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164 terms

SGU Physiology - Cardiovascular System

CVS flashcards for the SGU Physio midterm
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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
MSFP (mean systemic filling pressure)
Pressure that drives bl back to heart, inc w/ bl vol, venomotor tone, but has little change w/ change in TPR (since most bl found in vv)
postural orthostatic hypotension
Fg inc P above vv -> pool bl -> dec intrathoracic Vol -> dec CVP -> dec EDP -> dec SV -> dec PP -> dec MAP -> dec cerebral perfusion -> dizziness
Valsalva maneuver
forced expiration against a closed glottis -> inc intrathoracic P -> inc MAP -> Baroreceptor Reflex (dec HR, TPR) -> dec VR + SV => SNS reflex to stop fall of Bp -> bring intrathoracic P to normal (decompress aorta, retrigger) -> inc PP, inc MAP (due to inc VR) => inc SV => baroreceptor reflex stim again
essential
type of hypertension found in 95% of cases (few malignant or secondary), no single definable cause
hypovolemic
type of shock: dec bl vol -> dec preload -> dec SV -> dec CO
cardiogenic
type of shock: acute heart failure -> dec SV + CO
septic
type of shock: SIDS = systemic inflammatory response syndrome = massive TNF + NO release -> vasodil -> dec TPR
analphylactic
type of shock: allergic rxn -> dec TPR
internal transfusion
movement of interstitial fluid into blood, occurs during shock
syncope
(fainting) = sudden, transient loss of consciousness due to Bp fall resulting in reduced cerebral perfusion
CHF (chronic/congestive) heart failure
reduced myocardial contractility -> fail heart to pump bl at rate commensurate w/ reqs of metab tissues => exertional dyspnea, tiredness, pulm + systemic edema, 50% mortality w/in 5 years of Dx
digoxin (digitalis)
drug for cardiac failure that blocks the Na+/K+ ATPase in cardiac cells => inc [Ca2+]i -> inc contractile F
pheochromocytoma
disease: adrenal tumor that results in high catecholamine release
PND (paroxysmal nocturnal dyspnea)
when you wake up in the middle of the night to get some air because you have pulmonary edema
tachypnea
respirations > norm (12-20/min)