Pulmonary Circuit

Pulmonary
Pulmonary
arteries veins

Aorta and
branches
Venae
cavae

Left
atrium

Left
Right ventricle
atrium
Heart
Right
ventricle

Systemic Circuit

Capillary beds
of all body
tissues where gas
exchange occurs

Oxygen-rich,
CO2-poor blood
Oxygen-poor,
CO2-rich blood
Figure 14.6 In the embryo, the heart
develops from a single tube
Heart Valves Ensure One-Way Flow in the Heart
• Atrioventricular valves
– Between atria and ventricles
– Chordae tendineae prevent
eversion during ventricular
contraction
▪ Attached to valve flaps from
papillary muscles
– Tricuspid valve on the right side
– Bicuspid valve (mitral valve),
on the left side
• Semilunar valves
– Between ventricles and arteries
– Aortic valve
– Pulmonary valve

• The coronary circulation supplies

blood to the heart
– Coronary arteries vs. coronary
veins
Heart valves create one-
way flow through the heart
Heart valves create one-
way flow through the heart
Figure 14.8 The coronary circulation

A widowmaker heart attack happens when you have

a blockage in the biggest artery in your heart. That
means blood can't move through your left anterior
descending (LAD) artery, which provides 50% of
your heart muscle's blood supply. Immediate
treatment is crucial for a chance at survival.
Autorhythmic cells (pacemaker cells)

• Signal for contraction

• Smaller and fewer contractile fibers compared to contractile cells

• Do not have organized sarcomeres

Contractile cells Cardiac

– Striated fibers organized into sarcomeres
Muscle
Cardiac muscle vs. skeletal muscle
1. Smaller and have single nucleus per fiber Cells
2. Branch and join neighboring cells through intercalated disks
3. Gap junctions (electrical signal can cross)
Contract
4. T-tubules are larger and branch without
5. Sarcoplasmic reticulum is smaller
6. Mitochondria occupy one-third of cell volume!
Innervation
Cardiac Entry is a Feature of Cardiac EC Coupling
• Action potential starts with the heart pacemaker cells
• Ca2+ -induced Ca2+ release
– Voltage-gated L-type Ca2+ channels in the cell membrane open
– Ryanodine receptors (RyR) open in the sarcoplasmic reticulum (SR)
open in response to inflow of Ca2+
▪ Called Ca2+ spark
– Summed sparks create a Ca2+ signal
• Calcium binds to troponin

• Crossbridge cycle as in skeletal muscle

• Relaxation calcium removed from cytoplasm

– Into the SR with Ca2+ -ATPase
– Out of cell through the Na+ -Ca2+ exchanger (NCX)
Cardiac Muscle Contraction Can Be Graded
• Force generated is proportional to number of active crossbridges
– Determined by how much calcium is bound to troponin
• Sarcomere length affects force of contraction

Myocardial Action Potentials Vary

• Myocardial contractile cells
– Phase 4: resting membrane potential
– Phase 0: depolarization
▪ Due to Na+ inflow
AP skeletal muscle lasts 1-5
– Phase 1: initial repolarization msec.
▪ Na+ channels close
– Phase 2: plateau
▪ Long action potential due to Ca2+ inflow
▪ Sustains refractory period
and prevents tetanus
– Phase 3: rapid repolarization
▪ Due to K+ outflow
Myocardial autorhythmic cells
– Unstable membrane potential called pacemaker potential
– Depolarization is initially due to lf channel → Na+ inflow
– open
Depolarization → opening of voltage-gated Ca2+ channels → Ca2+
channel inflow
▪ → lf channels close → decreased Na+ inflow
– At threshold, 2nd type of voltage-gated Ca2+ channels open
steep depolarization →
– At peak, Ca2+ channels have closed, slow K+ channels open
+
→ decreased Ca inflow and increased K inflow
2+

▪ Pacemaker potential returns to lowest point

Table 14.3 Comparison of Action Potentials
in Cardiac and Skeletal Muscle
Blank Skeletal Muscle Contractile Myocardium Autorhythmic Myocardium
Unstable pacemaker
Membrane Potential Stable at – 70-80 mV Stable at –90 mV potential; usually starts at
–60 mV
+
+ Net Na entry through lf
Events Leading to Net Na entry through ACh- Depolarization enters via gap 2+
channels; reinforced by Ca
Threshold Potential operated channels junctions
entry
Rising Phase of Action Na+ Na+ entry
entry Ca2+ entry
Potential
Extended plateau caused by Ca+
+ +
Repolarization Phase Rapid; caused by K efflux entry; rapid phase caused byNa+ Rapid; caused by K efflux
efflux
+ Normally none; when
Due to excessive K efflux at
+ repolarization hits –60 mV,
high K permeability. When K
+
None; resting potential is –90
Hyperpolarization +
Na + the lf channels open again.
channels close, leak of K and mV, the equilibrium potential for
+ Ach can hyperpolarize the
restores potential to resting state K
cell
Duration of Action Variable; generally 150+
Short: 1–2 msec Extended: 200+ msec
Potential msec
Long because resetting of Na+
Not significant in normal
Refractory Period Generally brief Na+ channel gates delayed until
function
end of action potential
14.4 The Heart as Pump
• Electrical signals coordinate contraction
• Internodal pathway from sinoatrial node (SA node) to atrioventricular node (AV
node)
– Routes the direction of electrical signals so the heart ventricles contract
from apex to base
• Purkinje fibers transmit electric signals down the atrioventricular bundle (AV
bundle or bundle of His) to left and right bundle branches.
• SA node sets the pace of the heartbeat at 70 bpm (without autonomic 100 bpm)
– AV node (50 bpm) and Purkinje fibers (25–40 bpm) can act as pacemakers
under some conditions
– AV node delay with slower conductional signals through nodal cells 
• Pacemakers set the heart rate
14.4 The Heart as Pump
• Internodal pathway from
sinoatrial node (SA node) to
atrioventricular node (AV
node)
– Routes the direction of
electrical signals so the
heart contracts from apex
to base
• Purkinje fibers transmit electric
signals down the
atrioventricular bundle (AV
bundle or bundle of His) to left
and right bundle branches.
• SA node sets the pace of the
heartbeat at 70 bpm
– AV node (50 bpm) and
Purkinje fibers (25–40
bpm) can act as
pacemakers under some
conditions
– AV node delay with slower
conductional signals
through nodal cells 
The Electrocardiogram Reflects Electrical Activity

• Electrocardiogram (ECG)
– Show the summed electrical activity generated by all the cells of the heart
– Not the same as an action potential

• Components of the ECG

– Three waves
▪ P wave: depolarization of the atria
▪ QRS complex: wave of ventricular depolarization
– Atrial repolarization is part of QRS
▪ T wave: repolarization of the ventricle
– Two segments
▪ P-R segment: AV nodal delay
▪ T-P segment: ventricular and atrial relaxation

The Electrical Events of The Cardiac Cycle

• Mechanical events lag behind electrical events: contraction follows action potential

• ECG begins with atrial depolarization, atrial contraction at the end of P wave

• P-R segment electrical signal goes through AV node and AV bundle

• Q wave end: ventricular contraction begins and continues through T wave

Interpretat
ions of
ECGs

1. What is the heart rate?

– Heart rate: time between two P waves or two Q waves
– Faster than normal: tachycardia (greater than 100 bpm)
– Slower than normal: bradycardia (USUALLY lower than 60 bpm)

2 Is the rhythm of the heart regular or irregular?

3 Are the normal waves present in recognizable form?

4 Is there one QRS complex for each P wave? If yes, is the P-R segment
constant in length?
• Pathologies (cardiac arrhythmias) and ECGs
Figure 14.16g The Electrocardiogram
Physiology in Action: Electrocardiogram
The Heart Contracts and Relaxes during a Cardiac Cycle
• Diastole: cardiac muscle relaxes

• Systole: cardiac muscle contracts

• Five phases of the cardiac cycle

(1 – 2)

① The heart at rest: atrial and

ventricular diastole
– The atria are filling with blood
from the vein
– AV valves open  ventricles
fill

② Completion of ventricular filling:

atrial systole
– Atria contract
– Last 20% of blood volume
driven to ventricles
– End-diastolic volume
(EDV): volume in ventricle at
the end of ventricular
relaxation
Cardiac Cycle
• Five phases of the cardiac cycle (3 – 4)

③ Early ventricular contraction and the

first heart sound
– AV valves close
▪ Vibrations following closure of
the AV valves
– “Lub”
– No blood in or out (isovolumic
ventricular contraction)
– Increasing pressure due to
ventricular muscle contraction
– Concurrent atrial diastole
▪ Atria relax and blood flows in
the atria

④ The heart pumps: ventricular ejection

– Semilunar valves open
– Blood is ejected into arteries
– End-systolic volume (ESV):
volume in ventricle at the end of
ventricular contraction
The Heart Contracts and Relaxes during a Cardiac Cycle
• Five phases of the cardiac cycle (5)
⑤ Ventricular relaxation and the
second heart sound
▪ Arterial blood flows back
towards heart
– Semilunar valves shut 
second heart sound
• “Dup” (or “Dub”)
▪ Ventricular muscles relax
pressure drops (still higher
than atrial pressure)
▪ No blood enters or exits
(isovolumic ventricular
relaxation)
▪ AV valves open when
ventricular pressure drops
below atrial pressure

• Pressure-volume curves represent one

cardiac cycle
Watch: Cardiac Output
Stroke Volume is the Volume of Blood
Pumped per Contraction
• Stroke volume (SV) = EDV-ESV
– Volume of blood before contraction minus volume of blood after contraction
– Average  70 mL (70-kg man at rest)

• Cardiac output is a measure of cardiac performance (HR  SV)

– Volume of blood pumped by one ventricle in a given period of time (on minute)
– Cardiac output (CO)  heart rate  stroke volume
– Average  5 L/min
The Autonomic Division Modulates heart Rate
• Parasympathetic control
– DECREASES heart rate
+
– K permeability increases
▪ Pacemaker potential begins at a lower value
– Ca2+ permeability decreases
▪ Slows rate of pacemaker depolarization

• Sympathetic control
– INCREASES heart rate
– β1-adrenergic receptors on the autorhythmic cells
– Na+ & Ca2+ permeability increases
▪ Increases rate of pacemaker depolarization
• Tonic control
– Normally dominated by parasympathetic activity (without autonomic 100 bpm)
Multiple factors Influence Stroke Volume
• Contractility: intrinsic ability of a cardiac muscle fiber to contract at any given fiber length
• Length-tension relationships
– Determined by volume of blood at beginning of contraction (EDV)
– Degree of stretch is called preload
• Frank-Starling law of the heart
– Stroke volume is proportional to EDV
– The heart pumps all the blood that is returned to it
• Stroke volume and venous return
– EDV is determined by venous return which is affected by
1) skeletal muscle pump
2) respiratory pump
3) sympathetic innervation of veins
Contractility Is Controlled by the Nervous and Endocrine Systems
• Any chemical that affects contractility is an inotropic agent  inotropic effect

• Positive inotropes – increase contractility

– Epinephrine, norepinephrine, and digitalis (Digitalis purpurea (purple foxglove))
– Catecholamines increase
▪ Probability voltage-gated Ca2+ channels open, and open longer
▪ and also Ca2+ storage with phospholamban
–increase Ca2+-ATPase activity in the sarcoplasmic reticulum

• Negative inotropes – decrease contractility

• EDV and arterial blood pressure determine afterload

– Afterload: combined load of EDV and arterial resistance during ventricular
contraction
– Ejection fraction: percentage of EDV ejected with one contraction
Figure 14.22 Catecholamines increase cardiac contraction