CARDIOVASCULAR SYSTEM (Cont.

D. CORONARY BLOOD SUPPLY:

– Blood to cardiac tissues (Myocardium)
– Different from blood that goes through heart chambers
– Highest capillary concentration/unit tissue weight

Unit 6 – Cardiac muscles – very limited capacity for anaerobic respiration

– Most researched blood vessels in the human body

E. CIRCULATORY CIRCUITS:
Cardiovascular Physiology 1. Pulmonary – run by right ventricle; low pressure; less blood
2. Systemic – run by left ventricle; high pressure; more blood

CARDIOVASCULAR SYSTEM CARDIOVASCULAR SYSTEM (Cont.)

A. COMPONENTS OF THE SYSTEM: F. BLOOD FLOW: (Handout)
– Blood; Heart; Blood vessels
B. FUNCTIONS: – Bulk flow (all components move as one unit in one direction)
– Transport both the “good” and the “bad” stuff – Run by pressure difference
– Good stuff – oxygen, nutrients, chemical messengers, enzymes – F = ∆P/R
– Bad stuff - carbon dioxide, metabolic wastes (F = Blood Flow, ∆P = Pressure gradient; R = Resistance)
– Interacts with other systems – R = (VL/r4)(8/3.14)
(V = Viscosity; L = Length of blood vessels; r = radius)
C. BLOOD VESSELS:
– Most of the unknowns in the equation are constants except
– Size decreases away from heart radius
– Use: Arteries carry oxygenated blood; Veins carry deoxygenated – Therefore, Resistance to Blood Flow is mainly determined by
blood (1/r4) or the size of the blood vessels
– Exceptions - Pulmonary Vein and Artery – The smaller the blood vessel, the higher the Resistance

1
 HEART STRUCTURE INNERVATION OF THE HEART
1. STRUCTURAL LAYERS: 1. ANS (Sympathetics; Parasympathetics)
– Pericardium (sac), Epicardium, Myocardium, and Endocardium A. SYMPATHETICS:
– Innervates atria and ventricles
2. FOUR CHAMBERS: – Increase heart rate and contractility
– Neurotransmitter (Norepinephrine)
– Two Atria; Two Ventricles
– Receptors (Beta-adrenergic)
– Septum divides heart into left and right portions
– No horizontal “blood” flow
B. PARASYMPATHETIC: (Cranial Nerve X or Vagus nerve)
– Blood flow routes; Vertical “blood” flow – Mainly innervate the atria
– Decrease heart rate
3. “SKELETON”: – Little effect on ventricles and contractility
– Connective tissues & papillary muscles – Neurotransmitter (Acetylcholine)
– Used to anchor the valves firmly in place – Receptors (Muscarinic Cholinergic)

CONDUCTING SYSTEM OF HEART

A. COMPONENTS:
HEART STRUCTURE (Cont.)
• SA NODE Æ AV NODE Æ BUNDLE OF HIS Æ LEFT AND
4. VALVES:(Handout)
RIGHT BRANCHES Æ PURKINJE FIBERS
– 2 AVs or cuspids (blood into ventricles)
– 2 Arterials or semi-lunars (blood exit into aorta and pulmonary
artery) B. GENERAL POINTS:
– No valves by Venacava and Pulmonary veins entrances into the – Modified cardiac muscle cells acting as the “nervous system” of
heart
the heart; generally called nodal cells.
– Opening and closing depends on pressure differences and
directional blood flow) – SA and AV nodes located in right atrium
– Allow blood to move into one direction only – Conducting system (nodal cells) accounts for about 1% of all
5. MYOCARDIUM: cardiac cells
– Branched cardiac muscle cells – Nodal cells system are very excitable (create and conduct APs)
– Gap junctions (Quick Signal Transmission)
– Rest of cardiac cells pick up APs from conducting system and
– Desmosome junctions (strength & integrity) and Intercalated discs
transmit them fast via gap junctions
– Left ventricle wall thicker than right ventricle (WHY?)

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CONDUCTING SYSTEM OF HEART (Cont.)
C. SA NODE:
– Has pacemaker (spontaneous) cells (sets pace or rate of the heart)
– Creates potentials (100 APs/minute at rest) – the highest of all
nodal cells
– 1 AP Æ 1 heartbeat
– 100 APs = 100 beats/minute (“normal” basal heart rate)
– Normal heart rate – 70-80 beats/min at resting conditions (P>S)
– Innervation (ANS):
• Sympathetics (Norep., Epin.) - increase heart rate)
• Parasympathetics – the Vagus nerve (Ach.) - (reduce heart
rate)
CONDUCTING SYSTEM OF HEART (Cont.)
D. AV NODE:
– Slows transmission of AP within conducting system (0.1 secs)
– Coordinates cardiac function – Atria contracting before ventricles
(why?)
– Blocking AV nodal Action:
• Lose coordination of atria and ventricles
• Results into an inefficient heart pump
E. BUNDLE OF HIS:
– Transfers signals into the ventricles
F. BRANCHES AND PERKINJEE FIBERS:
– Spread the signals throughout the heart
HEARTBEAT
Heartbeat involves electrical activities (setting the pace) and
mechanical activities (contractions). Nodal cells are auto-rhythmic
(control HEART RATE); cardiac cells are contractile (control
CONTRACTILITY).
A. ELECTRICAL ACTIVITY:
– Within the conducting system:
• SA node (Pacemaker) cells are autorhythmic; spontaneously
self-excite using K+ , Na+ and Ca2+ ion channels; the cells
depolarize and repolarize to create pacemaker potentials
(PPs)
• Presence of leaky K+ channels; therefore Vm of cardiac muscles
is lower than – 70 mV
• Pacemaker potentials (PPs) are transmitted very fast along
the nodal cells of the conducting system. Nodal cells are
large diameter.
HEARTBEAT (cont.)
B. MUSCULAR ACTIVITY:
- Within myocardial cells:
• Cardiac cells next to conducting system pick up the signal
(AP); use gap junctions for fast transmission and distribution
of APs to other cardiac cells
• APs increase Ca2+ influx into cytosol from ECF and
sarcoplasmic reticulum (SR)
• Ca2+ from ECF also induces Ca2+ release from SR
• Ca removes Tropomyosin-Troponin blocking complex
• Myosin binds to Actin; Contraction by Sliding Filament
Mechanism
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SUMMARY OF ELECTRICALAND MECHANICAL ACTIVITIES
OF THE HEART
• It is the depolarization and repolarization of:
1. SA node
2. Atrial muscles (contraction and relaxation)
3. AV node
4. Bundle of His and the Branches
5. Purkinje fibers
6. Ventricular muscles (contraction and relaxation)
ELECTROCARDIOGRAMS (EKG OR ECG)
A. PRINCIPLE:
– Measures current generated in ECF by
electrical activities in cardiac muscles
B. USES OF EKGs:
– Detect Abnormal Rhythms (arrhythmia)
• (Bradycardia, Tachycardia)
– Detect Abnormal Conduction Patterns
• (Ectopic foci, Fibrillations, Flutters)
– Detect Cardiomyopathy
• (Death of cardiac tissue)
ELECTROCARDIOGRAMS (cont.)
C. MEASUREMENT AND WAVES: (Handout)
– Use a patient cable hooked on patient (electrodes) and
machine (adaptor)
– Normally, electrodes are placed on limbs (limb leads)
or on chest (chest leads)
D. MEASUREMENT AND ACCURACY:
– Best results – subject patient to some form of stress
– Accuracy is 60-65%; but can be improved to 90-95%
via the “before and after” echocardiography or nuclear
cardiac imaging
VECTOR CARDIOLOGY
A. COMMON LEADS:
(A Lead refers to electrode placement to create an EKG)
1. Chest – (V1 – V6) – Unipolar
2. Limb – (I, II, III) – Bipolar
3. There are other leads (placements and combinations)!
B. EINTHOVEN’S TRIANGLE:
– Created by the 3 Bipolar Limb Leads
– Used to Calculate Axis of the Heart (normal 60-70 o)
– Could be used as an indirect indicator of cardiomegaly
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 DIAGNOSTIC USE OF EKGs
HEART FUNCTION (SUMMARY)
A.VERY COMPLEX SUBJECT:
A. SEQUENCE:
– Leads used
– Atria contract as a unit; Ventricles contract as a unit
– Conditions under which EKG was taken
– Atria contract before ventricles to maximize EDV
B. BASIC TOOLS USED IN DIAGNOSIS:
1. Waves: (Size; Absence; Inversion)
B. REFRACTORY PERIOD OF CARDIAC MUSCLES
_ Absence of P-wave (Atrial fibrillation)
– Very long compared to skeletal muscles (300 vs 10 ms)
_ Inverted T-wave (Myocardial Ischemia)
– Cardiac muscle AP is different
• AP has a plateau due to Ca2+ influx
2. Abnormally long intervals between waves (Duration!).
• AP has 3 phases
– P-R = SA node blockage (AV Block)
– Importance:
– Q-S = Ectopic Focus ; problems with ventricular depolarization
• Prevents tetanization (cannot stimulate at close intervals)
– S-T = Myocardial Ischemia
• Maintains pumping efficiency (heart has time to fill and pump)
(CURRENTLY EKGs ARE COMPUTERIZED TO PROVIDE
INSTANT DIAGNOSIS)

STARLING’S LAW OF THE HEART ECTOPIC FOCUS

1. OBSERVATION: A. DEFINITION:
– Premature APs produced by other nodal cells in the conducting
– Blood in ventricle was related to SV (blood pumped/beat)
system not SA nodal cells due to:
• Localized ischemias and calcified plaques or drug toxic
2. THEORY: irritation
– Intrinsic (genetic) characteristic of cardiac muscles whereby B. CAN CAUSE:
increased muscle stretch leads to stronger force of contraction – Premature atrial or ventricular contractions (PAC, PVC)
– Delay (skip) in the heartbeat – compensatory pause
3. INCREASED EDV (VENTRICULAR FILL): C. CAN RESULT INTO:
– Increases (stretch of muscles; force of contraction; SV; CO) – Longer diastole (filling) leading to increased EDV
– Stronger systole (contraction) leading to increased SV (blood
ejected)
4. APPLICATION:
– Lethal ventricular fibrillations
– Exercise; Heart “Balance”

5
 CARDIAC CYCLE (Handouts)
A. LATE DIASTOLE:
– AV valves open; Arterial valves closed
– Filling with blood from Venacava/Pulmonary vein Æ Atria Æ
ventricles
– About (70-80%) full, SA node fires AP
– Atrial Depolarization and Contraction
– Rest of blood from Atria pushed into ventricles creating END-
DIASTOLIC VOLUME (EDV)
CARDIAC CYCLE: (Cont.)
B. SYSTOLE:
– Pressure changes; AVs valves close Æ LUB
– Isovolumeric ventricular contraction (IVVC) (all 4 valves are
closed)
– AV node fires AP
– Ventricular depolarization and contraction
– Arterials open due to pressure changes
– Blood ejection creating arterial or systolic pressure
– Some blood remains in the ventricles creating END-
SYSTOLIC VOLUME (ESV)
CARDIAC CYCLE: (Cont.)
C. EARLY DIASTOLE:
– Pressure changes; arterials close Æ DUB
– Isovolumeric ventricular relaxation (IVVR) (all 4 valves are
closed)
– Ventricular repolarization and relaxation
– AVs open due to pressure changes
– Begin refilling with blood once again
IMPORTANT POINTS ABOUT CADIAC CYCLE
A. STUDY:
– Relationships between Electrical and Mechanical phenomena
during Cardiac Cycle – (EKG, blood pressures,blood volumes,
heart sounds…)
B. TWO BRIEF PERIODS (IVVC, IVVR):
– When all 4 valves are closed; no period when all 4 valves are open
C. BLOOD EJECTION/FILLING:
– Blood Ejection fastest at beginning of SYSTOLE
– Blood Filling is Fastest at beginning of DIASTOLE
D. STROKE VOLUME (SV):
– SV is amount of blood pumped/ventricle/beat (EDV – ESV)
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 FACTORS AFFECTING CARDIAC OUTPUT
(CO = HR x SV)
HEART SOUNDS A. HEART RATE (HR):
– Sympathetics: ↑ HR by increasing Na+ influx into SA nodal cells Æ
A. NORMAL SOUNDS: (Handout) ↑ Depolarization Æ ↑ APs/unit time; (↑ AP speed of conduction on
– Include LUB, DUB, Venous pulse the nodal cells of the conducting system of the heart??)
B. ABNORMAL SOUNDS (MURMURS): – Hormones: Plasma Epinephrine (↑ HR)
– Presence of murmurs indicates some health problem – Parasympathetics: ↓ HR by increasing K+ efflux out of SA nodal
cells Æ Hyperpolarization Æ ↓ APs/unit time
– Can be caused by:
• Stenosis (narrowing of valves) B. STROKE VOLUME (SV):
• Insufficiency (Averted valves) – Sympathetics: ↑ SV by increasing Ca2+ influx into cardiac muscles
• Hole in cardiac septum Æ ↑ Strength of contraction.
– Murmurs during: – Hormones: Plasma Epinephrine (↑ SV)
• SYSTOLE usually indicate stenotic semi-lunar – EDV Æ Starling’s Law Æ ↑ SV
valves
• DIASTOLE usually indicate stenotic AV valves C. OTHER FACTORS:
– Exercise, Temperature, Age, Emotions, Stress

CARDIAC OUTPUT (CO) Cadiac Output: Applications

CO (L/min.) = SV (mL/beat) x HR (beats/min.)
D. VENOUS RETURN AND CARDIAC OUTPUT
A. DEFINITIONS:
– CO is the amount of blood pumped by each ventricle per minute 1. During Exercise:
– SV is the amount of blood pumped by each ventricle per beat – ↑ Venous Return Æ ↑ EDV Æ ↑ SV Æ ↑ CO
– HR is the number of heart beats/minute
B. FOR AN AVERAGE PERSON: 2. During Heart Failure:
– CO = 5-6 L per minute
– SV = 70-90 ml per beat – ↓ Venous Return Æ ↓ EDV Æ ↓ SV Æ ↓ CO
– HR = 60-80 beats per minute

7
 ENERGY REQUIREMENTS FOR CARDIAC
VASCULAR PRESSURES
FUNCTION
A. TWO PRESSURE SYSTEMS:
A. REQUIREMENT: – Arterial Pressure (used in Arterial portion of the circuits)
– Depends on Heart rate and Blood Pressure • Created by Heart Pumping Action
• Higher than Venous Pressure ( Pressure gradients 90 vs 15 mm
Hg)
B. ENERGY (ATP) PRODUCTION:
• Stored in big arteries (Pressure Reservoirs)
– Derived from nutrients and O2 supply to cardiac muscle (Coronary
blood supply) – Venous Pressure (used in Venous portion of the circuits)
– Myocardial ischemia effects are especially bad for people who: • Created by a bunch of factors:
– Suffer from hypertension (↑ MAP) – Sympathetic Stimulation to veins
– Have Tachycardia (↑ HR) – Muscular pumps
– Respiratory movements
– Blood volume
C. DEFINITIONS OF COMMON CARDIAC PROBLEMS: • Veins “store” blood (Blood Reservoirs)
(Handout)

BLOOD PRESSURE
VASCULAR SYSTEMS A. MEASUREMENT:
– Measured as systolic pressure (SP) and diastolic pressure (DP)
A. TWO CIRCUITS: (Handout)
– Pulmonary (low pressure circuit); Systemic (high pressure circuit) – Measured in mm Hg using sphygmomanometer; reported as
SP/DP(120/70)

B. ROLE OF PRESSURE: (Handout)

– Pulse pressure (PP) is the difference (SP – DP)
– To distribute blood into all parts of the body through the vascular
systems
BLOOD FLOW (F) = Pressure Gradient (∆P) – Magnitude of PP depends on:
Resistance (R) • Stroke volume (SV)
– This is the Poiseuille-Hagen’s Law • Elasticity of Arterial blood vessels
– R depends on: • Speed of blood ejection by left ventricle of the heart
• Size of blood vessel and viscosity of blood

8

BLOOD PRESSURE (Cont.)
B. MEAN ARTERIAL PRESSURE (MAP):
– Average pressure that drives blood throughout the body. It is
therefore used for diagnostic purposes.
– Calculated in 2 ways:
1. MAP = DP + (1/3)PP
2. MAP = CO x TPR (Total Peripheral Resistance)
3. MAP = [(2 x DP) + SP]/3
– Normal values (90-110 mm Hg):
1. Above normal – Hypertension (High blood pressure)
2. Below normal – Hypotension (Low blood pressure)
ARTERIAL BLOOD VESSELS
STRUCTURE OF BLOOD VESSELS: (Handout)
- Various walls (layers) and their respective uses
AORTA/ARTERIES:
– Large diameter -- ↓ resistance to blood flow
– Thick elastic tissue -- ↑ compliance
– Pressure reservoirs
ARTERIOLES:
– Small diameter -- ↑ resistance to blood flow
– Main determinants of blood flow in body
– Spontaneously constrict or dilate (lots of smooth muscles)
ARTERIOLES (Cont.)
CONTROL OF ARTERIOLAR SIZE
A. LOCAL CONTROLS OR FACTORS: eg CO2
_ Dilate arterioles to effect hyperemia (↑ blood flow) to an area or
organ
Factors ↑ build up of Local factors:
_ ↑ Metabolism Æ Active or Functional hyperemia
_ Vessel Occlusion Æ Reactive hyperemia
_ Tissue Injury and Localized Low Pressure Situations
B. SYMPATHETICS: (Norep & Epin)
_ Can Constrict or Dilate arterioles (receptors!)
C. HORMONES:
_ Constrict (Vasopressin or ADH, Plasma Epin., Angiotensin)
_ Dilate (Atrial Natrauretic)
CAPILLARIES:
A. STRUCTURE
– Narrow, Thin-walled (Endothelium); Highly permeable (porous)
– One capillary (high resistance to blood flow - narrow); capillary bed
(low resistance to blood flow – large cross-sectional area)
B. NUMBERS:
– Millions – each about 1mm long
– Total capillary length – 25,000/50,000 miles
– Large cross-sectional area (Slow Blood Flow)
– Cells close to capillaries (0.01mm)
– Capacity – 5-10% of total blood depending on level of activity
C. CAPILLARY BEDS: (Handout)
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 CAPILLARIES (Cont.)
C. FUNCTIONS:
– Nutrient, gases, waste products and fluid exchange REGULATING MAP (Handout)
NOTES ON NUTRIENT AND WASTE EXCHANGE: (Handout) A. BARORECEPTOR REFLEX:
– Diffusion and Carrier Mediated systems are involved. – Stimulus:
NOTES ON FLUID EXCHANGE: (Handout) • Change in MAP (Normal 90-110 mm Hg)
Hydrostatic and osmotic pressures involved – Receptors:
– Capillary hydrostatic pressure (dominant at arterial end; > plasma)
• Two barorecptors located in carotid sinuses
– Capillary osmotic pressure (dominant at venous end; > plasma proteins)
– More Filteration (arterial end); More Absorption (venous end) • One barorecptor located in Aortic arch
– Filteration > Absorption (4 L/day in adults) • Others in large arteries and veins, myocardial layer
– Returned into circulatory system via lymphatic system
– Integrating Centers:
– Edema (accumulation of fluid in tissues) if not returned.
– Interstitial osmotic pressure is the lowest • Medullary cardiovascular control centers in brain stem;
hypothalamus, cerebral cortex
LIKELY CAUSES OF EDEMA: (Handout) – Efferent Route: ANS (Sympathetic and Parasympathetic)
– Effectors : Heart, Blood vessels

STRUCTURE AND FUNCTION OF VEINS CORRECTING HYPOTENSION

• ↓ MAP Æ↓ receptor firing to control centers
A. STRUCTURE:
– Large diameter • ↑ Sympathetics; ↓ Parasympathetics

– Present low resistance to blood flow • ↑ HR; ↑ contractility Æ ↑ SV

– Highly elastic and distendable • Arterial constriction Æ ↑ TPR

– Act as blood reservoirs • Venous constriction Æ ↑ EDV Æ ↑ SV

↑ HR x ↑ SV = ↑ CO
– Have valves which help with venous return ↑CO x ↑ TPR = ↑ MAP

10
 CARDIAC PERFORMANCE IN EXERCISE CORONARY BLOOD SUPPLY IN EXERCISE
• Increase CO (5 to 35 L/min) (Handouts)
- Heart arterioles smooth muscles have
• Sympathetic action:
_ Blood shift (GIT Æ muscles; Dilate arterioles in skin, Alpha and Beta adrenergic receptors.
cardiac, skeletal muscles; and constrict those in GIT and - Sympathetics (NE) binds to Alpha to
kidneys)
cause vasoconstriction
_ Increase venous return through muscle pumps;
respiratory movements; sympathetics to veins; ↓ resistance - Adrenal medulla (plasma epinephrine)
to blood flow binds Beta to cause vasodilation.
_ Sympathetic action on the heart ↑ HR, SV.
• ↑ CO = (↑ HR X ↑ SV); ↓( BV, TPR)
- Epinephrine dominant to NE
MAP = ↑ CO x ↓ TPR (Exercise ↑ MAP slightly) - Adrenals “protect” the heart!

COMMON AILMENTS OF CARDIOVASCULAR

SYSTEM
CARDIAC PERFORMANCE IN UPRIGHT POSTURE 1. HYPERTENSION (↑ MAP):
• Can change blood pressure in extremities: ↓head; ↑ feet (gravity) - Most common ailment associated with the system! Usually
reflects ↑ CO, ↑ TPR
• Can reduce venous return Æ ↓ EDV Æ ↓ SV Æ ↓ CO
A. CAUSES:
• This can cause:
– Primary/idiopathic/essential; overweight (obesity); renal failure
– Fainting (↓ blood to the brain) – ↑ Na retention (Aldosterone) Æ ↑ water retention Æ ↑ blood
– Edema (↑ plasma filtration in feet capillary beds) volume
– Varicose veins (↑ blood build-up, and permanent vein distension) B. LEADS TO:
• Relief: – Heart attacks and failure; brain stroke; renopathy; left ventricle
– Muscle pumps; veins elasticity and valves hypertrophy
C. COMMON THERAPY:
– Keeping pressure distribution and venous return normal
– Vasodilating (↓TPR)
• Importance of resistance to blood flow (maintains normal blood and
– Anti-Aldosterone drugs (↓Na retention; ↓water retention)
blood pressure distribution)
– Exercise (↑sweating; ↓blood volume)
– Diuretics (↑urination; ↓blood volume)

11
 COMMON AILMENTS (Cont.) ATHEROSCELEROSIS (Cont.)
2. HYPOTENSION (↓ MAP):
C. DIAGNOSIS:
A. CAUSE:
– Angina Pectoris – pain
– Blood loss, Excessive Sweating, Extensive Burns
– EKG – Pronounced Q-wave
– Reduction in blood volume
– Plasma Cholesterol levels (Handout):
B. LEADS TO:
– Note the acceptable and danger levels!
1. ↓ Blood to Brain, Heart
– Increase in Creatine phosphokinase (CPK) and lactase
2. ↓ SV, ↑ HR, ↓ CO
dehydrogenase (LDH)
3. Circulatory Shock
D. TREATMENT:
C. RECTIFIED BY:
– Surgery – By-pass
– Baroreceptor reflex (Compensations – Blood distributions)
– Angioplasty – “Plumbing” with balloons
– Fluid exchange (Compensations - ↑ Vol by ↑ Plasma only)
– Exercise -- ↓ cholesterol, ↑ vessel diameter
– Blood transfusion (Compensations - ↑ Vol by ↑ Plasma and RBCs)
– Drugs – Ca2+ blockers and beta-adrenergic blockers
D. PRECAUTIONS:
– No alcohol, standing up, minimal clothes

COMMON AILMENTS (Cont.)

3. ATHEROSCLEROSIS: ATHEROSCLEROSIS AND “CARDIAC” ENZYMES

– disease of coronary blood vessels which narrows vessel lumens
– Lots of research on coronary blood vessels A.ATP PRODCTION IN CARDIAC MUSCLES:
– ↓ Blood flow (myocardial ischemia); ↓energy metabolites and O2
A. CAUSED BY: – ↓ ATP from aerobic glycolysis and oxidative phosphorylation
– Excess deposits of cholesterol B. COMPENSATIONS:
– Thickening of vessel walls due to over-proliferation in the smooth – Phosphagen System:
muscle and connective tissue layers ↑ Creatine
CP + ADP ---------------------------------------> C + ATP
B. PREDISPOSING FACTORS (MANY!!!): Phosphokinase (CPK)
– Overweight; Hypertension; High levels of plasma cholesterol – Anaerobic Glycolysis:
↑ latase
↑ Lactic Acid ----------------------------> Prevents Cardiac Fatigue
dehydrogenase (LDH)

12
 CARDIAC FIBRILLATIONS
A. ATRIAL FIBRILLATION
– Caused by stenosis of bicuspid valve Æ multiple ectopic firing (up
to 600 bpm) in atria
– About 100-160 impulses reach ventricles irregularly
– No P-wave in the ECG
– Use drug digitalis which slows impulses in Bundle of His
– Reduces # of signals reaching the ventricles

B. VENTRICULAR FIBRILLATION
– A very serious condition Æ death due to lack of blood to pump;
muscular fatigue
– Use electrical defibrillator to generate a normal cardiac conduction
patterns.

13