Physiology Cardio

Name the 3 overall functions of the CVS

homeostasis: exchange of blood with o2 and co2

communication: helping hormones control cells

temperature regulation: dilution of local heat and control skin blood vessels

what is the ultimate function of cvs

maintain adequate blood capillary perfusion to all body organs.

features of aorta and big arteries

High pressure
High elasticity

Whats the key feature that makes the wind Kessel mechanism possible

elasticity of the aorta

function of aorta and big arteries

allow intermittent blood flow to become pulsatile

features of medium muscular arteries

low resistance
low elasticity

function of medium muscular arteries

rapid blood flow without loss of any volume, pressure and time

function of narrow arteries and arterioles

act as stopcocks
control capillary blood flow
maintain high blood pressure

features of capillaries

very slow blood flow
very large TCSA
very thin, permeable walls

features of veins

distensible walls
high volume
low pressure

highest blood volume
highest elasticity

veins

aorta and big arteries

what connects 2 capillary networks in a portal circulation and function.

portal vessel

process and filter substances before entering systemic circulation

rules of flow in CVS

fluidity, continuous, unidirectional, closed system

What represents continuity of blood flow

2 features that allow unidirectional blood flow

venous return = cardiac output

valves and movement down pressure gradient

Intermittent blood flow

only comes from ventricles in systole

Pulsatile blood flow

elasticity of aorta and big arteries turns intermittent blood flow to pulsatile blood flow. High systole and low diastole

what vessel in the cvs has the lowest resistance

aorta and big arteries

drop of pressure across 
aorta - arteriole - capillary - vein

120
100 - 32 - 10 - 0

Order the vessels from highest resistance to the lowest

Arterioles, capillaries, aorta, vein

name high pressure components

All before the mean capillary pressure
L.V in systole
aorta, big arteries and distributing
arterioles
arterial end of capillary

name low pressure components

All after mean capillary pressure
Venous end of capillary
veins, svc
right and left atria
right and left ventricle in diastole
pulmonary circulation

whats the main factor that affects the velocity of the blood

write equation

TCSA

V=Q/A

what vessel has the lowest velocity

capillaries reaches 0.1cm/sec
highest TCSA

describe capacitance of blood

volume change per pressure change in a vessel 

high capacitance comes with low pressure - veins or low P comps

Low capacitances comes with high pressure - capillary or high P comps

characteristics of pericardium

inelastic
allow gradual physiological growth
not essential for cardiac function

an increase in intrapericardial pressure would cause

decrease in venous return
decrease in cardiac output and death

Main function of Sub valvular apparatus

papillary muscles and chorda tendinea dont allow bulging / eversion of valve back into the atria when there is high ventricular pressure.

Nerve supply of heart

Sympathetic : cervical and upper thoracic spinal cord segments

Parasympathetic : vagus nerve

Functions of aortic chamber

act as blood reservoir for venous return

produce ANP hormone to excrete excess sodium

give a boost pump and an atrial kick to the last 20% of blood to move from atrium to ventricle

volume stretch sensors, to balance cardiac output to venous return

What allows the action potential to move through to each muscle

gap junctions

Main difference between cardiac muscles and skeletal muslces

Uses extracellular calcium to release the calcium inside

calcium induced calcium release CICR (also only function of sarcoplasmic reticulum)

Difference between T tubule and sarcoplasmic reticulum from cardiac muscle to skeletal

T tubule more developed than skeletal

sarcoplasmic reticulum less developed

Main cells in SAN

P cells

Name non contractile Junctional fibers

and Function

His bundle

pirkunjie fibers

bundle branches

propagate rest of impulse from SAN to the rest of heart

Properties of cardiac muscle

excitability
autorrhythmicity
contractility
conductivity

Where is the property of excitability found

pace maker (self excitable)

junctional 

contractile

Where is the property of autorhythmicity found

pace maker

junctional, low only 3% of pirkinjie fibers

contractile, only when damaged

Where is the property of conductivity found

pace maker, very slow

junctional, rapid

contractile

Where is the property of contractility found

only contractile fibers. not in pace maker or junctional

What tissues produce a fast action potential

Atrial fibers
ventricular fibers (contractile)
pirkinjie fibers (junctional)

What stabilizes the RMP

balance between inward current of sodium (influx of sodium) and outward current of potassium (efflux of potassium)

Why is the depolarization and influx of sodium very rapid in fast Action potential

Large concentration gradient
Large electrical gradient

Why does the sodium keep on influx at 0mv

Only concentration gradient

How long does platue take in repolarization and what’s the main reason of this platue

200-300ms and the influx of Ca+ ion which balances release of K+ ion. Needed for muscle contraction

What causes the instability in the rest membrane potential of the slow response A.P

the accumulation of +cations inside the membrane

What completes the accumulation and prepotential in the Slow response A.P

calcium ions through transient T-type channels

(sodium ions already accumulation from previous hyperpolarization and potassium prevented from efflux and remains in the membrane with sodium and calcium)

Role of potassium in prepotential of slow repones A.P

Remain inside cell membrane by decrease of potassium permeability / prevention of potassium efflux

What starts the depolarization in the slow response A.P

influx of calcium ions through L calcium channels with little sodium influx

end at 0-10mv

what’s the firing level in the fast response A.P and slow response A.P

fast response A.P = -70

slow response A.P = -45

effect of sympathetic and para sympathetic

symp = increase Na influx to reach firing level faster

parasymp = decrease Na influx

symp = decrease potassium efflux to keep it in cell

parasymp= increase potassium efflux to leave cell

symp = increase camp which increases the L calcium channels in phase 0

parasymp = decrease camp which decreases the L calcium channels in phase 0

Define refractoriness

inability to respond to a stimulus

Where is the ARP in the fast response A.P

phase 0, 4, 1 , 2 and half of 3

function of the extensive refractory period

prolongs ARP to protect the heart from arrythmias 

important for cardioverter and the treatment of fibrillating heart, using 2k-3k volts and giving the heart 3-5seconds to wait for the fibers to reset and receive impulse from the SAN

What tissue is mainly affected by the supernormal period

prikinjie fibers,

end of phase 3 to 4

which of the periods are time dependent and which is voltage dependent in the slow response A.P

time dependent = RRP = end of phase 3 → 4

voltage dependent = ERP = phase 0→3

factors affecting SAN

temp 1C = 10-13/min

vagal tone decrease from 100 → 70/min. increase potassium permeability, decrease heart rate

hypokalemia and hypocalcemia decrease discharge (less prepotential)

parasympathetic decrease. sympathetic increase

SAN functions

1ry pacemaker due to it having the highest inherent automaticity 100/min

causes overdrive suppression, making only the SAN working and the rest dont

why does SAN have the slowest conductivity

protection against excitation by ectopic focus

time taken for atrial excitation

0.1

what region has the maximal delay of transmission in the AVN

AN region

What region has the lowest conduction velocity in the AVN

N region

what happens if the AVN is damaged whilst the SAN is normal

non nodal autorhythmic ventricular fibers act as pace maker for ventricles (idioventricular rhythm)

SAN takes control of atria only

AVN properties

unidirectional pacemaker

latent 2ry pacemaker, 40-60/min only

AV nodal delay of impulse until reach to ventricles by 100-150msec in order for atria to contract and release all blood before ventricle contract

block transmission by parasympathetic by av block = heart block

pathway of the impulse from SAN

SAN → atria → AVN → HIS bundle → bundle branches → pirkinjie fibers → ventricles

What’s the first part of the ventricle affected by the impulse

Whats the last part of the ventricle to be affected by the impulse

Left side of interventricular septum

posterbasal portion of ventricle. subepicardial surface

Sources of calcium

Small amount from ECF that enter by DHP receptors = depolarizing triggering Ca+

Large amount of Calcium from SR that is released through Ryanodine receptor.

mechanism of ECG

electrodes placed on body surface detect the electric activity of the heart through the body surface

what do bipolar limb leads measure 

the potential difference between 2 active points.

what do each of the limb leads measure

lead 1 = VL -VR

lead 2 = VF- VR

lead 3 = VF - VL

describe unipolar limb lead

absolute potential at a point

forms wilson point and is used as a better index for cardiac activity

unipolar augmented limb leads

at 150% of the normal it measures the difference between one limb and the 2 others

locations of the unipolar chest leads

v1 right 4th IC space

v2 left 4th IC space

v3 mid way v2 and v4

v4 left 5th IC mid clavicular

v5 left 5th IC anterior axillary

v6 left 5th IC midaxillary

which of the unipolar chest leads are best to show the left ventricle activity

v5 and v6

which of the unipolar chest leads are best to show the interventricular septum

v3 and v4

which of the unipolar chest leads are best to show the right ventricle activity

v1 and v2

which segment shows time of conduction of AVN

PR segment

what segment shows all repolarization of ventricle

ST interval

what segment shows all repolarization and depolarization of ventricle

QT interval

what segment shows atrial depolarization and AVN conduction and what is it prolonged and shortened by

PR interval

shortened: sympathetic and AV nodal rhythm

prolonged : vagal stimulation, atrial enlargement, AVN block

what segment shows all the ventricular muscles depolarized

ST segment

what can the ECG diagnose and be used for follow up

dysrhythmias

infarction and ischemia

electrolyte disturbance

pharmacological effect of a drug on the heart

what lead and electrode is best to view LAD

lead 3 and v6

what interval is important in figuring out a normal ecg

PR interval

what shows a normal SAN rhythm

a positive p wave from lead 2

a negative p wave from AVR

criteria for reentry of impulse

center of non excitable fibers

2 pathways for conduction of impulse

unidirectional block of one pathway due to ischemia, AVN block, electrolyte disturbance

other pathway is shortened by ischemia or prolonged by dilation of the heart

trigger by sympathetic stim, epinephrine

types of arrythmia caused by reentry

atrial fibrillation

ventricular fibrillation

atrial flutter

wolf Parkinson syndrome

AVNRT

what interval is used to identify the ARP in an action potential

QT interval

feature of partial first degree av block

delayed slow conduction

1:1 ratio of P-QRST

prolonged pr interval

features of partial 2nd degree av block. type 2

not all atrial impulse reach ventricle

dropped QRST

2:1 ratio of P-QRST

pr interval not prolonged

describe each of the QRS segments in the QRS complex

Q = septal depolarization -

R = myocardial depolarization, from endocardium to epicardium +

S = basolateral portion of the heart and pulmonary conus -

explain why the repolarization of the ventricle is shown as a positive wave

direction of repolarization is from epicardium to endocardium and repolarization is a negative wave and opposite of depolarization

features of complete heart block

disassociation between ventricle and atria

20-40 b/min , pirkinijie fibers take over damaged AVN

Stock Adams syndrome

loss of consciousness and anoxia due to decrease in the beats per minute 20-40, causing decrease of o2 to brain.

which part of the A.P does the action potential take place

20msec after peak of A.P

last 1/3 of platue

when is the peak of contraction/ tension in the A.P

at last 1/3 of platue

what determines the preload of the cardiac muscle before contraction

EDV

what determines the max contraction force and systolic tension

contractile element

what determines the passive stretch

parallel passive element

what occurs in isometric contraction

decrease in length of CE

increase in length of PE

no shortening of muscle

effect of increase of Calcium ion ECF

effect of decrease of Potassium ion ECF

increase in calcium stops the heart in systole

increase in potassium stops the heart in diastole