CARDIOVASCULAR SYSTEM OVERVIEW

CARDIOVASCULAR SYSTEM
OVERVIEW

Primary components

Primary functions

Primary methods of
regulation
1
Heart Tissue Layers
Pulmonary
trunk
Fibrous
pericardium
Pericardium
Myocardium
Epicardium
Myocardium
Endocardium
Heart chamber
2
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
Na+ channels inactivated; slow Ca2+ channels
activated; K+ permeability decreases
Na+/Ca2+ channels close; K+ permeability
increases
Ion restoration

Na+ / K + ion pump

Ca2+ pumps
Fig. 9-3
5
Membrane Permeability to Na+, K+, Ca2+
6
Transverse Tubule Role

Ca2+ enters via T-tubule

Activates calcium release channels in SR


Ryanodine receptor channels
Strengthens contractions
7
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
Fig 9-11
13
Sympathetic Regulation

Cardioacceleratory center

Increases Heart Rate

SA discharge & conduction

Increases inotropy

Overall increase in cardiac output: >100%

CO = HR * SV
14
Parasympathetic Regulation

Cardioinhibitory center

Vagus nerve

Vagal tone

Decreases SA rhythm & AV excitability
15
Autonomic Regulation

Effect on cardiac output


 with
 sympathetic
stimulus
 with
 parasympathetic
stimulus
Fig. 9-11
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)
Fig. 10-1
24
Intrinsic Cardiac Conduction System

Atrioventricular bundle


Bundle of His
Only “electrical” connection between atria &
ventricles
Fig. 10-1
25
Atrioventricular Junction & Conduction Delay
Fig. 10-3
26
Intrinsic Cardiac Conduction System

Bundle branches (L & R)
Fig. 10-1
27
Intrinsic Cardiac Conduction System

Purkinje fibers

Large fibers / fast transmission

Contraction direction: apex  atria

Autorhythmic (15-40x/min)
Fig. 10-1
28
Intrinsic Conduction Rates

Total conduction time 0.22
sec

SA node  AV node


AV node  AV bundle



0.03 sec
0.04 sec delay
Allows atria to
contract 0.16 sec
before ventricles
AV bundle  through
ventricles

Fig. 10-4
0.03 - 0.06 sec
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
Fig. 11-1
35
Normal Electrocardiogram

T wave

Electrical potential from repolarization of
ventricles

Slower  less amplitude than QRS

~ 0.2-0.3 mV; QT interval ~0.35s
Fig. 11-1
36
Ventricular vs. ECG Potentials
Fig. 11-3
37
Current Flow Around the Heart


Ventricles provide greatest influence
Ventricular septum 1st to depolarize; outer
Fig. 11-5
ventricular walls last
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
Fig. 11-6
41
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
Abnormal Rhythms from Conduction System
Blockages

Atrioventricular (AV) block

Causes

Ischemia of AV node or bundle fibers


Compression of AV bundle


Scarring
Inflammation of AV node or bundle


Lack of blood (coronary insufficiency)
Depresses conductivity
Extreme vagal stimulation
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


Capillaries


~62.5 cm2
~2,500 cm2
Venous

~338 cm2
Fig. 14-1
56
Circulation

Arterial system

Elastic


Conductance vessels


Expand and recoil
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
Fig. 14-3
66
Resistance vs. Conductance
Fig. 14-8
Poiseuille’s Law
Flow =
p*DPressure*r4
8*viscosity*length
4
pDPr
Flow =
8hl
67
Blood Pressure

Relationship between vessel area, flow rate
and pressure
Vessel
Aorta
CS area
Flow Rate
(cm2)
(cm/sec)
Mean Pressure
(mmHg)
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
Laminar flow
Turbulent flow
Turbulence =
Velocity * diameter * density
viscosity
ndr
Turbulence =
h
69
Resistance in Series vs. Parallel Circuits
Fig. 14-9
Series
Parallel
Series
Parallel
Rtotal = R1 + R2 + R3 + R4…
1
Rtotal
1 + 1 + 1 + 1
= R
R2 R3 R4
1
70
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
D Volume
D Pressure * Initial Volume

VD =

Veins ~8x more distensible than arteries

Thinner / weaker walls

Can expand and accommodate more volume
72
Vascular Distensibility & Compliance

Compliance (capacitance) = total quantity of
blood that a given portion of the circulation
can store
D Volume
D Pressure

VC =

Veins more compliant than corresponding arteries

Greater distensibility (~8x) and larger volume
(~3x) ~24x more compliant
73
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
Fig. 15-4
76
Pulse Pressure Damping
Fig. 15-6
77
Venous Pressure
Fig. 15-9
Fig. 15-10
78
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
Fig. 14-13
81
Local Control of Blood Flow

Local metabolic rate drives blood flow
Fig. 14-13
82
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+


 K+


Stimulates smooth muscle contraction  
vasoconstriction
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)
Fig. 18-1
91
Vasomotor Center

Vasomotor tone
Fig. 18-4
92
Vasomotor Center

Vasodilator area

Fibers project into
vasoconstrictor area and
inhibit vasoconstrictor
activity
Fig. 18-1
93
Vasomotor Center

Sensory area


Sensory signals from
vagus and
glossopharyngeal nerves
Role in reflex control
Fig. 18-1
94
Vasomotor Center

Input from higher brain areas
Fig. 18-3
95
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
Fig. 18-7
98
Baroreceptor Reflexes

Effect of baroreceptor denervation
Fig. 18-8
99
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
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

Pressure diuresis

Pressure natriuresis
Fig. 19-1
103
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
2
1
Fig. 19-3
106
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
Fig. 19-3
107
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
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Ischemic Heart Disease

Major causes of death after acute infarction

Decreased cardiac output

Blood damming in venous system

Rupture of infarcted areas

Fibrillation
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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)
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