CARDIOVASCULAR SYSTEM OVERVIEWclasspages.warnerpacific.edu/BDupriest/BIO 420/Unit 2...

CARDIOVASCULAR SYSTEM

OVERVIEW

Primary components

Primary functions

Primary methods of

regulation

1

Heart Tissue Layers

2

Fibrous

pericardium

Epicardium

Myocardium

Endocardium

Pulmonary

trunk

Heart chamber

Pericardium

Myocardium

Cardiac Muscle

Syncytium

Atrial vs. ventricular

Intercalated discs

Gap junctions

Fig. 9-2 3

Cardiac Muscle

4

Action Potentials in Cardiac Muscle

Voltage gated fast Na+ channels activated

5 Fig. 9-3

Na+/Ca2+ channels close; K+ permeability

increases

Ion restoration

Na+ / K + ion pump

Ca2+ pumps

Na+ channels inactivated; slow Ca2+ channels

activated; K+ permeability decreases

Membrane Permeability to Na+, K+, Ca2+

6

Transverse Tubule Role

7

Ca2+ enters via T-tubule

Activates calcium release channels in SR

Ryanodine receptor channels

Strengthens contractions

True or false: APs in cardiac muscle are the

same as those in neurons and skeletal muscle.

A) True

B) False

8

Which of these characteristics of cardiac

muscle allow for near-simultaneous contraction

of all cardiomyocytes?

A) AP plateau

B) Gap junctions syncytium

C) Ryanodine receptors

D) Drop in permeability to K+

9

Cardiac Cycle

Fig. 9-5 10

True or false: Isovolumic contraction and

isovolumic relaxation involve rapid increases

and decreases in pressure, respectively.

A) True

B) False

11

Regulation of Heart Pumping

Frank-Starling Mechanism (intrinsic

regulation)

Increased inflow increased output

Stretch-mediated contraction of cardiomyocytes

12

Regulation of Heart Pumping

Autonomic Control of Heart Pumping

Chronotropy vs. Inotropy

Sympathetic vs. parasympathetic

Cardiovascular center of medulla oblongata

13

Fig 9-11

Sympathetic Regulation

14

Cardioacceleratory center

Increases Heart Rate

SA discharge & conduction

Increases inotropy

Overall increase in cardiac output: >100%

CO = HR * SV

Parasympathetic Regulation

15

Cardioinhibitory center

Vagus nerve

Vagal tone

Decreases SA rhythm & AV excitability

Autonomic Regulation

Fig. 9-11

Effect on cardiac output

with

sympathetic

stimulus

with

parasympathetic

stimulus

16

Chemical Regulation of Heart Pumping

Ions

Potassium (K+) Excess

Decreases heart rate (depolarization)

Blocks conduction

Weakens heart

Calcium (Ca2+) Excess

Spastic contractions

Involvement in myofilament contraction

17

Which of the following is not an example of

extrinsic regulation?

A) Sympathetic control of heart rate

B) Vagal tone in heart rhythm

C) Excess K+ ions in extracellular fluid

D) Frank-Starling mechanism

18

CARDIOVASCULAR SYSTEM

ELECTRICAL CONDUCTION

Rhythmical Excitation of the Heart

Electrical Conduction System

19

Establishment of Heart Rate

Intrinsic cardiac conduction system

Autorhythmic cells (self-exciting)

Non-contractile

Relay action potentials

Spontaneous depolarization

Unstable resting potentials

20

Spontaneous Depolarization

Leaky Na+ channels: unstable resting potential

Na+ continually leaks in (K+ outflow reduced)

Reaches threshold

Fast Na+ & Ca2+ channels open

Repolarization

K+ permeability, Na+ & Ca2+ permeability

Fig. 10-2

21

Autorhythmicity of certain cardiac cells is due

primarily to which ions channels?

A) Ca2+

B) Cl -

C) K+

D) Na+

22

Intrinsic Cardiac Conduction System

Sinoatrial (SA) node

Depolarization rate 70-80x/min: Pacemaker

R atrium L atrium via gap junctions

R atrium AV node via internodal pathways

Fig. 10-1 23

Intrinsic Cardiac Conduction System

Atrioventricular (AV) node

Brief signal slowing

Autorhythmic (40-60x/min)

24 Fig. 10-1

Intrinsic Cardiac Conduction System

Atrioventricular bundle

Bundle of His

Only “electrical” connection between atria &

ventricles

25

Fig. 10-1

Atrioventricular Junction & Conduction Delay

Fig. 10-3

26

Intrinsic Cardiac Conduction System

Bundle branches (L & R)

27

Fig. 10-1

Intrinsic Cardiac Conduction System

Purkinje fibers

Large fibers / fast transmission

Contraction direction: apex atria

Autorhythmic (15-40x/min)

28 Fig. 10-1

Intrinsic Conduction Rates

Total conduction time 0.22

sec

SA node AV node

0.03 sec

AV node AV bundle

0.04 sec delay

Allows atria to

contract 0.16 sec

before ventricles

AV bundle through

ventricles

0.03 - 0.06 sec

Fig. 10-4

29

Electrical signals move from the atria to the

ventricles via which of these structures?

A) SA node

B) AV node

C) AV bundle

D) Bundle branches

30

CARDIOVASCULAR SYSTEM

ELECTROCARDIOGRAMS

31

Electrocardiograms (ECG/EKG)

Graphical recording of electrical changes

during heart activity

Heart generates electrical currents

Transmitted through body

Monitor to evaluate heart function

See Fig. 11-1

32

Electrocardiogram & Voltage

Fig. 11-2 33

Normal Electrocardiogram

P wave

Electrical potential from depolarization of atria

~0.1-0.3 mV; PQ interval ~ 0.16s

Fig. 11-1 34

Normal Electrocardiogram

QRS wave

Electrical potential from

depolarization of ventricles

~ 1 mV; RR interval ~0.83s, ~72bpm

35 Fig. 11-1

Normal Electrocardiogram

T wave

Electrical potential from repolarization of

ventricles

Slower less amplitude than QRS

~ 0.2-0.3 mV; QT interval ~0.35s

36 Fig. 11-1

Ventricular vs. ECG Potentials

Fig. 11-3

37

Current Flow Around the Heart

Ventricles provide greatest influence

Ventricular septum 1st to depolarize; outer

ventricular walls last Fig. 11-5

38

Current Flow & Voltage

Fig. 11-4

39

Measurements Using Bipolar Limb Leads

Bipolar = electrocardiogram recorded

from 2 electrodes on different sides of

heart

Fig. 11-6 40

Measurements Using Bipolar Limb Leads

Based on work of Einthoven

Einthoven’s triangle

Einthoven’s law

41

Fig. 11-6

Chest (Precordial) Leads

Six standard chest leads

Leads very close to heart

surface

Useful for identifying

ventricular abnormalities

Attached to positive terminal

Measure one lead at a time

RA, LA, LL all attached to

negative terminal

Fig. 11-8,9 42

Cardiac Arrhythmias

Arrhythmia = abnormal rhythm of the heart

Typically due to defects in cardiac

conduction system

43

Abnormal Sinus Rhythms

Tachycardia

Increased heart rate (>100-150 bpm)

Causes

Sympathetic stimulation

Increased body temp (fever)

Increased metabolism

18 beats / °C

Fig. 13-1 44

Abnormal Sinus Rhythms

Bradycardia

Depressed heart rate <60 bpm)

Causes

Increased heart strength (fitness)

Larger stroke volume per beat fewer beats

required

Vagal stimulation (parasympathetic)

Fig. 13-2 45

Abnormal Rhythms from Conduction System

Blockages

Sinoatrial (SA) block

Prevents atrial contraction

Loss of P wave

AV node sets rhythm

Decreased heart rate

Fig. 13-4 46

Abnormal sinus rhythm looks like what on an

ECG?

A) Long R-R intervals

B) Long Q-T intervals

C) Short Q-T intervals

D) Irregular R-R intervals

47

Atrioventricular (AV) block

Causes

Ischemia of AV node or bundle fibers

Lack of blood (coronary insufficiency)

Compression of AV bundle

Scarring

Inflammation of AV node or bundle

Depresses conductivity

Extreme vagal stimulation

Abnormal Rhythms from Conduction System

Blockages

48

Abnormal Rhythms from Conduction System

Blockages

Atrioventricular (AV) block

Effects

First degree blockage

Increased P-R interval

Fig. 13-5 49

Abnormal Rhythms from Conduction System

Blockages

Atrioventricular (AV) block

Effects

First degree blockage

Second degree blockage

Dropped beats

Fig. 13-6 50

Abnormal Rhythms from Conduction System

Blockages

Atrioventricular (AV) block

Effects

First degree blockage

Second degree blockage

Third degree (complete) blockage

Dissociation of P-QRS complex

Ventricles contract at slower rate (AV pace)

Fig. 13-7 51

Ventricular Fibrillation

Uncoordinated signals

Out-of-sequence / incomplete contractions

Large areas contracting simultaneously

Blood not pumped

Typically fatal if not stopped within 2-3 min

Typical causes

Electrical shock

Ischemia of heart muscle

Fig. 13-16 52

Ventricular Fibrillation

Defibrillation

Apply electric shock (~100 V AC or 1000 V DC)

Simultaneously depolarize entire myocardium

Interrupt twitching and reestablish sinus rhythm

Fig. 13-17 53

Which condition could cause death fastest if left

untreated?

A) Atrial fibrillation

B) Ventricular fibrillation

C) Bradycardia

D) Tachycardia

54

CARDIOVASCULAR SYSTEM

INTRODUCTION TO CIRCULATION

55

Circulation

Blood distribution

Cross sectional areas

Arterial

~62.5 cm2

Capillaries

~2,500 cm2

Venous

~338 cm2

Fig. 14-1 56

Circulation

Arterial system

Elastic

Expand and recoil

Conductance vessels

Aorta, large arteries

Resistance vessels

Small arteries, arterioles

Regulate flow

57

Arterial System

58

Circulation

Venous system

Capacitance vessels

Accommodate blood volume

Major blood reservoir

59

Venous System

60

Venous Valves

Fig. 15-11 61

Circulation

Capillaries Site of exchange

Fluids, nutrients, ions, wastes, etc.

Simple squamous epithelium

Continuous vs. fenestrated vs. sinusoidal

62

Circulation

Capillary beds

Flow regulated through sphincter muscles

Allow shunting of blood to areas needed

Autonomic control

See Fig. 17-3 63

Which layer is common to arteries, veins, and

capillaries?

A) Internal elastic lamina

B) External elastic lamina

C) Tunica externa

D) Endothelium

64

Blood Pressure

Fig. 14-2

65

Circulatory Biophysics

Flow is proportional to the

Change in Pressure / Resistance

66

Fig. 14-3

Resistance vs. Conductance

Fig. 14-8

67

Flow = p*DPressure*r4

8*viscosity*length

Poiseuille’s Law

pDPr4

8hl Flow =

Blood Pressure

Relationship between vessel area, flow rate

and pressure

CS area Flow Rate Mean Pressure

Vessel (cm2) (cm/sec) (mmHg)

Aorta 2.5 33 100

Capillaries 2,500 0.03 17

Vena cava 8 10 0

Fig. 14-9

68

Types of Flow

Fig. 14-2

69

Turbulent flow

Laminar flow

Turbulence = Velocity * diameter * density

viscosity

Turbulence = ndr

h

Resistance in Series vs. Parallel Circuits

Fig. 14-9

70

Rtotal = R1 + R2 + R3 + R4…

Series

Parallel

Series

Parallel 1

Rtotal

1

R1

1

R2

1

R3

1

R4 + + + =

Autoregulation

Attenuates effect of arterial pressure on

tissue blood flow (perfusion)

Involves locally acting factors

Metabolic theory

Myogenic theory

71

Vascular Distensibility & Compliance

Distensibility = ability to expand and

accommodate increased pressure or volume

VD =

Veins ~8x more distensible than arteries

Thinner / weaker walls

Can expand and accommodate more volume

72

D Volume

D Pressure * Initial Volume

Vascular Distensibility & Compliance

Compliance (capacitance) = total quantity of

blood that a given portion of the circulation

can store

VC =

Veins more compliant than corresponding arteries

Greater distensibility (~8x) and larger volume

(~3x) ~24x more compliant

73

D Volume

D Pressure

Vascular Distensibility & Compliance

Volume-pressure curves: Arterial vs. venous

See Fig 15-1 (ELMO/textbook)

74

Vascular Distensibility & Compliance

Delayed compliance

Stress-relaxation of vessels

75

Pulse Pressure

Arterial pressure pulsations

Pulse pressure = Systolic BP – Diastolic BP

Stroke volume & compliance

76

Fig. 15-4

Pulse Pressure Damping

77

Fig. 15-6

Venous Pressure

78

Fig. 15-10

Fig. 15-9

Regulation of Blood Pressure

79

Blood Pressure

Force exerted on the wall of a blood vessel by the blood within it

MAP = CO x TPR

Where:

MAP = Mean Arterial Pressure, mmHg

CO = Cardiac Output, mL/min

TPR = Total Peripheral Resistance (units?)

80

Regulation of Blood Pressure and Flow

Approaches to control

Alter blood distribution

Alter vessel diameter

Timing of control

Acute

Long-term

Mechanisms of control

Local, humoral, nervous, kidney

81

Fig. 14-13

Local Control of Blood Flow

Local metabolic rate drives blood flow

82

Fig. 14-13

Local Control of Blood Flow

Metabolic control

Oxygen lack theory

Vasodilator theory

Adenosine?

Endothelial-derived factors

Nitric oxide

Endothelin

83

Local Control of Blood Flow

Long-term regulation

Tissue vascularity (Fig 17-6: ELMO/textbook)

84

Acute local control of blood pressure and flow

can be accomplished by all of the following

except:

A) Nitric oxide

B) Metabolic control (autoregulation)

C) Increased vascularity of tissue

D) Endothelin

85

Humoral Control of Blood Pressure

Vasoconstrictor agents

Norepinephrine (1°) & epinephrine

HR & BP (vasoconstriction by stimulation of receptors)

Epinephrine may cause vasodilation (vessels with receptors)

E.g., coronary arteries

Antidiuretic hormone (ADH; vasopressin)

Angiotensin II

Endothelin

86

Humoral Control of Blood Pressure

Vasodilator agents

Bradykinin

Arteriolar dilation

Increased capillary permeability

Histamine

Released due to tissue damage or allergic reaction

Mast cells and basophils

Arteriolar dilation

Incr. capillary permeability

87

Humoral Control of Blood Pressure

Misc. ions & compounds

Ca2+

Stimulates smooth muscle contraction

vasoconstriction

K+

Inhibits smooth muscle contraction

vasodilation

H+ (pH)

[ H+ ] or intense [ H+ ] causes vasodilation

88

True or false: Humoral control of blood

pressure and flow is usually specific to one

particular capillary bed.

A) True

B) False

89

Nervous Regulation of Blood Pressure

Vasomotor center

Controls HR and vascular constriction

Part of cardiovascular center

Inferior pons and reticular substance of medulla

Fig. 18-1

90

Vasomotor Center

Vasoconstrictor area

Sympathetic impulses to

systemic blood vessels

Innervates nearly all blood

vessels except

capillaries

Sets “sympathetic tone” of

blood vessels

(vasomotor tone)

91

Fig. 18-1

Vasomotor Center

Vasomotor tone

92

Fig. 18-4

Vasomotor Center

Vasodilator area

Fibers project into

vasoconstrictor area and

inhibit vasoconstrictor

activity

93

Fig. 18-1

Vasomotor Center

Sensory area

Sensory signals from

vagus and

glossopharyngeal nerves

Role in reflex control

94

Fig. 18-1

Vasomotor Center

Input from higher brain areas

95

Fig. 18-3

The primary part of the cardiovascular control

center responsible for vasomotor tone is the…

A) Cardioacceleratory center

B) Vasoconstrictor area

C) Vasodilator area

D) Sensory area

96

Rapid Control: Baroreceptor Reflexes

Detects & responds to short-term BP changes

Fig. 18-5

97

Baroreceptor Reflexes

Effect of baroreceptors

98

Fig. 18-7

Baroreceptor Reflexes

Effect of baroreceptor denervation

99

Fig. 18-8

Bainbridge Reflex

Increased atrial pressure stretches SA node

Direct result - increased HR (10-15%)

Increases SA depolarization rate

Indirect result - Bainbridge reflex

Stimuli sent from SA node through vagal afferents

to medulla

Stimuli from medulla sent through vagal and

sympathetic efferents back to SA node

Increases HR (40-60%)

Helps prevent damming of blood in veins,

atria, pulmonary circulation

10

0

The Bainbridge reflex sensors are located in

the…

A) Carotid sinus

B) Right atrium

C) Aortic arch

D) All of the above

101

Kidney Regulation of Arterial Pressure

Renal-body fluid system for arterial pressure

regulation

Fig. 19-6 102

Renal Output Curve

Fig. 19-1 103

Pressure diuresis

Pressure natriuresis

Kidney Regulation of Arterial Pressure

Fig. 19-2 104

Kidney Regulation of Arterial Pressure

Water/salt output must equal water/salt intake

Infinite feedback gain principle

Fig. 19-3 105

Infinite Feedback Gain Principle

Example: increased arterial pressure H2O/Na+ intake remains constant but arterial

pressure increases

Renal output increases due to increased

pressure

Body will lose fluids/salts (blood volume drops)

until pressure returns to equilibrium

Fig. 19-3 106

1

2

Infinite Feedback Gain Principle

Example: decreased arterial pressure H2O/Na+ intake remains constant but arterial

pressure decreases

Renal output decreases due to decreased

pressure

Blood volume will rise (reabsorption) to bring

pressure back to equilibrium

107 Fig. 19-3

Long-term Changes to Arterial Pressure

Renal output

Abnormal kidney

function

Salt/water intake

Fig. 19-4

108

Kidneys respond to increased mean arterial

pressure by…

A) Increasing urine volume (urine output)

B) Reducing urine volume (urine output)

C) Increasing urine osmolality

D) Decreasing urine osmolality

109

The physiological basis for the result of the

previous question is that higher arterial

pressure causes…

A) increased filtration

B) reduced reabsorption

C) increased secretion of sodium, with water

following by osmosis

D) all of the above

110

Hypertension

High blood pressure

Mean arterial pressure > 110

Systolic pressure > 135

Diastolic pressure > 90

May lead to shortened life expectancy

Excess workload on heart

Vessel rupture (stroke)

Kidney damage - glomerulosclerosis (failure)

111

Hypertension

Volume-loading hypertension

Excess accumulation of extracellular fluids due to…

Decreased renal mass

Increased salt levels

112

Volume-loading Hypertension

Fig. 19-9 113

Pressure Control via Renin-Angiotensin System

Fig. 19-10 114

Pressure Control via Renin-Angiotensin System

Effect of angiotensin II

Vasoconstricting agent

Direct action on kidney

Salt & water retention

Indirect action on kidney

Stimulates aldosterone release from adrenal

cortex

Increases salt & water retention by kidneys

Fig. 19-10 115

Pressure Control via Renin-Angiotensin System

Effect of angiotensin levels

Fig. 19-11 116

“The College Try”

The pepperoni pizza challenge (increased Na+

intake)

Relative to infinite feedback gain principle

Fig. 19-3 117

“The College Try”

The pepperoni pizza challenge (increased Na+

intake)

Relative to infinite feedback gain principle

Relative to the renin-angiotensin mechanism

Fig. 19-12 118

What is the primary controller of long-term

arterial pressure?

A) Local factors

B) Humoral factors

C) Nervous system

D) Kidneys

119

What is the primary controller of short-term

arterial pressure?

A) Local factors

B) Humoral factors

C) Nervous system

D) Kidneys

120

What is the primary controller of short-term

capillary bed blood flow?

A) Local factors

B) Humoral factors

C) Nervous system

D) Kidneys

121

Coronary Circulation

122

Ischemic Heart Disease

Atherosclerosis

Cholesterol deposited beneath arterial endothelium forms plaques Fibrous tissue invasion; calcification

Protrude into lumen and restrict blood flow

May rupture: Rough surfaces cause clots

Thrombus vs. embolus

Common sites Coronary arteries

123

Ischemic Heart Disease

May lead to myocardial infarction

Infarction = sudden loss in blood flow to point

where myocardial cells cannot sustain function

Acute infarction

Tissue recovery

Zones surrounding

point of occlusion

Replacement of dead

cells with fibrous tissue

Hypertrophy of healthy tissue

Ischemia/reperfusion injury

Fig. 21-8

124

Ischemic Heart Disease

Accommodation by collateral coronary

circulation

Form anastomoses

Fig. 21-6 125

Ischemic Heart Disease

Major causes of death after acute infarction

Decreased cardiac output

Peripheral ischemia (cardiac shock)

May involve systolic stretch

Fig. 21-7 126

Ischemic Heart Disease

Major causes of death after acute infarction

Decreased cardiac output

Blood damming in venous system

Inefficient pumping of heart

Leads to pulmonary edema

Plasma from pulmonary capillaries perfuses

into alveoli

Decreased O2/CO2 exchange

Tissues (heart) weaken

127

Ischemic Heart Disease

Major causes of death after acute infarction

Decreased cardiac output

Blood damming in venous system

Rupture of infarcted areas

Dead tissues degenerate, weaken, rupture

128

Ischemic Heart Disease

Major causes of death after acute infarction

Decreased cardiac output

Blood damming in venous system

Rupture of infarcted areas

Fibrillation

129

What do all the four causes of death following

myocardial ischemia have in common?

A) They all can only result from

atherosclerosis developing over time.

B) They all involve weakening or death of

cardiomyocytes.

C) They all involve other organs (lungs,

kidneys)

130