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CARDIOVASCULAR

PHYSIOLOGY

STUDENT MANUAL
Dr. Guido E. Santacana
CARDIOVASCULAR
PHYSIOLOGY
LECTURES

STUDENT LECTURE NOTEBOOK


Guido E. Santacana Ph.D.
DEPT. of PHYSIOLOGY
INTRODUCTION TO
CARDIOVASCULAR
PHYSIOLOGY
GENERAL ASPECTS OF
THE CARDIOVASCULAR
SYSTEM
MAIN FUNCTIONS OF THE
CIRCULATORY SYSTEM
 Transport and distribute essential
substances to the tissues.
 Remove metabolic byproducts.

 Adjustment of oxygen and nutrient


supply in different physiologic states.
 Regulation of body temperature.

 Humoral communication.
THE MAIN CIRCUIT

COLLECTING
PUMP TUBULES

DISTRIBUTING THIN
TUBULES VESSELS
Pressure Profile of the Circulatory
System

ELASTIC TISSUE
MUSCLE
Distribution of Blood in the
Circulatory System
Organization in the
Circulatory System

SERIES AND

PARALLEL CIRCUITS
CARDIAC
ELECTROPHYSIOLOGY

LECTURE NOTEBOOK
Guido E. Santacana Ph.D.
GENESIS OF THE MEMBRANE
POTENTIAL AND EQUATIONS TO
REMEMBER!!

EK = -60 LOG ([Ki]/[Ko])


= -94mv
ENa = -60 LOG ([Nai]/[Nao])
= +70mv

PK (K+)o + PNa(Na+)o + PCl(Cl-)i


Em = RT/F ln
PK (K+)I + PNa(Na+)i + PCl(Cl-)o
THE RESTING MEMBRANE POTENTIAL
OF THE CARDIAC CELL

If membrane
permeable
only to K+
If membrane
permeable
To both Na+ and
K+

If membrane permeable
To Na+, K+ plus with
A Na+/K+ Pump
WHY NOT Na+ 0R Ca++ FOR THE CARDIAC CELL
MEMBRANE POTENTIAL ?

EXTRA INTRA-
CELL. CELL.
Em

Na+ 145Mm 15Mm 70mv

Ca++ 3Mm 10-7 M 132mv

K+ 5Mm 145Mm -100mv


ACTION POTENTIALS FROM DIFFERENT
AREAS OF THE HEART

ATRIUM VENTRICLE
0 0
mv

mv
-80mv
-80mv

0
mv

SA NODE
-80mv
time
ELECTROPHYSIOLOGY OF THE FAST
RESPONSE FIBER
PHASE 0 OF THE FAST FIBER ACTION
POTENTIAL
Na+
Na+
A m B m
m
h h
-90mv -65mv

Na+ Na+
C m m
h
D h
0mv +20mv

Chemical Na+
Gradient m
E h
Electrical +30mv
Gradient
K+ CURRENTS AND REPOLARIZATION

 PHASE 1-TRANSIENT OUTWARD


CURRENT (TOC) Ito
 PHASE 1-3-DELAYED RECTIFIER
CURRENT IK
 PHASE 1-4-INWARDLY
RECTIFIED CURRENT IKl
THE PLATEAU PHASE AND
CALCIUM IONS

OPEN CLINICAL VALUE

L Ca++ Ca++
+10MV
CHANNELS BLOCKERS

T Ca++
CHANNELS -20MV NO (physiological)
EFFECTS OF Ca++ CHANNEL BLOCKERS
AND THE CARDIAC CELL ACTION
POTENTIAL

CONTROL DILTIAZEM
10 uMol/L
10 30 uMol/L
30
FORCE

CONTROL
10
30
TIME
Clinical Correlation
Early After-Depolarizations

Torsades de Pointes

0mV

-60mV

-90mV

Early After-Depolarization
OVERVIEW OF SPECIFIC EVENTS IN THE
VENTRICULAR CELL ACTION POTENTIAL
Overview of Important Channels in Cardiac
Electrophysiology

Sodium
Channels
Fast Na+ Phase 0 depolarization of non-pacemaker cardiac action potentials
Slow Na+ "Funny" pacemaker current (If) in cardiac nodal tissue
Potassium
Channels
Inward
rectifier (Iir Maintains phase 4 negative potential in cardiac cells
or IK1)
Transient
Contributes to phase 1 of non-pacemaker cardiac action potentials
outward (Ito)

Delayed
Phase 3 repolarization of cardiac action potentials
rectifier (IKr)
More Channels!

Calcium
Channels

Slow inward, long-lasting current; phase 2 non-pacemaker cardiac action


L-type (ICa-L) potentials and phases 4 and 0 of SA and AV nodal cells; important in
vascular smooth muscle contraction

Transient current that contributes to phase 4 pacemaker currents in SA and AV


T-type (ICa-T)
nodal cells
ELECTROPHYSIOLOGY OF THE
SLOW RESPONSE FIBER

0
2
0
mvs -40 3
4

-80 ERP RRP

time (msec)

RECALL: INWARD Ca++ CURRENT CAUSES DEPOLARIZATION


CONDUCTION OF THE ACTION
POTENTIAL IN CARDIAC FIBERS

LOCAL CURRENTS
- ------- +++++++
++++++++ --------

FIBER A FIBER B

DEPOLARIZED POLARIZED
ZONE ZONE
CONDUCTION OF THE ACTION
POTENTIAL
 FAST RESPONSE: Depends on
Amplitude,Rate of Change,level of
Em.
 SLOW RESPONSE: Slower
conduction.More apt to conduction
blocks.
 WHAT ABOUT MYOCARDIAL
INFARCTS AND CONDUCTION?
EFFECTS OF HIGH K+ ON CONDUCTION
AND AP OF FAST FIBERS
AP-AMP

0MV

Em
K+=3mM K+=7mM K+=14mM
0MV

K+=16mM
K+=3mM
WHAT HAS VARIED? LOOK AT: Em,AP SLOPE-AMPLITUDE
HIGH K+ AND m/h Na+ GATES

LOWER
HIGH K+ Em

CLOSED h GATES
(SOME)

LOWER AP LOWER Na+ ENTRY


AMPLITUDE
EXCITABILITY OF FAST AND SLOW
FIBERS

FAST m/h GATES COMPLETE RESET AFTER


PHASE 3
CONSTANT AND COMPLETE
RESPONSE IN PHASE 4

SLOW LONG RELATIVE REFRACTORY


PERIOD.
POST-REPOLARIZATION
REFRACTORINESS
AFTER THE EFFECTIVE OR
ABSOLUTE REFRACTORY
PERIOD (FAST FIBER)

MV

ARP

-80 RRP
TIME
POST-REPOLARIZATION
REFRACTORINESS (SLOW FIBER)

200 MSEC C
0
B

MV A
-60

POSTREPO

TIME
AUTOMATICITY RHYTMICITY

SA NODE

AV NODE
IDIOVENTRICULAR- ectopic
PACEMAKERS foci
THE SA NODE PACEMAKER POTENTIAL
CHARACTERISTICS OF THE
PACEMAKER POTENTIAL

RECALL: PHASE 4-PACEMAKER POTENTIAL(PP) OBSERVED HERE.


FREQUENCY DEPENDS ON: THRESHOLD,RESTING POTENTIALS
AND SLOPE OF THE PP
CAUSES OF THE PACEMAKER
POTENTIAL

K+
if iCa OUT

IN
iK

Na+ Ca++
THE PACEMAKER POTENTIAL
CURRENTS AFTER
DEPOLARIZATION

if iCa

iK
WHICH CURRENT WILL BE MORE AFFECTED BY
ADRENERGIC STIMULATION? WHICH BY CHOLINERGIC
STIMULATION?
LOOKING AT THE PACEMAKER
CURRENTS

voltage

iK

if
ionic currents
iCa
EFFECTS OF Ca++ CHANNEL
BLOCKERS ON THE PACEMAKER
POTENTIAL

NIFEDIPINE
CONTROL
(5.6 X 10-7 M)
0

MV

-60

TIME
OVERDRIVE SUPRESSION AND
AUTOMATICITY OF PACEMAKER CELLS
 Na+/K+ ATPase ENHANCEMENT
BY HIGH FREQUENCY.
 CONSEQUENT
HYPERPOLARIZATION.
 SUPRESSION OF AUTOMATICITY.

 RECOVERY TIME REQUIRED.

 ECTOPIC FOCI/SICK SINUS


SYNDROME.
THE CONDUCTION SYSTEM OF THE
HEART
ATRIAL AND ATRIOVENTRICULAR
CONDUCTION

BACHMANS PATH
RA SAN LA
INTERNODAL PATHS AN REGION

AV NODE
N REGION
NH REGION

BH
LV
RV
RIGHT BUNDLE LEFT BUNDLE
BRANCH BRANCH
NODAL DELAY

AV NODE
NA REGION
REGION OF LONGER PATH
FAST CONDUCTION
DELAY
N REGION SLOW CONDUCTION SHORTER PATH

NH REGION
FAST CONDUCTION

REFLECTED IN THE P-QRS INTERVAL


OF THE ECG
UNI AND BIDIRECTIONAL BLOCK
CLINICAL IMPLICATIONS

B
A
ANTEGRADE
NORMAL
BLOCK

C D
REENTRY
UNIDIRECTIONAL
BI
BLOCK
Clinical Correlation
Re-entry Tachycardias
Paroxysmal Supraventricular Tachycardia
Ischemic Tissue

Slow Fast Fast


Slow
Pathway Pathway Pathway
Pathway

Normal Conduction Re-Entry Circuit


AV NODE AND AV BLOCKS
FOCUS ON N REGION
NORMA ECG
L

1ST DEGREE
PROLONGUED AV
CONDUCTION TIME

2ND DEGREE
1/2 ATRIAL IMPULSES
CONDUCTED TO VENTRICLES

3RD DEGREE

VAGAL MEDIATION
IN N REGION/COMPLETE
BLOCK
CONDUCTION IN THE VENTRICLES

 PURKINJE FIBERS WITH LONG


REFRACTORY PERIODS.
 PROTECTION AGAINST PREMATURE
ATRIAL DEPOLARIZATIONS AT SLOW
HEART RATES.
 AV NODE PROTECS AT HIGH HEART
RATES.
QUICK QUIZ
Which of the following is not true about the effect of
acetylcholine (Ach) in the electrophysiology of the cardiac pacemaker
cell:
A. Ach lowers the magnitude of the minimum repolarization potential.
B. Ach lowers the slope of the pacemaker potential.
C. Ach decreases the SA node frequency.
D.Ach increases the ik current of the pacemaker cell.
E. Ach decreases the iCa++ current of the pacemaker cell.

The main reason why the AV node filters out high stimulation
frequencies from the SA node is:
A. The long pathway that the stimulus must traverse in the AV node.
B. Post Repolarization Refractoriness of AV nodal cells.
C. The AV nodal cell is always hyperpolarized
D. Ca++ is the main ion in Phase 0 of the AV nodal cell.
E. I need to review this section very fast.
CARDIAC
MECHANICS
MAIN THEMES
THE HEART AS A PUMP
THE CARDIAC CYCLE
CHAPTER 3 B&L
CARDIAC OUTPUT
LENGHT/ TENSION AND THE FRANK-
STARLING RELATION
LEFT VENTRICULAR
PRESSURE

INITIAL MYOCARDIAL FIBER LENGHT


LEFT VENTRICULAR END-DIASTOLIC VOLUME
PRELOAD AND AFTERLOAD IN THE
HEART

 INCREASE IN FILLING
PRESSURE=INCREASED PRELOAD
 PRELOAD REFERS TO END
DIASTOLIC VOLUME.
 AFTERLOAD IS THE AORTIC
PRESSURE DURING THE EJECTION
PERIOD/AORTIC VALVE OPENING.
 LAPLACES’S LAW & WALL STRESS,
WS = P X R / 2(wall thickness)
LEFT VENTRICULAR PRESSURE AND
AFTERLOAD AT CONSTANT PRELOADS

EFFECT OF INCREASED
LEFT VENTRICULAR

PRELOAD
PRESSURE

PEAK
ISOMETRIC
FORCE

AFTERLOAD (aortic pressure)


NOTE: WHAT HAPPENS IN THE NORMAL HEART VS ONE IN THE LAST
PHASES OF CARDIAC FAILURE?
CONTRACTILITY:THE VENTRICULAR
FUNCTION CURVE

EFFECT?

CHANGES IN
CONTRACTILITY
dP/dt AS A VALUABLE INDEX OF
CONTRACTILITY
MAX dP/dt

B
LEFT VENTRICULAR

120
PRESSURE (mmHg)

40

.2 TIME (s) .6
opens

Mitral
Aortic

Closes

CARDIAC CYCLE
Atrial Systole
Isovolumic contract.

S1
Rapid Ejection

Reduced Ejection

S2
Isovolumic Relax.
Rapid Ventricular
Filling

Reduced Ventricular
Filling

Atrial Systole
opens
closes
Mitral
Aortic
QUICK QUIZ
How to find out that you know
the Cardiac Cycle.
150

Atrial Mitral
systolecloses Aortic
opens

Aortic
Mitral
closes
opens

50

TIME (SEC)
Clinical Correlation
Diagnosis of Aortic Stenosis by Pressure
Graphs

Normal Aortic Stenosis

Aorta Aorta

Ventricle Ventricle
LEFT VENTRICULAR PRESSURE (mmHg) LEFT VENTRICULAR
PRESSURE/VOLUME P/V LOOP
END OF SYSTOLE

120 F
E

80 D

40

A B END OF DIASTOLE
C
0
50 100 150
LEFT VENTRICULAR VOLUME (ml)
EFFECT OF PRELOAD ON
THE VENTRICULAR P/V
LOOP
ESV
PRESSURE (mmHg)
VENTRICULAR

2 3
1
LEFT

EDVs

VOLUME (ml)
EFFECT OF AFTERLOAD IN
THE LEFT VENTRICULAR
P/V LOOP
ESV
ESV
3
PRESSURE (mmHg)

ESV
2
VENTRICULAR

1
LEFT

EDV

VOLUME (ml)
EFFECT OF CONTRACTILITY
ON THE LV P/V LOOP
PRESSURE (mmHg)
VENTRICULAR
LEFT

1
2

VOLUME (ml)
QUICK QUIZ

PRELOAD AFTERLOAD CONTRACTILITY


CARDIAC OUTPUT AND THE FICK
PRINCIPLE
BODY O2 CONSUMPTION

Lungs
250mlO2/min
PULMONARY PULMONARY
ARTERY VEIN

PaO2 PvO2
0.15mlO2/ml blood 0.20mlO2/ml blood
Pulmonary capillaries

O2 CONSUMPTION (ml/min)
CARDIAC OUTPUT=
PvO2 - PaO2
HEMODYNAMICS
 VELOCITY,FLOW,PRESSURE

 LAMINAR FLOW
 POISEUILLE’S LAW

 RESISTANCE(SERIES-PARALLEL)

 TURBULENT FLOW AND


REYNOLD’S NUMBER

CHAPTER 5 B&L
REQUIRED CONCEPTS

VELOCITY = DISTANCE / TIME


V = D / T

FLOW = VOLUME / TIME


Q = VL / T

VELOCITY -FLOW- AREA

V = Q / A
CROSS SECTIONAL AREA AND
VELOCITY

A= 2cm2 10cm2 1cm2

Q=10ml/s a b c

V= 5cm/s 1cm/s 10cm/s

V=Q/A
HYDROSTATIC PRESSURE

136cm 100
0 200
100
0 200
P=pxgxh
0
100mmHg

136cm 100
0 200
P = Pressure mmHg
100
p = density 0 200

g = gravity
h = height 0
ENERGY OF A STATIC VS A DYNAMIC
FLUID

TOTAL ENERGY= POTENTIAL E. + KINETIC E.


TE = PE + KE

FLUID AT REST (HYDROSTATIC )

FLUID IN MOTION (HYDROSTATIC


+ HYDRODYNAMIC)
VELOCITY AND PRESSURE

100
0 200

0
POISEUILLE’S LAW GOVERNING FLUID
FLOW(Q) THROUGH CYLINDRIC TUBES

4
(Pi - Po) r
(FLOW)Q =
8nL

DIFFERENCE
IN PRESSURE VISCOSITY LENGHT RADIUS
RESISTANCE TO FLOW IN THE
CARDIOVASCULAR SYSTEM
BASIC CONCEPTS
Rt = R1 + R2 + R3…. SERIES RESISTANCE

1/Rt = 1/R1 + 1/R2 + 1/R3… PARALLEL RES.


R1
SERIES PARALLEL R2
R1 R2 R3 R3
WHAT REALLY HAPPENS IN THE CVS?

LOWER R HIGHER R LOWER R

ARTERY CAPILLARIES

ARTERIOLES
LAMINAR VS TURBULENT FLOW
THE REYNOLD’S NUMBER

LAMINAR TURBULENT
FLOW FLOW

p = density
D = diameter
Nr = pDv / n v = velocity
n = viscosity
laminar = 2000 or less
QUICK QUIZZ
1. Which of the following vessels will produce a dramatic
decrease in blood flow through the tissues by a change in
radius?

A. Aorta
B. Venules
C. Arterioles
D. Capillaries

3. After a bout with hemorrhagic Dengue you would expect


to find a heart murmur at a lower level than before the
disease.
A. True B. False
PV Loop Refresher

B A

B
A

What happens from A to B?


ARTERIAL SYSTEM
 COMPLIANCE

 MEAN ARTERIAL PRESSURE


 PULSE PRESSURE

 PRESSURE MEASUREMENT

CHAPTER 26 B&L
THE CONCEPT OF THE HYDRAULIC
FILTER
SYSTOLE DIASTOLE

COMPLIANT

RIGID
EFFECTS OF PUMPING THROUGH A
RIGID VS A COMPLIANT DUCT
O2 CONSUMPTION (mlO2/100g/beat)

0.1

PLASTIC TUBING

NATIVE AORTA

0
5 STROKE VOLUME (ml) 15
STATIC P-V RELATIONSHIP IN
THE AORTA
% INCREASE IN VOLUME

PRESSURE (mmHg)
ELASTIC MODULUS OR
ELASTANCE

Ep= ELASTIC MODULUS


Da= MAX. CHANGE IN
Ep = P / Da/Db AORTIC DIAMETER.
Db= MEAN AORTIC DIAM.

ELASTANCE COMPLIANCE
P V V P
EP IS INVERSELY PROPORTIONAL TO C
MEAN ARTERIAL PRESSURE (MAP)

REMEMBER OHMS LAW?

CARDIAC OUTPUT PERIPHERAL RESISTANCE

INSTANTANEOUS
INCREASE

STEADY STATE
INCREASE
EFFECT OF COMPLIANCE ON
MAP
Qh- inflow (CO)
Qr- outflow
Ca- Compliance
ARTERIAL PRESSURE (mmHg)

Pa = Qh - Qr / Ca Pa- MAP

SMALL Ca

LARGE Ca

INCREASE CARDIAC OUTPUT

TIME
PULSE PRESSURE

STROKE VOLUME COMPLIANCE

V4

VB
VOLUME V3

V2
VA
V1
P1 PA P2 P3 PB P4 PRESSURE
PULSE PRESSURE
EFFECTS OF:

COMPLIANCE TOTAL PERIPHERAL RESISTANCE


TPR

A B
CHAPTER 9 B&L
COUPLING OF THE HEART AND BLOOD VESSELS

VASCULAR FUNCTION CURVE

HOW CARDIAC OUTPUT REGULATES


CENTRAL VENOUS PRESSURE

CARDIAC FUNCTION CURVE

HOW CENTRAL VENOUS PRESSURE (PRELOAD)


REGULATES CARDIAC OUTPUT
VASCULAR FUNCTION CURVE
HOW CHANGES IN CARDIAC OUTPUT INDUCE
CHANGES IN CENTRAL VENOUS PRESSURE?

8
Pmc
CENTRAL VENOUR PRESSURE (mmHg)

VASCULAR FUNCTION
B CURVE

-1
0 8
CARDIAC OUTPUT (L/min)
HOW BLOOD VOLUME AND VENOMOTOR
TONE CHANGE THE VASCULAR FUNCTION
CURVE?
CENTRAL VENOUR PRESSURE (mmHg)

VASCULAR FUNCTION
8 CURVE

-1
0 8
CARDIAC OUTPUT (L/min)
TOTAL PERIPHERAL RESISTANCE
AND THE VASCULAR FUNCTION
CURVE.
8
CENTRAL VENOUR PRESSURE (mmHg)

VASCULAR FUNCTION
CURVE

-1
0 8
CARDIAC OUTPUT (L/min)
THE CARDIAC FUNCTION CURVE
CARDIAC OUTPUT (L/min)

CENTRAL VENOUS PRESSURE (mmHg)


EFFECTS OF SYMPATHETIC STIMULATION
ON THE CARDIAC FUNCTION CURVE
CARDIAC OUTPUT (L/min)

CENTRAL VENOUS PRESSURE (mmHg)


HOW BLOOD VOLUME AND PERIPHERAL
RESISTANCE CHANGE THE CARDIAC
FUNCTION CURVE?
VOLUME RESISTANCE
CARDIAC OUTPUT (L/min)

CENTRAL VENOUS PRESSURE (mmHg)


THE CARDIAC FUNCTION CURVE IN
HEART FAILURE
CARDIAC OUTPUT (L/min)

CENTRAL VENOUS PRESSURE (mmHg)


HEART - BLOOD VESSELS
COUPLING
MORMAL FUNCTION
VEINS PUMP ARTERIES

Qh 5L/min

Pa

CPV=2mmHg=Pv
COMPLIANCES MPA=102mmHg
Cv = 19Ca
Cv>>>>Ca

5L/min Qr
PERIPHERAL R= Pa - Pv / Qr
R = 20mmHg/L/min
CARDIAC ARREST!
INMEDIATE EFFECT
FLOW STOPS HERE

VEINS PUMP ARTERIES

Qh 0L/min

Pa
FLOW CONTINUES HRE
CPV=2mmHg=Pv
TRANSFER ART-->VEINS

5L/min Qr
Qr CONTINUES AS LONG AS
R = 20mmHg/L/min A PRESSURE GRADIENT
Qr= Pa - Pv/20 IS SUSTAINED
CARDIAC ARREST
STEADY STATE
FLOW STOPPED

VEINS PUMP ARTERIES

Qh 0L/min

Pa = 7mmHg

Pv = 7mmHg = MEAN CIRCULATORY PRESSURE OR Pmc


95mmHg

5mmHg FLOW STOPPED

0L/min Qr
Qr = 0 ( NO Pa - Pv DIFFERENCE)
WE START PUMPING!
INMEDIATE EFFECT
SOME VENOUS BLOOD FLOW STARTS

VEINS PUMP ARTERIES

Qh 1L/min

Pa = 7mmHg

Pv = 7mmHg

NO FLOW HERE YET

0L/min Qr
FLOW RETURNS AT Qr AT
THE NEW Qh
VEINS PUMP ARTERIES

Qh 1L/min

Pa = 26mmHg

Pv = 6mmHg

FLOW STARTS

1L/min Qr
R = 20mmHg
Qr = Pa - Pv / 20 = 1L/min
THE END