CARDIOVASCULAR PHYSIOLOGY

Dr. Keith MugaruraDept of Pediatrics Mulago Hospital

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.

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").

CARDIOVASCULAR SYSTEM

HEART(PUMP)

VESSELS(DISTRIBUTION SYSTEM)

RE

GU

LA

TIO

N

AUTOREGULATION

NEURAL

HORMONAL

RENAL-BODY FLUIDCONTROL SYSTEM

PHYSIOLOGY OF THE HEARTPHYSIOLOGY OF THE HEART

Cardiac Pump Dynamics

• Overview on Anatomy of the heart.

• Electrophysiology of the heart

• Cardiac Cycle

• Pressure

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

• 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

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

Electrophysiology of the Electrophysiology of the HeartHeart

Cardiac Conduction System

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

Aps Skeletal vs Cardiac

1

2

3

Electrical and Mechan Connections

Peak of vent contraction

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

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

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

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

LARA

LL

ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly)

3 Bipolar Limb Leads:

I = RA vs. LA (+)

LARA

LL

ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly)

3 Bipolar Limb Leads:

I = RA vs. LA (+)

II = RA vs. LL (+)

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 (+)

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(+)

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(+)

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(+)

V1 V2

V3

V4

V5

V6

6 PRECORDIAL (CHEST) LEADS

Spine

Sternum

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.

Cardiac CycleCardiac Cycle

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

CARDIAC OUTPUT = STROKE VOLUME x HEART RATE

Autoregulation (Frank-Starling “Law of the Heart”)

Contractility

SympatheticNervous System

ParasympatheticNervous System

LATE DIASTOLE

ATRIALSYSTOLE

ISOMETRIC VENTRICULARCONTRACTION

VENTRICULAR EJECTION

ISOMETRICVENTRICULARRELAXATION

THE CARDIAC CYCLE

DIASTOLE

PRES

SURE

DIASTOLICPRESSURE CURVE

SYSTOLIC PRESSURE CURVE

HEART

End Diastolic VolumeEnd Systolic Volume

IsovolumetricPhase

Isotonic (Ejection) Phase

StrokeVolume

Pre-load

After-load

PRES

SURE

DIASTOLICPRESSURE CURVE

SYSTOLIC PRESSURE CURVE

HEART

End Diastolic VolumeEnd Systolic Volume

IsovolumetricPhase

Isotonic (Ejection) Phase

StrokeVolume

Pre-load

After-load

INCREASED

CONTRACTILITY

PRES

SURE

DIASTOLICPRESSURE CURVE

SYSTOLIC PRESSURE CURVE

HEART

End Diastolic VolumeEnd Systolic Volume

IsovolumetricPhase

Isotonic (Ejection) Phase

StrokeVolume

Pre-load

After-load

DECREASED

CONTRACTILITY

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

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

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

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

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

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.

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.

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

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”

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

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

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

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

Physiology of Blood VesselsPhysiology of Blood Vessels

• Flow

• Resistance

• Elastance/Compliance

Flow

• Blood circulates by going down a pressure gradient

• to understand circulation we must understand blood pressure

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

Control of Blood Pressure

• Baroreceptor • Baroreflex• Renin-angiotensin system

– Renin– Angiotensin

• Juxtaglomerular apparatus• Aortic body and carotid body• Autoregulation

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

Veins

• Pressure inside is 35 to 15 mmHg

• 60-70 % of the blood is in veins

• Transport of blood to heart for oxygenation

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

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

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

Metarteriole

Arteriole

PrecapillarySphinctersCapillaries

Venule

?

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

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

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

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

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