Xphys Circulatory responses to exercise

relative changes in blood flow

large

absolute changes in blood flow

small

nitric oxide

released by muscles during contraction to vasodilate

lowest pressure

right atrium

highest pressure

left ventricle

arteries

carry blood away from heart

veins

carry blood to heart

capillaries

exchange of materials

bulkflow

large push out and slightly smaller pull back in

afterload

keeps semilunar valve closed

tricuspid valve

between R atrium and ventricle

bicuspid valve

between L atria and ventricle

pulmonary circuit

pumps deoxygenated blood to lungs

systemic circuit

pumps oxygenated blood to tissues

epicardium

outer layer

myocardium

muscle

endocardium

blood-proof layer

myocardium blood supply

coronary arteries

myocardial infarcation

heart attack

pericardial sac

decreases friction

signal sharing in cardiac muscle

intercalated discs and branching

LDH in cardiac

favors pyruvate

ejection of blood

2/3 in systole

distole at rest

0.5 sec

systole at rest

0.3 sec

allows for shorter diastole with exercise

greater venous return

semilunar valves open

ventricular pressure > atrial pressure

first heart sound

closing of AV valve

second heart sound

closing of aortic and pulmonary valves

ESV

1/3 of blood left in heart after systole

hypertension BP

above 140/90 mmHG

primary hypertension

multifactoral, more common

secondary hypertension

result of some other disease process

normal BP

less than 120/80

prehypertension

120-129 and less than 80

hypertension stage 1

130-139 or 80-89

hypertension stage 2

140+ or 90+

SA node

pacemaker, intitiates depolarization

AV node

passes depolarization to ventricles

bundle branches

connects atria to left and right ventricle

purkinji fibers

spread wave of depolarization throughout ventricles

long-term regulation of MAP

kidneys

short-term

SNS, baroreceptors in aorta and carotid arteries

P wave

atrial depolarization

QRS complex

ventricular depolarization and atrial repolarization

R

start of ventricular contraction

T wave

ventricular repolarization, contraction stops

PR interval

AV nodal delay

Peak P

atrical contraction

atherosclerosis

fatty plaque narrows coronary arteries

ST depression

indicates myocardial ischemia

PSNS impacts HR by

inhibiting AV and SA node

SNS impacts HR by

using catecholamines and stimulating SA and AV nodes

increase of HR with onset of exercise is due to

PSNS withdraw

nerve associated with HR

vagus nerve

Heart rate variability

time between R-R intervals

EDV increases due to

increased venous return

frank-starling mechanism of the heart

greater EDV results in a more forceful contraction

venous return increased by

skeletal muscle pump, respiratory pump, vasoconstriction

plasma

liquid portion of blood

hematocrit

RBC, WBC, platelets

untrained individuals SV

plateaus at 40-60% VO2max

artreiovenous difference

amount of O2 taken up from 100ml of blood

CO to muscles at rest

15-20%

CO to muscles with submax exercise

80-85%

nitric oxide

increases vasodilation

autoregulation of blood flow

dictated by local metabolities

HR with arm exercises

greater than legs

double product

HR*SBP

baroreceptors in aorta and carotid bodies

sensitive to arterial BP