Download Cardiac Conducting System AND Cardiac cycle

Cardiac Conducting System
Cardiac muscle tissue contracts on its own
No neural nor hormonal control
“autorhythmicity’
Specialized cells: initiate and distribute depolarization
1. Sinoatrial node (SA node)
a. Near entrance of superior vena cava/posterior wall of
R. atrium
b. “pacemaker cells” establish heart rate
c. Connected to AV node via conducting pathways
d. Stimulus affects only ATRIA
i. Fibrous skeletal separates atria from ventricle
2. AV node:
a. Floor of right atrium
b. Near opening of coronary sinus
c. From AV node to bundle of His( Left and right bundle
branches) which run along interventricular septum
d. Delay at AV node allows atria to complete contraction
before ventricular contraction begins
3. Bundle branches(bundle of His)
a. Impulse reaches bundle branches- travels along
septum, splits between L & R bundle branches
b. Purkinje fibers – where the bundle branches diverge
into smaller branches
i. Cause ventricular contraction
ii. Wave action from apex(bottom) to base(top)
toward right ventricle first
iii. Blood is pushed out aortic and pulmonary trunk
ELECTROCARDIOGRAM
Monitors electrical activity of heart
1. P wave: small bump, atria contract after start of P wave –
depolarization of atria(SA node)
2. QRS complex: ventricles depolarize – STRONG electrical
signal – ventricles contract AFTER peak at R (AV node)
3. T wave small bump after QRS – ventricles relax
4. Do not “see” atrial relaxation due to strong QRS
Problems detected:
Extension of P-R interval = damage to conducting pathways or
damage to AV node
Extension of Q-T interval = myocardial damage
HEART ATTACK – myocardial infarction
Infarct = nonfunctional area of myocardium
Enzymes that detect MI= LDH; SGOT; CPK(creatine
phosphokinase)
Systole – contraction
Diastole – relaxation
Interpretation of heart sounds via stethoscope
Lubb- AV valves close – start of ventricular systole
Dupp – semilunar valves close, ventricular diastole begins
Patients upper area right of sternum – hear pulmonary
semilunar valve
Lower right of sternum – hear right atrioventricular valve
(tricuspid)
Upper right of sternum – hear aortic semilunar valve
Lower right of sternum – left atrial ventricular valve – bicuspid
CARDIAC CYCLE
Heart beat to heartbeat – period of contraction(systole) and
relaxation(diastole)
Start of cycle: atrial systole – atria contract forcing a small
amount of blood into ventricles to fill to capacity(already 70%
full due to passive flow during diastole of both atria and
ventricles following ventricular systole)
Atrial diastole  ventricular systole
Ventricular pressure exceeds arterial pressure and semilunar
valves open  blood flows into pulmonary trunk or aorta
Ventricular diastole pressure lowers in ventricles causing
higher pressure in arteries(pulmonary trunk/aorta) causes Semi
lunar valves to close
BOTH atria and ventricles in diastole – blood flows passively
from the veins into atria then to ventricles
Before systole of atria begins again the ventricles are 70% filled
with blood!
If atria are damaged, the heart can still function!
Stroke volume: amount of blood ejected by a single ventricle
Cardiac output : amount of blood pumped by each ventricle in
1minute – provides idea of amount of peripheral blood flow –
regulated so that all tissues are receiving an adequate blood
supply
CLINICAL NOTES –
1. Caffeine – acts directly on the conducting system
increasing the rate of depolarization at SA node
2. Nicotine – stimulates the sympathetic neurons that
innervate the heart – stress, speed, strength of contraction
3. Hypo or hyper kalemia (K+) concentrations – hyper polarize
or depolarize the cell membrane – can result in death
4. Hypo or hyper calcium ion concentrations – prevent
polarization – death
5. Low body temperature – lowers heart beat and
contractility strength – until it stops…
6. High body temp – increases heart beat, contractility
7. Epinephrine – Norepinephrine – and thyroid hormones
increase contractility – (positive inotropic effects) –
sympathetic stimulation (cardiac nerve)
8. Ach – parasympathetic stimulation (vagus nerve) negative
inotropic effect) – hyperpolarization/inhibition – slows
heart
9. Cardiac center of medulla oblongata (regulated by reflex
pathways from hypothalamus)
a. Cardioaccelatory center – sympathetic neurons –
increase heart rate
b. Cardioinhibitory center – parasympathetic neurons –
slow heart rate
10.
Heart attack? – diagnostic blood test – enzymes
enter blood if cardiac cells are imploding – cardiac
troponin T, cardiac troponin 1, CK-MB(creatine
phosphokinase)
11.
3 weeks – 21 days after conception – a beating heart!