conduit artery - stressed volume

Resistant artery (60%)

microcirculation

vein - unstressed volume

Mean Arterial pressure

MAP = diastolic pressure + 1/3 pulse pressure

MAP = HR x SV x TPR; CO  = HR x SV

MAP = (Ps + 2Pd)/3 -- so MAP is 2/3 diastolic pressure and 1/3 systolic pressure

Arterial compliance is also a component of MAP bc the aorta can stretch and absorb some of the pressure during a heartbeat. Loss of this compliance during aging is what causes elderly persons to have higher pulse pressure

aterial systolic pressure

arterial diastolic pressure

pulse pressure

Properties of conduit arteries like the aorta.

Compliance: The ability of a material to stretch when external force is applied to it. as BP rises duirng a heart beat (Systole), the aorta expands to accommodate the extra blood that is in it at the time.

Elastic recoil: The opposite of compliance. As the aorta relaxes during diastole, its hgihly elastic wall recoils to push the blood out and return to its previous shape

Compliance = dV/dP; P is distending/transmural pressure

Aortic compliance = SV/pulse pressure

Transmural pressure = Pin - Pout

Transmural pressure is the pressure difference between the inside and outside of a vessel... has nothing to do wtih downstream pressure

INtrinsic: autoregulation. caused by alteration of BP or regional metabolic vaso-activator. Is important for distribution of blood fow to tissues and organs

Extrinsic: changes in arteriorlar radius caused by neural (sympathetic nerve innervation) and humoral (Angiotensiin II) factors. it is important for control of MAP

ACE inhibitor regulates BP by targetting angiotensin II

Organ BF = dP / Organ resistance

increased BP activates mechanical stretch receptors on vascular smooth muscle cells (VSMC). This results in VSMC contraction and leads to a steady state of relatively constatn blood flow after an immediate, transient increase in flow

This process makes flow independent of pressure

When O2 consumption > O2 supply, the tissues become hypoxic or ischemic

When this happens, metabolic vasodilators are released from the surrounding tissue and vasocontrictor release is reduced. This decreases vascular resistance and increases blood flow.

Ex of this situation: during exercise

Hypoxia - reduced oxygen tension

Ischemia - reduced oxygen flow

active hyperemia

reactive (passive) hyperemia

Difference: they have different tirggers, everything after that is th same (vasodilation response)

Perfusion pressure

4 factors:

Autonomic NS control (mainly sympathetic to control heart rate)

Baroreceptor reflex detects CO2 concentration in blood and pH

Chemoreceptors

Hormonal control

Sympathetic: Brain gets signal that body needs more blood.

Medulla sends signal to SA node to increase HR, increase myocardial contractility and induce vasoconstriction.

"Signal" = Norepinephrine release at sympathetic nerve terminals and binds to a-adrenergic receptors on resistant and capacitant vessels.

Parasympathetic: decreates HR

Located in aortic arch and carotid sinus

Increase in MAP causes vessels to stretch. Baroreceptors detect stretching or lack thereof and send a signal to the medulla to increase either sympathetic or parasympathetic activity and derease the other

Located in aortic arch and carotid bodies

Activated by decrease in arterial PO2 & pH, or increase in arterial PCO2. Activated receptors induce vasoconstriction, resulting in an increase in BP.

located in the walls of large systemic veins and the right atrium. Respond to stretch the same as baroreceptors but also respond to changes in blood volume bc the change in volume will stretch the walls.

When the wall stretches, it induces ANP secretion, which causes increase kindey capillary permeability and thus increased glomerular filtration rate (GFR) and increased Na excretion (Increased water retention)

Renin-Angiotensin-Aldosterone system:

1. Reduced renal arterial pressure and blood volume cause the release of angiotensinogen from the liver and renin from juxtaglomerular cells. in the blood, these combine to form angiotensin I

2. Angiotensin I combines with ACE to form angiotensin II

3. Angiotensin II does 3 things: induces aldosterone release from adrenal cortex, decreases sodium excretion in proximal convoluted tubules, and increases TPR in peripheral arterioles.

All of these things ultimately result in increased blood volume and arterial pressure.

allow for efficient gas and solute exchange between tisues and blood

Continuous - found in CNS, lungs, skin, skeletal muscle

Fenestrated - found in intestinal mucosa, exocrine glands, renal glomeruli, choroid plexus

Discontinuous - found in liver, spleen, bone marrow.

Absorption - inward force, driven by capillary oncotic pressure

Filtration - outward force, driven by interstitial oncotic pressure

Collect fluids and solutes from the interstitium and return them to circulation. They carry absorbed substances and nutrients from the GI tract into circulation.

Defense fxn: filter lymph at lymph nodes and remove foreign proteins

Because veins are very compliant (not very resistant)

This results in veins having a huge reservoir of blood (60% of total body blood)

 Skeletal muscle pump: valves in peripheral veins close twhen the muscle surrounding it contracts

Resp Pump: During inhalation, thoracic cavity pressure decreases, which sucks blood from periphery into thoracic cavity. During exhalation, blood is driven toward the heart It is never driven backward into periphery

Venomotor tone: Sympathetic activity promotes constriction, which increase vasomotor tone which immediately increases venous pressure and increases venous wall tension (reduces compliance) and raises venous pressure

Central (intrathoracic) blood volume: SVC, IVC, right atrium and ventricle, left atirum, pulm circulation.

At a given depth or height of column, pressure will be the same no matter what shape the vessel is

Gravity increases pressure - which is why there is more pressure in the feet than there is in the head

Pressure gradient: proportional to flow, so increase pressure = increase flow

Tube length: inverse to flow, so increase tube length = decreased flwo

Radius: most important determinant. Because Poisuille's law has r^4, a 2x increase in radius results in an 16x increase in flow, and so on.

Resistance (viscosity): increased resistance decreases flow

It cannot be directly measured, so it has to be indirectly measured as a factor of pressure and flow

TPR= (Pmean - Pright atrium)/CO

Series: Rt = R1 + R2 + R3....

Parallel: 1/Rt = 1/R1 + 1/R2 + 1/R3

Rt<Ri, even when Ri is the lowest of the resistances. So the advantage of parallel vessels in a greatly reduced resistance

Changes in Ri lead to little changes in Rt. So if one vessel is blocked, it won't greatly influence the system.

Laminar flow - velocity center > velocity edges

Turbulent flow - random, chaotic

velocity increases

diameter increases

denisty increases

viscosity decreases

Good: ensure adequate mixing of blood, creates heart sounds

Bad: thrombus formation = plaques, aneurysms

Anemia promotes turbulence (decreased viscosity)

P - depolarizaiton of atria during atrial systole

QRS complex - depolarization of left ventricle during isovolumetric contraction

ST segment - ejection

T wave - ventricular repolarization

S1 - mitral valve closing

S2 - aortic valve closing

S3 - aortic valve opening

Systole: begins at beginning of isovolumetric contraction, ends at beginning of isovolumetric relaxation

Diastole: begins in isovolumetric relaxation, ends at isovolumetric contraction

Preload is the pressure of the ventricle while it's filling.

It icnreases SV by increasing end diastolic volume.

Afterload is the pressure of the aorta. It decreases stroke volume by increasing end systolic volume.

Contractility increases SV by decreasing ESV.

Compliance is the slope of the diastole curve decreases SV by decreasing EDV.

Preload (filling pressure)

Afterload (aortic pressure)

Contractility

hypertrophy: HTN (chronic) due to increased work load over several months

dilation: persistant elevated preload over several days (acute)

Both create a mechanical disadvantage

CO drops dramatically at very low HR (<50 bpm)

CO drops at very high HR (>180 bpm) bc there is not enough time for the ventricle to fill during diastole

CO remains constant at normal HR (50-180 bpm)

Ejection fraction

velocity index

end systolic pressure-volume curve

ventricular function curve

mechanical compression - with each beat, the contracting heart squeezes the coronary arteries and increases their resistance to flow

Metabolic:

increasing contractility increases CBF

decreasing contractility (Beta blocker) decreases CBF

heart attack (acute myocardial infarction)

usually caused by thrombus

treated with thrombolytic agent (tPA)

size of ischemic area

level fo collateral flow

duration of ischemia

maintain force generation

create a long refractory period

absolute refractory period - 0-3 - allow for ventricular filling

relative refractory period - 3-4

Na

cardiac myocytes will be paralyzed

sympathetic - Adreneric B1 receptors

Parasymp (vagal) - muscarinic acetylcholin

AV bundle (40-55 bpm)

If AV bundle is ablated, it goes to the next highest pacemaker (purkinje fibers) which are dangerously slow (25-40 bpm)

AV block

Bundle branch block

abnormal, non=specific

MI

Long QT

1500 mm/min/RR

Vary: HR = # of RR in 10 sec x 6

first > 0.2 sec

second - 2 p waves for each QRS complex

third - atria and vet beat independently

smaller size

less t-tubules (skeletal has 2/sarcomere, cardiac has 1)

intercalated disk in cell-cell jxn

aerobic metabolism

intercalated disks

desmosomes

gap jxns

desmosomes and gap jxns are in intercalated disk

1. blocks Na/K pumps, resultsi n intracellular Na accumulation

2. Increase in intracellular Na causes Na-Ca exchanger to not work bc cell doesn't want to take up more Na, and thus it takes up more Ca

Increase in Ca cuaes an increase in contractility

Increases it- more AP per min, more Ca in flux per min, more Ca in Sr, increased contraction

Positive staircase or bowditch effect

compliance

edv

preload dramatically increases in herat failure bc of decreased myocyte contractiltiy

Afterload is the pressure that the heart ejects against (pressure of aorta)

Afterload dramatically increases in HTN?

maximum velocity of heart muscle shortening

contractility

length

afterload