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

systole

contraction phase of heart (around 0.3 sec)

diastole

relaxation phase of the heart (around 0.5 sec)

viscosity

part of peripheral resistance. Higher viscosity = increased BP

Poiseuilles Law (know equation and variables)

(Q) = change in Pr^4 (pi)/nL(8).

Blood flow is proportional to a pressure gradient/resistance

MAP — mean arterial pressure (120/80 —> 93 mmHg)

MAP=diastolic pressure + ⅓ (systolic pressure - diastolic pressure)

arteries

Contains a lot of elastin and expands during systole and recoils during diastole. During diastole it helps to maintain smooth blood flow

arterioles

Cause a drop in BP. They dilate and constrict in response to changes in CO2 levels.

capillaries

only made of endothelial cells (only vessels that have no smooth muscle around them)

venules

very small blood vessels that collect deoxygenated blood and and waste products from capillary beds and channel them into larger veins

veins

arteries + vins have 3 layers: external (connective tissue), media (mostly smooth muscle), internal (made of endothelium, basement membrane, and elastin)

endothelium

innermost layer of all vessels

tunica interna

made of endothelium, basement membrane, and elastin

elastin

found it large arteries to help them expand and contract

precapillary sphincters

determines how much blood flow an area recieves

skeletal muscle pump

Blood is moved toward heart by contraction of surrounding skeletal muscles (skeletal muscle pump)

length tension relationship (more you stretch out the harder you can contract). Also affected by venous return which is aided by the skeletal muscle pump + respiratory pump

LDL (low density lipoprotein)

from the liver to the tissues (ApoB – 100

Apo B-100

Liver – Apo B-100 → LDL

is a protein

HDL (high density lipoprotein)

HDL = healthy, excess cholesterol from tissues is “properly” disposed of or stored in the liver for future use

tissues/Blood vessels – Apo A-1 —> HDL

atherosclerosis

Plaque begins at sites of damage to endothelium

Ex. from hypertension, smoking (vaping), high cholesterol, or diabetes

When you have a buildup of cholesterol it will start to crystallize

arteriosclerosis

hardening of the arteries. Accounts for 50% of deaths in the US

atheroma

As plaque forms and crystallizes you constrict vessels therefore need more blood pressure to drive blood flow and it forms an area where a clot can form (atheroma)

Plaque is called the atheroma and the actual clot is called a thrombus

angiogram

medical imaging test that uses X rays and a special contrast dye to see inside your blood vessels (arteries + veins)

ischemia

occurs when blood supply to tissue is deficient — most commonly due to atherosclerosis in coronary arteries

Buildup of lactic acid so you don't have the blood flow to remove things

determined on an ECG through an elevated/depressed ST segment

angina pectoris

chest pain

MI (myocardial infarction)

can tell by an enhanced ESR, change in ST segment, and high levels of CPK (creatine phosphokinase), LDH (lactate dehydrogenase), and troponin

creatine phosphokinase (CPK)

converts creatine to phosphocreatine (is found in skeletal + cardiac muscle). igh levels of it could be indicative of an MI

lactate dehydrogenase (LDH)

used to diagnose an MI

myogenic regulation

When BP increases, cerebral arterioles  constrict; when BP decreases, arteriole dilate (=myogenic regulation)

metabolic regulation

Arterioles are very sensitive to increases in local neural activity ( = metabolic regulation) Areas of the brain with the highest metabolic activity recieved the most blood

cutaneous

closer to the surface

thermoregulation

maintining body core temp at a homeostatic level

Angioplasty

Place a stent in the vessel to give it a better shape that was disrupted by the plaque

thrombus

A clot that can become dislodged and go to smaller and smaller vessels – this is the case in CAD

embolus

a thrombus that’s free in the blood but its usually going to a smaller and smaller vessel

stent

used in an angioplasty to give the vessel better shape

baroreceptors

stretch receptors that are activated by changes in BP and they are located in the aortic arch and carotid sinuses

vasomotor control center

where the baroreceptors send APs in the medulla

cardiac control center

where the baroreceptors send APs in the medulla

carotid sinus baroreceptor

a specialized stretch receptor located in the wall of the carotid sinus

aortic arch baroreceptor

a specialized stretch receptor located in the adventitia of the aortic arch

atrial stretch receptor

baroreceptors in the atria to detect ventricular overflow/topping off

ANP-atrial natriuretic peptide

a hormone that has multiple affects — all of these mechanisms are to prevent overfilling the atria which would tend to overfill the ventricles

primary/essential hypertension

high BP that is caused by complex and poorly understood processes

secondary hypertension

caused by known disease processes

Ex. kidneys important in maintaining BP – kidney problems/kidney failure we can expect secondary hypertension

congestive heart failure

hypertension causes increased workload of the heart leading to ventricular hypertrophy and CHF

hypovolemic shock

shcok that ovvurs when the body loses more than 20% of blood or fluid supply

septic shock

due to infection (sepsis) – often bacteria release endotoxins that can cause excess production of NO (nitric oxide causes vasodilation) and massive vasodilation (high mortality rate)

sepsis

bacteria int eh blood stream causing systemic infection

endotoxin

Pyrogens are released by WBCs in response to endotoxin from gram-bacteria. Is believed to be beneficial to the body because it slows down the growth of bacteria

anaphylactic shock

severe life threatening allergic rxn that occurs when there’s a massive flood of chemicals like histamine

neurogenic shock

shock that occurs when theres damage to the central nervous system that disrupts normal Sympathetic NS

cardiogenic shock

common following MI (heart attack): heart just can’t pump blood and generate pressure

colloid osmotic pressure - AKA oncotic pressure

pressure exerted by proteins in the blood plasma (ex. albumin) that pulls water back into he blood vessels

starling forces

The more volume you add the more that's pumped out up until a certain point (at a certain point volume pumped out decreases)

(Ultra) filtration

pressure-drriven membrane separation process that uses semipermeable membranes

reabsorption

process by which the body or a physical system absorbs a substance again

asymptomatic

no symptoms. Typically in hypertension there’s no symptoms until substantial vascular damage (silent killer)

lymphatic system

Lymph nodes filter lymph before returning it to veins via thoracic duct or right lymphatic duct