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Physio Lecture 7 – Physio Lecture 7 – Introduction to Cardiovascular Introduction to Cardiovascular
PhysiologyPhysiology
Prof. dr. Željko Dujić
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MAIN FUNCTIONS OF THE CIRCULATORY SYSTEMMAIN FUNCTIONS OF THE CIRCULATORY SYSTEM
-Transport and distribute essential substances Transport and distribute essential substances to the tissuesto the tissues (most important to the vital (most important to the vital organs – brain and heart)organs – brain and heart)..
-Remove metabolic byproducts.Remove metabolic byproducts.
-Adjustment of oxygen and nutrient supply in Adjustment of oxygen and nutrient supply in different physiologic states.different physiologic states.
-Regulation of body temperature.Regulation of body temperature.
- - Humoral communicationHumoral communication by maintaining by maintaining tissue perfusiontissue perfusion..
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Pressure Profile of the Circulatory System
ELASTIC TISSUE
MUSCLE
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THE SYSTEMIC CIRCULATION
CAPACITY VESSELS
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Distribution of Blood in the Circulatory System
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PULMONARYCIRCULATION
1. LOW RESISTANCE2. LOW PRESSURE
(25/10 mmHg)
SYSTEMICCIRCULATION
1. HIGH RESISTANCE2. HIGH PRESSURE
(120/80 mmHg)
PARALLELSUBCIRCUITS
UNIDIRECTIONALFLOW
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VEINS
CAPACITYVESSELS
HEART
80 mmHg 120 mmHg
SYSTOLE
DIASTOLE
ARTERIES (LOW COMPLIANCE)
CAPILLARIES
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Membrane potential and critical equations
EK = -60 LOG ([Ki]/[Ko]) = -94mv
ENa = -60 LOG ([Nai]/[Nao]) = +70mv
Em = RT/F ln
PK (K+)o + PNa(Na+)o + PCl(Cl-)i
PK (K+)I + PNa(Na+)i + PCl(Cl-)o
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CARDIAC ELECTROPHYSIOLOGY UPDATE
Na+
EXTRACELL.
INTRA-CELL. Em
145Mm 15Mm 70mV
Ca++ 3Mm 10-7 M 132mV
K+ 5Mm 145Mm -100mV
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Action potentials from different heart areas
mv
0
-80mv
mv
0
-80mv
mv
0
-80mv
ATRIUM VENTRICLE
SA NODE
time
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ME
MB
RA
NE
PO
TE
NT
IAL
(m
V)
-90
0
0
12
3
4
TIME
PHASE0 = Rapid Depolarization (inward Na+ current) 1 = Overshoot2 = Plateau (inward Ca++ current)
3 = Repolarization (outward K+ current)4 = Resting Potential
Mechanical Response
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K+ CURRENTS AND REPOLARIZATION
• Phase 1- transient outward current (TOC) Ito
• Phase 1-3 - delayed rectifier current IK
• Phase 1-4 – inwardly rectifier current IKl
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THE PLATEAU PHASE AND CALCIUM IONS
L Ca++ CHANNELS
L Ca++ CHANNELS
T Ca++ CHANNELS
T Ca++ CHANNELS
OPEN
+10mV
-20mV
CLINICAL VALUE
Ca++ BLOCKERS
NO (physiological)
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OVERVIEW OF SPECIFIC EVENTS IN THE VENTRICULAR CELL ACTION
POTENTIAL
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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
or IK1)Maintains phase 4 negative potential in cardiac cells
Transient outward (Ito)
Contributes to phase 1 of non-pacemaker cardiac action potentials
Delayed rectifier (IKr)
Phase 3 repolarization of cardiac action potentials
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Cont’ed with Channels
Calcium Channels
L-type (ICa-L)Slow inward, long-lasting current; phase 2 non-pacemaker cardiac action
potentials and phases 4 and 0 of SA and AV nodal cells; important in vascular smooth muscle contraction
T-type (ICa-T) Transient current that contributes to phase 4 pacemaker currents in SA and AV nodal cells
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ELECTROPHYSIOLOGY OF THE SLOW RESPONSE FIBER
RECALL: INWARD Ca++ CURRENT CAUSES DEPOLARIZATION
0
-80
-400
2
34
ARP RRP
time (msec)
mV
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CONDUCTION OF THE ACTION POTENTIAL IN CARDIAC FIBERS
- ------- - -
---- --+ ++ + + + + + +
+ + + ++ +
FIBER A FIBER B
DEPOLARIZEDZONE
POLARIZED ZONE
LOCAL CURRENTS
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CONDUCTION OF THE ACTION POTENTIAL
• FAST RESPONSE: Depends on AP Amplitude, Rate of Potential Change,level of Em.
• SLOW RESPONSE: Slower conduction. More apt to conduction blocks.
• WHAT ABOUT MYOCARDIAL INFARCTS AND CONDUCTION?
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AFTER THE EFFECTIVE OR ABSOLUTE REFRACTORY
PERIOD (FAST FIBER)
TIME
MV
-80
0
RRP
ARP
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POST-REPOLARIZATION REFRACTORINESS (SLOW FIBER)
A
B
C
mV
TIME
-60
0
200 MSEC
POSTREPO
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CHARACTERISTICS OF THE PACEMAKER POTENTIAL
PHASE 4-PACEMAKER POTENTIAL(PP).FREQUENCY DEPENDS ON: THRESHOLD, RESTING POTENTIALSAND SLOPE OF THE PP
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THE CONDUCTION SYSTEM OF THE HEART
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PACEMAKERS (in order of their inherent rhythm)
• Sino-atrial (SA) node (HR 60-70)
• Atrio-ventricular (AV) node (HR 40)
• Bundle of His (HR 15-40)
• Bundle branches
• Purkinje fibers
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CARDIAC MECHANICS
MAIN THEMES
THE HEART AS A PUMP
THE CARDIAC CYCLE
CARDIAC OUTPUT
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THE HEART AS A PUMP• REGULATION OF CARDIAC OUTPUT
– Heart Rate via sympathetic & parasympathetic nerves– Stroke Volume
• Frank-Starling “Law of the Heart”
• Changes in Contractility
• MYOCARDIAL CELLS (FIBERS)– Regulation of Contractility– Length-Tension and Volume-Pressure Curves– The Cardiac Function Curve
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LENGHT/ TENSION AND THE FRANK-STARLING RELATION
LE
FT
VE
NT
RIC
UL
AR
PR
ES
SU
RE
INITIAL MYOCARDIAL FIBER LENGHTLEFT VENTRICULAR END-DIASTOLIC VOLUME
Diastole
Systole
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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)
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CONTRACTILITY:THE VENTRICULAR FUNCTION CURVE
CHANGES INCONTRACTILITY
EFFECT?
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CARDIAC FUNCTION CURVE
CA
RD
IAC
OU
TP
UT
(L
/min
)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
Volume
Pre
ssur
e
THE FRANK- STARLING “LAW OF THE HEART”
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CARDIAC FUNCTION CURVE
CA
RD
IAC
OU
TP
UT
(L
/min
)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
THE FRANK- STARLING “LAW OF THE HEART”
IncreasedContractility
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CARDIAC FUNCTION CURVE
CA
RD
IAC
OU
TP
UT
(L
/min
)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
THE FRANK- STARLING “LAW OF THE HEART”
DecreasedContractility
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ISOVOLUMETRIC RELAXATIONRAPID INFLOW
DIASTASISATRIAL SYSTOLE
EJECTION
ISOVOLUMETRICCONTRACTION
SYSTOLE DIASTOLE SYSTOLE
AORTICPRESSURE
ATRIALPRESSURE
VENTRICLEPRESSURE
ECG
PHONO-CARDIOGAM
VO
LU
ME
(m
l)P
RE
SS
UR
E (
mm
Hg)
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HEART - BLOOD VESSELSCOUPLING AT REST
PUMP ARTERIESVEINS
Qh 5L/min
Qr5L/min
PERIPHERAL R= Pa - Pv / Qr
R = 20mmHg/L/min
MPA=102mmHgCPV=2mmHg=Pv
COMPLIANCESCv = 19CaCv>>>>Ca
Pa
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CARDIAC ARREST!INMEDIATE EFFECT
PUMP ARTERIESVEINS
Qh 0L/min
Qr5L/min
CPV=2mmHg=Pv
Pa
FLOW STOPS HERE
FLOW CONTINUES HERETRANSFER ART-->VEINS
R = 20mmHg/L/minQr= Pa - Pv/20
Qr CONTINUES AS LONG ASA PRESSURE GRADIENT IS SUSTAINED
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CARDIAC ARRESTSTEADY STATE
PUMP ARTERIESVEINS
Qh 0L/min
Qr0L/min
Pv = 7mmHg = MEAN CIRCULATORY PRESSURE OR Pmc
Pa = 7mmHg
FLOW STOPPED
FLOW STOPPED
Qr = 0 ( NO Pa - Pv DIFFERENCE)
95mmHg
5mmHg
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WE START PUMPING!INMEDIATE EFFECT
PUMP ARTERIESVEINS
Qh 1L/min
Qr0L/min
Pv = 7mmHg
Pa = 7mmHg
FLOW STARTS
NO FLOW HERE YET
SOME VENOUS BLOOD
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FLOW RETURNS AT Qr AT THE NEW Qh
PUMP ARTERIESVEINS
Qh 1L/min
Qr1L/min
Pv = 6mmHg
Pa = 26mmHg
FLOW STARTS
R = 20mmHg
Qr = Pa - Pv / 20 = 1L/min
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HEMODYNAMICS
• VELOCITY, FLOW, PRESSURE
• LAMINAR FLOW
• POISEUILLE’S LAW
• RESISTANCE (SERIES-PARALLEL)
• TURBULENT FLOW AND REYNOLD’S NUMBER
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REQUIRED CONCEPTS
VELOCITY = DISTANCE / TIME V = D / T
FLOW = VOLUME / TIME Q = VL / T
VELOCITY =FLOW/ AREA
V = Q / A
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CROSS SECTIONAL AREA AND VELOCITY
Q=10ml/s
A= 2cm2 10cm2 1cm2
V= 5cm/s 1cm/s 10cm/s
V = Q / A
a b c
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POISEUILLE’S LAW GOVERNING FLUID FLOW(Q) THROUGH CYLINDRIC
TUBES
(FLOW)Q(FLOW)Q = (Pi - Po) r
DIFFERENCEIN PRESSURE RADIUS
8nL
VISCOSITY
4
LENGHT
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LAMINAR VS TURBULENT FLOWTHE REYNOLD’S NUMBER
LAMINARFLOW
TURBULENTFLOW
Nr = pDv / n
p = densityD = diameterv = velocityn = viscosity
laminar = 2000 or less
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Right coronary blood flow
Left coronary blood flow
* The peak left coronary flow occurs at the end of isovolumetric relaxation
*
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Cessation of Myocardial Blood Flow
Cessation of Myocardial Blood Flow
mitochondria
cellular pO2 < 5mmHg within seconds
oxidative phosphorylation stops
cytosol
anaerobic glycolysis
glycogen
glucose-6-phosphate
pyruvate
lactate
cellular acidosis
depletion of ATP
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Blood Vessel
• Intima primarily the endothelial lining
• Mediavascular smooth muscle, collagen, elastin
• Adventitiaconnective tissue
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Vascular Endothelium
Vasodilators Vasoconstrictors
Nitric OxideProstacyclinEndothelium-derived hyperpolarizing factorBradykinin
Endothelin-1 Angiotensin II
Wilson SH, Lerman A.Heart Physiology and Pathophysiology, Academic Press(edited by Sperelakis N.) 473-480
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L-Arginine is converted to NO by the enzyme nitric oxide synthase (NOS)
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Nitric Oxide (NO)Function
• Vasodilator• Inhibitor of vascular smooth muscle cell
proliferation• Inhibitor of platelet adherence/aggregation• Inhibitor of leukocyte/endothelial interactions
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Endothelin-1(ET-1)
• Peptide first sequenced in 1988• Most potent vasoconstrictor in humans
• Maintenance of basal arterial vasomotor tone
• Strong chemoattractant for circulating monocytes and macrophage activation “proatherogenic”
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Endothelial Dysfunction
• Imbalance of endothelium-derived relaxing and contracting factors
Atherosclerotic risk factors
Decreased NO bioavailabilityIncreased levels of ET-1