Heart Excitation

Heart Excitation Cardiac muscle cells are

excitable (with electrical stimulation they will contract, leading to the contraction of the heart)–Contraction of heart leads to

pumping of blood

Specialized Tissues (important in the regulation and coordination of electrical activity)

Sinoatrial node (SA node) – located in wall of right atrium– hearts pacemaker– where electrical signals originate and lead

to contraction, sets the rate of contraction, at rest about 72-84 bpm

– causes atria to contract force blood into ventricles

Atrioventricular Node (AV node) passes electrical signal to ventricles

from the atria passes electrical signal to bundle of

His

Bundle of His (atrioventricular bundle)

special tissue within ventricular septum

Splits to form the right and left bundle branches

pass signals to Purkinje fibres

Purkinje fibres pass signal to myocardium in

ventricles

Atria initiate contraction from top down, push blood into ventricles

Ventricles contract bottom up – push blood into aorta and pulmonary arteries

SA node can be influenced by another source and can increase or decrease force of contraction (HR) – eg. exercise, increased adrenaline,

drugs If SA node is damaged the AV node

takes control

Electrocardiogram An electrocardiogram (ECG or EKG, abbreviated

from the German Elektrokardiogramm) is a graphic produced by an electrocardiograph, which records the electrical voltage in the heart in the form of a continuous strip graph.

It is the prime tool in cardiac electrophysiology, and has a prime function in the screening and diagnosis of cardiovascular diseases.

The electrocardiogram does not assess the contractility of the heart.

A typical ECG tracing of a normal heartbeat consists of a P wave, a QRS complex and a T wave.

P wave – atrial depolarization (spreading of the electrical signal to contract through the atria). – Both the left and right atria contract

simultaneously. – Immediately after depolarization of the atria

there is repolarization (readies for another contraction)

Normal ECG

QRS complex – depolarization of ventricles– contraction of the left and right

ventricles, which is much more forceful than that of the atria and involves more muscle mass, thus resulting in a greater ECG deflection.

– Slight dip, followed by steep peak, then a quick return back to near baseline levels

– The duration of the QRS complex is normally less than or equal to 0.10 second.

Normal ECG

T wave – represents the repolarization of the ventricles.

Electrically, the cardiac muscle cells are like loaded springs.

A small impulse sets them off, they depolarize and

contract. Setting the spring up again is repolarization

ECG abnormalities may indicate heart problems or disease

Current that causes Left and right atrial contraction

“atrial depolarization”

Current that causes Left and right ventricle contraction

“ventricular depolarization”

Current that causes “repolarization” of the ventricle contraction

Coronary Veins/ArteriesArteries Veins

-blood is supplied through 2 major arteries that branch off and divide several times

-they branch off the aorta and supply the myocardium with oxygen.

-blood moves from coronary capillaries, venules, to veins

-All veins come together at the CORONARY SINUS

-this drains into the right atrium to be “re-oxydenated”

Heart Complications Atherosclerosis = narrowing of coronary

arteries caused by plaque

Angina = chest pain caused by atherosclerosis

Myocardial infarction = part of the myocardium not receiving blood supply

Cardiac arrest = heart stops

Aneurysm =a balloon-like bulge in an artery that weakens and bursts

Components of Blood

Plasma– Liquid portion of blood– Contains ions, proteins, hormones

Cells– Red blood cells (erythrocytes)

Contain hemoglobin to carry oxygen– A protein that gives blood the ability to – Deliver oxygen and take out carbon dioxide

– White blood cells (leukocytes) Important for fighting infection and your immune

system– Platelets (thrombocytes)

Important in blood clotting

Blood Pressure

Purpose?– To measure the efficiency of the heart

and the condition of the blood vessels

HOW DO WE MEASURE BLOOD PRESSURE?

Measuring Blood Pressure

Use a sphygmomanometer cuff and a stethoscope on the brachial artery

Increase pressure to about 150mmHg

Release the pressure and listen for the first “lub dub” sound (systolic pressure)

Wait until the artery returns silent (diastolic pressure)

Cardiac CycleIs a series of events that occurs

through one heart beat.

Systole ~ phase of contraction – ventricles contract - the heart ejects the blood

Diastole ~ phase of relaxation – ventricles relax - heart is filling with blood

Blood Pressure Readings

Average: 120/80mmHg Hypotension: lower than 90/60mmHg Pre-hypertension: 120-139/80-

89mmHg Hypertension: 140-149/90-99mmHg Severe hypertension: 160/100mmHg

plus

Hypotension

Not usually a concerns unless dizziness, light-headedness and fainting occur

Caused by: – bleeding or haemorrhaging– Allergic reaction– pregnancy

Risk Factors of High Blood Pressure/Hypertension

Age Race Gender Heredity Diet (high fat) Stress Inactivity Alcohol and smoking

Treatments

1. Medication– Diuretics to lower blood volume– Inhibitors to relax blood vessels

2. Diet– Decrease fat and sodium intake

3. Exercise– Strengthens heart muscle– Releases endorphins (decrease stress)– Gradual increase in activity is important

Cardiovascular Dynamics

How the heart adapts to meet the demands of increased workload

Cardiac Output (Q) volume of blood pumped out of the left ventricle in

1 minute measured: L/min at rest ~ 5-6 L/min

Two factors that contribute to cardiac output:

1. Stroke Volume (SV)2. Heart Rate (HR)

Q = SV x HR

Stroke Volume amount of blood that is ejected from

the left ventricle in a single beat measured in mL

Heart Rate The number of times the heart

contracts in a minute (beats/min)

Calculating Cardiac Output

Cardiac output is the product of stroke volume and heart rate:

Q (L/min) = SV (mL) X HR (beats/min)

Example: HR at rest ~72 beats/min, SV at rest ~71 mLQ resting (L/min) = 72 beats/min X 71 mL

= 5112 mL/min (5.11 L/min)

Cardiac Output and Exercise

Q increases to 15-25 L/min (depending on intensity of exercise)

Q increases then becomes constant SV increase occurs early in exercise

and plateaus HR increases early (same as above) Prolonged exercise SV might decline

late in exercise (due to excessive fluid loss from body – sweating)– Q is maintained because HR increases

What happens with training?

Q (cardiac ouput)– Rest 5-6 L/min– Exercise 35-45 L/min

Stroke volume– Untrained male at rest 70-80 mL/beat– Highly trained male 100-110 mL/beat– Highly trained endurance 150-170 mL/beat

Therefore, with training we can pump out more blood with less beats = more efficient system

What enables the increase of SV?

Frank starling Law: the ability of the heart to stretch and increase the force of the contraction and thus the amount of blood that is ejected.

– This is mostly effected by the amount of blood returned to the heart

VENOUS RETURN

VENOUS RETURN

(VR) increases during exercise by– Venoconstriction– The skeletal muscle pump– The thoracic pump– Nervous stimiulation (increased HR)

Ejection Fraction

Measures the efficiency of SV EF is recorded in a % The portion of blood that is ejected

from the left ventricle EF at rest = 50-60% EF max ex. = 85%

EF % = SV x 100LVEDV

Athlete’s Heart vs Diseased Heart

Athlete’s Heart

Volume Load Endurance athlete’s Increase size of the

ventricle chamber Little change to

ventricle wall

Pressure Load Anaerobic activities Ventricle wall

thickness increases to push blood out faster

Little change to ventricle chamber size

Hypertrophic Cardiomyopathy (HCM)

Enlarged ventricle wall Muscle fibres of the heart are not

connected properly and become intertwined and enlarged

Present at birth Kills with no symptoms