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
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