yes interdependent sides

-right outworks the left the pulmonary system overdoes and can drown in own fluids

output of the left heart and imperil the blood supply to all systemic organs

-backs up into the superior and inferior vena cava

-left exceeds the right then person can bleed out

not in most cases except for portal ciculation and the kidneys

-allows for adjustment of blood flow to meet ind organ needs without creating major disturbances in blood supply

In the CV system energy is known as?

pressure 

-pressure gradient between two points in a system

endothelium

-single layer of epithelial cells

smooth muscle

-contraction and relaxation widen or reduce the lumen diameter

-arranged in circular layers

adventitia

-composed of collagen and elastin fibers

-transmural pressure- difference in pressure inside v. outside a hollow structure

-degree of flexibility within vascular wall

veins- large tmp creating very large intervascular volume and more flexible walls

arteries- small tmp more stiff walled and small intervascular changes

decreases

-veins highly distendable and has higher compliance and capacitance compared to stiff vessels of the same size

force that opposes the force within the vessel that keeps vessel from ripping apart

equal to the products of the transmural pressure and the vessel radius

higher

-because wall stress is lower in thicker walls

principle that the volume of a homogenous fluid passing per unit time through a capillary tube is

-directly proportional to the pressure difference between its ends and to the fourth power of its internal radius

-inversely proportional to its length and to the viscosity of the fluid

Poiseuill Law

doubling the pressure ____the flow

Poiseuille Law

halving the pressure______ the flow?

Poiseuille Law

doubling the length of the tube ___ the flow by _____

Poiseuille Law

doubling the tube radius ______ flow by 16fold

Poiseuille Law

do thick sticky fluids flow more or less easily than a thinner watery-like fluid

BP= CO * TPR

cardiac output * total peripheral resistance

striated muscle

-doesn't require innervation to be activated

-muscle contraction coupled with action potential from within cells

automaticity

-ability to generate their own action potential

rhythmicity

-ability to generate action potentials in a regular repetitive manner

functional syncytium

-as if it were one large cell

pacemaker

specialized rapidly conducting tissues (purkinje fibers)

ventricular and atrial muscle cells

ventricular

atrial

purkinje

sinoatrial (SA) node

atrioventricular (AV) node

in cardiac cells at rest, prior to excitation, the resting potential is the electrical charge differential b/w the inside and outside of cell

--90mV

change in membrane potential cell interior becomes relatively less negative than the cell exterior

-transmitted from cell to cell creating a wave or impulse of electrical activity

change in membrane potential returning to the initial resting (polarized) state

-cell interior becomes more - than cell exterior

5

0-4

phase 4

-associated with diastole (at rest)

-rapid depolarization phase

-rapid influx of NA+ into cell

-threshold potential of cardiac cells -70mV

have self sustaining inward Na+ current

membrane potential neutralizes to 0 and into positive range (Na influx)

-transient outward K+ current responsible for partial repolarization

-returns membrane to 0mV

-slow Ca++ influx and relatively low K+ efflux results in plateau

-maintains a voltage of approximately 0mV

-Ca++ channels slowly inactivate and efflux of K+ begins to exceed influx of Ca++

-rapid repolarization

returns transmembrane voltage back to -90 mV

-largely results from K+ efflux

3 ways:

-max - voltage is -60mV

-phase 4 isn't flat but has an upward slope representing spontaneous gradual depolarization

-phase 0 upstroke is less rapid and reaches lower amplitude relying solely on Ca++ influx

K+

-high plasma K+ hyperkalemia depolarize cardiac cells (cardiac arrest)

-low plasma K+ conc. hypokalemia hyperpolarizes the tissue

-enhance Ca++ movements & increase size of action potential

-Norepi increases phase 3 K+ conductance shortening cardiac refractory period

SA node, initiates an action potential

.05m/sec (.1sec)

-important bc without delay the ventricles wouldn't have time to fill after diastole

splits into left and right bundle branches

-bundle branches give rise to Purkinje fibers

purkinje fibers

atria- 60-80 bpm

AV junction- 40-60 bpm

ventricles- 20-40 bpm

amplified, timed recording of the electrical activity of the heart

-detected from the surface of the body

-plot of voltage as a function of time

-heart rhythm abnormalities

-myocardial ischemia and infarction

-electrolyte inmalances

-effect of certain medications

-anatomic orientation of heart

-size of atria/ventricles

-path take by action potentials

depolarization of both ventricles

represents the beginning of ventricular contraction

plateau phase of ventricular repolarization

-follows QRS complex

amount of time the action potential takes to travel from SA node through the AV node

.12-.20 seconds

interval of time action potential takes to travel from the end of the AV node through the ventricles

.06-1.0 sec

time

.04 seconds in each small box

distance between 2 heavy boxes is .2 seconds

12

-6 limb and 6 chest

-lead I (-) right arm (+) left arm

-lead II (-) right arm (+) foot

-lead III (-) left arm (+) foot

AVF- left foot +

AVR- right arm +

AVL- left arm +

V1-V6

successive steps from the patient's right to the left side of the chest

true

-allcells that can contract during a single activation do so; there are no spare units to recruit

conc. of Ca++

-increased Ca++ conc. enhances contractile force

-decreased Ca++ conc reduces contractile force

raises; exceeds; mitral

(S1)

exceeds; atrium; aortic

isovolumic contraction

Interventricluar pressure rised until it exceeds that in the aorta.

_____ and ______ valves are forced open and ejection of blood in ____begins.

A2- produced by aortic valve closure

P2- produced by pulmonic valve closure

children or young adults from rapid deceleration of the column of blood against ventricular wall

-pathologic in older adults indicates change in ventricular compliance

atrial contraction or pathologic change in ventricular compliance

-always pathologic

1) preload

2) afterload

3) contractility (inotropic state)

4) inotropic effect )of increased heart rate)

product of stroke volume and the heart rate

CO= SV * HR

passive stretch is proportional to the amount of filling (volume) of the heart during diastole

-increased filling increases the potential isometric contractile force that can be generated in the heart

accounts for changes in the force generated by the myocardium for a given set of preload and afterlad

-change in contractility moves curve up or down (Frank-starling curve)

the mores the ventricle is filled with blood during diastole the greater the volume of ejected blood will be during the resulting systolic contraction

"more heart fill, more it pumps"

heart unable to maintain sufficient output to meet body's normal metabolic needs

load presented to weakened heart is too high for muscle, therefore, muscle can't shorten as far and with normal velocity

-stroke volume and cardiac output reduced because of inability of heart to pump blood

muscle resistant to stretch that must take place during diastole

-muscle can't sufficiently lengthen, begins its contraction at too short a length

-muscle unable to shorten sufficiently to pump an adequate volume of blood with each beat

Small arteries and arterioles together regulate what percent of total vascular reistance?

Where is the remainder equally divided?

70-80

between capillaries and venules

What type of capillary junction are found in the brain and the spinal cord?

What type of molecules may pass?

tight

smallest water soluble 

Capillaries in intestines, liver, and glomerulus of kidney have capacities for larger/small water transport?

At rest is there more blood volume in the arteries or veins? 

Where is most of the at rest blood located?

veins

1/2 of which is within the venules

GI tract, liver and skin

pulmonary circualtion

When compressed or actively contracted the lymph vessels are allowed to?

Why?

passively relax

pressure in the lumen becomes slightly lower than in the interstitial space and tissue fluid enters the lymph vessel

Are lymphatic valves one-way?

Why or why not?

one-way

allow lymph to flow only from the tissue toward the progressively larger lymphatic vessels and finally into large veins in the chest cavity

diffusion

filtration

vesicular transport

the more capillaries spaced out around the cell the more exchange takes place and increases the rate of diffusion

-especially important because becomes impaired in many disease state- diabetes, atherosclerosis

_____favors the pressurized filtration of water through pores?

Why?

hydrostatic pressure

hydrostatic pressure on the blood side is higher than on the tissue side

What does the colloid osmotic pressure provide?

Where is the pressure generated by?

Does it act with or opposite the hydrostatic pressure?

provides force pulling water into capillaries

pressure generated by plasma proteins

opposite

When does edema occur?

When does dehydration occur?

-interstitial fluid volume exceeded hydrostatic pressure elevated hydrostatic pressure goes to tissues

-negative hydrostatic tissue pressure water loss from tissues

Does edema increase/decrease diffusion distances? 

• Loss of protein from the plasma will result in?

What are some causes of this?

• edema
• liver disease- production issue, kidney-excessive loss of protein disease, burns, and hives- destruction of the capillary integrity increase in amount of protein coming through
• obstruction

-veins: increase in pressure on venous side forces back increases interstitial fluid (DVT)

-lymph channels: fluid not going back to lymph system instead remaining in interstitial space

What is released from all arteries, microvessels, veins, and lymphatic endothelial cells?

Why is it important?

endothelium-derived relaxing factor (EDRF)

important contributors to local vascular regulation

NO

causes vasodilitation

acetylcholine

histamine

ATP & ADP

hypoxia

adenosine

prospasmodic: spasm of the arteries constricting it down decreasing blood flow

prothrombotic: risk of clots

proatherogenic: risk of atherosclerosis lipid collection in the vessel 

mean arterial pressure

systolic arterial pressure

diastolic arterial pressure

pulse pressure

The difference between the maximum and minimum blood pressures produced during one heart beat.

What does this represent?

pulse pressure

represents the force that heart generates each time it contracts

diastolic pressure + 1/3 (pulse pressure)

ex.

BP 120/80

pulse pressure 40mmHg

80+ 1/3(40)= 93

stiffness and reduced elasticity of the aorta

-HTN, atherosclerosis, sever anemia, hyperthyroidism

BP=CO * SVR

CO= HR * SV (contractility, preload, afterload)

The pressure corresponding to 1st korotkoff sound is?

Pressure at which the korotkoff sounds cease is?

-systolic pressure

-diastolic pressure

age

race

diet

gender

body weight

large

-systemic veins  20 times more compliant than systemic arteries

central blood volume

-constitutes 25% of total blood volume

extrathoracic blood volume

Changes in central venous pressure at a good reflection of?

Is this an invasive to measure? 

central blood volume

yes measured by placing the tip of a  catheter in the right atrium

-overhydration which increases venous return

-heart failure which limit venous outflow and leads to venous congestion

-positive pressure breathing, straining

-hypovolemic shock from hemorrhage, fluid shift, dehydration

-negative pressure breathing which occurs sometimes with spinal cord injuries

-changes in total blood volume

-changes in distribution of total blood volume between central and extrathoracic regions

Arginine vasopressin

andiotensin II

aldosterone

atrial natriuretic peptide

norepinephrine

-SA node, AV node, Specialized conducting tissue, all cardiac muscles including the ventricles

oppose each other

increase in one=decrease in other

low

decreasing

- generating tonic(maintenance) excitatory signals to spinal sympathetic pregangionic fibers

-intergrating cardiovascular reflexes

-integrating signals from supramedullary neural networks and from circulation hormones and drugs

yes

when wall is stretched by increased transmural pressure (inside vessel), firing rate of nerves from mechanoreceptors increases

parasympathetic

-decreased sympathetic activity

-results in increased AVP

-AVP vasoconstrictor causing water retention by kidneys

-increase in blood volume

-increase in BP causes decreased AVP release and increased water excretion by kidneys

BP

-only works from moment to moment not long term

cardiopulmonary: unloading (decreased stretch) results in _____sympathetic nerve activity to heart and blood vessels and _____ parasympathetic nerve activity.

increased; decreased

-also activate RAAS and increased release of AVP

ventilation

-also affect cardiovascular system through neurogenic reflexes

-PO2 or pH or arterial blood is low

-PCO2 of arterial blood increased

-flow through bodies is low or stopped

-chemical given that blocks oxidative metabolism in chemoreceptor cells

chemoreceptors: increased firing leads to?

-profound peripheral vasoconstriction/dilation

-elevation/decrease arterial pressure

vasoconstriction

elevation

-if respiratory movement voluntarily stopped, vasoconstriction more intense and a striking bradycardia and decreased cardiac output occur

-decreased blood flow through bodies

-chemoreceptor firing increases

-serves as secondary emergency reflex if BP continues to fall despite baroreceptor reflex action

increased sympathetic activity to heart and blood vessels

decreased parasympathetic activity to heart

Cardiovascular response to pain leads to?

Is known as?

increased cardiac output, SVR, and mean arterial pressure

-cold pressor response

diminished sympathetic activity

-enhanced parasympathetic activity with

-decreased cardiac output, SVR, and BP

-contributes to cardiovascular shock from severe trauma

psychological stress can raise blood pressure, increase atherogenesis, and predispose person to fatal cardiac arrhythmias

-results from activation of fight or flight

EPI- adrenal medulla

AVP- posterior pituitary

Renin- kidneys

atrial natriuretic peptide- cardiac atrium

baroreceptor reflex bc it causes vasocontriction and increases mean arterial pressure

-also actos on a1 receptros in skeletal muscles and get vasoconstriction

-NE increases cardiac parasympathetic tone

Low concentration of EPI causes

-vasco_____ in skeletal muscle bc activates B2 over A1 receptors of the arterial system

-SVR may fall/rise and mean arterial BP does not rise

-baroreceptor reflex in activted/not activated

dilation

fall

not activated

binding to A1 receptors and causes peripheral vasocontriction

-only reached when administered as a drug

B2 vasodilation

A1 vascocontriction

-arteriolar vasconstriction

-reduced Na secretion by increased Na reabsorption by proximal tubule of kidneys

-release of aldosteron from adrenal cortex which promotes Na reabsorption in distal convoluted tubules

-causes release of AVP from post pituitary gland promoting water reabsorption 

-enhances NE release, reducing NE uptake potentiating sympathetic nervous system effect

atria are stretched

-increase blood volume increases stretch

-leads to higher Na excretion and reduction in blood volume

activation of neural reflexes

hormonal control mechanisms

kidneys- responsible for setting mean arterial pressure values

depends upon salt and water excretion by kidneys

it lowers blood volume and cardia output sufficiently to return mean arterial pressure to original set levels

-decrease in arterial pressure has the opposite effect

compensated shock

progressive shock

irreversible shock

compensated shock

-ex donation of blood

progressive shock

-ex car accident and bleeding out in shock, must give meds to increase BP 

compromise

decreases

drop

acidotic

neurogenic shock

-secondary to inhibition or dysfunction of CNS

septic shock

-blood poisoning