Download Heart Ch 18-PPT-STUDENT-2015

Document related concepts

Heart failure wikipedia , lookup

Management of acute coronary syndrome wikipedia , lookup

Cardiac contractility modulation wikipedia , lookup

Hypertrophic cardiomyopathy wikipedia , lookup

Artificial heart valve wikipedia , lookup

Coronary artery disease wikipedia , lookup

Lutembacher's syndrome wikipedia , lookup

Mitral insufficiency wikipedia , lookup

Cardiac surgery wikipedia , lookup

Myocardial infarction wikipedia , lookup

Quantium Medical Cardiac Output wikipedia , lookup

Electrocardiography wikipedia , lookup

Atrial fibrillation wikipedia , lookup

Arrhythmogenic right ventricular dysplasia wikipedia , lookup

Dextro-Transposition of the great arteries wikipedia , lookup

Heart arrhythmia wikipedia , lookup

Transcript
THE CIRCULATORY SYSTEM
 Ch. 18 The HEART
PARTS OF THE CARDIOVASCULAR SYSTEM
 1.
2.
3.
I. Heart Anatomy
A. Size, Location, and Orientation
 Size:
STUDY QUESTION EXAMPLES:
1. Describe the Heart’s Size, Location,
 Location:
Orientation, Coverings, and Wall Layers
 Orientation of Apex & Base
Midsternal line
2nd rib
Sternum
base
Diaphragm
apex
Point of
maximal
intensity
(PMI)
B. Coverings of the Heart
 2A Review
Serous Membranes
- P_________
- V_________
- for Heart named:
Cavity
- in M__________
B. Coverings of Heart …
1. Pericardium = double-walled sac
Outer
Sac
Inner
Sac



Fibrous pericardium – Function:
Parietal pericardium
Visceral Pericardium
= epicardium =
 Serous fluid:
Figure 11.1a–b
The Heart = pump of the cardiovascular system
Superior
vena cava
Aorta
Parietal
pleura (cut)
Pulmonary
trunk
Left lung
Pericardium
(cut)
Diaphragm
Apex of
heart
(c)
Figure 18.1c
C. Layers of the Heart Wall
1. Epicardium
2. Myocardium
 Connective tissue:
3. Endocardium – endothelium
Figure 11.2b
D. Fibrous Skeleton of Heart
 Layer Within:
2. What is the Fibrous Skeleton
and what is its purpose?
 Connective Tissue
 Anchors:
 Supports:
 Electrical
Characteristics:
 Conduction ?:
 Importance:
Cardiac
muscle
bundles
E. Chambers and Associated Great Vessels
Overview
 Atria:
 Auricles
 Ventricles:
 Interatrial Interventricular
Septum
 Sulci
 Coronary Sulcus
 Anterior Interventricular
Sulcus
 Posterior Interventricular
Sulcus
E. Chambers and Associated Great Vessels …
1. Atria
 Pectinate Muscles
 Fossa Ovalis
 Foramen Ovale
 Right
 Superior Vena
Cava
 Inferior Vena Cava
 Coronary Sinus
 Left
 Pulmonary
Veins
3. Give the general function of the atria and state
which blood vessels connect to them. Include a
description of the Foramen Ovale.
2. Ventricles – 2 pumps
4. …
• Right vs. Left
• Shapes:
• Thickness
• Trabeculae carneae
• Papillary Muscles
• Right: Pulmonary Trunk 
• Left: Aorta & Coronary Arteries
Figure 11.4
F. Pathway of Blood Through
the Heart
1. 2 PUMP SYSTEM with two
circulations
 Blood Flow Direction:
a. Pulmonary Circulation:
b. Systemic Circulation:
2. Blood Vessels in Pathway
5. Describe the path a blood cell would take
starting with the Right Atria and ending back at
the RA.
6. Explain how the heart is like 2 pumps.
G. Coronary Circulation
 Heart muscle has lots o’
mitochondria,
 can burn:
 O2 supply:
 uses how much blood:
 VESSELS:
- Coronary Arteries
- Cardiac Veins
Figure 11.2a
G. Coronary Circulation …
2. Coronary Arteries:
a. Branch from:
b. Function
3. Left Coronary Artery & Branches
4. Right Coronary Artery & Branches
Right
coronary
artery
Right
marginal
artery
Posterior
interventricular
artery
Aorta
Left
coronary
artery
Circumflex
artery
Anterior
interventric
artery
Figure 18.7a
G. Coronary Circulation …
5. Cardiac Veins
- Function
- Coronary Sinus
Superior
vena cava
Anterior
cardiac
veins
Aorta
Pulmonary
Trunk
Great
cardiac
vein
Coronary
sinus
Small cardiac vein
Middle cardiac vein
(b) The major cardiac veins
Figure 18.7b
6. Homeostatic Imbalances
STUDENTS DO
 Angina pectoris
 Myocardial Infarction (heart attack)
H. FETAL CIRCULATION
 Foramen Ovale
 Fossa Ovalis
 Ductus Arteriosis
 Ligamentum Arteriosum

Umbilical Cord:
I. Heart Valves
1. Function: prevent backflow of blood
2. Atrioventricular (AV) valves—between ________________
 Bicuspid (mitral) valve __________ side
 Tricuspid valve ___________side
 Parts: Cusps, Chordae Tendinae, Papillary muscles
 When ventricles contract:
H. Heart Valves …
 Parts
 Cusps
 Chordae Tendinae
 Papillary muscles
Operation of the AV valves
Returning blood fills
relaxed atria and
ventricles (open AV
valves)
AV valves open
Ventricles
(a)
Figure 11.5a, step 1
Operation of the AV valves
Returning blood
fills relaxed atria
and ventricles
(open AV valves)
Atria contract –
more blood forced
into ventricles
AV valves open
Relaxed
Ventricles
(a)
Figure 11.5a, step 2
Operation of the AV valves
Chordae tendineae
prevent valve flaps
from everting
3. Ventricles contract,
blood forced
against AV flaps / into
arteries
4. AV valves close
preventing backflow
to atria (LUB of LUBdup sound)
(a)
Figure 11.5a, step 4
H. Heart Valves …
3. Semilunar valves
Function:
 Pulmonary semilunar valve – ____side
 Aortic semilunar valve – ______side
3 cusps each
 When Ventricles contract:
Figure 11.2c
Operation of the semilunar valves
Aorta
Pulmonary
trunk
As ventricles contract
semilunar valves are
forced open
Semilunar valve
open
(b)
Figure 11.5b, step 1
Operation of the semilunar valves
All this to ensure that…
Aorta
Pulmonary
trunk
Semilunar valve
open
(b)
As ventricles relax, blood
flows back from arteries,
forcing semilunar valves
to close
‘dup’ of LUBdup sound
Semilunar valve
closed
Figure 11.5b, step 2
II. Cardiac Muscle Fibers
A. Microscopic Anatomy
* Review Skeletal Muscles
A. Microscopic Anatomy …
1. Cardiac muscle cell characteristics:
2. Endomysium anchored to:
3. T tubules:
and No
4. SR:
. Source of Ca+2:
.
.
5. Mitochondria:
Intercalated
disc
Cardiac
muscle cell
Mitochondrion
T tubule
Mitochondrion
Sarcoplasmic
reticulum
Z disc
Nucleus
Sarcolemma
A. Microscopic Anatomy …
6. Intercalated discs =
7. Functional Syncytium:
 Autorhythmic Cells =
 Function:
8. Long Absolute Refractory Period
 Function:
Intercalated discs
Gap junctions
Desmosomes
B. Mechanism and Events of Contraction
 AP in Skeletal Muscle Cells– review
Skeletal Fiber
Cardiac Cells
Action
Potential
Plateau
Muscle
Tension
B. Mechanism and Events of Contraction …
1. Stimulus: comes from Autorhythmic Cells 
Pacemaker Potential
2. Action Potential
a. Depolarization in Cardiac Muscle Cells 1 in figure
i) Na+ channels open
ii) slow Ca2+ channels open 
iii) Influx of extracellular Ca2+ causes
Na+
Slow Ca2+
Ca2+
2. Action Potential …
a. Depolarization in Cardiac Muscle Cells …
iv) Contraction begins
v) Plateau Phase
2
in figure
 Ca+ channels slow to
close:
 Contraction
 K+ channels closed
Figure 18.12 AP in Cardiac
Muscle Cells
3
/Contraction
Cardiac
Muscle
b. Repolarization
 Ca channels close
 K+ channels open
 Ca+ pumped back to SR
and extracellular
 Muscle Contraction ends
d. Hyperpolarization– none
e. Energy: almost exclusively
and depends on
.
.
Respiration
III. Heart Physiology
A. Electrical Events: Heart Activity
1. Setting the Basic Rhythum
SA Node
a. Not Dependent on:
b. Intrinsic Ability Due to:
i) ___________Junctions
ii) Intrinsic Conduction System with
Autorhythmic Cells
c. Intrinsic Conduction System
 = Autorhythmic Cells: NonContractile; all linked together
 Functions:
i)
ii)
AV Node
III. Heart Physiology …
A. Electrical Events: Heart Activity
…
d. AP initiation by Autorhythmic Cells SA Node
i) Unstable Resting Potential Causes
 During Hyperpolarization: None
Na+ Channels:
 Speed of initial Depolarization:
AV Node
3
3
2
1
2
1
AP in Autorythmic Cells …
ii) At Threshold get Fast Depolarization = Pacemaker
Potential:
 AP triggered
iii) Repolarization
Ca close & K
open
3
3
iv) Repeat a-b-d
2
1
2
1
Heart Physiology …
Autorhythmic Cells …
Figure 18.13 Action Potentials of
Autorhythmic Cells
Threshold
Action
potential
Ca2+
channels
open
2
2
3
1
1 Pacemaker potential
Slow depolarization due to
opening of Na+channels and
closing of K+ channels.
Membrane potential is never
a flat line.
Na+
channels
open
2
3
1
Pacemaker
potential
Depolarization Action
potential begins when
pacemaker potential reaches
threshold. Depolarization
due to Ca2+ influx through
Ca2+ channels.
3 Repolarization due to Ca2+
channels inactivating and K+
channels opening. This allows K+
efflux, brings membrane potential
back to its most negative voltage.
 REVIEW– Action Potentials
 Autorhythmic Cells
 Slow Na Channels open = Pacemaker Potential
 Threshold: fast Depolarize = due to Ca+ coming in
from outside
 AP triggered
 Repolarization: as normal &
then Na Channels open
 Cardiac Muscle Cells
 Na+ Channels open
 Depolarization Ca+ Channels open let Ca in from
outside  Triggers Action Potential
 Plateau Phase: Ca channels slow to close
 Repolarization: as normal and
Na channels closed
 Hyper: none
2. Sequence of Excitation
i)
Sinoatrial (SA) node– Function:
 Normal75 beats/min = Sinus Rhythm: Needs help of:
 Intrinsic Rate:
 Moves to:
ii) Atrioventricular (AV) node– functions:
 Location: Interatrial septum, inferiorly and just above Tricuspid
Valve
2. Sequence of Excitation …
iii) Atrioventricular Bundle = AV bundle (bundle of His) 
 Location: Very short in:
iv) Bundle branches: carry impulses what direction:
v) Purkinje fibers:
 Location:
 Function:
Action potential succession during one heartbeat.
Superior vena cava
Right atrium
1 sinoatrial (SA)
node (pacemaker)
generates impulses.
Internodal pathway
2 Impulses
Left atrium
pause (0.1 s) at
atrioventricular
(AV) node.
3 atrioventricular
(AV) bundle
connects atria
to ventricles.
Purkinje
fibers
4 bundle branches
conduct impulses thru
interventricular septum.
5 Purkinje fibers
Interventricular
septum
depolarize contractile
cells of both ventricles.
(a) Anatomy of the intrinsic conduction system showing the
sequence of electrical excitation
Autonomic Innervation of the HEART
 Parasympathetic NS
 Cardioihibitory Center
Vagus
Nerve
Medulla
 Vagus Nerve
 Function:
 Mechanism:
 Sympathetic NS
 Cardioacceleratory Center
 Function:


 Mechanism:
Sympathetic
Cardiac Nerves
Autonomic innervation of the heart.
The vagus nerve
(parasympathetic)
decreases heart rate.
Dorsal motor nucleus of vagus
Cardioinhibitory center
Cardio-acceleratory center
Medulla oblongata
Sympathetic trunk ganglion
Thoracic spinal cord
Sympathetic trunk
Sympathetic cardiac
nerves increase heart rate
and force of contraction.
AV node
SA node
Parasympathetic fibers
Sympathetic fibers
Interneurons
A. Electrical Events …
4. Electrocardiography
= Picks up:
i) Electrodes, Leads: pick up
electrical activity
 Clinically: 12 leads
ii) Electrocardiogram, ECG
or EKG =
 Vertical axis =
 Horizontal axis =
Figure 18.6 Electrocardiogram
An electrocardiogram (ECG a.k.a. EKG) tracing
QRS complex
Sinoatrial
node
Atrial
depolarization
Ventricular
depolarization
Ventricular
repolarization
Atrioventricular
node
P-Q
Interval
S-T
Segment
Q-T
Interval
0.1
Electrocardiography …Waves
R
P-Q
SA node
& Intervals– sequence of
Depolarization
interval
Repolarization
T
P
QS
1
Atrial depolarization, initiated by
the SA node, causes the P wave.
R
AV node
T
P
Q S
2
With atrial depolarization complete,
the impulse is delayed at the AV node.
R
T
P
Q
3
0.1 s just after it
begins, Atria
Contract
S
Ventricular depolarization begins
at apex, causing the QRS complex.
Atrial repolarization occurs.
= P-Q interval (or
P-R interval), begin
atrial excitation to
begin ventricle
excitation; includes
Atrial depolarization
and depolarization
through rest of
conduction pathway
Sequence of deflection waves of an ECG tracing
Depolarization
Repolarization
R
T
P
Q
4
S
Ventricular depolarization is
complete.
= S-T segment,
ventricles completely
depolarized, all cells in
plateau phase
R
T
P
Q
5
S
Ventricular repolarization begins
at apex, causing theQ-T
T wave.
R Segment
T
P
Q-T Segment = Ventricular
6 Ventricular repolarization is Depolarization through
complete.
Ventricular Repolarization
Q
S
An electrocardiogram (ECG a.k.a. EKG) tracing
QRS complex
Sinoatrial
node
Atrial
depolarization
Ventricular
depolarization
Ventricular
repolarization
Atrioventricular
node
P-Q
Interval
S-T
Segment
Q-T
Interval
Begin V. Depolarization to end
V. Repolarization
 Abnormalities in EKG
 Q-T interval: if elongated or shortened  Repolarization
Abnormal
 R: enlarged  Enlarged Ventricles
 S-T segment: if elevated or depressed Cardiac Ischemia
 Normal
Junction Rhythum:
Nonfunctional SA node
 2nd Block: missing P waves
Ventricular Fibrillation
Heart Attack
Electrical Shock
B. Heart Sounds: Valves Students do
Know:
Heart Murmur
Incompetent
Stenotic
Aortic valve sounds heard
in 2nd intercostal space at
right sternal margin
Pulmonary valve
sounds heard in 2nd
intercostal space at left
sternal margin
Mitral valve sounds
heard over heart apex
(in 5th intercostal space)
in line with middle of
clavicle
Tricuspid valve sounds typically
heard in right sternal margin of
5th intercostal space
C. Cardiac Cycle: Mechanical Events
 Systole =
 Diastole =
 BP =
Atrioventricular valves
Aortic and pulmonary valves
Phase
Left atrium
Right
atrium
Left
ventricle
Right
ventricle
Open
Closed
Open
Closed
1
Open
2b
Closed
1
2a
3
Ventricular
Atrial
Isovolumetric Ventricular Isovolumetric Ventricular
ejection
filling contraction contraction
relaxation
filling
phase
phase
1
Ventricular filling
(mid-to-late diastole)
2a
2b
Ventricular systole
(atria in diastole)
3
Early diastole
1. Ventricular Filling
- Valves are:
a. Ventricles are:
- Valves are:
- Pressure is:
- Atria are:
Left atrium
Right atrium
Left ventricle
Right ventricle
Ventricular
filling
Ventricles
and atria fill…
Figure 11.7, step 1a
Cardiac Cycle …
1. Ventricular Filling …
b. late diastole– atria are:
Follows P-wave
Left atrium
Right atrium
Left ventricle
Right ventricle
Ventricular
filling
Atrial
contraction
Atrial systole
1
… then atria contract
Atrioventricular valves
Aortic and pulmonary valves
Phase
Open
Closed
1
Figure 11.7, step 1b
Cardiac Cycle …
2. Ventricular Systole
a. Ventricles:
- Isovolumetric Contraction =
- Pressure:
AND Valves:
- End Diastolic Volume =
b. Ejection Phase:
Atrioventricular valves
Aortic and pulmonary valves
Phase
Closed
Open
2b
2a
Isovolumetric Ventricular
ejection
contraction
phase
phase
2a
2b
Ventricular systole
(atria in diastole)
Stage 2: ventricular systole
Cardiac Cycle …
3. Early Diastole
a. Ventricles completely closed again = -- ------ Isovolumetric Relaxation
- End Systolic Volume =
b. Ventricular filling
- Valves:
Atrioventricular valves
Aortic and pulmonary valves
Phase
Left atrium
Right
atrium
Left
ventricle
Right
ventricle
Open
Closed
Open
Closed
1
Open
2b
Closed
1
2a
3
Ventricular
Atrial
Isovolumetric Ventricular Isovolumetric Ventricular
ejection
filling contraction contraction
relaxation
filling
phase
phase
1
Ventricular filling
(mid-to-late diastole)
2a
2b
Ventricular systole
(atria in diastole)
3
Early diastole
Cardiac Cycle …
Homeostasis– Students Do:
 Tachycardia
 Bradycardia
Figure 11.7, step 3
D. Cardiac Output (CO)
Definition of Terms
- CO = Volume of blood pumped by:
- Stroke Volume (SV) =
HR =
CO = heart rate (HR) x stroke volume (SV)
= 5.25 L/min
- Cardiac Reserve
=
D. Cardiac Output …
Control of CO: 2 methods– SV and HR Regulation
1. Regulation of Stroke Volume to control CO
a. SV = EDV – ESV
(intrinsic factor)
b. Three main factors affect SV
i) Preload (is intrinsic) =
(1) Frank Starling Law of the Heart:
MOST
IMPORTANT
(2) Venous Return:
(MOST IMP FACTOR FOR SV regulation)
↑ Venous Return 
Preload 
contraction 
Ventricular
volume (ml)
(3) Affect of Heart Rate: ↓heart rate  ↑ venous return
EDV
SV
ESV
EDV
Cardiac Output Control … 1. Regulation of SV …
b. Three main factors affect SV …
ii) Contractility –(is extrinsic)
(ALSO IMPORTANT)
 Mechanism:
 Sym. N. S. (Cardioacceleratory Center)
 Ca2+ influx 
(see next slide)
 Hormones: Glucagon, Thyroxine, and Epinephrine all
increase contractility
 + Inotropic Agents =
 - = decreasing contractility
iii) Afterload –
(LOWEST IN IMPORTANCE—mainly affecting unhealthy people)
 ↑ Blood Pressure  ↑ ESV  ↓ SV
 (hypertension = )
Sympathetic input boosts Ca2+ = ↑Contractility = ↑SV
Extracellular fluid
Norepinephrine
Adenylate cyclase
Ca2+
b1-Adrenergic
receptor
G protein (Gs)
Ca2+
channel
ATP is converted
Cytoplasm
to cAMP
a
GDP
Inactive protein
kinase A
Enhanced
actin-myosin
interaction
Troponin
Cardiac muscle
force and velocity
Phosphorylates SR Ca2+ channels,
increasing intracellular Ca2+
b
release
binds Ca2+
to
Active
Phosphorylates
plasma membrane
Ca2+ channels,
increasing extracellular Ca2+ entry
protein
kinase A
Phosphorylates SR Ca2+
pumps, speeding Ca2+
c
removal and relaxation
Ca2+
Ca2+ uptake
pump
SR Ca2+
channel
Sarcoplasmic
reticulum (SR)
Figure 18.21
Overview: Autonomic Control
 Cardiovascular Center in Medulla
 Parasympathetic: Cardioinhibitory Center
normally in control of Heart at rest:
  Vagus nerve (= Vagal Tone)
 Stroke volume controlled by EDV
 Sympathetic:
 Cardioacceleratory Center takes over Heart
during stress and emergencies 
 ↑ HR via stimulation of SA node
 ↑ SV via ↑ Contractility (which ↓ ESV)
 Vasomoter Center-- normally in control of
blood vessel diameter at rest
Factors involved in regulation of cardiac output.
Exercise (by
skeletal muscle and
respiratory pumps;
see Chapter 19)
Heart rate
(allows more
time for
ventricular
filling)
Bloodborne
epinephrine,
thyroxine,
excess Ca2+
Venous
return
Contractility
EDV
(preload)
ESV
Exercise,
fright, anxiety
Sympathetic
activity
Heart
rate
Stroke
volume
Stroke Volume Regulation
Initial stimulus
Physiological response
Result
Parasympathetic
activity
Cardiac
output
Negative inotropic agents decrease
contractility = Acidosis, ↑extracellular
K+, Ca channel blockers
D. Cardiac Output Control …
2. Regulation of Heart Rate To Control CO
a. Not very important in healthy individuals:
– Relevant for:
b. STRESS: extrinsic factors regulate
i) Autonomic N.S. (NEXT SLIDE)
 Sympathetic (via cardioacceleratory & Vasomoter
centers): Overrides Parasymp
Results: (1) Threshold:
(2) SA node:
 HR
(3) Contractility
 Sensory Sympathetic Reflexes: (1) Baroreceptors
(2) Atrial (Bainbridge) reflex –
 Parasympathetic(via cardioinhibitory Center): functions
as
Vagal Tone:
c. Chronotropic factors
 + = Sympathetic input, thyroxine, heat
Autonomic innervation of the heart.
The vagus nerve
(parasympathetic)
decreases heart rate.
Dorsal motor nucleus of vagus
Cardioinhibitory center
Cardio-acceleratory center
Medulla oblongata
Sympathetic trunk ganglion
Thoracic spinal cord
Sympathetic trunk
Sympathetic cardiac
nerves increase heart rate
and force of contraction.
AV node
SA node
Parasympathetic fibers
Sympathetic fibers
Interneurons
REVIEW OF FACTORS AFFECTING CO
 Stroke Volume
Venous Return– intrinsic
Contractility: via Symp
- using Cardioaccel C.
- Adrenal Medulla Hormones
 Heart Rate
Symp using
- Cardioaccel. Center
- Adrenal Medulla Hormones
Para using Cardioinhibitory Center
Factors involved in regulation of cardiac output.
Exercise (by
skeletal muscle and
respiratory pumps;
see Chapter 19)
Heart rate
(allows more
time for
ventricular
filling)
Bloodborne
epinephrine,
thyroxine,
excess Ca2+
Venous
return
Contractility
EDV
(preload)
ESV
Stroke
volume
Exercise,
fright, anxiety
Sympathetic
activity
Parasympathetic
activity
Heart
rate
Heart Rate
Cardiac
Stroke Volume
output
Regulation
Regulation
Initial stimulus
Negative inotropic agents decrease
Physiological response
contractility = Acidosis, ↑extracellular
Result
K+, Ca channel blockers
Regulation of Heart Rate
 Chronotropic factors
d. OTHER FACTORS: Age, gender, ion imbalances also effect HR
END OF PPT
NEXT
 Review Questions
 Extra Slides
Review Questions
Which of the following is true
about the heart…
A. Only O2 rich blood leaves the
heart.
B. O2 rich blood leaves the left
side, but not the right
C. Only O2 poor blood enters
the heart
D. O2 poor blood enters the
right side and leaves the
right side
Review Questions
Atrioventricular (AV) valves prevent blood from
__________________
semilunar
going back into the atria while ______________
valves open to allow blood into arteries during
pulmonary circuit
ventricular contraction. The ___________
systemic
delivers blood to the lungs and the ____________
circuit delivers to the rest of the body.
Review Questions
SA node
Heart rate is controlled primarily by the _____
because it spontaneously depolarizes at a faster rate
than any other part of the conduction system.
decreases
Parasympathetic fibers ____________
heart rate by
hyper - polarizing the typical lower limit of the
______
opening extra K+
pacemaker potential by ____________
channels.
Sympathetic fibers increase
________ heart rate by, among
depolarizing the pacemaker potential.
other things, ____________
Review Questions
If the impulse from the SA node to the AV node is
delayed, how would that effect the ECG?
P-Q interval takes longer
What does the QRS complex indicate?
Ventricular depolarization
Interference of signal transmission from SA to AV
heart block
node is known as ________________.
Review Questions
sinoatrial (SA)
The pacemaker of the heart is known as the _____________
atrioventricular (AV) node coordinates the slightly
node. The ____________________
delayed contraction of the ventricles. Blood then travels away
aorta
from the heart via the ____________
to the systemic system and
pulmonary _____________
artery
the _______________
to the lungs.
Figure 11.6
Review Questions
End Diastole Vol (EDV) - _______________
End Systole Vol (ESV)
Stroke volume = ________________
What are 3 factors that effect SV?
Preload, Contractility, Afterload
Positive chronotropic
____________
_____________ factors include anything
that increases heart rate like heat or the Atrial Reflex.
Review Questions
Contraction of heart muscles is clinically referred to
systole
as _____________;
relaxation is referred to as
diastole
_____________.
Maximum blood pressure occurs during…
A. Ventricular diastole
B. Atrial systole
C. Atrial diastole
D. Ventricular systole
What is EDV?
End Diastole Volume
Electrocardiography …
• Waves and Intervals
An electrocardiogram (ECG a.k.a.
QRS EKG)
complextracing
Sinoatrial
node
Atrial
depolarization
SA
Ventricular
depolarization
AV
Ventricular
Bundle & repolarization
Purkinje
AV
Plateau
Phase
Atrioventricular
node
P-Q
Interval
S-T
Segment
Q-T
Interval
Atria
Contract
Ventricles
Contract
 CO = SV X HR
REVIEW
 SV = EDV - ESV

Use substitution:
CO = (EDV - ESV) X HR
Most

Important
Preload = VENOUS FILLING
* 1) ↑ Venous Filling = ↑ EDV  ↑ Stretching
* 2)  ↑ V. Contraction  ↓ ESV
STARLING’S LAW
3) ↓ HR  ↑ Venous Filling

Important
Contractility = V. CONTRACTION
 ↑ V. Contraction  ↓ ESV
(↑ Sym. Innervation)
Low 
Important
Afterload = BLOOD PRESSURE

↑ BP  ↑ ESV