ANP 1105A - Anatomy & Physiology I
•
Lecture 14 – Heart part 2/2
Presented by: Michael Downey
Faculté de médecine | Faculty of Medicine
uOttawa.ca
What you will learn to do:
4.2.6 Explain extrinsic innervation
4.2.7. Explain what is an ECG tracing and the nature of the
information it is providing
4.2.8. Explain the events occurring during each phase of the
cardiac cycle
4.2.9. Define cardiac output in terms of heart rate and stroke
volume
4.2.10. Describe in detail the mechanisms for the regulation of
heart rate & stroke volume
Relevant sections of the text: Chapter 18
Web Extras: https://www.youtube.com/watch?v=xIZQRjkwV9Q
https://www.youtube.com/watch?v=kwLbSx9BNbU
Images used are generally from the textbook assigned
for the course. Other images are credited on the slide
or in the notes section.
Review from last class! - Know the flow!
https://pediatricheartspecialists.com
Review from last class! Intrinsic system sets ‘pace’ of the heart
Pacemaker cells are
concentrated in a
specific area called
the SA node and are
connected to (and
part of) the intrinsic
conduction system
SA node->AV Node->AV Bundle->Bundle Branches->Purkinjie Fibres
Objective: 4.2.6B
Extrinsic Innervation of the Heart
Modifying the Basic Rhythm
• Heartbeat modified
by ANS via cardiac
centers in medulla
oblongata
See notes for details!
Objective: 4.2.6B
What are the functions of these two
centres
Cardioacceleratory centre: sends signals through
sympathetic trunk to increase both rate and force
Stimulates SA and AV nodes, heart muscle, and
coronary arteries
Cardioinhibitory centre: parasympathetic signals
via vagus nerve to decrease rate
Inhibits SA and AV nodes via vagus nerves
There is a lot of electrical activity in the heart…
How can we measure that and why do we care?
Objective: 4.2.7
Electrocardiography
• Electrocardiograph can detect electrical currents
generated by heart
• Electrocardiogram (ECG or EKG) is a graphic recording of
electrical activity
Electrocardiogram
Electrocardiograph
Objective: 4.2.7
Electrocardiography
Electrocardiogram is a composite of all action
potentials at given time; not a tracing of a single AP
How: Electrodes are placed at various points on body
to measure voltage differences; 12 lead ECG is most
typical
Objective: 4.2.7
Electrocardiograph (the machine)
Things can get complicated . . .
You don’t need to know this slide –
its to illustrate the ECGs can be complicated.
Objective: 4.2.7
So let’s keep it simple
Main features:
– P wave: depolarization of SA
node and atria
– QRS complex: ventricular
depolarization and atrial
repolarization
– T wave: ventricular
repolarization
– P-R interval: beginning of
atrial excitation to beginning of
ventricular excitation
– S-T segment: entire
ventricular myocardium
depolarized
– Q-T interval: beginning of
ventricular depolarization
through ventricular
repolarization
Objective: 4.2.7
Electrocardiogram (the output)
This is simply a different way of looking at the
same information presented in the previous slide.
It shows: The sequence of depolarization and
repolarization of the heart related to the
deflection ECG waves.
Objective: 4.2.7
And one more time with the first one…
Main features:
– P wave: depolarization of SA
node and atria
– QRS complex: ventricular
depolarization and atrial
repolarization
– T wave: ventricular
repolarization
– P-R interval: beginning of
atrial excitation to beginning of
ventricular excitation
– S-T segment: entire
ventricular myocardium
depolarized
– Q-T interval: beginning of
ventricular depolarization
through ventricular
repolarization
Objective: 4.2.7
Electrocardiogram issues (why we care!):
Normal/healthy
Junctional Rhythm
Junctional Rhythm: SA node nonfunctional. AV node takes
over and paces heart at 40-60 beats per minute.
P waves absent.
Objective: 4.2.7
Electrocardiogram issues:
Second degree heart block
Ventricular fibrillation
2nd degree heart block: AV node fails to conduct some SA node impulses. More P values
than QRS waves. In this tracing there are usually two P waves for each QRS.
Ventricular fibrillation: electrical activity is disorganized. Action potentials occur
randomly throughout ventricles
• results in chaotic grossly abnormal ECG deflections, seen in acute heart attack and
after electrical shocks
Objective: 4.2.7
Electrocardiogram issues:
Changes in patterns or timing of ECG may reveal diseased or
damaged heart, or problems with heart’s conduction system
Problems that can be detected:
• Enlarged R waves may indicate enlarged ventricles
• Elevated or depressed S-T segment indicates cardiac
ischemia
• Prolonged Q-T interval reveals a repolarization
abnormality that increases risk of ventricular arrhythmias
Objective: 4.2.8
Mechanics of heart function
Lets start with some definitions!
Systole: period of heart contraction
Diastole: period of heart relaxation
Cardiac cycle: blood flow through heart during one complete
heartbeat.
Objective: 4.2.8 - Cardiac Cycle
Our goal is to understand this figure!
Objective: 4.2.9
Regulation of heart pumping:
Let’s start with some definitions:
Cardiac output: amount of blood pumped out by a single
ventricle in 1 minute. Equals heart rate (HR) times stroke
volume (SV)
Stroke volume: volume of blood pumped out by one
ventricle with each beat
Objective: 4.2.9
Sample calculation for cardiac output:
Cardiac Output
Heartrate
CO  ml / min   HR  75 beats / min  SV  70 ml / beat 
5.25 L / min
=5250
mls/min
= 5.25 L/min
Stroke volume
We can think about resting and reserve cardiac output
Maximal CO is 4–5 times resting CO in non-athletic people (20–25 L/min)
Maximal CO may reach 35 L/min in trained athletes
Cardiac reserve: difference between resting and maximal CO
Objective: 4.2.10
Stroke volume
Mathematically: SV = EDV  ESV
• EDV – End diastolic volume – amount of blood flowing into the ventricles
when relaxed
• ESV – End Systolic volume – amount left after contraction
– EDV is affected by length of ventricular diastole and venous pressure
(~120 ml/beat)
– ESV is affected by arterial BP and force of ventricular contraction (~50
ml/beat)
– Normal SV = 120 ml (EDV)  50 ml (ESV) = 70 ml/beat
Objective: 4.2.8 - Cardiac Cycle
Objective: 4.2.10
Cardiac Output
Heartrate
CO  ml / min   HR  75 beats / min  SV  70 ml / beat 
5.25 L / min
=5250
mls/min
= 5.25 L/min
Regulation of stroke volume
• Three main factors that affect SV:
1. Preload
2. Contractility
3. Afterload
Let’s look at these 1 and a time!
Stroke volume
Objective: 4.2.10
A-1 Regulation of stroke volume by preload
• Preload: degree of stretch of heart muscle
– Preload: degree to which cardiac muscle cells are stretched just
before they contract
• Changes in preload cause changes in SV
– Affects EDV
– Relationship between preload and SV called FrankStarling law of
the heart
– Cardiac muscle exhibits a length-tension relationship
• At rest, cardiac muscle cells are shorter than optimal length;
leads to dramatic increase in contractile force
Objective: 4.2.10
A-1 Regulation of stroke volume by preload
What is Frank-Starling lab of the heart?
• Within defined
limits, the heart will
pump whatever
volume of blood it
receives
•
Over a fairly wide
range, there is a
proportional
relationship
between EDV and
stroke volume
J. Carnegie
Objective: 4.2.10
A-1 Regulation of stroke volume by preload
What regulates preload:
• Most important factor in preload stretching of cardiac
muscle is venous return—amount of blood returning to
heart
• Slow heartbeat and exercise increase venous return
Increased venous return distends (stretches) ventricles
and increases contraction force
Objective: 4.2.10
A-2 Regulation of stroke volume by contractility
Contractility - Contractile strength at given muscle length
Independent of muscle stretch and EDV
Points to note
• Increased contractility lowers ESV; caused by:
Sympathetic epinephrine release stimulates increased Ca2+
influx, leading to more cross bridge formations
• Positive inotropic agents increase contractility - Thyroxine,
glucagon, epinephrine, digitalis, high extracellular Ca2+
• Decreased by negative inotropic agents - Acidosis (excess
H+), increased extracellular K+, calcium channel blockers
Objective: 4.2.10
A-2 Regulation of stroke volume by contractility
(Nor)Epinephrine Increases Heart
Contractility Via a Cyclic AMP
Second Messenger System
Objective: 4.2.10
A-3 Regulation of stroke volume by afterload
Afterload: back pressure exerted by arterial blood
– This must be overcome by ventricles to eject blood
• Back pressure from arterial blood pushing on SL
valves is major pressure
– Aortic pressure is around 80 mm Hg
– Pulmonary trunk pressure is around 10 mm Hg
– Hypertension increases afterload, resulting in increased
ESV and reduced SV
Objective: 4.2.10
Cardiac Output
Heartrate
CO  ml / min   HR  75 beats / min  SV  70 ml / beat 
5.25 L / min
=5250
mls/min
= 5.25 L/min
B. Heart rate can be impacted by:
1. Autonomic nervous system
2. Chemicals
3. Other factors
Let’s look at these 1 and a time!
Stroke volume
Objective: 4.2.10
B-1 Heart rate regulation by autonomic nervous system:
• Sympathetic nervous system can be activated by emotional or
physical stressors
• Norepinephrine is released and binds to β1-adrenergic receptors
on heart, causing:
• Pacemaker to fire more rapidly, increasing HR
• Increased contractility
Objective: 4.2.10
B-1 Heart rate regulation by autonomic nervous system:
Parasympathetic nervous system opposes sympathetic effects
• Acetylcholine hyperpolarizes pacemaker cells by opening
K+ channels, which slows HR
• Has little to no effect on contractility
Heart at rest exhibits vagal tone due to parasympathetic
• Parasympathetic is dominant influence on heart rate
• Decreases rate about 25 beats/min
• Cutting vagal nerve leads to HR of ~100
Parasympathetic acts here
Objective: 4.2.10
B-1 Heart rate regulation by autonomic nervous system:
Two additional Points:
Crosstalk: when sympathetic is activated, parasympathetic is
inhibited, and vice-versa
Atrial (Bainbridge) reflex: Sympathetic reflex initiated by
increased venous return, hence increased atrial filling
• Atrial walls are stretched with increased volume
• Stimulates SA node, which increases HR
• Also stimulates atrial stretch receptors that activate
sympathetic reflexes
Objective: 4.2.10
B-2 Heart rate regulation by hormones and ions
– Hormones
• Epinephrine from adrenal medulla increases heart rate
and contractility
• Thyroxine increases heart rate; enhances effects of
norepinephrine and epinephrine
– Ions
• Intra- and extracellular ion concentrations (e.g., Ca2+
and K+) must be maintained for normal heart function
– Imbalances are very dangerous to heart
Objective: 4.2.10
B-3 Heart rate regulation by other factors
– Age
• Fetus has fastest HR; declines with age
– Sex
• Females have faster HR than males
– Exercise
• Increases HR
• Trained atheles can have slow HR
– Body temperature
• HR increases with increased body temperature
Objective: 4.2.10
Defective (?) control of heart rate
• Tachycardia: abnormally fast heart rate (>100 beats/min)
– If persistent, may lead to fibrillation
• Bradycardia: heart rate slower than 60 beats/min
– May result in grossly inadequate blood circulation in
nonathletes
– May be desirable result of endurance training
33 bpm
> 33 bpm
Objective: 4.2.10
Defects in cardiac output (CO) can
lead to congestive heart failure:
Definition: CO is so low that blood circulation
is inadequate to meet tissue needs,
progressive condition
Objective: 4.2.10
All together now:
Erin Mulhivill
Alomgir Hossain
Ben Rotstein
Wenbin Liang
Katey Rayner
Mireille Ouimet
True or False: Tachycardia is an increase in systolic
pressure
What is true about electrocardiograms?
A. The P wave represents ventricle depolarization
B. The atrial repolarization is hidden in the QRS peak
C. The P wave is always half the height of the QRS peak
D. The T wave represents atrial repolarization
E. None of the above are true statements
F. All of the above are true statements
Cardiac Output:
A. Is equal to HR/SV
B. Is affected by ESV but not EDV
C. Is equal to SV x HR
D. Is not impacted by calcium
Your doctor listens to your chest. She hears a clicking
sound around your heart.
This could be due to:
a)
b)
c)
d)
Decreased Cardiac output
Stenotic AV valve
Incompetent SL valve
Low levels of calicum
Summary
We followed up intrinsic regulation of heart studied in the
last class by focusing on extrinsic regulation. We then
learned about the electrocardiograph and how it can be
used to investigate heart function. We learned briefly about
the cardiac cycle before looking at the concept of cardiac
output in detail.
up next class
We will begin looking in depth at blood vessels beyond the
heart.
mdowne2@uottawa.ca