more term based for cariovasular system

Venecava

connected to right atrium

pulmonary veins

connected to left atrium

valve between LA and LV

bicuspid valve, also called mitrial valve

valve between RV and RA

tricuspid valve

pulmanary valve

RV

aortic valve

LV

papilary muscles

contract when valves are open

endocardium

inside heart

myocardium

cardiac muscle, solid

pericardium

outside of heart

corinary circulation

small amount of blood exits LV

Chordae tendineae

cable like straps attached to papilary muscle

papilary muscle

portion of cardiac wall growing into chamber

perkinji system

conductive

helps system go from bottom up

sinoatrial node

heart pacemaker, causes atria to contract

atrioventricular node

recieves electrical impulse from sinoatrial node

delays signal to let ventricles fill with blood, passes signal to bundle of his

bundle of his

go to bottom of heart

carries impulse from AV node to ventricles

purkinje pathway

SA node—→AV node—→ bundle of his—→ perkinje fibers

conductive contractile cells

myocardial cells

conductive noncontractile cells

perkinje system

nonconductive noncontractile cells

skeleton of the heart

SA node beats

100/min

atrial beats

40-60/min

AV node beats

25-40/min

vent. m. beats

20/min

average resting heart rate

70/min

what can raise heart rate

parasympathetic

max impulses/min

240

depolarization

systole

repolarization

diastole

cardiogram

measures wave of electricity that travels through heart every beat

P wave

start of atrial systally (depolarization)

QRS complex

start of ventricular systally (depolarize) and atrial dyastaly (repolarization)

peak of T

start of ventricular diastally

blood pressure

systolic/diastolic

contraction happens when

when depolarized

AV block

slowing of conduction between AV node and bundle of his

1st degree block

slower but no skipped beats

2nd degree block

some skipped beats

3rd degree block

severed communication between top and bottom

lets ventricles beat on own rhythm

atrial flutter

rapid weak sawtooth pattern

asynchronous QRS

rhythm=250-250 bpm

ventricles can’t keep up with atria

myocardial interaction

after heart attack

clogging of coronary arteries leading to decreased blood flow, myocardial death

fibrilation

random, wandering isoelectric line, no clear P or QRS events

fibrillation can either be atrial or ventricular

atrial feels like racing

ventricular triggered by heart attack

defibrillator

not fixing dead part just want SA node to dodge dead spot

atrial diastole from

—->p and R—→

atrial systole from

mid p—>R

ventricular diastole from

—→r mid and T—→

ventricular systole from

R mid —→ T mid

crosses on important chart mean

a valve opens

causes sound

valve closing

isometric contract

all chambers closed pressure skirockets

isometric relaxation

chambers closed, pressure decreases

P and R align with

first action potential in atrial muscles

depolarization of atria and ventricles

T align with

steep repolarization of ventricles

which side is weaker

right side is weaker

normal open valve

laminar flow=quiet

not normal open valve

stenotic valve: narrowed valve, turbulent flow= murmer

valve does not open all the way

normal closed valve

no flow=quiet

not normal closed valve

unsufficient valve: leaky valve, turbulent backflow=murmer

blood leaking valve, damaged whne tries to close can’t fully

prolase

valve fails entirely, closes then pressure bursts it open the wrong way

aortic stenosis

aortic valve is narrow, hard for blood to leave left ventricle

mitral regurgitation

mitral valve doesn’t close properly, blood leaks to left atrium

aortic regurgitation

aortic valve doesn’t clse properly, allowing blood to leak to left ventricle

patent ducts arteriosus

fetal blood vessel vessel open after birth, abnormal blood flow between aorta and pulmonary artery

mitral valve prolapse

mitral valve bulges backward into the left atrium

how to increase heart pumping

by either increasing heart rate or volume

EDV: starling’s law of the heart

heart muscle has stretch receptors in it

can strengthn beat not start one

contracts more forcefully, puts more blood in

trained heart

work longer, still needs same amount of blood

lower heart rate even at rest

more efficient, pumps more blood

untrained heart

beats more often and less efficient

leaving the heart, blood flow

blood can’t flow backwards through aortic valve or pulmonary valve during diastate

aorta elasticity

as age, elastic of connective tissues break down

collesteral also stiffins it