SGU Physiology - Cardiovascular System

164 terms by pdolan 

Create a new folder

Advertisement Upgrade to remove ads

CVS flashcards for the SGU Physio midterm

systole

contraction of the heart, when ventricles contract and eject

diastole

relaxation of the heart, when AV valves are open (and everything else that is NOT ventricles contracting and ejecting)

5 (to 5.5L)

normal blood volume

portal circulation

parallel bl flow to receive venous outflow, found in liver, kidney, and brain

Tunica intima

innermost endothelial layer found in all blood vessels (capps consist solely of a single endothelial layer), secretes vasoactive agents like NO

Tunica media

elastic laminar layer that supplies mech strength + contractile power to bl vessel

Tunica adventitia

CT layer of bl vessels that holds it in place (where vasa vasorum lie and nociceptive fibers are in vv)

capillaries

part of systemic circ that has greatest overal cross-sectional Area due to parallel bl flow=> least velocity

capacitance

class of bl vessel: vv, where 2/3rds of bl in circ resides

exchange

class of bl vessel: capps

resistance

class of bl vessel: arterioles

conduit

class of bl vessel: aa

elastic

class of bl vessel: large aa + aorta

arterioles

bl vessels that have highest resistance and lowest capacitance, largest pressure drop

veins

bl vessels that have lowest resistance and highest capacitance

SA node

pacemaker/slow diastolic potential of heart due to if and ica, betw -60 to -40mV (-40 triggers Ap)

AV node

where cardiac Ap delay occurs to give atria time to contract before ventricles

cardiac

type of Ap that lasts 300-400ms and opens various ion chans like Ca2+

myocytes

have RMP = -85mV

inward rectifier

ik1 current where K+ flows spont out of since gk is high

background current

due to ib, Na+ drives Na+Ca2+ exchanger (antiport) => Ca2+ influx

Phase 0

ventricular myocyte Ap phase: rapid depol due to iNa

Phase 4

ventricular myocyte Ap phase: resting @ -85mV

Phase 1

ventricular myocyte Ap phase: initial rapid depol due to ito chans = transient outward K+ current, Na+ chans close

Phase 2

ventricular myocyte Ap phase: plateau due to ica2+ = L-type Ca2+ chans

Phase 3

ventricular myocyte Ap phase: rapid repol due to ik = delayed rectifiers

absolute

type of refractory period consisting of inactivated Na+ chans, much longer in cardiac cells to prevent tetanus => rhytmic contraction

relative

type of refractory period consisting of mostly closed Na+ chans but K+ chans still open => large Ap necc to overcome

Phase 4

SA node Ap phase: if (inward funny since open even though polarized) = Na+ chans and ica = T-type Ca2+ chans (T for Transient), spont depol

Phase 0

SA node Ap phase: ica = L-type Ca2+ rapid depol

Phase 3

SA node Ap phase: ik and some if = rapid repol

Phase 2 (plateau)

phase of Ap that is present in ventricular myocytes, shortened in atrial myocytes, and completely absent in SA node

sinus rhythm

the normal SA firing rate of 60-75/minute

P wave

ECG: atrial depolarization

QRS complex

ECG: ventricular depol, if wide = bundle block

PR interval

ECG: interval from depol -> ventric myocardium, extended in AV block

RR interval

ECG: used to calc HR

T wave

ECG: ventricular repol, inverted w/ Angina (or MI's)

QT interval

ECG: interval of ventricular systole (inc in arrythmias since delayed repol)

ST segment

ECG: period when ventricular cells in plateau and entire ventricular surface is depol, inc w/ MI's

0.1 mV

the value of each small square on y-axis of ECG

0.2s

the value of each large square on x-axis of ECG

Lead I

bipolar limb lead: RA -> LA, 0deg on circle of axes

Lead II

bipolar limb lead: RA -> LL, 60 deg on circle of axes

Lead III

bipolar limb lead: LA -> LL, 120 deg on circle of axes

aVR

augmented limb lead: E = RA, negative since wave of depol (mean QRS vector) is opp of E, -150 deg on circle of axes

aVL

augmented limb lead: E = LA, -30deg on circle of axes

aVF

augmented limb lead: E = LL, 90 deg on circle of axes

V

symbol used for indifferent electrode in augmented leads

V1

precordial chest lead: IC4 -> R sternum, negative

V2

precordial chest lead: IC4 -> L sternum, negative

V3

precordial chest lead: betw V2 + V4

V4

precordial chest lead: IC5 -> Mid-Clavicular, negative

V5

precordial chest lead: L Ant Axillary -> L V4

V6

precordial chest lead: Mid Ax -> L V5

left axis deviation

when mean axis is >-30 deg on circle of axes, corresponds to left ventricular hypertrophy/ conduction block or right ischemia

right axis deviation

when mean axis is > 90 deg

Bundle of Kent

accessory conducting pathway that bypasses AV node=> supraventricular tachy char of Wolff-Parkinson-White syndrome

1st degree

AV block: slow AV node conduction w/ long PR interval

2nd degree

AV block: conduction occasionally fails and P wave does not result in QRS complex, 3 types: Mobitz I + II, Bundle Branch

Mobitz I

AV block: type of 2nd degree where increased vagal, beta blockers, or Ca2+ chans cause long PR intervals w/ occasional skipping of QRS, gen aS/S

Mobitz II

AV block: type of 2nd degree block that is problematic because there is no QRS complex most of the time due to problems w/ Purkinjes or Bundle of His, Tx = pacemaker

Bundle Branch Block

AV block: type of 2nd degree block char by wide QRS due to uncoord Ap spread because the HR is too high => dec Fcontract

3rd degree

AV block: no impulse goes through AV node => Purkinjes are beating at a slow rate and atria has indy beat -> dec CO + Bp -> Tx = emergency

atrial fibrillation

irreg RR intervals and some sections of NO P waves due to rapid Ap frequency, causes bl to pool in atria and form clots

ventricular fibrillation

medical emergency char by lack of coordinated ventricular contraction -> dec CO + MAP => Tx = defib/cpr

apex beat

when LV contracts and twists forward to tap against the chest wall

incinsura

column of blood in aorta bounces back against closed valve

A wave

atrial wave: "atrial wave" where atria contract -> inc P

C wave

atrial wave: "Carotid" wave where closed AV valves bulge into the atria and carotid a expands

X descent

atrial wave: atria relax

V wave

atrial wave: "ventricular" systole -> inc Atrial P

Y descent

atrial wave: rapid emptying of atria after AV valves open

1

heart sound: close AV valves

2

heart sound: close SL valves, split since aortic valve closes before pulm valve due to inc P downstream

3

heart sound: bl rushing to relax ventricles in early diastole, common in young

4

heart sound: atrial systole, before 1

EDV (end diastolic volume)

max Vol bl in ventricle, before contraction

CVP (central venous pressure)

pressure in VC as it enters RA => atrial P, sim to Atrial pressure due to reflux of bl into vv

Ejection fraction

SV/EDV, meas of LV Fx, inc w/ contractility

diastasis

dec rate of filling since ventricle is reaching its natural resting volume

8 (mmHg)

LA mean systolic P

3 (mmHg)

RA mean systolic P

120/9(mmHg)

LV mean systolic/diastolic P

25/4 (mmHg)

RV mean systolic/diastolic P

25/10 (mmHg)

Pulm a mean systolic/diastolic P

diastolic interval

determines the minimum EDV to get the minimum CO, gen = 0.13s => max HR

incompetence

failure of valve to seal properly

stenosis

narrowing of valve

aortic valve stenosis

heart murmer: narrowed aortic valve causes crescendo-decrescendo murmer betw HS1 + HS2

tricuspid (or mitral) incompetence

heart murmer: tricuspid or mitral valve fails to seal properly => pansystolic murmur

aortic valve incompetence

aortic valve fails to close properly -> early diastolic decrescendo murmur after HS2

PP (pulse pressure)

Systolic P - Diastolic P

mitral (or tricuspid) stenosis

narrowed mitral (or tricuspid) valve causes diastolic murmur

CICR (Ca2+ Induced Ca2+ Release)

mechanism where Ca2+ rel from SR in response to Ca2+ transport in cardiac mm

Ca transient

slow increase in [Ca2+]I when L-type Ca2+ chans slowly open

Inotropy

Fcontract, inc w/ inc [Ca2+]i

Lusitropy

Relaxation, inc w/ ability to get rid of Ca2+ (ex: SERCA)

Chronotropy

contraction rate

Frank Starling Law

rule that contraction E of fiber is proportional to initial m fiber length

Starling Mechanism

rule that ventricular ejection volume dep on EDV

preload (heart)

meas of myocardial end diastolic wall stress, inc w/ EDV, inc SV

cardiac performance curve (ventricular function curve)

meas index of resting fiber length (RAP, P, EDV, EDP) vs Econtract (Fcontract, Ventric P, SV, CO)

stroke work

work done to eject bl into aorta against R = SV * MAP = A of PV loop

Kinetic work

work done to accelerate bl to ejection velocity, oft ignored (1% of total work output of heart) but inc w/ stenosis

afterload (cardiac)

F overcome to eject bl into arterial sys, higher in people w/hypertension, inc w/ PR, TPR, Aortic P, decreases SV => dec Ejection Fraction

contractility (cardiac)

intrinsic ability of myocardial fibers to dev F from given length, corresponds to inotropism, inc SV

negative inotropic agents

things that decrease contractility of the heart by dec [Ca2+]I, ex: Ca-chan blockers, beta blockers, MI + cardiac failure

positive inotropic agents

inc contractility by inc [Ca2+]I (by inc ica, Ca2+ reuptake, inhib Ca-ATPase, inhib NaCaexchanger

ESPVR (End-Systolic P-V Relation)

max P gen @ any volume, line on PV loops that is drawn from norm PV loop to theoretical maximal isovolumetric P

Laplace's Law

P = 2T/R

MAP (mean arterial pressure)

CO * TPR = Bpdiastolic + PP/3 = arithmetic mean of systolic + diastolic P under A of P wave

2000

Reynolds number above which corresponds to shift from laminar -> turbulent flow

fick's method

meas rate at which circ absorbs O2 from lungs to calc CO

Indicator dilution

technique that takes known amount of indicator and the time it takes for it to dissapear to meas CO

Compliance

V/P (mL/mm Hg)

unstressed

type of volumes in vv (due to high compliance)

stressed

type of volume in aa (due to low compliance)

1st Korotkoff sound

transient spurt of artery opening briefly during systole, vibrates arterial wall and taken as systolic P w/sphygmomanometer

endothelial cells

function to govern bl-tissue exchange, reg vasc tone, possess ACE, secrete anti-hemostatic agents and clotting factor, release NO

continuous

type of capp w/ cont BM, found in most tissues

fenestrated

type of capp w/ perforated endoth, very permeable to water and small solutes, found in tissues spec in fl exch

discontinuous

type of capp w/ large junctions in BM, highly permeable, found in organs where RBCs and WBCs need to migrate betw bl + tissue

filtration

leaving capps, fav by Pc, Pif (since neg) and TTif

absorption

the act of entering capps, fav by TTp

Pc

capillary hydrostatic P, favors filtartion, P due to bl in capp, higher at arterial end but more affected by changes in venous P

Pif

interstitial fl P, favours absorption, hydrostatic P exerted by interstial fluid

πp

plasma colloid osmotic pressure, favors absorption, effective osmotic pressure of capp bl due to presence of some bl constituents

πif

interstitial fluid colloid osmotic P, favors filtration, due to small amounts of leaked plasma proteins in interstial fluid

Starling's Law

law: amount of fl filtered out from ends of capps = amount of fl returned to circ by absorption (N.b. there is a small difference due to lymph drainage)

ascites

accum fluid in perioneal cavity

myogenic response

increase Bp => vessel contracts, reason why bl flow to brain is rel const

vasoconstrict

action of Endothelin, 5-HT (Serotonin), TX's, LTs

vasodilate

action of NO, Prostacyclins, Histamine, Bradykinin, metabolic (H+, Hypoxia, Adenosine, Interstitial K+)

IHD (Ischemic Heart Disease)

leading cause of death in the west, due to insuff coronary bl flow

Angina Pectoris

pain due to Inc SNS, inc Coronary vasoconstiction => dec O2 to heart

intermittent claudication

ischemic pain on walking

baroreceptor reflex

reflex: sensor -> aortic depressor + carotid sinus nn -> medullary CVS center -> SNS + PSNS -> heart, arterioles, aa, vv affected

Baroreceptors

detect Bp changes, gen Aps

a1 antagonists

drugs: can cause decrease in baroreceptor reflex since cause marked postural hypotension (since they prevent NE-mediated vasoconstriction)

chemoreceptor reflex

reflex: MAP < 80mmHg -> dec PaO2, inc PaCO2, inc H+ (dec pH) => stim vasomotor centers -> inc SNS -> inc Bp

cerebral ischemic response

VERY low Bp -> low pH + high PaCO2 => directly stimulate VMC (VasoMotor Center) -> inc SNS -> inc Bp

Cushing Reaction

CSF P > Bp => cerebral ischemic resonse -> inc Bp

renin-angiotensin system

for long term control of Bp: dec Bp -> dec renal perfusion -> inc Renin -> Angiotensinogen conv to Angiotensin I --ACE--> A-II -> vasoconstriction, inc thirst, inc ADH (inc H2O retention), inc Aldosterone (inc Na+ reabsorption) -> return Bp to norm

cardiopulmonary (low pressure, volume) receptors

receptors located in vv, pulm a, atria, detect bl Volume differences (loc in vv since that's where most of the Volume of the systemic circulation resides)

Bainbridge Reflex

increase in HR in response to cardiopulm/low P/ volume receptors = inc ANF, HR, dec ADH

CO (cardiac output)

volume of blood pumped into aorta each minute or volume of blood flows around circ/min

VR (venous return)

volume of blood flowing from vv to RA/minute

increase

effect of B1 + M2 agonists on heart rate

See More

Please allow access to your computer’s microphone to use Voice Recording.

Having trouble? Click here for help.

We can’t access your microphone!

Click the icon above to update your browser permissions above and try again

Example:

Reload the page to try again!

Reload

Press Cmd-0 to reset your zoom

Press Ctrl-0 to reset your zoom

It looks like your browser might be zoomed in or out. Your browser needs to be zoomed to a normal size to record audio.

Please upgrade Flash or install Chrome
to use Voice Recording.

For more help, see our troubleshooting page.

Your microphone is muted

For help fixing this issue, see this FAQ.

Star this term

You can study starred terms together

NEW! Voice Recording

Create Set