Physiology

• oxygen
• nutrients
• warmth
• water
• hormones
• ions

• carbon dioxide
• chemical wastes
• heat
• water
• toxins from liver

• red (darker when deoxygenated)
• pH 7.4
• 37 degrees C
• amiable
• 5 liters

• plasma (55%)
• WBCs/platelets (buffy coat)
• RBCs (45%)

• erythrocytes
• packed with hemoglobin (oxygen transport)
• 15 grams of Hb per 100 ml blood
• decreased RBC count = anemia
• increased RBC count = polycythemia

oxygen content in the blood

• iron and amino acids
• vitamin B12
• folic acid
• oxygen content of blood

120 days, recycled in the spleen (or liver)

• the amount of RBCs that settle out of blood in a single hour.
• elevated during infection, arthritis, and inflammatory diseases

• made of water and plasma proteins
• made in the liver
• main function of plasma proteins: plasma colloidal osmotic pressure

• most common plasma protein
• contributes to plasma colloidal osmotic pressure
• -prevents excessive fluid filtration
• carrier function

• carrier proteins
• clotting factors
• lipids
• steroid-binding proteins
• bilirubin
• clotting factors

• carrier proteins
• LDLs
• iron (transferrin)
• beta 1 and beta 2 subtypes

anatibodies

• protein precursor to clot
• precursor to fibrin which polymerizes to form an insoluble mesh (coagulation)

ability of blood to maintain its volume

• trauma induces vasoconstriction
• vasoconstrictive factors (endothelin-1) released
• platelets stimulate vasoconstriction by releasing thronboxane A₂ and serotonin

• thromboxane and thrombin both promote platelet aggregation causes adherence, aggregation, and secretion
• adherence promoted by damaged endothelial and exprosed tissue proteins
• simultaneous aggregation forms platelet plug
• ongoing secretions of serotonnin promotes vasoconstriction

• initiation of the conversion of fibrinogen to fibrin
• -clotting cascade causes amplification

• prothrombin turned into thrombin by prothrombin activator
• fibrinogen turned into fibrin by thrombin
• fibrin threads aggregate forming a clot

• requires Factor 9
• requires Factor 8a as a cofactor
• slower system but greater amplification
• converts X into Xa (prothrombin activator)
• once thrombin is produced it works as positive feedback to keep the system going

• requires Factors 7 and 3
• fast pathway with less amplification (weak)
• converts X into Xa (prothrombin activator)

• endothelial linings- minimize clotting
• consumption of clotting factors- alpha-globulin plasma protein called antithrombin 3 binds to thrombin and inactivates it
• Fibrinolysis- fibrin destruction by plasminogen (protease) --> plasmin (destroys clotting factors)

• produced by intestinal bacteria
• required for the synthesis of several clotting factors

competative inhibitor for vitamin K sites in hepatocytes

• blood clotting factors are improperly made
• hemophilia A from a lack of Factor 8

• abnormal clot that forms in vessel called thrombus
• -can break away and freely float as an embolism and get stuck in a vessel

• clotting problem with purple spots (from bruises)
• decreased platelet numbers
• prolonged bleeding time, deficient clot retraction, platelet antibodies, anemia

the radius of the vessel

• efficient, smooth, quiet
• faster in the center

• occurs when the streamlines are disturbed
• inefficient, rough, noisy
• sounds called murmers/bruits
• due to obstructions and high velocity flow
• forms eddy currents

• the point when turbulence happens
• velocity is usually destabilizing factor

• normally minimal but increases with turbulent flow
• causes further damage to vessel walls
• causes clotting, altered endothelial behavior, injury

• blood vessels stretching in proportion to the intravascular pressure put on them
• give them the ability to absorb more blood
• a change in volume per a change in pressure

• arteries not compliant
• veins very compliant

2/3 of blood is stored in the veins (capacitance vessels)

• variably compliant (arteries)
• initial pressure of blood causes arteries to constrict, will eventually loosen to allow more blood (compliance)

• a sound heard during the eection of blood from a normal heart
• due to unusually powerful ejections of blood from the left ventricle causing turbulence in the aortic arch
• usually harmless

• the arterial system
• specifically the arterioles (regulators)
• smooth muscle forms the tunica media

• vasoconstriction- decrease in flow, decrease in radius
• vasodilation- increase in flow, increase in radius

• passive streching causes contraction
• expansion of a vessel causes depolarization
• autoregulation becuase it stabilizes flow, quick!
• increase flow causes vasoconstriction
• decrease flow causes vasodilation

voltage-dependent Ca⁺² channels

• main source of regulation
• contraction by: norepinephrine, angiotensin 2, vasopressin, endothelin-1, serotonin, thromboxane A₂
• relaxation by: nitric oxide, prostacyclin, and local metabolites
• vascular smooth muscle cells are covered with receptors

• alpha 1 receptors for norepinephrine from axons of sypathetic fibers causes vasoconstriction
• beta 2 receptors cause vasodilation

cause vasoconstriction

• for acetylcholine
• cause vasodilation

• released by endothelial cells when stimulated by blood-borne agents and shear forces
• induces intracellular Ca⁺² levels to fall
• causes vasodilation

• released by endothelial cells when stimulated by blood-borne agents
• causes vasodilation

• rapid vasoconstriction
• can not secrete nitric oxide

• induces vasodilation
• extra sources of nitric oxide

• production of CO₂ as well as other cellular wastes inhibit the ability of vascular smooth muscle to contract
• causes vasodilation

• cause vasodilation
• from LOCAL paracrine agents
• increase metabolism causes increase flow
• -active hyperemia (produces rubor-blushing)
• fast/rapid

• carbon dioxide
• hydrogen ion
• adenosine
• potassium ion
• lactic acid

• depriving tissues of nutrients, especially oxygen
• tissue turn blue = cyanosis
• produces pain in tissues
• extrinsic control used to maintain order

vasoconstriction

vasodilation

• brief period of ischemia wherein the blood flow is restored in a massive way that nearly matches what would have been delivered during the entire time of ischemia
• all the accumulated metabolites are washed away

• nervous system and endocrine system
• dependednt on the sensitivity of vascular smooth muscle
• autonomic nerves
• -spinal sympathetic chain axons, norepinephrine causes vasoconstriction
• constant low level vasomotor tone
• no parasympathetic innervation

• epinephrine and nor epinephrine released becuase of sympathetic innervation
• lands on alpha-1 adrenergic receptors causing vasoconstriction
• powerful, slow body wide effect
• increases blood pressure

• release of renin causes angiotensin 2
• lands on angiotensin 2 receptors causing endothelin-1 production and vasoconstriction
• powerful, slow effect

• releases vasopressin
• lands on vasopressin receptors causing production of endothelin-1 causing vasoconstriction

• external agent causes localized inflammation response in the integument
• -irritant and allergens
• skin becomes itch, red, and may blister
• release of histamine promotes arteriolar vasodilation and capillary leaky-ness

striated muscle cells anchored by intercalated disks which have low electrical resistance

allowing action potential to move from cell to cell

• depolarization- influx of Na
• plateau-cell is resistanct to stimulation- absolute refractory period, release of Ca
• repolarization- the relative refractory period, influx of K

inhibits Na/K pump in cardiac muscles, causes stronger heart beat

SA node to atrial muscle to AV node to bundle branches to Perkinje fibers to ventricular muscle

• spontaneous action potentials cause contractions
• membranes of the heart are naturally leaky and dont need nerves to send action potentials and contract

• bind norepinephrin and epinephrin
• primarily beta-1 receptors
• norephinephrine released from sympathetic fibers
• increase excitability, strength, and rate of contraction

• Ach muscarinic receptors sensetive to Acetylcholine released from parasympathetic fibers
• causes decreased excitability, strength and rate of contraction

to the body, supplied by the left ventricle

short, to the lungs for oxygenation, supplied by the right ventricle

contraction and ejection of the blood

relaxation and filling of the blood

• ventricular pressure
• aortic pressure
• ventricular volume
• electrocardiogram
• phonocardiogram
• atrial pressure

• 75% passive
• 25% by the atria

• isovolumetric relaxation- no filling but continued relaxation of ventricular muscles
• rapid inflow- 1/3 of the time, filling of ventricles (passive)
• diastasis- 1/3 of the time, minimal filling (passive)
• atrial systole- 1/3 of the time, filling via atrial contraction (active)

• isovolumetric contraction- contraction with valves closed
• ejection- releasing of blood

130 ml

60 ml (always some blood in the ventricles)

end-diastolic volume - end-systolic volume = 70 ml

• indicator of performace
• Stroke volume/end-diastolic volume
• should be greater than 50%

highest point of aortic pressure

lowest point of aortic pressure

• "lub"
• closure of the AV valves

• "dup"
• closure of the semilunar valves

• difficulty pushing blood thru the aortic valve
• loud murmur heard thru systole
• "thrill" of chest

• valve fails to prevent backflow
• "blowing" murmur during diastole

• difficulty pushing blood thru mitral valve
• murmur during second half of diastole

• valve allows blood back up into the left atrium
• murmur during systole

• stroke volume X heart rate
• normal 5000 ml/min

• Frank-Starling Mechanism- increase diastolic filling causes increased EDV causes increased strength of contraction causing decreased ESV causing increased stroke volume
• increase venous return = increase cardiac output (no nerves needed!!)
• tops out at 15 l/min

• doesnt affect cardiac output
• AFTERLOAD- pressure at aortic valve at end-systolic volume

• mediated by nerves
• anticipatory
• max 30 l/min
• sympathetic nerves: stress response, mostly to ventricles, from sympathetic chain
• parasympathetic nerves: restorative resoponse, from the X nerves to nodal tissues

• conduction speed = dromotropic effect
• rate of contraction = chronotropic effect
• strength of contraction = inotropic effect

• cause positive dromotropism, chronotropism, and inotropism
• increases heart rate and stroke volume
• occurs during exercise
• maximum efficiency 140-160 bpm
• can reduce CO if inhibited

heart rate greater than 100 bpm

competitively inhibits the receptors, governors heart rate

• present on SA and AV nodal cells
• creates negative dromotropism, chronotropism, and inotropism
• decreases heart rate down to 30 bpm and stroke volume to 25%

• heart fails to adequately pump blood
• presents with dyspnea, peripheral edema, and fatigue
• abnormal electrocardiogram, enlarged heart
• abnormal echocardiogram, low ejection fraction
• from a decompensated heart
• heart has coronary artery disease, valvular problems, high resistance in vessels

• SA nodal tissue
• it is the pacemaker of the heart
• produces a sinus rhythm

gives the atria time to contract before the ventricles do

monitors the electrical behavior of the heart

atrial depolarization

ventricular depolarization

ventricular repolarization

• due to AV nodal slowdown
• elongation is bad, shows that there is AV heart block

• due to absolute refractory period
• when segment is longer shows that the ventricles are bad

• summation of the QRS voltages shows the direction of electrical current flow
• normal is -10 to 100 degrees

asynchronous contractions of the heart

• abnormal rhythmicity of the pacemaker
• blocks in the conducting system
• abnormal impulse pathways
• spontaneous generation of impulses

• low heart rate
• can be normal in athletes
• abnormal when caused by excessive parasympathetic stimulation

when the heart rate changes with breathing changes

• due to ischemia of the AV node or bundle branches
• 1st degree: minor lengthening of PR interval
• 2nd degree: serious lengthening of PR interval, occasional dropped beat in ventricles
• 3rd degree: complete, ventricular escape

problem in the purkinje system causing abnormal QRS interval

electrical event out of sequence

• if in the atria it is harmless
• in the ventricle can be deadly
• caused by hyper-excitablility of myocardial tissue
• -over use of stimulants
• -local ischemia
• may cause fibrillation

• electrical chaos of impulses
• tolerable in atrias
• deadly in ventricles in minutes
• due to myocardial ischemia
• from circus entry - impuse rentry

• shocking the heart
• stops it, allows it to reset, and hopefully restarts on its own

• arrhythmia due to blockage in electrical conduction system
• different degrees
• caused by: coronary artery disease, inflammation of nodal tissue
• treatment: medication or pacemaker

• the force excerted on the container
• BP = cardiac output X peripheral resistance

• blood
• vascular tree
• heart

systolic BP - diastolic BP

• distributes blood
• absorbs shock

summation of pulse wave-forms

arterioles

• combination of valves and skeletal muscles
• the "second pump" of the systemic system

• gravity effects atrial and venous pressures
• venous pressure rises to 90 mmHg in the feet while standing, lower while walking due to musculature

sphygmomanometry-blood pressure cuff and stethoscope

• blood volume
• blood viscosity
• size of vascular container

averages 100mmHg

• nervous control system using aortic and carotid baroreceptors
• alters BP thru efferent innervation to the heart and vasculature
• fast acting, high gain, not long-term
• used for changes in body position

• nervous system control using aortic and carotid chemoreceptors (in aortic and carotid bodies)
• fast acting, high bain, lasts a few hours
• involved in control of respiration

• nervous system control using atrial stretch receptors
• fast acting, unknown gain
• can increase heart rate
• "Bainbridge reflex"
• activates baroreceptors
• competition minimizes venous damming of blood
• hormonal effect from atrial natriuretic factor
• -increases atrial pressure
• -decreases blood volume

• nervous system control using neurons of the cardiovascular control center
• fast acting, high gain, lasts for an hour
• rare reflex

• evokes vasoconstriction, cardiac acceleration, enhanced myocardial contractility
• vasoconstrictor sub-areas are tonically active

evokes inhibition of teh pressor area causing decreased sympathetic outflow and increased parasympathetic activity

• humoral control using hormones from the adrenal medulla
• -epinephrine and norepinephrine
• land on alpha and beta adrenergic receptors
• cause vasoconstriction and increased cardiac output
• release caused by sympathetic innervation
• fast acting, unknown gain, long lasting

• delayed compliance
• slow-acting, low gain,

• changing pressure of the capillary walls will change filtration of the blood
• slow acting, low gain

• humoral system using hormones from the kidney and blood
• -renin and angiotensin 2
• slow acting, low gain

• cardiac myocyte hypertrophy
• thirst
• direct stimulation of nephron to retain Na and H2O
• efferent arteriolar vasoconstriction
• increased glomerular filtration
• stimulate the release of ADH from pituitary

• blocks angiotensin converting enzyme
• used for management of hypertension/heart failure

• humoral control using hormones from the adrenal cortex
• -aldosterone
• slow acting, low gain

• humoral control using osmotically sensitive neuons in the hypothalamus to produce a hormone in the posterior pituitary
• -vasopressin
• slow acting, unknown gain

• fluid and humoral system that uses the kidney
• -uses the nephron and renin-angiotensin system
• slow acting, high gain
• the ultimate mechanism
• adjusts the amount of fluid in the vascular compartment
• relies on diuresis (formation of urine)

• level of water and salt intake
• behavior of kidneys as represented in the acute renal output curve

• salt levels directly related to extracellular fluid volume
• angiotensin acts directly on kidneys to retain salt and water
• angiotensin acts on adrenal glands to increase aldosterone secretion causing increased water and salt retention in kidneys

• resting SBP above 140 or DBP above 90
• usually due to kidneys not secreting enough salt and water

causes kidneys to make more urine

• short term alter cardiac output and peripheral resistance
• long term alter blood volume

• vascular stenosis to the kidneys- atherosclerosis
• renal vascular hypertension
• ischemic nephropathy
• cant regulate long-term blood pressure

kidneys, GI tract

• sympathetic fibers cause vasodilation (beta 2 receptors)
• local metabolic factors from cardiac myocytes cause vasodilation
• -release of CO2 and H, some adenosine

intense pain from obstruction of coronary artery

• chest pain from myocardial ischemia
• not a heart attack

• progression of myocardial ischemia
• death of cardiac muscle tissue
• compromises cardiac output

coronary artery blockage and death of myocardial tissue

• 4 ml/min/100g of tissue at reast
• up to 80 ml/min/100g of tissue during exercise

• sympathetic fibers cause vasoconstriction or vasodilation
• local metabolites cause vasodilation (main mechanism)

• increase cardiac output and vasoconstriction = better delivery of blood
• thinking about exercise can cause increase heart rate

• area given the highest priority
• 700 ml/minute
• least tolerant area for ischemia

• due to blockage of a cerebral blood vessel
• preceded by a transient ischemic attack

• local metabolic factors from neurons cause vasodilation
• release of CO2 and H

• ultrafiltrate
• plasma: increased Na, decreased glucose and K

given the lowest priority

• local metabolic factors form GI tissues cause vasodilation
• sympathetic fivers cause vasoconstriction
• -parasympathetic stimulation promotes glandular activity which causes vasodilation

maifestation of ischemia due to lack of priority

• fluid derived form GI vasculauture
• excessive fluid can cause ascites

• 75% of blood from the hepatic portal vein
• 25% of blood from hepatic artery

flow determined by local intestinal factors

• red pulp can store up to 50 ml of concentrated RBCs
• cleanse blood of old cells

• huge supply of cardiac output to maintain filtration rate
• sympathetic innervation produces vasoconstriction and a drop in flow

• priority for temperature regulation
• many arteriovenous anastomoses (cold areas)
• controls core body temperature
• -increase core temp = vasodilation and sweating
• -decrease core temp = vasoconstriction

• sympathetic fibers cause vasoconstriction
• parasympathetic fibers cause vasodilation
• cholinergic sympathetic fibers innervate sweat glands

when cold gets into dermis arterioles beome paralized causing vasodilation

• vasodilation of arterioles in extremely cold weather
• leads to frostbite
• -tissues freeze

• due to atherosclerosis affecting arteries of the leg
• causes ischemic pain due to loss of circulation and drainage
• -intermittent becuase gets worse during exercise when muscles call for oxygen

metabolizing tissues of the body

• cardiac output: from the left ventricle
• tissue output: from the body, coupled with the venous pump

the size of the vascular compartment

• total pressure could fall decreasing total flow
• blood flow is reduced to non-essential areas to keep up pressure

• must pump the same amount of blood as systemic circulation/unit of time
• 22 SBP/8 DBP, creates negative intrapleural pressure
• not compliant

• decreased O2 causes vasoconstriction
• venous return to R ventricle sets pulmonary flow
• -increased metabolism in tissue cause vasodilation allowing more blood back to the right atrium/ventricle causing an increase in pulmonary flow

• inadequate blood flow causing tissue damage
• 3 origins
• 1. decrease blood volume= hypovolemic shock
• 2. decrease peripheral resistance= low-resistance shock
• 3. decrease cardiac output= Cardiogenic shock
• problem of systemic circulation

• diffusion extremely important
• fluid diffuses out of capillaries into the interstitium, becomes lymph

• colubility
• size
• capillary permeability
• concentration
• pressure

• 1. small molecule/lipid soluble movememnt. most common
• 2. lots of leakage, filter is a function of pressure
• 3. wholesale leakage

• capillary pressure- outward pushing force (fluctuates)
• interstitial free fluid pressure- inward pushing force
• plasma colloidal osmotic pressure- inward pulling
• interstitial fluid colloidal osmotic pressure- outward pulling

• summation of all forces acting on a capillary
• total is 28 in and 28 out = 0

• net out at the arteriole end
• net in at the venule end

midpoint in the capillary where net force is 0

flux from plasma to interstitium causing systemic vascular filtered plasma loss of approx 2-3 ml/min

skeletal muscle contracts, lymph fluid flows

• interstitial free fluid pressure is stable due to natural tension of tissues
• fluids leave capillaries and promptly enter the lymphatic system

nromal pressure has a range, if it reaches 0 mmHg thats BAD!

fluid accumulation in tissues

from damaged endothelia

• from altered BP/flow dynamics
• caused from venous obstruction, acute arteriolar dilation or cardiac failure

• changed in blood
• from nephrosis, starvation, burns

• from parasite, surgery
• causes lymphodemea
• blockage of the drainage from the lymphatic system

• accumulation of lymphatic fluid causing swelling
• severity variable depending upon fluid accumulation
• disease of capillary dynamics and lymphatic circulation