Transcript Ch 14: Cardiovascular Physiology

Ch 14: Cardiovascular Physiology
concepts:
Fluid flow
 APs in contractile & autorhythmic
cells
 Cardiac cycle (electr. & mech. events)
 HR regulation
 Stroke volume & cardiac output

Overview of Cardiovascular
System
3 basic components: ?
The heart is a dual pump!
Blood Flow

Why does blood flow through cardiovascular system?
(teleological vs. mechanistic answers)

Mechanistic approach:
Blood Flow Rate  P/ R

Pressure gradient (P) is main driving force
for flow through the vessels
Fig 14-4

Pressure of fluid in motion decreases over
distance because of energy loss due to
friction
Fig 14-2
Resistance Opposes Flow
3 parameters determine
resistance (R):
1.
Tube length (L)
2.
Tube radius (r)
3.
Fluid viscosity ()
Poiseuille’s law
8L 
R=
r4

Constant in human body
R
1 / r4
Fig 14-5
Velocity of Flow
Depends on Flow Rate and Cross-Sectional
Area:

Flow rate = volume of blood passing
one point in the system per unit of time
– If flow rate   velocity 

Cross-Sectional area (or tube diameter)
– If cross sectional area   velocity 
Velocity = flow rate / cross section area
Cardiac Muscle & Heart

Review heart and
circulatory system anatomy

One way flow in heart is
ensured by ?

Heart muscle cells:
– 99% contractile
– 1% autorhythmic
Fig 14-1
Follow Path of Blood through
Heart
Compare to Fig 14-7
Microanatomy of Contractile
Cardiac Muscle Cells
Intercalated discs
sSR smaller than in skeletal
muscle, indicates ?
Abundant mitochondria
extract about 80% of O2
Cardiac Muscle Cell Contraction is
Graded

Skeletal muscle cell: all-or-none contraction
in any single fiber for a given fiber length. Graded
contraction in skeletal muscle occurs through?

Cardiac muscle:
– force  to sarcomere length (up to a
maximum)
Fig 12-16
– force  to # of activated crossbridges
(Function of intracellular Ca2+: if [Ca2+]in
low  not all crossbridges activated)
Foxglove for a Failing Heart
See cardiac glycosides p. 492

Cardiac glycosides from
Digitalis purpurea
digitoxin

Highly toxic in large
dosage: destroys all
Na+/K+ pumps

In low dosage: partial
block of Na+ removal from
myocardial cells
Explain mechanism of
action !
APs in Contractile Myocardial Cells

Similar to skeletal muscle

Stable resting pot. ~ -90 mV

Rapid depolarization due to voltage
gated Na+ channels (Na+ movement?)

Repolarization due to voltage gated K+
channels (K+ movement?)

What is unique?
Fig 14-13

Flattening of AP into plateau phase due to
K+ perm.  and Ca2+ perm.

Flattening of AP into
plateau phase due to K+
perm.  and Ca2+ perm.

Much longer AP

Refractory period and
contraction end
simultaneously - Why
important?
Fig 14-14
AP in skeletal muscle :
1-5 msec
AP in cardiac muscle
:200 msec
Refractory Period of Skeletal Muscle
Fig 14-14
Summation and Tetanus
Fig 14-14
Refractory Period of Cardiac
Muscle
guarantees chamber filling!
No summation and tetanus possible
Fig 14-14
APs Autorhythmic Cells

Anatomically distinct from contractile
cells – Also called pacemaker cells

Spontaneous AP generation (Do not need
___________)

Unstable resting membrane potential (=
pacemaker potential)
Pacemaker potential starts at ~
-60mV, slowly drifts to threshold
AP
Fig 14-15
Heart Rate = Myogenic
Skeletal Muscle contraction = ?
If-channel Causes Mem. Pot. Instability

Autorhythmic cells have different membrane
channel: If - channel
allow
current
(= I ) to flow
f = “funny”
researchers didn’t
understand initially

If channels let K+ & Na+ through at -60mV

Na+ influx > K+ efflux (why??)

slow depolarization to threshold
Channels involved in APs of
Cardiac Autorhythmic Cells

Slow depolarization due to If channels

As cell slowly depolarizes: If -channels
close & Ca2+ channels start opening

At threshold: lots of Ca2+ channels open
 AP to + 20mV

Repolarization due to?
Modulation of Heart Rate by NS



NS can alter permeability of autorhythmic
cells to different ions
NE/E:  flow through If and Ca2+
channels – Rate AND force of
contraction go up
Ach:  flow through K+ channels
 flow through Ca2+ channels
Fig 14-16
– Consequence?
Sympathetic Heart Rate Modulation
Parasympathetic Heart Rate Modulation
The Heart as a Pump

Move from events in single cell to
events in whole heart

Cardiac cycle
1. electrical events
2. mechanical events

Electrical conduction in heart
coordinates contraction
Electrical Conduction in Heart
Fig 14-18
Leads to
Pacemaker sets HR
SA node firing rates set HR
Why?
If SA node defective?
AV node: 50 bpm
Implant
ventricular cells: 35 bpm  mechanical
pacemaker!
Electrocardiogram ECG (EKG)

Reflects electrical activity of whole heart not of
single cell!

Surface electrodes record electrical activity
deep within body - How possible?
Fig
14 20


EC fluid = “salt solution” (NaCl)  good
conductor of electricity to skin surface
Signal very weak by time it gets to skin
– ventricular AP = ? mV
– ECG signal amplitude = 1mV

Fig 14-22
EKG tracing =  of all electrical potentials
generated by all cells of heart at any given
moment
Since:
Depolarization = signal for contraction
Segments of EKG reflect mechanical heart events
Components of EKG
Waves (P, QRS, T)
 Segments (PR, ST)
 Intervals (wave- segment combos:
PR, QT)
Fig 14-20

Mechanical events
lag slightly behind
electrical events.
Why neg. tracing for
depolarization ??
Net electrical current
in heart moves towards
+ electrode
Net electrical current in
heart moves towards
- electrode
EKG tracing goes
up from baseline
EKG tracing goes
Down from baseline
Einthoven’s Triangle and the 3 Limb Leads:
+
I
RA –
–
Fig 14-19
II
III
+
+
LL
LA
–
Info provided by EKG:
1.
2.
3.
HR
Rhythm
Relationships of EKG components
 each P wave followed by QRS
complex?
 PR segment constant in length? etc.
etc.
For the Expert:
Find subtle changes in shape or
duration of various waves or
segments.
Indicates for example:
 Change in conduction velocity
 Enlargement of heart
 Tissue damage due to ischemia
(infarct!)
Prolonged QRS complex
Injury to AV bundle can increase duration of
QRS complex (takes longer for impulse to
spread throughout ventricular walls).
Fig 14-23
Mechanical Events of Cardiac Cycle

Systole (time during which cardiac
muscle contracts)
– atrial
– ventricular

Diastole (time during which cardiac
muscle relaxes)
– atrial
– ventricular
Compare to Fig 14-24
Summary

Heart at rest: atrial &
ventricular diastole

Completion of ventricular
filling: atrial systole

Ejection: ventricular systole
Heart Sounds (HS)


1st HS: during early ventricular contraction
 AV valves close
2nd HS: during early ventricular relaxation 
semilunar valves close
Fig 14-26
Gallops, Clicks and Murmurs
(clinical focus)
Turbulent blood flow produces heart
murmurs upon auscultation
Cardiac Output (CO) – a
Measure of Cardiac Performance
CO = HR x SV

calculate for average person!
HR controlled by ANS
– parasympathetic influence ?
– sympathetic influence ?
– without ANS, SA node fires 90-100x/min

What happens with ANS when resting HR goes
up (e.g. during exercise)?
Stroke Volume (SV)
= Ventricular blood volume pumped in
one contraction
= mL / beat
= EDV - ESV
For average person:
SV
= EDV - ESV
70mL = 135 mL - 65 mL
CO = HR x SV
Force of contraction
Fig 14-28
Length of muscle fibers (Starling
curve/law) due to venous return,
influenced by skeletal muscle pump and
respiratory pump
Sympathetic activity (and adrenaline)
venous constriction by sympathetic NS and
Increased Ca2+ availability
Myocardial Infarction