Cardiovascular 2

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backman’s bundle

conducts action potentials from the SA pacemaker into the left atrium causing contraction

anterior, middle and posterior internodal pathways

conduct the action potential from the SA node to the AV node, depolarizing right atrial muscle along the way

speed of atrial conduction

relatively slow, 80-100ms

ventricular conduction

layer of connective tissue prevents conduction directly from atria to ventricle

conduction slows down through the AV node to allow blood from atria to empty into ventricles

bundle of HIS in ventricle conduction

depolarization proceeds through the septum to the apex

purkinje fibres in ventricular conduction

spreads up the walls to the ventricles from the apex to the base

direction of ventricular conduction

SA node → AV node → Bundle of His → bundle branches → purkinje fibres

ventricular muscles in contraction

have a spiral arrangement that ensures that blood is squeezed upward from the apex of the heart

complete conduction block

caused by damage in conduction pathway, block at the bundle of his results in a complete dissociation between the atria and the ventricles

blockage at the bundle of his

the SA node continues to be pacemaker for the atria but electrical activity does not make it to the ventricles so the purkinje fibres take over as the pacemaker for the ventricles

electrocardiograms

electrodes placed on the skin surface record the electrical activity of the heart. shows electrical activity summed from all the cells of the heart.

how does ECG work

salt solutions like our NaCl- based extracellular fluid are good conductors of electricity allowing the electrodes to pick up signals from the fluid

speed of ventricle conduction

occurs more rapidly, 60-100ms

Einthoven’s triangle

a hypothetical triangle created around the heart when electrodes are placed on both arms and the left leg to measure the heart's electrical activity.

leads

pairs of electrodes where one electrode acts as a positive electrode and one acts as a negative electrode

upward ECG deflection

if the electrical activity of the heart is moving towards the positive electrode

downward ECG deflection

electrical activity is moving away from the positive electrode

no deflection ECG

electrical activity is moving perpendicular to the axis of the electrodes

ECG waves

appear as deflections above of below the baseline

ECG segments

sections of the baseline between two waves with no detection of current flow

ECG intervals

the combination of waves and segments

P wave

atrial depolarization, contraction doesnt start until about halfway through the P wave

PQ or PR segement

conduction through the AV node and AV bundle

Q wave

depolarization of interventricular septum

R wave

contraction of outer walls of the septum

QRS complex

ventricular depolarization

ST segment

represents the plateau phase when the ventricle starts to contract upwards

T wave

ventricular repolarization, movement of K out of the cells

Tachyardia

faster than normal heart rate

bradycardia

slower than normal heart rate

changes in heart rate detection ECG

P wave to P wave or R to R

heart rhythm detection ECG

arrhythmia can be a result of many issues detectable on an ECG

QRS complex for every P wave ECG

there must be one QRS complex for every P wave, elongated segments indicative of damage

premature ventricular contractions

purkinje fibres randomly kick in as pacemaker, can be due to insufficent oxygen to myocardium, excessive Ca2+, hypokalemia, medications, exercise or high levels of adrenaline

shown as a skipped beat or palpitation

Long QT syndrome

inherited channelopathy

delayed repolarization of the ventricles, palpitations, fainting and sudden death due to ventricular fibrillation

cardiac cycle

one complete contraction and relaxation of the heart

diastole

the time durirng which cardiac muscle relaxes

systole

the time during which cardiac muscle contracts

late diastole

both sets of chambers are relaxed and ventricles fill passively

atrial systole

atrial contraction forces a small amount of additional blood into ventricles

isovolumetric ventricular contraction

first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves

ventricular ejection

as ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected

isovolumetric ventricular contraction

as ventricles relax, pressure in ventricles fall, blood flows back into cusps of semilunar valves and snaps them closed

A A’ segment

starts at end systolic volume, pressure in ventricles drops below the pressure in the atria and the AV valve opens causing the ventricle to fill with blood

A’ B segment

atria contracts forcing more blood into the ventricle and slightly increasing volume and pressure. at the end, the max amount of blood is in the ventricles

B-C segment

the ventricle begins contracting closing AV valve, continued contraction causes a large increase in pressure within the ventricle

C-D segment

Once pressure in the ventricle rises above 80 mmHg it exceeds the aorta and the aortic valve opens causing a rapid ejection of blood

the ventricle begins to relax and pressure begins to drop but blood still flows due to inertia

DA segment

pressure in aorta begins to exceed ventricle causing semi-lunar valve to close, ventricle continues to relax

End of wiggers diagram

ventricle relaxes, pressure in atria begins to exceed ventricle

AV valve opens and you get the passive filling of the ventricle

Start of wiggers diagram

ventricle begins to contract, increasing pressure within ventricle causing the AV valves to snap shut

end diastolic volume

the maximum volume in the ventricle after ventricular filling

end systolic volume

the minimal amount of blood in the ventricles, blood left after ventricular contraction

stroke volume

amount of blood ejected during a single ventricular contraction

stroke volume equation

stroke volume = end diastolic volume - end systolic volume

End systolic volume purpose

leaves a small amount of blood in the ventricle, providing a safety margin

increase of stroke volume

can be caused by the autonmic nervous system, venous return and by certain medications

ejection fraction equation

ejection fraction = stroke volume/ end diastolic volume

cardiac output

the flow of blood delivered from one ventricle in a given time period str

cardiac output equation

cardiac output = heart rate x stroke volume

unbalanced cardiac outputs of circuits

if balance of cardiac outputs is offset, blood tends to pool in the healthy circuit feeding the weaker side of the heart

how can cardiac output be changed

through adjusting heart rate in pacemaker cells. slowing down depolarization, starting at a more negative value

contractility of the heart factor

the intrinsic ability of a cardiac muscle fibre to contract at any given fibre length and is a function of Ca2+ entering and interacting with the contractile filaments

the length of fibres factor

determined by the volume of blood in the ventricle at the beginning of contraction, creates more force when stretched

inotropic agent

any chemical that affects contractility

positive inotropic effect

chemicals increasing contractility

negative ionotropic effect

chemicals decreasing contractility

norepinephrine ionotropic effect

released from the sympathetic neurons or adrenal medulla cause a positive iontotropic effect regardless of EDV

sympathetic modulation of stroke volume step 1

phosphorylation of Ca2+ channels increases calcium conductance during action potentials causing greater calcium entry

sympathetic modulation of stroke volume step two

phosphorylation of ryanodine receptors enhances sensitivity to Ca2+ increasing release of Ca2+ from sarcoplasmic reticulum

sympathetic modulation of stroke volume step 3

increases rate of myosin ATPase which speeds up myosin head binding

sympathetic modulation of stroke volume step 4

phosphorylation of serca increases the speed of Ca2+ reuptake which increases Ca2+ storage creating a bigger calcium pool in SR

frank starling law of the heart

the amount of force developed by the cardiac muscle of a ventricle depends on the initial stretch of the ventricle walls by ventricle filling

preload

the degree of myocardial stretch prior to contraction on the heart

heart stretch

indicated by ventricular end diastolic volume

skeletal muscle pump

skeletal muscle activity compresses veins in the extremeties pushing blood back to the heart increasing venous return

respiratory pump in venous return

during breathing in the chest expands and the diaphragm moves down creating a subatmospheric pressure in the thoracic cavity, this draws blood into the vena cava increasing venous return

sympathetic constriction of veins

decreases their volume squeezing blood back towards the heart

afterload

the end load against which the heart contracts to eject blood

primarily determined by the combination of the EDV and the pressure in the outflow artery prior to contraction

afterload increase

can be increased in pathological situations like hypertrophy where the heart decreases the cavity size decreasing the EDV

inadequate lymph drainage

cause of edema

can occur from obstructions in the lymphatic system and lymph nodes

disruption in normal capillary filtration and absorption

cause of edema

increased capillary hydrostatic pressure, decrease in plasma protein concentration or increase in interstitial protiens

Cross sectional area of vessels

with each branching of a vessel, the two new branches always have a higher total cross sectional area than the parent vessel

velocity of blood formula

velocity of blood = flow rate/ cross sectional area