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206 Cards in this Set

  • Front
  • Back
Pulmonary circuit
Pulmonary truck carries
oxygenated blood to lungs.
it is returned via pulmonary veins

Systemic circuit

aorta and other arteries carry oxygenated blood to the body.
comes back via vena cave veins.

Parietal pericardium

outside of heart


serous inner simple squamous epithelium layer


fibrous outer layer

pericardial cavity

contains pericardial fluid

visceral pericardium other name?

epicardium

visceral pericardium

outer serous simple squamous epithelium


Loose areolar connective tissue


adipose tissue.

myocardium

cardiac muscle tissue.


+ fibrous skeleton of collagen and elastin fibers

Functions of the myocardium fibrous skeleton

structural support.


anchors myocytes


electrical insulation and direction.


(support, myocytes, electrical)

endocardium

simple squamous epithelium

what separates the chambers


and what are they covered with

sulci superficially


covered by adipose and coronary vessels.

pectinate muscles

ridges in the atria that allow it to expand.

atria

receive blood and pump it to ventricles.


thin.

ventricles

pump blood out of heart.


bottom.

left ventricle

thicker then right ventricle because it has to pump blood allover the body.

trabeculae carneae

ridges in the ventricles


atrioventricular valve



prevent backflow of blood from ventricles to atria.


open when pressure of ventricles is less then pressure in atrium (when atriums fill up)

right atrioventricular valve.

tricuspid valve


because it has a lot of pressure coming from the body. (vena cavas)

left atrioventricular valve

bicuspid or mitral valve


only has two because it receives blood from the lungs (pulmonary veins)

tendinous cords/chordae tendinae

prevent valvular prolapse of atrioventricular valves.


(disfunction = backflow + edema)

Papillary muscles

brace the tendinous cords in the AV valves.

Semilunar valves.

are between ventricles and aorta/pulmonary trunk.


open when ventricles are contracting.


closed when pressure of ventriles is less than pressure in arteries.

R semilunar valve

pulmonary semilunar valve.


prevents backflow from pulmonary trunk into right ventricle.

L semilunar valve.

aortic semilunar valves


prevents backflow from aorta into L ventricle.

Blood flow through the chambers.

starts from superior and inferior vena cava.
right atrium -> right tricuspid AV valve.
right ventricle -> pulmonary semilunar valve
pulmonary trunk
lungs
pulmonary veins
left atrium -> left bicuspid (mitral) valve
left ventricle -> left Aortic semilunar valve.
Aorta - Body

heart accounts for body weight?


how much blood does it receive?

0.5% of body weight


receive 5% of blood.

Arteries in the heart.

Left and


right coronary artery.



Left coronary artery branches into.

Anterior interventricular A


and Circumflex A



Anterior interventricular artery supplies


comes form

supplies : anterior ventricles.


comes from: left coronary artery.

Circumflex A branches to

left marginal Artery.

Left marginal artery supplies


came from?

supplies : left atrium and posterior L ventricle
came from : circumflex and left coronary artery

Right coronary artery supplies

R marginal artery and


posterior interventricular artery



R marginal artery supplies


came from

Supplies : R atrium and posterior right ventricle.


came from right coronary artery



posterior interventricular artery supplies


came from

supplies posterior ventricles


came from right coronary arteries.

explain the interventricular Heart arteries in simple form

Both start with Coronary arteries.


Left does anterior interventricular artery which supplies left ventricles.


right does posterior interventricular artery which does posterior ventricles.


Left is Anterior (front) interventricular + ventricle


Right posterior (back) interventricular + ventricle.

Explain the left and Right Marginal arteries.

Both start with Coronary arteries.


Left has a circumflex first, right doesnt.


both supply atrium of same side, also


posterior ventricle of same side.

MI

Myocardial infarction - heart attack.


death of myocardium due to ischemia

angina pectoris

Pain from transient (short) ischemia


early indicator of impending MI.

Anastomoses

Overlap in blood supply


also called collateral circulation

What is the function of anastomoses

If blockage occurs, allows a second route which


reduces the risk of blockage

Two venous drainage vessels.

Great cardiac Vein (beside interventricular A)


post interventricular vein



Great cardiac vein drains into

anterior heart.

posterior interventricular vein drains into

posterior hear.

where do both venous drainages end up?

anterior/posterior heart.


coronary sinus


Right Atrium

SB1 SIRF


what is it?

Structure of cardiac muscle cells


acronym

SB1 ISRF


actual

Striated


Branched


1 nucleus per cell.


Intercalated discs.


sarcoplasmic reticulum (store CA) but can get from ECF!!


Fibrosis only repair.

Inter Mehcollect


what is this?

Intercalated disks acronym

Inter Mehcollect


actual

Interdigitating folds


mechanical junctions


electrical junctions



Interdigitating folds

folded plasma membrane

mechanical junctions

fascia adherens and desmosomes.

electrical junctions

gap junctions

GMS FOL


What is it.

Cardiac muscle highly resistant to fatigue


acronym



GMS FOL


actual

Glycogen storage, where glucose comes from.


Mitochondria A LOT


Stores oxygen as Myoglobin


Fuels, variety, Fatty acid + gluc + others


O2 deficiency vulnerability.


Little anaerobic respiration - less lactate accumulation

Myoglobin

Stores oxygen.


when your tissues, heart use oxygen, they run out of oxygen and can get some from this.

Cardiac conduction system


function

Elelectrical wiring of the heart that coordinate cardiocyte contraction

cariac conduction sytem Structure.

Specialized myocytes that are


noncontractile and autorhythmic;




Ie. depolarize spontaneously.

Myocyte

muscle cells.


can be specialized.

Purkinje Fibers.

Specialized fibers in heart that send nerve signals to the cells in the ventricles of the heart and cause them to contract to pump blood to the lungs or the rest of the body.

Sa node.

Sinatrial node. (pacemaker)

Cardiac conduction system


Route.

Sinoatrial (SA) node (pacemaker) thru both atria.


-> atrioventrical (av) node (signal pauses)


-> AV bundle


-> R and L bundle branches


-> Purkinje fibers


-> around ventricular myocardium such that the heart contracts from the bottom upwards.

Heart BPM without nervous system

100 bpm

What happens at the atrioventricular node?

Signal pauses.

Sympathetic nervous system supply to the heart


origin.

nerves originate from the


lower cervical, upper thoracic region

Parasympathetic nervous system supply to the heart origin.

Input to hear via Right and Left vagus nerve.

Sympathetic nervous system cardiac nerve input to these


locations

Myocytes


SA and AV node


Coronary Blood vessels.

Sympathetic nervous system cardiac nerve input to Myocyte function

Increase contraction strength.(sympathetic)

Sympathetic nervous system cardiac nerve input


to Sa and Av node


function

Increase HR (sympathetic)

Sympathetic nervous system cardiac nerve input to Coronary blood vessels


function

Regulates blood flow of heart. (sympathetic)

Parasympathetic Right vagus nerve innervates
this

SA node (parasympathetic)

Parasympathetic left vagus nerve innervates


this

AV node (parasympathetic)

Baseline stimulation of the parasympathetic nervous system


is called

Vagal tone


brings resting heart rate to 75 BPM

Systole (noun)

Contraction of the ventricles

Diastole (noun)

Relaxation of the ventricles.

Sinus rhythm


Full

pacemaker rhythm


75 bpm


resting HR


Initiated by SA node.


modified by parasympathetic nervous system.

Nodal rhythm


info

40-50 bpm

Nodal rhythm


control

Occurs when AV node takes over Sa node.

Nodal rhythm


Full

40-50 bpm


occurs when AV node take over SA node.

Strong midgets cardios were


rated nodes above the rest.


their vessel flow had to be regulated


what is this?

Sympathetic nervous system nerves to the heart


phrase





Strong midgets cardios were


rated nodes above the rest.


their vessel flow had to be


Explain

Cardiac nerves to myocytes increase contraction strength


cardiac nerves to SA & AV node increase HR


input to Coronary blood vessels regulates flow of the heart.

Sinus Rhythm


Info

pacemaker rhythm


75 bpm


resting HR

Sinus Rhythm


Control

Initiated by SA node.


modified by parasympathetic nervous system.

SNECA


What is this?

Cardiac Rhythms


acronym

SNECA


Names

Sinus rhythm


Nodal rhythm


Ectopic focus


Arrhythmia

Ectopic focus


info

20-40 bpm


may be due electrolyte imbalance, hypoxia, drugs.

Ectopic focus


Full

20-40 bpm


may be due electrolyte imbalance, hypoxia, drugs.


occurs when another part of conduction system thats not SA or AV node control HR.


Is insufficient to maintain life.


requires artificial pacemaker

Ectopic focus


control

another part of the conduction system that is not the SA or AV node control HR.

SA AV node function.

Control HR

Artifical pacemaker

required to maintain life if your heart is in


ectopic focus (20-40 bpm)

Arrythmia


definition

abnormal rhythm

Arrythmia


cause

may be due to heart block


(damage to conduction system)

Atrial Fibrillation

death and must be shocked back to sinus rhythm.


contains little waves between beats.

SA node cells do not have this

Stable resting membrane potential.


(what about it)

Pacemaker potential in the SA node cells is due to


scientific steps.

Slow Na inflow - MP goes from -60MV -> -40MV


At -40mV: fast Ca2+ channels open -> trigger AP


at 0 mV: K channels open -> repolarize cell

Pacemaker potential in the sa node


basic.

slow sodium inflow brings membrane potential from -60mV to -40mV where calcium channels open and an Action potential is triggered.


at 0mV potassium channels open and repolarize the cell.

Pacemaker potential impulse conduction to myocardium steps full.

1. Sa node fires, Atria contract


2. signal travels to AV node where its delayed while ventricles fill.


3. signal spread to adjacent myocardium(slow) and down AV bundle and bundle branches (very quick) to purkinje fibers.


4. all ventricular myocytes contract, starting with myocytes at the apex of the heart.

Pacemaker potential impulse conduction to myocardium step 1

SA node fires, Atria contract.

Pacemaker potential impulse conduction to myocardium step 2

Signal goes to AV node where its delayed while ventricles fill

Pacemaker potential impulse conduction to myocardium step 3

Signal spreads to adjacent myocardium (slowly) and down av bundle and bundle branches (very quickly) to purkinje fibers.

Pacemaker potential impulse conduction to myocardium step 4

All ventricular myocytes contract, starting with myocytes at the apex of the heart.

Cardiac conduction system electrical signal route starting place

Sinoatrial (sa) node (pacemaker) through both atria



Cardiac conduction system electrical signal route after SA node through both atria.

Atrioventricular (AV) node (signal pauses)

Cardiac conduction system electrical signal route after AV node signal pauses.

AV bundle

Cardiac conduction system electrical signal route after AV bundle

Right and left bundle branches. (very quickly)

Cardiac conduction system electrical signal route after right and left bundle branches.

purkinje fibers.

Cardiac conduction system electrical signal route after Purkinje fibers.

Around ventricular myocardium such that the heart contracts from the bottom(apex) upwards.

Action potential in a myocyte steps full.

Start at -96mV


1. Na channels open -> depolarization (action potential trigger) (rapid) Peaks at almost 30mV


2. Na close, Ca channels open, cause Ca to leave SR (long depolarizatio) Ca closes (at around 0mv)


3. K channels open shoot out rapidly, repolarization occurs. happens at about 0mV and 200ms



Action potential in a myocyte


starting mV?


peak mV?


Calcium closes mV?

-96mV


almost 30 mV


around 0 mV

Muscle tension is unlike a skeletal muscle in this way



long lasting vs twitch.

Action potential in a myocyte


time?

200 ms.

Action potential in a myocyte


heart contraction plateau time?


heart back to normal time?

200 ms


300 ms

Action potential in a myocyte step 1

1. Starts at -.96 mV Na channels open(RAPID) depolarization (action potential trigger) Peaks at almost 30mV

Action potential in a myocyte step 2

2. Na close, Ca channels open, cause Ca to leave SR (long, steady depolarization) Ca closes (at around 0mV)

Action potential in a myocyte step 3

3. K channels open and shoot out rapidly, repolarization occurs happens at about 0mV and 200ms

Electrocardiogram

Record of all electrical activity of the heart.

PQRST

waves of parts of the heart.

P wave

Atrial depolarization


first up and down bump

QRS complex

Ventricular depolarization.


Atrial repolarization (hidden)

T wave

Ventricular repolarization.

Atria Contracting


(PQRST wave)

Top of P wave until start of Q wave

Ventricle Contracting


(PQRST wave)

Top of R wave until just before top of T wave

Nodal rhythm


(PQRST wave)

Sa node is not functional so p wave is missing on EKG

Premature ventricular contraction (PVC)


(PQRST wave)

Extra beat, looks like the wave goes down far at the qrs complex.

Ventricular fibrillilation


(PQRST wave)

Requires immediate intervention.


looks like up and down randomly.

Cardiac cycle

One complete cycle of contraction/relaxation of all 4 chambers. both contract then relax.

Unit of measure of pressure

mm of mercury


mm Hg

How fluid flows

from high pressure to low pressure.

S1 sound is

closure of Atrioventricular valves


heard just before peak of R.

S2 sound is

closure of semilunar valves.


heard half way down t wave.

S3 may be hear in

children and adolescents ECG

cardiac cycle starts

Semilunar valves have just closed (S2) and AV valves just opened

VIVI


what is this

phases of the cardiac cycle acronym

VIVI actual

Ventricular Filling


Isovolumetric contraction


Ventricular Ejection


Isovolumetric relaxation.

Cardiac filling phase 1 + QRST wave

Ventricular filling. essentially filling the ventricle up. until AV valves close.


End of T until top of R.



Ventricular filling states

1 Rapid filling


2 diastasis


3 atrial systole

Rapid filling (cardiac cycle)


(PQRST complex)

end of T wave(end of S2) until diastasis.(end of S3)


first stage of ventricular filling of the cardiac cycle

Diastasis (cardiac cycle)


(PQRST complex)

End of rapid filling(end of S3) until top of P wave (atrial systole)


second stage of ventricular filling of the cardiac cycle

Atrial Systole (cardiac cycle)


(PQRST complex)

top of P wave until top of R wave.


final stage of ventricular filling.

Ventricular filling


ESV (end systolic volume)

60mL


(how much was left over after it contracted)

Ventricular filling


EDV (end diastolic volume)

60ml End systolic volume +


30ml passively added +


40ml from atrial systole =


130mL

Cardiac filling phase 2

Isovolumetric contraction




Comes after Ventricular filling.


ventricles contract, pressure builds, AV valves close and you hear S1 sound, no blood leaves



Isovolumetric contraction
(PQRST Wave)

Top of R wave (S1)


until end of S wave.

Cardiac filling phase 3

Ventricles continue to contract until pressure in ventricles is greater then pressure in arteries so Semilunar valves open.

Ventricular ejection


(PQRST Wave)

End of s wave until just past top of t wave.


can still hear s1

Ventricular ejection formulas

Stroke volume and ejection fraction

Stroke volume

amount ejected out of ventricle during ventricular ejection

ejection fraction

Stroke volume(how much ejected)


divided by End diastolic volume (how much was here.



If there was 130ml in the ventricles, and they ejected 70ml. what are we calculating and what is it?

Ejection fraction = 70/130 = 54%

Cardiac filling phase 4

isovolumetric relaxation


ventricles relax, pressure in ventricles is less than pressure in arteries so semilunar valves close (S2)

isovolumetric relaxation
(PQRST Wave)

Near end of T until end up T.


S2 heard



Left and right ventricle stroke volume

these are equal to each other.

L heart failure

edema in the lungs


(more common)

R heart failure

edema in the body.

Cardiac output

amount of blood ejected from each ventricle/minute.



cardiac output formula

Heart rate x Stroke volume

Maximum Cardiac output

220 - your age = BPM

Values for CO at rest

75 bpm x 70 ml = 5250 ml/min.

cardiac reserve

difference between maximum and resting CO.

Heart rate pulse is measured here

radial and common carotid arteries.

resting hr


in infants


females


males

120 bpm


75 bpm


70 bpm

tachycardia

persistent hr > 100 bpm.

causes tachycardia

stress, anxiety, stimulants.

Blood loss might do this

Tachycardia


light, fast pulse


from a decrease in SV.

bradycardia

persistent hr < 60.



bradycardia due to

hypothermia, sleep, athletes.

well condition hearts might get this

bradycardia as SV is greater.

Chronotopes

things that effect heart rate

stress, coffee

postive chronotropes

meditating, drugs

negative chronotropes.

Homeostatic mechanisms that control heart rate sensors


control centers


effectors

sensors : proprioceptors, baroreceptors, chemoreceptors.




control centers : cardioaccelatory (sympathetic ouput) + cardio inhibitory centers in the medulla (parasympathetic output)




Effectors: heart, sa node, or muscle. heart is big one.

Proprioceptors

sense your muscle and joints moving


tell your heart that you are moving/ exercising



proprioceptors are here

muscle spindle,


lamellar corpusce (nerve ending in skin)


golgi tendon organ.

baroreceptors are here

located in carotid sinuses and aortic arch

baroreceptors do this

pressure sensors (blood pressure)


if bp decrease, these send signal to increase HR via cardio stimulation center.

Chemoreceptors are here

in carotid bodies in carotid arteries and aortic arch, medulla

Chemoreceptors do this

pH sensors.

Chemoreceptors formula

CO2 + H2O <-CAH-> H2CO3 <-> H + HCO3



Chemoreceptors does what during exercise

Increase in CO2 means increase in H so pH goes down so hR goes up via cardio stimulation center.

Cardioaccelatory center is here


it stimulates this.

Medulla


output to sympathetic nervous system

Cardioinhibitory center is here


it stimulates this.

Medulla


output to parasympathetic nervous system

Proprioceptors, baroreceptors, and chemoreceptors are what?

sensors.

cardioaccelatory and cardioinhibitory are this

control centers.

Heart, sa node, muscle are this

effectors.

EPI and NE increase HR via this

cAMP

K and CA imbalance

these can lead to arrythmia

caffeine, nicotine, epi, NE are this

positive chronotropes.

three things that effect stroke volume

Preload


Contractility


afterload.

preload

amount of tension in the ventricle before contraction.

preload varies with

venous return

if more blood returns to heart this happens

larger the volume of blood in the heart.

exercise does what to preload

increases it by increasing SV and CO

Frank starling law of the heart states this

SV varies with end diastolic volume


the more blood enters the heart, the more blood leaves.

contractility

force of contraction for a given preload.

increase contractility does this to SV and CO

increase SV so increase CO

Contractility is changed by

ionotropes

positive ionotropes

increase contractility such as calcium

these decrease contractility

negative ionotrope

athletic hearts have this type of contractility

higher contractility

Afterload

blood pressure in the aorta and pulmonary trunk that opposes the opening of those valves.




resistance the heart has to overcome in order to push blood out of the left ventricle.

an increase in in afterload does this to stroke volume and cardiac output

decreases stroke volume and cardiac output

this happens to afterload if arterial circulation is impeded

increased afterload.

on a graph, what happens to stroke volume as afterload increases

it decreases.

exercise


stimulus


receptor


control center


effector

stimulus: muscle contraction


receptor: proprioceptor (were moving)


control center: cardio stimulating center(medulla)


effector: sa node, which results in increase hr.

hypertrophy

increase in volume of an organ.

a bigger heart does this

(hypertrophy)


which increases stroke volume and CO



a stronger heart does this

increase contractility so increase CO

SAID principle

your body will adapt to stress you put on it.

sv and contractility are bigger rest, this must be done to constant CO

decrease resting HR.