Physiology Exam 3

Pulmonary

pertaining to the lungs

systemic

body wide

atria

1st and 3rd chambers of the heart

ventricle

2nd and 4th chambers of the heart. Pushes blood out to the lungs and out the aorta.

septum

separates the chambers of the heart (separating oxygenated/deoxygenated blood)

myocardium

thick musular layer of the heart wall that pumps blood throughout the body

aorta

three branches that pumps blood out to the rest of the body

pulmonary artery

artery that takes blood from the rt ventricle and transfers it to the lungs to get oxygenized

pulmonary vein

brings oxygenized blood to the lft atria

AV valves

1st lub sound is produced by the closing of the AV valves

tricuspid

btwn rt atrium + rt ventricle

bicuspid

btwn left atrium + left ventricle

semilunar valves

Aortic + pulmonary semilunar valves blood goes out ot

CO-cardiac output

volume of blood pumped/min by each ventricle

SA (sinoatrial node)

pacemaker cells extend out towards the atria and these will make a pathway called the interatrial path

internodal pathway

electrical activity goes rapidly to AV node via the internodal pathway

AV node

junction btwn the 2 atria and ventricles — go through bundle of his and then go through septum and activate cells when they activate the purkinjie fibers

bundle of his

cardiac muscle fibers that transmit electrical impulse from the AV node down the ventricle of the heart

purkinjie fibers

serve as the final rapid conduction pathway of the hearts electrical system, ensuring the synchronized contraction of the ventricles.

HCN-hyperpolarization activated syslic nucleotide gated

non selective voltage gated cation channels that open in response to membrane hyperpolarization.

absolute refractory period

brief time span during + immediately after an AP when neuron/muscle cell can’t generate another AP no matter the strength of the stimulus

plateau phase (Ca)

extended refractory period when Ca comes into the cell and at the same time K leaves the cell

CO-cardiac output

total volume of blood pumped by the heart per minute Stroke volume x Heart rate. Regular Co is 70 ml/beat x 75 bpm

SV-stroke volume

blood pumped/beat by each ventricle

EDV-end diastolic volume

the maximum amount of blood in ventricules occurs at the end of ventricular relaxation. EDV=around 135 mL

ejection fraction

stroke volume/EDV

Frank starling law of the heart

the more volume you add the more blood that’s pumped out

SV-stroke volume

volume of blood ejected by a ventricle of the heart during each single cardiac contraction.

determined by 3 variables:

EDV— volume of blood in ventricles at end of diastole

total peripheral resistance (TPR) — impedence to blood flow in arteries

contractility — strength of ventricular contraction

Chronotropic effect

effect timing of HR (symp + parasymp effect influences it)

inotropic

NE+Epi produce an increase in contraction strength

intrinsic

if its more local its an intrinsic control mech.

extrinsic

damage outside blood vessels releases tissue thromboplastin that triggers a clotting shortcut

skeletal pump

collection of skeletal muscle (mainly in calves+legs) that help push venous blood back to the heart against gravity

venous return

veins hold most of blood in body (70%) and thus called capacitance vessels (vessels that hold energy)

capacitance vessels

vessels that hold energy. veins hold most blood in body (70%)

compliance

have thin walls and stretch easily to accommodate more blood without increased pressure (=higher compliance)

isovolumetric contraction

brief phase in early ventricular systole where the hearts ventircles contract without any change in blood volume

isovolumetric relaxation

short phase in the cardiac cyc;e where the ventricles relax and pressure drops rapidly, while all heart valves remain closed

heart murmurs

abnormal sounds produced by abnormal patterns of blood flow in heart. Many caused by defectiv heart valves

rheumatic fever

fever that occurs from an inflammatory disease such as streptococcus infection/strep throat

mitral stenosis

mitral valve becomes thickened and calcified very often due to secondary damage. Thickened valve does not open fully, impairing blood flow from the left atrium to the left ventricle

TPR-total peripheral resistance

impedence to blood flow in arteries