Cardiovascular Physiology and Monitoring Tariq Alzahrani M.DAssistant Professor College of Medicine King Saud University

Coronary Circulation Blood Supply RCA LCA

Conduction System SAN AVN

Coronary Perfusion Pressure (50-120mmHg)

ADBP – LVEDP

Cardiac Cell Types• Electrical cells Generate and conduct impulses rapidly• SA and AV nodes• Nodal pathways• No contractile properties

• Muscle (myocardial) cells Main function is contraction• Atrial muscle• Ventricular muscle• Able to conduct electrical impulses• May generate its own impulses with certain types of stimuli

PURKINJE FIBERS

BUNDLEBRANCHES

Sino-atrial(SA) node

Atrio-ventricular (AV) node

INTERCALATED DISC (TIGHT JUNCTION)

Nerve impulse Terminology• Resting state The relative electrical charges found on each

side of the membrane at rest • Net positive charge on the outside • Net negative charge on the inside

• Action PotentialChange in the electrical charge caused bystimulation of a neuron

Action Potential Terms• DepolarizationThe sudden reversal of electrical chargesacross the neuron membrane, causing thetransmission of an impulse• Minimum voltage must be met in order to do this

• Repolarization Return of electrical charges to their originalresting state

Automaticity (P Cells)• Prepotential, Resting Potential,

Diastolic Depolarization• Action Potential• Repolarization

Factors That Affect Automaticity:Sympathetic and parasympathetic outflow will affect the prepotential phaseTemperatureRA and SAN stretchHormonesDrugs

Distribution Of P Cells

Conduction SpeedA-V nodal conduction:One way conductionA-V nodal Delay (0.1 sec)

Factors Affecting Conductivity:Sympathetic and vagal infuinceTemperatureHormonsIschemiaAcidosisDrugs

MEM

BRAN

E P

OTE

NTI

AL (m

V)

-90

0

0

12

3

4

TIME

PHASE0 = Rapid Depolarization (inward Na+ current) 1 = Overshoot (outward K+ current)

2 = Plateau (inward Ca++ current)

3 = Repolarization (outward K+ current)

4 = Resting Potential

Mechanical Response

(outward K+ current)(inward Na+ current)

MEM

BRAN

E P

OTE

NTI

AL (m

V) 0 0

-50 -50

-100 -100

SANVENTRICULULARCELL

ACTION POTENTIALS

0

12

3

4

4

0 3

Cardiac MyocyteStructureCa++ ReleaseExcitation-Contraction

Coupling

The Fibrous A-V Ring

THE ANATOMY OF BLOOD VESSELS

• Layers:1. Tunica interna (intima)

2. Tunica media

3. Tunica externa (adventitia)

Comparison of Veins and Arteries

Arteries: Veins:

The Distribution of Blood

Cardiac Output CO = SV x HR• The amount of blood ejected from theventricle in one minute• Stroke volume Amount of blood ejected from the ventricle inone contraction• Heart rateThe # of cardiac cycles in one minute

Determination of Stroke Volume• Preload 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• Contractility The efficiency and strength of contraction Frank Starling’s Law• Afterload Resistance to forward blood flow by the vessel walls

• End-diastolic volume (110-120 mL)• End-systolic volume (40-50 mL)• Stroke volume (70 mL)• Ejection fraction (60%)

Pressure-Volume Loops

Volume Load ►

Pressure Load ►

Regulation of Cardiovascular System

• Neural Mechanisms–Vasoconstriction

–Vaosdilation

–Baroreceptors

–Chemoreceptors

Nerve Supply of the Conduction System

SANReceives right vagal and right sympathetic supply

AVNReceives left vagal and left sympathetic supply

The rest of the conduction system receive sympathetic supply (like ventricle)

HORMONAL REGULATION

• 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• ANP from RA

BP (Kidney) Renin

Angiotensinogen (renin substrate)

Angiotensin

Aldosterone

Kidney

sodium & water retention

Vasoconstriction

Venoconstriction

RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM

HypothalamicOsmoreceptors

BP via Posterior Pituitary Vasopressin (ADH)

Vasoconstriction WaterVenoconstriction Retention

VASOPRESSIN(ANTIDIURETIC HORMONE)

How To interpret ECG?

1. Rate?

2. QRS Duration?

3. Stability?

ECG limb leads

Normal ECG

• P wave corresponds to depolarization of SA node

• QRS complex corresponds to ventricular Depolarization

• T wave corresponds to ventricular repolarization

• Atrial repolarization record is masked by the larger QRS complex

Measurements

Small square = 0.04 sec.

Large square = 5 small square = 0.2 sec.

One second = 5 large square.

One minute = 300 large square.

P duration = 3 small sqs = 0.12 sec.

P height = 3 small sqs = 0.12 sec.

QRS duration=3 small sq=0.12 sec.

P-R interval = 5 small sq = 0.2 sec.

Remember This 3, 3, 3 and 5

Right ventricular hypertrophy (precordial leads)

Left ventricular hypertrophy (precordial leads)

QRS voltage decrease

• Myocardial infarction (decrease of excitable myocardium mass)• Fluids in the pericardium (short-circuits of currents within pericardium)• Pulmonary emphysema (excessive quantities of air in the lungs)

J-point:

ST-segment shift –sign of current ofinjury

-Time point of completeddepolarization (zero reference)-The junction of the QRS and the ST segment

Injury currents: constant source

• Mechanical trauma• Infectious process• Ischemia

• Ischemia= ST depression or T-wave inversion Represents lack of oxygen to myocardial tissue

• Injury = ST elevation -- represents prolonged ischemia; significant when > 1 mm above the baseline of the segment in two or more leads

• Infarct = Q wave — represented by first negative deflection after P wave; must be pathological to indicate MI

What part of the heart is affected ?II, III, aVF =

Inferior Wall

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Which part of the heart is affected ?

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

• Leads V1, V2, V3, and V4 =

Anterior Wall MI

What part of the heart is affected ?

I, aVL, V5 and V6 Lateral wall of left

ventricle

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

• I, aVL, V5 + V6 = Lateral Wall = Circumflex Artery Blockage

RateIf regular: Divide 300/ number of large squares between 2 Rs = HR

If irregular: count number of complexes in 6 sec. and multiply by 10

- Normal 60 -100

- Bradycardia < 60

- Tachycardia > 100

P = Sinus

No P = Non sinus

Rate > 100.

QRS: Narrow.

Stable or unstable.

Rate < 60.

QRS: Narrow.

Stable or unstable.

Sinus tachycardia.

PSVT.

Atrial flutter.

Atrial fibrillations.

Sinus bradycardia.

1st degree HB.

2nd degree HB.

Complete HB.

Supraventricular Rhythm

Supraventricular Rhythm: Tachycardia

Sinus Tachycardia

Paroxysmal SVT

Supraventricular Rhythm: Tachycardia

Atrial Flutter

Supraventricular Rhythm: Tachycardia

Atrial Fibrillations

Supraventricular Rhythm: Tachycardia

Supraventricular Rhythm: Bradycardia

Sinus Bradycardia

Normal Sinus Rhythm

Supraventricular Rhythm: Bradycardia

1st Degree HB

Supraventricular Rhythm: Bradycardia

2nd Degree HB: Mobitz 1 Wenckebach.

Progressive lengthening of the P-R interval with intermittent dropped beat.

Supraventricular Rhythm: Bradycardia

Sudden drop of QRS without prior P-R changes

2nd Degree HB: Mobitz 2

Supraventricular Rhythm: Bradycardia

3rd Degree HB

The right bundle brunch block (precordial leads)

Left bundle branch block (precordial leads)

Characteristics of PVCs• QRS prolongation due to slower conduction in

the muscle fibers• QRS high amplitude due to lack of synchrony of excitation of RV and LV which causes partial neutralization of their contribution to the ECG• QRS and T-wave have opposite polarities, again

due to slow conduction which causes repolarization to follow depolarization.

Ventricular Rhythm

Idioventricular Rhythm.

Ventricular Rhythm

Accelerated Idioventricular Rhythm.

Ventricular Rhythm

Ventricular Rhythm

Pacer Rhythm

Ventricular Rhythm

Stability

* Stable patient: think of drug therapy.

* Unstable patient: think of electric therapy.

Treatment

Supraventricular Rhythm:

Stable = Drugs

Adenosine.

B blocker.

Ca channel blocker.

Digoxin.

Unstable = Electric

DC, Synchronized

Treatment

Ventricular Rhythm:

Stable = Drugs

Amiodarone.

Lidocaine.

Procainamide.

Unstable = Electric

DC, Non Synchronized

Normal Venous Tracing

a ► Atrial Contraction

c ► Isometric (V) Contraction

x ► Mid-Systole

v ► Venous Filling (Atrial)

y ► Rapid Filling (Ventricular)

THANK YOU