Physiology Exam 4

Stroke Volume

Amount of blood pumped each cycle

SV = End Diastolic Volume - End Systolic Volume

EDV = affected by the length of vent contraction & venous pressure (increased ventricular loading) 

ESV = affected by the arterial blood pressure and force of ventricular contraction 

Factors that effect SV

• Preload (EDV)

• Contractlity

• Afterload (ESV)

Cardiac Output

volume of blood pumped in each ventricle per minute 

CO = Heart Rate X SV

Resting CO= 5.25 L/Min

Max CO is 4-5 times resting

Maximal CO is met by increasing HR and SV 

Starlings Law

Preload

The SV of heart increases from an increase of volume of blood filling in heart.

Heart sarccomeres are extra overlapped

Greater filling = Greater force of contraction

Venous return is amount of blood returning to heart

Slow heart rate or increase in blood pressure (exercise) = increased venous return = increased contraction force.

Contractility

Contractile strength at given muscle length

Muscle length stays the same when contracting! 

Increased by sympathetic stimulation and positive inotropic agents. Ca2+

Decreased by negative inotropic agents (weaken contraction) 

Afterload

The pressure that the ventricles must overcome to eject blood through the semilunar valves 

Hypertension: High blood pressure in systemic circulation 

increases afterload = increased End Systolic Volume = decreased Stroke Volume 

Peristalsis

alternation contractions of smooth muscle layers that mix and squeeze substances through tube 

Single-unit (visceral) smooth muscle

Act like cardiac muscle

Gap junctions - synchronicity

spontaneous depolarization 

In all hollow organs besides the heart 

Autonomic nervous system (varicosities) 

Respond to multiple chemical stimuli

Multi-unit smooth muscle

Acts like skeletal muscle

Large airways, arteries, goosebumps, iris of eye

Rarely ever gap junctions or spontaneous depolarization 

independent muscle fiber innervated by the autonomic nervous system - graded potential 

 

Varicosities

autonomic nerves that innervate smooth muscle into diffuse junctions

Smooth muscle

thin and short 

only one nucleus

No sarcomreres, myofibrils, or T-tubules 

Thick filament has myosin heads all over

pouchlike infoldings called caveolae 

No troponin - calmodulin instead 

Calmodulin activates light chain kinase 

Dense bodies - like Z disks 

Can contract in the absence of electrical depolarization 

Relaxation only occurs after phosphate is removed from the myosin light chain 

contraction of smooth muscle

Slow ATPases

slow to contract but stays contracted for a long time

Either action or graded potential 

no electrical change (G-protein)

responds to stretch briefly, then adapts to new length 

Some smooth muscles have no nerve supply. depolarize spontaneously or respond to physical stimuli or chemical stimuli from G-protein-linked receptors. 

3 wall layers of Arteries and veins

Tunica intima = endothelium (lining)

Tunica media = smooth muscle and elastin

Tunica externa = collagen fibers

Lumen - central blood containing space

Elastic Arteries

large thick-walled arteries with elastin in all three tunics

Aorta is the major branch

Large lumen has low resistance and is inactive in vasoconstriction.

Aorta expands and recoils as blood is ejected from the heart (Pressure reservoirs)

Muscular Arteries 

downstream of elastic arteries 

thick tunica media with more smooth muscle

Active in vasoconstriction  

Arterioles 

Smallest arteries to capillary beds

Contain smooth muscle for controlling flow to capillary beds and determining MAP

uses vasodilatation and vasoconstriction 

No gas or nutrient exchange! walls to thick, meant for regulation. 

Capillaries

in all tissues Except: cartilage, epithelia, cornea, and lens of eye. 

make up about 80% of the length of blood vessels 1 red blood cell in diameter to ensure only single RBC pass at a time. 

Walls are very thin 

Functions: exchange gas, nutrients, wastes, hormones, etc. 

Venules

formed when capillaries unite

very porous, allow fluids and WBC into tissues. 

act like capillaries 

lower pressure than in capillaries and still thin walls 

larger venules have one or two layers of smooth muscle. 

Veins

formed when venules converge

have thinner walls and larger lumens compared to similar arteries 

thin tunica media but still have smooth muscle which undergoes constriction 

Thick tunica externa of collagen fibers 

Blood pressure lower than in arteries 

Adaptations ensure retern of blood to heart depsite low pressure 

large diameter lumens offer little resistance 

Capacitance vessels

blood reservoirs

contain up to 60% of blood supply 

Venous valves 

prevent backflow of blood. 

most abundant in veins of limbs

(muscle surrounding vein)

Blood volume

80% of blood volume in systemic circulation

60% of that is in veins and venules 

15% of that is in arteries and arterioles 

Resistance

increase length and blood viscocity = increase resistance

increase radius = decrease resistance 

(top same - bottom opposite) 

Length and blood viscosity do not change. (relatively constant) 

Flow rate

Flow rate decreases with larger cross sectional area (more branches)

Arterial blood pressure

Systolic pressure: pressure exerted in the aorta during ventricular contraction 

Diastolic pressure: the lowest level of aortic pressure 

blood pressure near the heart is pulsatile 

regulation of systemic blood flow

Local Control of Systemic Circulation Autoregulation

Arterioles 

The tissue doesn’t need instructions from the brain to get more blood. If it’s low on O₂, the arterioles automatically open up

independent of MAP and neural/hormonal control 

(smaller goal)

Systemic Control of system-wide 

Neural & hormonal

Arteries 

blood need to go back to heart 

(bigger goal)

Metabolic controls

Local chemicals short term autoregulation

Vasodilation - Nitric oxide (NO)

Nitrates like nitroglycerin and viagra increase NO for vasodilation 

active tissue is using O2 and relasing CO2, H+, K+, and adenosine 

Vasoconstriction - Endothelins from the endothelium 

inactive tissue high O2 and low CO2, K+, H+

NO and Endothelin are balanced unless blood flow is bad, then NO wins. 

Myogenic controls

Local stretch short-term autoregulation

keep blood flow to tissue relatively constant despite most fluctuations in systemic pressure 

vascular smooth muscle response to stretch 

protects the weaker capillaries downstream

Stretch (increase pressure) = vasoconstriction 

low stretch (low pressure) = vasodialation and increase blood flow 

Long-term local autoregulation

Short-term autoregulation can’t meet tissue nutrient requirements 

Angiogenesis: The number of vessels to the region increases, and existing vessels enlarge. Blood vessels grow into anoxic tissue (low O2)

Oxygen tank in premature - 

1. Too much O2 = reduced retinal capillary growth 

2. When high O2 was removed, the retina didn’t have oxygen and capillaries didn’t grow there = can’t see anymore 

Metabolic control in Pulmonary

Perfusion = change of pulmonary O2 in alveoli changes the diameter of arterioles 

Ventilation = change in pulmonary CO2 in alveoli changes the diameter of bronchioles

Collapsed lung = pulmonary arteriole dilation directs blood to the alveolar region, where O2 is high. 

Neural Control of Systemic blood flow and pressure 

Short term: neural controls

change Cardiac Output and Peripheral Resistance to alter Blood Pressure. 

Reflexes (neural): 

Baroreceptors - mechanical sensors in carotid sinus and the aortic arch 

Chemoreceptors - carotid bodies in the aortic arch and neck arteries 

Hormonal control of systemic blood flow and pressure 

Long-term regulation: changes in blood volume (kidney) 

Short-term regulation: changes in resistance and Cardiac Output 

Increased secretion increases blood pressure: 

• Epinephrine and Norepinephrine increase CO and PR (vasoconstriction) almost everywhere. (Except heart, skeletal muscle, and liver)

• ADH increases blood volume and causes vasoconstriction 

• Aldosterone increases Na+ and blood volume 

• Angiotensin II increases aldosterone 

Increased secretion lowers blood pressure:

• Atrial natriuretic peptide (ANP) causes vasodilatation and decreases blood volume by lowering blood Na+ and inhibiting aldosterone and ADH

High blood pressure stretches the heart and leads to ANP

Capillary exchange

1. Diffusion - high to low concentration

2. Vesicle transport - proteins/hormones are endocytosed and exocytosed on the other side

3. Bulk flow - distribution of extracellular fluid volume thru pressure. 20 L in bulk flow daily 

Pressure in capillaries 

Capillary Hydrostatic pressure pushes fluid out of the capillary 

Interstitial Hydrostatic pressure pushes fluid into the capillary (little effect) 

Capillary Osmotic pressure pulls fluid into the capillary 

Interstitial Osmotic pressure pulls fluid out of the capillary (little effect)

airway resistance 

Resistance is greatest in medium sized bronchi 

Resistance is lowest at the terminal bronchioles, where the total cross-sectional area increases the most. 

Surfactant

detergent-like lipoprotein complex 

reduces surface tension of alveolar fluid and no alveolar collapse 

helps normalize pressures between different alveoli 

Infant respiratory distress syndrome: insufficient quantity of surfactant, alveoli collapse after each breath. 

Lung compliance

A measure of the lungs’ ability to stretch and expand for breathing 

can’t do it if low flexibility in thorasic cage,

scar tissue (not elastic like it should be),

reduced production of surfactant 

Pressure

Negative intrapleural pressure is caused by elastic recoil of the lungs and surface tension of alveoli. BUT the elasticity of the chest wall pulls the thorax out

Surface tension between the parietal and visceral pleura keeps the lungs inflated 

Intrapleural pressure cannot be the same as the atmospheric pressure or intrapulmonary pressure, or the lung will collapse. The parietal pleura or visceral pleura can be punctured for that to happen. 

Intrapleural pressure must be lower than the pulmonary and atmosphere pressures 

Transpulmonary pressure must stay positive so lung stays inflated 

Atelectasis = lung collapse due to

1. plugged broncheoles → collapse of alveoli 

2. pneumothorax → air in plural cavity

Dead Space

anatomical dead space

No contribution to gas exchange 

The air remaining in passageways is 10% of the residual volume 

Alveolar dead space - non-functional alveoli due to collapse, lack of capillaries or obstruction 

Total dead space - sum of anatomical and alveolar dead space 

dead space normally constant, difficult to measure 

Rhabdomyolysis

muscle damage allows myoglobin to leak into the bloodstream and then nephron, where it gets clogged then causes renal falure and death

urine 

180 L of fluid processed each day. only 1.5L is urine