physio

Página 1

session 40

page 78 [ch.??]

vent. fun. curves

[preload vs systolic performance i.e. frank starling=directly proportional]

[inc. contractility or dec. afterload]

[change in performance without a change in preload would be a change in afterload or contractility]

vectors:

[what happened to performance?]

[what happened to preload?]

[dec. performance and dec. preload=frank starling]

[shifted to another curve = reflex inc. in contractility]

[clinical e.g.: dec preload: bleed[dehydration, diarrhea, vomiting], venodilators[nitrates], standing up-right]

[dec. performance, inc. preload, i.e. not frank starling, so inc. afterload [e.g. arteriolar vasoconstriction] or dec. contractility [e.g. heart failure, MI, beta blocker, acidosis, ischemia{immediate}]

*phenylephrine OD would stop a heart

*HTN could depress vent. output

*HF pt in HTN crisis --> reduced ejection

[inc. preload {esp. acute} with reduced performance can be due to pump failure {blood backs up} e.g. ?pulm. edema]

[inc. performance, dec. preload, i.e. not frank starling, so inc. contractility (dopamine, intropes {digoxin=Na/K pump inhibitor, inamrinone & milrinone=PDE inhibit.}, sympathetics {NE,Epi}, beta 1 agonist {dobutamine=selective, isproteronol=non-selective} or dec. afterload (arterolar vasodilation {ACE-I, hydralazine, etc.}]

[inc. performance, inc. preload {vol. load=infusion, pregnancy (contractility won't dec.), venoconstriction, lying down/flt, space travel=no gravity} i.e. frank starling. with reflex dec. contractility or inc. afterload

vent. vol.

EDV = preload

ESV

Stroke vol = vol. of blood ejected {EDV-ESV}

EF=SV/EDV {clinical marker of contractility} {normal >60%}

in systole the heart pressurizes and ejects

systolic dysfun. = dec. stroke vol. [problem ejecting]

in diastole, the heart de-pressurizes and refills

dystolic dysfun. = inc. diastolic pressure {dec. filling <=stiffness/dec. compliance}

heart overload: pressure or volume

pressure overload:

acute --> hypertrophy [concentric=thicker with less diameter = stiff=diastolic dysfun.]

chronically: systolic dysfun

vol. overload

e.g.

slowly devloped usu. well tolerated

acute: descending frank [maintaining dystolic fun.]

chronic: eccentric hypertrophy {like seen with exercise}

systolic dysfun. over time --> HF [the heart get worn out]

cardiomyopathy

dilated: inc. vol. and poor ejection --> inc. preload--> systolic dysfun. -->dilation -->failure

[S3 in dilated]

[lateral displacement of point of max. impulse]

path. causes: alcool, chagas, preg., doxirubicin, cocaine, coxakie virus, idiopathic, wet beriberi [b1, vol. owerload]

restrictive: dec. compliance [stiffer] --> diastolic dysfun. --> inc. heart pressure-->inc. venous and cap. pressure

sys. fun. maintained till late stages

e.g. -'osis' and loefloer

hypertrophic: septal or LVh not related to pressure overload

dystolic dysfun. [stiff]

causes: genetic, [young athletes die suddenly]

---break---

ch. 1 section v

??CVS notes: HY relationships

overview

left heart-->body [high o2 &low co2=venous blood] [pulm. a. and systemic v. to the RA]]

Rt heart --> lungs [low o2&high co2 = arterial blood] [pulm. v. and systemic a. to the body]

CO is the same in both pumps [closed loop]

hemodynamics: Q= [p1-p2] / R {core}

[pressure, flow, resistance]

flow directly proportional to pressure gradient

MAP is the upstream pressure in the body

MAP is well regulated!

resistance inversely proportional to radius [4x]

radius = vasoconstriction/dilation

inc. resistance= dec. blood flow and dec. downstream pressure and inc. upstream pressure [inc. pressure gradient]

{R=[p1-p2]/Q}

pressure gradient is directly proportional to resistance

dec. resistance= dec. upstream pressure and inc. downstream pressure [dec. gradient], inc. blood flow

[p2 related to blood flow?]

[p1 related to resistance?]

----