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4-1 The Heart

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The Cardiovascular System: �The Heart

  • STOP! Listen to the Cardiac Anatomy lecture before proceeding!
  • Beats over 39 million times and pumps over 1 million gallons per year
  • Over 60,000 miles of blood vessels

​

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Functions of the CV System

  • Transportation
    • O2, CO2, metabolic wastes, nutrients, heat, cells, & hormones
  • Regulation
    • helps regulate pH through buffers
    • helps regulate body temperature
      • coolant properties of water
      • vasodilatation of surface vessels dump heat
    • helps regulate water content of cells by interactions with dissolved ions and proteins
  • Protection from disease & loss of blood

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4 Chambered heart

R. Atrium

L. Atrium

R. Ventricle

L. Ventricle

  • Systemic venous blood
  • ↓O2 ↑CO2
  • ↓pH
  • ↓P
  • Pulmonary arterial blood
  • ↓O2 ↑CO2
  • ↓pH
  • ↑P
  • Systemic arterial blood
  • ↑O2 ↓CO2
  • ↑pH
  • ↑P
  • Pulmonary venous blood
  • ↑O2 ↓CO2
  • ↑pH
  • ↓P

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Cardiovascular System

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Structure of Cardiac Muscle Cell

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Structure of Cardiac Muscle

  • Short, thick, branched cells, 50 to 100 μm long and 10 to 20 μm wide with one central nucleus
  • ↓ Sarcoplasmic reticulum, large T tubules
    • must admit more Ca2+ from ECF during excitation
  • Intercalated discs, join myocytes end to end
    • interdigitating folds - ↑ surface area
    • mechanical junctions tightly join myocytes
      • fascia adherens: actin anchored to plasma membrane
      • desmosomes
    • electrical junctions - gap junctions form channels allowing ions to flow directly into next cell

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Metabolism of Cardiac Muscle

  • Aerobic respiration
  • Rich in myoglobin and glycogen
  • Large mitochondria
  • Organic fuels: fatty acids, glucose, ketones
  • Fatigue resistant

Intercalated discs

Cardiac muscle tissue

LM × 575

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Coronary Flow

  • Must have its own supply of blood
  • Reduced during ventricular contraction
    • arteries compressed
  • Increased during ventricular relaxation
    • openings to coronary arteries, just above aortic semilunar valve, fill as blood surges back to valve

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Myocardial Infarction

  • Sudden death of heart tissue caused by interruption of blood flow from vessel narrowing or occlusion
  • Anastomoses defend against interruption by providing alternate blood pathways
    • circumflex artery and right coronary artery combine to form posterior interventricular artery
    • anterior and posterior interventricular arteries combine at apex of heart

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4-2 Cardiac Conduction System

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Conduction System of Heart

  • The heart is myogenic and autorhythmic
    • Cardiomyocytes repeatedly generate spontaneous APs that trigger coordinated contractions through the conduction system

​

Action

potential

Pacemaker

potential

Threshold

Slow Na+

inflow

K+ outflow

Ca2+–Na+

inflow

0

.4

.8

1.2

1.6

–70

–60

–50

–40

–30

–20

–10

0

+10

Membrane potential (mV)

Time (seconds)

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Conduction System of Heart

Coordinates contraction of heart muscle.

SA node fires.

Excitation spreads through

atrial myocardium.

AV node fires.

Excitation spreads down AV

bundle.

Subendocardial conducting

network distributes excitation

through ventricular

myocardium.

Left

atrium

Subendocardial

conducting network

Bundle

branches

Right atrium

Sinuatrial node

(pacemaker)

Atrioventricular

node

Atrioventricular

bundle

Subendocardial

conducting network

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Rhythm of Conduction System

  • Systole=contraction; Diastole=relaxation
  • SA node fires spontaneously 90-100 times per minute
  • AV node fires at 40-50 times per minute
  • If both nodes are suppressed fibers in ventricles by themselves fire only 20-40 times per minute
  • Artificial pacemaker needed if pace is too slow
  • Extra beats forming at other sites are called ectopic pacemakers
    • caffeine & nicotine increase activity

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Cardiomyocyte Action Potentials

Plateau

Myocardial

relaxation

Myocardial

contraction

Absolute

refractory

period

Action

potential

Voltage-gated Na+ channels open.

Na+ inflow depolarizes the membrane

and triggers the opening of still more Na+

channels, creating a positive feedback

cycle and a rapidly rising membrane voltage.

Na+ channels close when the cell

depolarizes, and the voltage peaks at

nearly +30 mV.

Ca2+ entering through slow Ca2+

channels prolongs depolarization of

membrane, creating a plateau. Plateau falls

slightly because of some K+ leakage, but most

K+ channels remain closed until end of

plateau.

Ca2+ channels close and Ca2+ is transported

out of cell. K+ channels open, and rapid K+

outflow returns membrane to its resting

potential.

0

.15

.30

–80

–60

–40

–20

0

+20

Membrane potential (mV)

Time (seconds)

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1

Rapid Depolarization

Cause: Na+ entry

Duration: 3–5 msec

Ends with: Closure of

voltage-gated fast

sodium channels

+30

0

1

mV

Absolute refractory

period

0

Stimulus

100

Time (msec)

200

Relative

refractory

period

–90

KEY

Absolute refractory

period

300

Relative refractory

period

a

Step 2

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1

Rapid Depolarization

Cause: Na+ entry

Duration: 3–5 msec

Ends with: Closure of

voltage-gated fast

sodium channels

2

The Plateau

Cause: Ca2+ entry

Duration: ~175 msec

Ends with: Closure

of slow calcium

channels

3

+30

0

2

1

mV

Absolute refractory

period

0

Stimulus

100

Time (msec)

200

Relative

refractory

period

–90

KEY

Absolute refractory

period

300

Relative refractory

period

a

Step 3

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1

Rapid Depolarization

Cause: Na+ entry

Duration: 3–5 msec

Ends with: Closure of

voltage-gated fast

sodium channels

2

The Plateau

Cause: Ca2+ entry

Duration: ~175 msec

Ends with: Closure

of slow calcium

channels

3

Repolarization

Cause: K+ loss

Duration: 75 msec

Ends with: Closure

of slow potassium

channels

+30

0

2

1

mV

Absolute refractory

period

0

Stimulus

100

Time (msec)

200

3

Relative

refractory

period

–90

KEY

Absolute refractory

period

300

Relative refractory

period

a

Step 4

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Depolarization & Repolarization

  • Depolarization
    • Cardiac cell resting membrane potential is -90mv
    • excitation spreads through gap junctions
    • fast Na+ channels open for rapid depolarization
  • Plateau phase
    • 250 msec (only 1msec in neuron)
    • slow Ca+2 channels open, let Ca +2 enter from outside cell and from storage in sarcoplasmic reticulum, while K+ channels close
    • Ca +2 binds to troponin to allow for actin-myosin cross-bridge formation & tension development
  • Repolarization
    • Ca+2 channels close and K+ channels open & -90mv is restored as potassium leaves the cell
  • Refractory period
    • very long so heart can fill

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Contraction of Myocardium

  • Myocytes have stable resting potential of -90 mV
  • Depolarization (very brief)
    • stimulus opens voltage regulated Na+ gates, (Na+ rushes in) membrane depolarizes rapidly
    • action potential peaks at +30 mV
    • Na+ gates close quickly
  • Plateau - 200 to 250 msec, sustains contraction
    • slow Ca+2 channels open, Ca+2 binds to fast Ca+2 channels on SR, releases ↑Ca+2 into cytosol: contraction
  • Repolarization - Ca+2 channels close, K+ channels open, rapid K+ out returns to resting potential

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Electrocardiogram (ECG)

  • Composite of all action potentials of nodal and myocardial cells detected, amplified and recorded by electrodes on arms, legs and chest

​

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ECG

  • P wave
    • SA node fires, atrial depolarization
  • PQ segment
    • Conduction time from SA to AV nodes
    • atrial systole occurs here
  • QRS complex
    • AV node fires, ventricular depolarization
    • ventricular systole intiated
    • (atrial repolarization and diastole - signal obscured)
  • T wave
    • ventricular repolarization
  • QT interval
    • Total time of ventricular depolarization
    • Shortens with increased HR
  • ST segment
    • Ventricular systole during this time
    • Plateau phase

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Normal Electrocardiogram (ECG)

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Diagnostic Value of ECG

  • Invaluable for diagnosing abnormalities in conduction pathways, MI, heart enlargement and electrolyte and hormone imbalances

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ECGs, Normal & Abnormal

No P waves

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Abnormal ECGs

Extrasystole : note the inverted QRS complex, misshapen QRS and �T and absence of a P wave preceding this contraction.

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Abnormal ECGs

Arrhythmia: conduction failure at AV node

No pumping action occurs

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  • Ventricular fibrillation
  • Atrial fibrillation

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4-3 Cardiac Cycle

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Cardiac Cycle

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Wigger’s diagram

  • AKA the most painful figure in the book.

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ONE CARDIAC CYCLE

QRS

complex

Electro-

cardiogram

(ECG)

P

T

QRS

complex

P

ATRIAL

DIASTOLE

ATRIAL

SYSTOLE

VENTRICULAR

DIASTOLE

120

Aortic valve

opens

ATRIAL DIASTOLE

VENTRICULAR

SYSTOLE

VENTRICULAR DIASTOLE

ATRIAL

SYSTOLE

Aortic valve

closes

90

Aorta

Dicrotic

notch

1

Pressure

(mm Hg)

60

Left

ventricle

Left AV

valve opens

30

Left atrium

Left AV

valve closes

1

0

130

Left�ventricular

Volume (mL)

​

End-diastolic

volume

1

Stroke

volume

End-systolic

volume

50

0

6

100

200

300

400

Time (msec)

500

600

700

800

Atrial contraction begins.

Step 2

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© 2018 Pearson Education, Inc.

ONE CARDIAC CYCLE

QRS

complex

Electro-

cardiogram

(ECG)

P

T

QRS

complex

P

ATRIAL

DIASTOLE

ATRIAL

SYSTOLE

VENTRICULAR

DIASTOLE

120

Aortic valve

opens

ATRIAL DIASTOLE

VENTRICULAR

SYSTOLE

VENTRICULAR DIASTOLE

ATRIAL

SYSTOLE

Aortic valve

closes

90

Aorta

Dicrotic

notch

1

Pressure

(mm Hg)

Atria eject blood into ventricles.

60

Left

ventricle

Left AV

valve opens

30

Left atrium

Left AV

valve closes

1

0

130

Left�ventricular

Volume (mL)

​

2

End-diastolic

volume

1

2

Stroke

volume

End-systolic

volume

50

0

100

200

300

400

Time (msec)

500

600

700

800

Atrial contraction begins.

2

Step 3

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ONE CARDIAC CYCLE

QRS

complex

Electro-

cardiogram

(ECG)

P

T

QRS

complex

P

ATRIAL

DIASTOLE

ATRIAL

SYSTOLE

VENTRICULAR

DIASTOLE

120

Aortic valve

opens

ATRIAL DIASTOLE

VENTRICULAR

SYSTOLE

VENTRICULAR DIASTOLE

ATRIAL

SYSTOLE

Aortic valve

closes

90

Aorta

Dicrotic

notch

1

Pressure

(mm Hg)

Atria eject blood into ventricles.

60

Left

ventricle

Atrial systole ends; AV valves close.

Left AV

valve opens

30

Left atrium

Left AV

valve closes

1

0

130

Left�ventricular

Volume (mL)

​

2

3

End-diastolic

volume

3

1

2

Stroke

volume

End-systolic

volume

50

0

100

200

300

400

Time (msec)

500

600

700

800

Atrial contraction begins.

2

3

Step 4

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© 2018 Pearson Education, Inc.

ONE CARDIAC CYCLE

QRS

complex

Electro-

cardiogram

(ECG)

P

T

QRS

complex

P

ATRIAL

DIASTOLE

ATRIAL

SYSTOLE

VENTRICULAR

DIASTOLE

120

Aortic valve

opens

ATRIAL DIASTOLE

VENTRICULAR

SYSTOLE

VENTRICULAR DIASTOLE

ATRIAL

SYSTOLE

Aortic valve

closes

90

Aorta

Dicrotic

notch

1

Pressure

(mm Hg)

Atria eject blood into ventricles.

60

Left

ventricle

4

Atrial systole ends; AV valves close.

Isovolumetric ventricular contraction occurs.

Left AV

valve opens

30

Left atrium

Left AV

valve closes

1

0

130

Left�ventricular

Volume (mL)

​

2

3

End-diastolic

volume

3

1

2

Stroke

volume

End-systolic

volume

50

0

100

200

300

400

Time (msec)

500

600

700

800

Atrial contraction begins.

2

3

4

Step 5

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© 2018 Pearson Education, Inc.

ONE CARDIAC CYCLE

QRS

complex

Electro-

cardiogram

(ECG)

P

T

QRS

complex

P

ATRIAL

DIASTOLE

ATRIAL

SYSTOLE

VENTRICULAR

DIASTOLE

120

Aortic valve

opens

ATRIAL DIASTOLE

VENTRICULAR

SYSTOLE

VENTRICULAR DIASTOLE

ATRIAL

SYSTOLE

5

Aortic valve

closes

90

Aorta

Dicrotic

notch

1

Pressure

(mm Hg)

Atria eject blood into ventricles.

60

Left

ventricle

4

Atrial systole ends; AV valves close.

Isovolumetric ventricular contraction occurs.

Ventricular ejection occurs.

Left AV

valve opens

30

Left atrium

Left AV

valve closes

1

0

130

Left�ventricular

Volume (mL)

​

2

3

End-diastolic

volume

3

1

2

Stroke

volume

End-systolic

volume

50

0

100

200

300

400

Time (msec)

500

600

700

800

Atrial contraction begins.

2

3

4

5

Step 6

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ONE CARDIAC CYCLE

QRS

complex

Electro-

cardiogram

(ECG)

P

T

QRS

complex

P

ATRIAL

DIASTOLE

ATRIAL

SYSTOLE

VENTRICULAR

DIASTOLE

120

Aortic valve

opens

ATRIAL DIASTOLE

VENTRICULAR

SYSTOLE

VENTRICULAR DIASTOLE

ATRIAL

SYSTOLE

5

Aortic valve

closes

6

90

Aorta

Dicrotic

notch

1

Pressure

(mm Hg)

Atria eject blood into ventricles.

60

Left

ventricle

4

Atrial systole ends; AV valves close.

Isovolumetric ventricular contraction occurs.

Ventricular ejection occurs.

Semilunar valves close.

Left AV

valve opens

30

Left atrium

Left AV

valve closes

1

0

130

Left�ventricular

Volume (mL)

​

2

3

End-diastolic

volume

3

1

2

Stroke

volume

End-systolic

volume

50

0

6

100

200

300

400

Time (msec)

500

600

700

800

Atrial contraction begins.

2

3

4

5

6

Step 7

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ONE CARDIAC CYCLE

QRS

complex

Electro-

cardiogram

(ECG)

P

T

QRS

complex

P

ATRIAL

DIASTOLE

ATRIAL

SYSTOLE

VENTRICULAR

DIASTOLE

120

Aortic valve

opens

ATRIAL DIASTOLE

VENTRICULAR

SYSTOLE

VENTRICULAR DIASTOLE

ATRIAL

SYSTOLE

5

Aortic valve

closes

6

90

Aorta

Dicrotic

notch

1

Pressure

(mm Hg)

Atria eject blood into ventricles.

60

Left

ventricle

4

7

Atrial systole ends; AV valves close.

Isovolumetric ventricular contraction occurs.

Ventricular ejection occurs.

Semilunar valves close.

Left AV

valve opens

30

Left atrium

Left AV

valve closes

Isovolumetric relaxation occurs.

1

0

130

Left�ventricular

Volume (mL)

​

2

3

End-diastolic

volume

3

1

2

Stroke

volume

End-systolic

volume

50

0

6

100

200

300

400

Time (msec)

500

600

700

800

Atrial contraction begins.

2

3

4

5

6

7

Step 8

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ONE CARDIAC CYCLE

QRS

complex

Electro-

cardiogram

(ECG)

P

T

QRS

complex

P

ATRIAL

DIASTOLE

ATRIAL

SYSTOLE

VENTRICULAR

DIASTOLE

120

Aortic valve

opens

ATRIAL DIASTOLE

VENTRICULAR

SYSTOLE

VENTRICULAR DIASTOLE

ATRIAL

SYSTOLE

5

Aortic valve

closes

6

90

Aorta

Dicrotic

notch

1

Pressure

(mm Hg)

Atria eject blood into ventricles.

60

Left

ventricle

4

7

Atrial systole ends; AV valves close.

Isovolumetric ventricular contraction occurs.

Ventricular ejection occurs.

Semilunar valves close.

Left AV

valve opens

30

Left atrium

Left AV

valve closes

Isovolumetric relaxation occurs.

AV valves open; passive ventricular

filling occurs.

1

0

130

Left�ventricular

Volume (mL)

​

2

3

End-diastolic

volume

8

3

1

2

Stroke

volume

End-systolic

volume

50

0

6

100

200

300

400

Time (msec)

500

600

700

800

Atrial contraction begins.

2

3

4

5

6

7

8

Step 9

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Figure 20–18 Heart Sounds.

© 2018 Pearson Education, Inc.

120

Valve

location

Sounds

heard

Valve

location

Sounds

heard

Semilunar

valves open

Semilunar

valves close

Aortic

valve

Pulmonary

valve

Pressure

(mm Hg)

90

Aorta

60

Right

AV

valve

Valve

location

Sounds

heard

Valve

location

Sounds

heard

Left

ventricle

Left

atrium

AV valves

close

AV valves

open

Left

AV

valve

30

0

S4

S1

S2

S3

S4

Heart

sounds

Placements of a stethoscope for

listening to the different sounds

produced by individual valves

“Lubb”

“Dupp”

The relationship between heart sounds

and key events in the cardiac cycle

a

b

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One Cardiac Cycle

  • At 75 beats/min, one cycle requires 0.8 sec.
    • systole (contraction) and diastole (relaxation) of both atria, plus the systole and diastole of both ventricles
  • End diastolic volume (EDV)
    • volume in ventricle at end of diastole, about 130ml
  • End systolic volume (ESV)
    • volume in ventricle at end of systole, about 60ml
  • Stroke volume (SV)
    • the volume ejected per beat from each ventricle, about 70ml
    • SV = EDV - ESV

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Heart Sounds

  • Auscultation - listening to sounds made by body
  • First heart sound (S1), louder and longer “lubb”, occurs with closure of AV valves
  • Second heart sound (S2), softer and sharper “dupp” occurs with closure of semilunar valves
  • S3 - rarely heard in people > 30

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Phases of Cardiac Cycle

  • Diastole
    • all chambers relaxed
    • AV valves open
    • blood flowing into ventricles
  • Atrial systole
    • SA node fires, atria depolarize
    • P wave appears on ECG
    • atria contract, force additional blood into ventricles
    • ventricles now contain end-diastolic volume (EDV) of about 130 ml of blood

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Isovolumetric Contraction of Ventricles

  • Atria repolarize and relax
  • Ventricles depolarize
  • QRS complex appears in ECG
  • Ventricles contract
  • Rising pressure closes AV valves - heart sound S1 occurs
  • No ejection of blood yet (no change in volume)

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Ventricular Ejection

  • Rising pressure opens semilunar valves
  • Rapid ejection of blood
  • Reduced ejection of blood (less pressure)
  • Stroke volume: amount ejected, 70 ml at rest
  • SV/EDV= ejection fraction, at rest ~ 54%, during vigorous exercise as high as 90%, diseased heart < 50%
  • End-systolic volume: amount left in heart

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Isovolumetric Relaxation of Ventricles

  • T wave appears in ECG
  • Ventricles repolarize and relax (begin to expand)
  • Semilunar valves close (dicrotic notch of aortic press. curve) - heart sound S2 occurs
  • AV valves remain closed
  • Ventricles expand but do not fill (no change in volume)

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Ventricular Filling - 3 phases

  • Rapid ventricular filling - AV valves first open ↑pressure
  • Diastasis - sustained lower pressure, venous return
  • Filling completed by atrial systole
  • Heart sound S3 may occur

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Unbalanced Ventricular Output

Right ventricular

output exceeds left

ventricular output.

Pressure backs up.

Fluid accumulates in

pulmonary tissue.

Pulmonary edema

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Unbalanced Ventricular Output

Left ventricular

output exceeds right

ventricular output.

Fluid accumulates in

systemic tissue.

Pressure backs up.

Systemic edema

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Pressure-Volume Loops

  • A & D = ESV
  • B = EDV
  • A🡪B = Diastole
  • B🡪C = IsoV contraction
  • C🡪D = Systole
  • D🡪A = IsoV relaxation

​

​

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4-4 Regulation of Cardiac Output: HR

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Factors Affecting

Heart Rate (HR)

Autonomic

innervation

Hormones

Factors Affecting

Stroke Volume (SV)

End-diastolic

volume (EDV)

End-systolic

volume (ESV)

HEART RATE (HR)

STROKE VOLUME (SV) = EDV — ESV

CARDIAC OUTPUT (CO) = HR x SV

Cardiac Output (CO)

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Heart Rate

Measured from pulse

    • Infants have HR of 120 beats per minute or more
    • Young adult females avg. 72 - 80 bpm
    • Young adult males avg. 64 to 72 bpm
    • HR rises again in the elderly

​

​

Factors affecting HR:

    • Nervous system
    • Hormones
    • Ions
    • Age
    • Gender
    • Fitness
    • Temperature

Evaluation of Heart Rate in Daily Life Based on 10 Million Samples Database

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HR Effects

  • Chronotropic effects alter HR
    • Positive chronotropic agents ↑ HR
    • Negative chronotropic agents ↓ HR
    • Cardiac center of medulla oblongata
      • an autonomic control center with 2 neuronal pools: a cardioacceleratory center (sympathetic), and a cardioinhibitory center (parasympathetic)
  • Tachycardia
    • HR > 100
    • Exercise, stress, anxiety, drugs, heart disease or ↑ body temp.
  • Bradycardia
    • HR < 60
    • common in sleep and endurance trained athletes (↑ SV)

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HR: Sympathetic Nervous System

  • Cardioacceleratory center of Medulla
    • stimulates sympathetic cardiac accelerator nerves to SA node, AV node and myocardium
    • these nerves secrete norepinephrine, which binds to β-adrenergic receptors in the heart (+ chronotropic effect)
    • Sympathetic NS can ↑ HR up to 230 bpm
      • limited by refractory period of SA node
    • But CO peaks at HR of 160 to 180 bpm due to ↓ SV

​

​

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HR: Parasympathetic Nervous System

  • Cardioinhibitory center of medulla
    • stimulates vagus nerves
      • right vagus nerve - SA node
      • left vagus nerve - AV node
    • secrete Ach (acetylcholine), binds to muscarinic receptors
      • opens K+ channels in nodal cells, hyperpolarized, fire less frequently, HR slows down
    • vagal tone: background firing rate holds HR to sinus rhythm of 70 to 80 bpm
      • severed vagus nerves - SA node fires at intrinsic rate-100bpm
      • maximum vagal stimulation ↓ HR as low as 20 bpm

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HR: Sympathetic vs PS

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Inputs to Cardiac Center

  • Higher brain centers affect HR
    • sensory and emotional stimuli - rollercoaster, IRS audit
    • cerebral cortex, limbic system, hypothalamus
  • Proprioceptors
    • inform cardiac center about changes in activity, HR ↑ before metabolic demands arise
  • Baroreceptors
    • pressure sensors in aorta and internal carotid arteries send continual stream of signals to cardiac center
      • if pressure drops, signal rate drops, cardiac center ↑ HR
      • if pressure rises, signal rate rises, cardiac center ↓ HR

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Inputs to Cardiac Center

  • Chemoreceptors
    • sensitive to blood pH, CO2 and oxygen
    • aortic arch, carotid arteries and medulla oblongata
    • primarily respiratory control, may influence HR
    • ↑ CO2 (hypercapnia) causes ↑ H+ levels, may create acidosis (pH < 7.35)
    • Hypercapnia and acidosis stimulates cardiac center to ↑ HR

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Chronotropic Chemicals

  • Neurotransmitters - with cAMP as 2nd messenger
    • norepinephrine and epinephrine (catecholamines) are potent cardiac stimulants
    • cAMP ↑Ca2+ entry into cell and SR Ca2+ reuptake
  • Drugs
    • caffeine inhibits cAMP breakdown
    • nicotine stimulates catecholamine secretion
  • Hormones
    • TH ↑ β-adrenergic receptors in heart, ↑ sensitivity to sympathetic stimulation, ↑ HR
    • Glucagon ↑ cAMP production
  • Electrolytes - K has greatest chronotropic effects
    • Hyperkalemia: ↑[K+] 🡪 myocardium less excitable 🡪 ↓ & irregular HR
    • Hypokalemia: ↓[K+] 🡪 cells hyperpolarized, requires ↑ stimulation
    • Hypercalcemia: ↑[Ca2+] 🡪 ↓HR
    • Hypocalcemia: ↓[Ca2+] 🡪 ↑HR

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HR: Autonomic Regulation

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4-5 Regulation of Cardiac Output: SV

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© 2018 Pearson Education, Inc.

Factors Affecting

Heart Rate (HR)

Autonomic

innervation

Hormones

Factors Affecting

Stroke Volume (SV)

End-diastolic

volume (EDV)

End-systolic

volume (ESV)

HEART RATE (HR)

STROKE VOLUME (SV) = EDV — ESV

CARDIAC OUTPUT (CO) = HR x SV

Cardiac Output (CO)

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Stroke Volume

3 factors regulate stroke volume:

    • Preload = SV ∝ EDV
      • Amount of tension in the myocardium before systole
      • Driven by venous return
      • Frank-Starling Law of the Heart

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Stroke Volume

3 factors regulate stroke volume:

    • Preload = SV ∝ EDV
    • Contractility = SV ∝ Contractility
      • Strength of contraction for a given preload
      • Influenced by inotropic agents
        • + inotropy 🡪 ↑SV
        • - inotropy 🡪 ↓SV
      • Ca2+ is strong + inotrope
        • Hypercalcemia: ↑contractility 🡪 ↑SV 🡪 ↑CO
        • Hypocalcemia: ↓contractility 🡪 ↓SV 🡪 ↓CO
        • NE and E ↑cAMP🡪↑Ca2+

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Stroke Volume

3 factors regulate stroke volume:

    • Preload = SV ∝ EDV
    • Contractility = SV ∝ Contractility
    • Afterload = SV ∝ 1/Afterload
      • Resistance to blood flow
        • Sum of all forces opposing ventricular ejection

​

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Figure 20–23 Factors Affecting Stroke Volume.

© 2018 Pearson Education, Inc.

Factors Affecting Stroke Volume (SV)

KEY

Venous return (VR)

VR =

VR =

Filling time (FT)

FT =

FT =

= increased

= decreased

Preload

End-diastolic

volume (EDV)

End-systolic

volume (ESV)

EDV =

EDV =

SV

SV

STROKE VOLUME (SV)

ESV =

ESV =

SV

SV

EDV

EDV

EDV

EDV

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Figure 20–23 Factors Affecting Stroke Volume.

© 2018 Pearson Education, Inc.

Factors Affecting Stroke Volume (SV)

KEY

Venous return (VR)

VR =

VR =

Filling time (FT)

FT =

FT =

Sympathetic

stimulation

increases

Parasympathetic

stimulation

decreases

E, NE, glucagon,

thyroid hormones

increases

= increased

= decreased

Preload

Contractility (Cont)

of muscle cells

Cont =

Cont =

End-diastolic

volume (EDV)

End-systolic

volume (ESV)

EDV =

EDV =

SV

SV

STROKE VOLUME (SV)

ESV =

ESV =

SV

SV

ESV

ESV

EDV

EDV

EDV

EDV

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Figure 20–23 Factors Affecting Stroke Volume.

© 2018 Pearson Education, Inc.

Factors Affecting Stroke Volume (SV)

KEY

Venous return (VR)

VR =

VR =

Filling time (FT)

FT =

FT =

Sympathetic

stimulation

increases

Parasympathetic

stimulation

decreases

E, NE, glucagon,

thyroid hormones

increases

= increased

= decreased

Preload

Contractility (Cont)

of muscle cells

Cont =

Cont =

Vasoconstriction

increases

Vasodilation

decreases

End-diastolic

volume (EDV)

End-systolic

volume (ESV)

Afterload (AL)

AL =

AL =

EDV =

EDV =

SV

SV

STROKE VOLUME (SV)

ESV =

ESV =

SV

SV

ESV

ESV

ESV

ESV

EDV

EDV

EDV

EDV

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Exercise and Cardiac Output

  • Effect of proprioceptors
    • HR ↑ at beginning of exercise due to signals from joints, muscles
  • Effect of venous return
    • muscular activity ↑ venous return causes ↑ SV
  • ↑ HR and ↑ SV cause ↑CO
  • Effect of ventricular hypertrophy
    • caused by sustained program of exercise
    • ↑ SV allows heart to beat more slowly at rest, 40-60bpm
    • ↑ cardiac reserve, can tolerate more exertion

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Stroke Volume and Heart Rate

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4-6 Cardiac Pathologies

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Risk Factors for Heart Disease

  • Risk factors in heart disease:
    • Age
    • Sex
    • Genetics
    • Smoking
    • Cholesterol
    • Hypertension
    • Obesity
    • Fitness
    • Diabetes mellitus
    • High blood levels of fibrinogen
    • Ventricular hypertrophy

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Congestive Heart Failure

  • Causes of CHF
    • coronary artery disease, hypertension, MI, valve disorders, congenital defects
  • Left side heart failure
    • less effective pump so more blood remains in ventricle
    • heart is overstretched & even more blood remains
    • blood backs up into lungs as pulmonary edema
    • suffocation & lack of oxygen to the tissues
  • Right side failure
    • fluid builds up in tissues as peripheral edema

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Plasma Lipids and Heart Disease

  • Risk factor for developing heart disease is high blood cholesterol level.
    • Correlated with growth of fatty plaques
    • Most lipids are transported as lipoproteins
      • low-density lipoproteins (LDLs)
      • high-density lipoproteins (HDLs)
      • very low-density lipoproteins (VLDLs)
    • HDLs remove excess cholesterol from circulation
    • LDLs are associated with the formation of fatty plaques
    • VLDLs contribute to increased fatty plaque formation
  • There are two sources of cholesterol in the body:
    • in foods we ingest & formed by liver

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Desirable Levels of Blood Cholesterol for Adults

  • TC (total cholesterol) under 200 mg/dl
  • LDL under 130 mg/dl
  • HDL over 40 mg/dl
  • Normally, triglycerides are in the range of 10-190 mg/dl.
  • Among the therapies used to reduce blood cholesterol level are exercise, diet, and drugs.

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Exercise and the Heart

  • Sustained exercise increases oxygen demand in muscles.
  • Benefits of aerobic exercise (any activity that works large body muscles for at least 20 minutes, preferably 3-5 times per week) are;
    • increased cardiac output
    • increased HDL and decreased triglycerides
    • improved lung function
    • decreased blood pressure
    • weight control.

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Coronary Artery Disease

  • Heart muscle receiving insufficient blood supply
    • narrowing of vessels---atherosclerosis, artery spasm or clot
    • atherosclerosis--smooth muscle & fatty deposits in walls of arteries
  • Treatment
    • drugs, bypass graft, angioplasty, stent

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Clinical Problems

  • MI = myocardial infarction
    • death of area of heart muscle from lack of O2
    • replaced with scar tissue
    • results depend on size & location of damage
  • Blood clot
    • use clot dissolving drugs streptokinase or t-PA & heparin
    • balloon angioplasty
  • Angina pectoris----heart pain from ischemia of cardiac muscle

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By-pass Graft

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Percutaneous Transluminal Coronary Angioplasty

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Stent in an Artery

  • Maintains patency of blood vessel