cardiac physiology dr keith mugarura
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TRANSCRIPT
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CARDIOVASCULAR PHYSIOLOGY
Dr. Keith MugaruraDept of Pediatrics Mulago Hospital
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OBJECTIVES
• Explain the physiology of circulation and perfusion
• Describe the electrical and mechanical events involved in the cardiac cycle.
• Discuss the factors that alter or impact the electrical and mechanical events of the cardiac cycle.
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Definition
Cardiovascular physiology is the study of Cardiovascular physiology is the study of
the the circulatory system. More specifically, . More specifically,
it addresses the it addresses the physiology of the of the heart
("cardio") and ("cardio") and blood vessels ("vascular"). ("vascular").
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CARDIOVASCULAR SYSTEM
HEART(PUMP)
VESSELS(DISTRIBUTION SYSTEM)
RE
GU
LA
TIO
N
AUTOREGULATION
NEURAL
HORMONAL
RENAL-BODY FLUIDCONTROL SYSTEM
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PHYSIOLOGY OF THE HEARTPHYSIOLOGY OF THE HEART
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Cardiac Pump Dynamics
• Overview on Anatomy of the heart.
• Electrophysiology of the heart
• Cardiac Cycle
• Pressure
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Overview on Histo- Anatomy of the Heart:Overview on Histo- Anatomy of the Heart:• cardiac muscle fibers are relatively short, thick branched cells, 50-100
μm long
• striated myofibrils are highly ordered usually 1 nucleus per cell and rather than tapering cells are bluntly attached to each other by gap junctions (intercalated discs)
• myocardium behaves as single unit and atrial muscles separated from ventricular muscles by conducting tissue sheath (atria contract separately from ventricles)
• need constant supply of oxygen & nutrients to remain aerobic and hence greater dependence on oxygen than skeletal muscles
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• cardiac muscle cells are not individually innervated like skeletal muscle cells, they are self stimulating
• rhythmic beating of the heart is coordinated and maintained by the heart conducting system
• heart has some specialized fibers that fire impulses to coordinate contraction of heart muscle innervated by autonomic NS
• sympathetic stimulation can raise rate
• parasympathetic stimulation can lower rate
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Electrical cells Muscle (myocardial) cells
•Generate and conduct impulses rapidly
•SA and AV nodes
•Nodal pathways
•Interventricular septum
•No contractile Properties
•Main function is contractionAtrial muscleVentricular muscleAble to conduct electrical impulses
•May generate its own impulses with certain types of stimuli
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Electrophysiology of the Electrophysiology of the HeartHeart
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Cardiac Conduction System
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Overview on Nerve TermsResting stateResting state• The relative electrical charges found on each
side of the membrane at restNet +ve charge on the outsideNet -ve charge on the insideAction PotentialAction Potential• Change in the electrical charge caused by
stimulation of a neuron
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Aps Skeletal vs Cardiac
1
2
3
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Electrical and Mechan Connections
Peak of vent contraction
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Summary of APsRestingResting DepolarizationDepolarization RepolarizationRepolarization
Sodium stays outside of the cell
Potassium mostly stays inside
Massively negative charges never leave the cell
The stimulus hits the cell
Sodium channels open up and sodium pours in then the charges reverse:Positive insideNegative outside
Sodium channels close
Potassium channels Open- Potassium pours out Allows for a quick return to a resting state
Sodium is kicked out of the cell- Active transport Sodium-potassium pump
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OVERVIEW ON ECG
P wave = passage of current through atria from SA Node (conduction through atria is very rapid)
QRS wave = passage of current through ventricles from AV Node – AV Bundle – Purkinje Fibers (impulse slows as it passes to ventricles)
T wave = return to “resting” conditions
ECG is a record of the electrical activity of the conducting system.ECG is NOT a record of heart contractions
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EKG Waves and Intervals
P
Q
R
S
T
P-Rinterval
Q-T interval
QRS length
Normal: PR interval: 0.12-0.2 secQRS length: <0.10 secQT interval: 0.3-0.4 sec
Abnormalities in:QRS – ventricular
depolarizaton problemsP-R interval – A/V
conduction problems
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Pediatric Vs Adult ECGs
• Pediatric ECGs findings that may be normal:• HR >100BPM• Shorter PR, QT Int and QRS Duration• Inferior and Lateral small Q waves• RV Larger than LV in neonates, so: RAD Large Precordial R Waves Upright T Waves
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LARA
LL
ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly)
3 Bipolar Limb Leads:
I = RA vs. LA (+)
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LARA
LL
ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly)
3 Bipolar Limb Leads:
I = RA vs. LA (+)
II = RA vs. LL (+)
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LARA
LL
ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly)
3 Bipolar Limb Leads:
I = RA vs. LA (+)
II = RA vs. LL (+)
III = LA vs. LL (+)
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LARA
LL
ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly)
3 Bipolar Limb Leads:
I = RA vs. LA (+)
II = RA vs. LL (+)
III = LA vs. LL (+)
3 Augmented Limb Leads:
aVR = (LA-LL) vs. RA(+)
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LARA
LL
ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly)
3 Bipolar Limb Leads:
I = RA vs. LA (+)
II = RA vs. LL (+)
III = LA vs. LL (+)
3 Augmented Limb Leads:
aVR = (LA-LL) vs. RA(+)
aVL = (RA-LL) vs. LA(+)
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LARA
LL
ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly)
3 Bipolar Limb Leads:
I = RA vs. LA (+)
II = RA vs. LL (+)
III = LA vs. LL (+)
3 Augmented Limb Leads:
aVR = (LA-LL) vs. RA(+)
aVL = (RA-LL) vs. LA(+)
aVF = (RA-LA) vs. LL(+)
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V1 V2
V3
V4
V5
V6
6 PRECORDIAL (CHEST) LEADS
Spine
Sternum
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ECG Recordings: (QRS vector---leftward, inferiorly and posteriorly
3 Bipolar Limb Leads I = RA vs. LA(+) II = RA vs. LL(+) III = LA vs. LL(+)3 Augmented Limb Leads aVR = (LA-LL) vs. RA(+) aVL = (RA-LL) vs. LA(+) aVF = (RA-LA) vs. LL(+)
6 Precordial (Chest) Leads: Indifferent electrode (RA-LA-LL) vs.chest lead moved from position V1 through position V6.
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Cardiac CycleCardiac Cycle
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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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CARDIAC OUTPUT = STROKE VOLUME x HEART RATE
Autoregulation (Frank-Starling “Law of the Heart”)
Contractility
SympatheticNervous System
ParasympatheticNervous System
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LATE DIASTOLE
ATRIALSYSTOLE
ISOMETRIC VENTRICULARCONTRACTION
VENTRICULAR EJECTION
ISOMETRICVENTRICULARRELAXATION
THE CARDIAC CYCLE
DIASTOLE
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PRES
SURE
DIASTOLICPRESSURE CURVE
SYSTOLIC PRESSURE CURVE
HEART
End Diastolic VolumeEnd Systolic Volume
IsovolumetricPhase
Isotonic (Ejection) Phase
StrokeVolume
Pre-load
After-load
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PRES
SURE
DIASTOLICPRESSURE CURVE
SYSTOLIC PRESSURE CURVE
HEART
End Diastolic VolumeEnd Systolic Volume
IsovolumetricPhase
Isotonic (Ejection) Phase
StrokeVolume
Pre-load
After-load
INCREASED
CONTRACTILITY
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PRES
SURE
DIASTOLICPRESSURE CURVE
SYSTOLIC PRESSURE CURVE
HEART
End Diastolic VolumeEnd Systolic Volume
IsovolumetricPhase
Isotonic (Ejection) Phase
StrokeVolume
Pre-load
After-load
DECREASED
CONTRACTILITY
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PRES
SURE
DIASTOLICPRESSURE CURVE
SYSTOLIC PRESSURE CURVE
HEART
End Diastolic VolumeEnd Systolic Volume
IsovolumetricPhase
Isotonic (Ejection) Phase
StrokeVolume
Pre-load
After-load
INCREASE
DFIL
LING
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Influences of the Cardiac CycleMaster controller: the medullaMaster controller: the medullaIncoming input• Chemoreceptors- Sense changes in pH, PaCO2
and PaO2• Baroreceptors- Sense changes in arterial
pressureResponse of the medulla• Stimulate the autonomic nervous system
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Autonomic Nervous SystemAutonomic Nervous SystemSympatheticSympathetic Nervous System- Nervous System- Extensively
innervates the SA node and ventricular cells Increase in heart rate Increase in conduction and contractility in the
ventricles
ParasympatheticParasympathetic Nervous System- Nervous System- Innervates the SA and AV nodes
• Decreases heart rate• Decreases conduction times through the AV node
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HormonesHormones• Epinephrine & Norepinephrine
– From the adrenal medulla
• Renin-angiotensin-aldosterone– Renin from the kidney– Angiotensin, a plasma protein– Aldosterone from the adrenal cortex
• Vasopressin (Antidiuretic Hormone-ADH)– ADH from the posterior pituitary
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Determination of Stroke VolumePreloadPreload• Amount of blood delivered to the chamber• Depend upon venous return to the heart• Also dependent upon the amount of blood delivered
to the ventricle by the atrium
ContractilityContractility• The efficiency and strength of contraction• Frank Starling’s Law
AfterloadAfterload• Resistance to forward blood flow by the vessel walls
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Preload and Afterload• Preload: Wall tension at EDV (analogous to EDV or
EDP– As Preload increases, so does Stroke Volume. This is a
regulatory mechanism.– Factors that increase venous return, or preload:
• the muscular pump (muscular action during exercise compresses veins and returns blood to the heart), an increased venous tone, and increased total blood volume.
• Afterload: A sum of all forces opposing ventricular ejection. Roughly measured as Aortic Pressure.
– As Afterload increases, stroke volume decreases.
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Starling’s Law of the Heart
• The heart adjusts its pumping rate to the rate of blood return. How?– More blood returning stretches the atria and ventricles
more. – Stretching heart SA node muscle causes faster rhythmicity. – Stretching heart muscle causes faster conduction. – Stretching heart muscle causes stronger, more complete
contraction.
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Contractility
• Increased by increasing myocardial Ca++• Means greater shortening of fibers at a given
fiber length.• Increased contractility = Increased CO (SV)
– Positive Inotropy:• Increased HR (more Ca++ in the cell)• using1 agonists or cardiac glycosides (digoxin)
Inhibit Na/K ATPaseDecrease Ca export
Increases inward CaCauses PLB phosphorylationActivates SERCA
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CARDIAC FUNCTION CURVE
CARD
IAC
OU
TPU
T (L
/min
)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
Volume
Pres
sure
THE FRANK- STARLING “LAW OF THE HEART”
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CARDIAC FUNCTION CURVE
CARD
IAC
OU
TPU
T (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
CARD
IAC
OU
TPU
T (L
/min
)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
THE FRANK- STARLING “LAW OF THE HEART”
DecreasedContractility
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CARDIAC FUNCTION CURVE
CARD
IAC
OU
TPU
T (L
/min
)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
THE FRANK- STARLING “LAW OF THE HEART”
IncreasedHeart Rate
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CARDIAC FUNCTION CURVE
CARD
IAC
OU
TPU
T (L
/min
)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
THE FRANK- STARLING “LAW OF THE HEART”
DecreasedHeart Rate
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Physiology of Blood VesselsPhysiology of Blood Vessels
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• Flow
• Resistance
• Elastance/Compliance
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Flow
• Blood circulates by going down a pressure gradient
• to understand circulation we must understand blood pressure
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Blood Pressure
Blood Pressure is created by1. The force of the heart beat• the heart maintains a high pressure on the
arterial end of the circuit2. Peripheral resistance• back pressure, resistance to flow• eg atherosclerosis inhibits flow so raises
blood pressure
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Control of Blood Pressure
• Baroreceptor • Baroreflex• Renin-angiotensin system
– Renin– Angiotensin
• Juxtaglomerular apparatus• Aortic body and carotid body• Autoregulation
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MOTOR CORTEXHYPOTHALAMUS
VASOMOTOR CENTERPRESSOR AREA
DEPRESSOR AREACARDIOINHIBITORY AREA
Vagus
HEARTArterioles
VeinsAdrenalMedulla
BaroreceptorsCarotid SinusAortic Arch
ChemoreceptorsCarotid BodiesAortic Bodies
Bainbridge Reflex ( Heart Rate)Atrial Receptors Volume Reflex ( Urinary OUTPUT)
a. Vascular Sympathetic Toneb. ADH Secretionc. Aldosterone Secretion
Chemosensitive Area
GlossopharyngealNerve
SympatheticNervous
System
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Veins
• Pressure inside is 35 to 15 mmHg
• 60-70 % of the blood is in veins
• Transport of blood to heart for oxygenation
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Flow in Veins•Flow of blood in veins is due to way valves and venous pumps
Way valves•prevent backflow•most abundant in veins of limbs•quiet standing can cause blood to pool in veins and may cause
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venous pumpsMuscular pump (=skeletal muscle pump)• during contraction veins running thru muscle are compressed• and force blood in one direction (toward heart)Respiratory pumpInspiration:• creates pressure gradient in Inferior Vena Cava to move blood
toward heartExpiration:• increasing pressure in chest cavity forces thoracic• blood toward heart
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CAPILLARIES
• Pressure inside is 35 to 15 mmHg
• 5% of the blood is in capillaries
• exchange of gases, nutrients, and wastes
• flow is slow and continuous
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Metarteriole
Arteriole
PrecapillarySphinctersCapillaries
Venule
?
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Capillary Beds•Capillaries ( usually 10 –100) are organized into capillary beds
•Functional groupings of capillaries functional units of circulatory system
•Arterioles and venules are joined directly by metarterioles (become thoroughfare channels after capillaries branch off)
•Capillaries branch from metarterioles 1-100/bed cuff of smooth muscle surrounds origin of capillary branches = precapillary sphincter
Amount of blood entering a bed is regulated by:a. vasomotor nerve fibersb. local chemical conditions
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VASOMOTION = Intermittent flow due to constriction-relaxation cycles of precapillary shpinctersor arteriolar smooth muscle (5 - 10/min)
AUTOREGULATION OF VASOMOTION:
1. Oxygen Demand Theory (Nutrient Demand Theory)O2 is needed to support contraction (closure)
2. Vasodilator TheoryVasodilator substances produced (via O2)e.g. Adenosine Heart CO2 Brain Lactate, H+, K+ Skeletal Muscle
3. Myogenic Activity
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Vasoactive Substances
• Local– Metabolites (adenosine, K+, CO2)– Neurotransmitters (1- constriction, 2-dilation)– Hormones (Histamine, Bradykinin)
• General– Renin-Angiotensin-Aldosterone System – conserves water
and salt, constricts arterioles– ADH (Vasopressin) – vasoconstrictor and water conservation– ANP (Atrial Natriuretic Peptide) – arteriolar dilator and
increased salt/water excretion
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Resistance
• Parallel– Most vascular beds– Lower total Resistance– Independent control
• Series– Sequential pressure drops– Portal circulations(Hepatic, Hypothalamic
Hypophyseal, etc)
nRRRR
1111
21
nRRRR 21
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Name of circulation
% of cardiac output
Autoregulation Perfusion Comments
pulmonary circulation
100% (deoxygenated) Vasoconstriction in response to hypoxia
cerebral circulation 15% high under-perfusedFixed volume means intolerance of high pressure. Minimal ability to use anaerobic respiration
coronary circulation 5% high under-perfused
Minimal ability to use anaerobic respiration. Blood flow through the left coronary artery is at a maximum during diastole (in contrast to the rest of systemic circulation, which has a maximum blood flow during systole.)
Splanchnic circulation 15% low Flow increases during digestion.
hepatic circulation 15% Part of portal venous system, so oncotic pressure is very low
renal circulation 25% high over-perfused Maintains glomerular filtration rate
skeletal muscular circulation 17% Perfusion increases dramatically during
exercise.
Cutaneous circulation 2% over-perfused Crucial in thermoregulation. Significant
ability to use anaerobic respiration