G3iii / 18B18: Describe the factors affecting LV function

18B18: Exam Report

Describe the factors affecting left ventricular function.

12% of candidates passed this question.

Candidates often misinterpreted the question and described determinants of cardiac output. The answer should have focussed on factors affecting/contributing to normal LV function – not pathological states. Some answers showed a lack of appreciation that normal left ventricular function is afterload independent, due to compensatory reflexes. Answers needed to consider intrinsic and extrinsic factors affecting LV function – the latter (e.g. SNS, PSNS, hormones, drugs) was often left out. Answers needed to consider both systolic and diastolic function. An excellent answer included physiological phenomena such as the Treppe effect, Anrep effect and baroreceptor and chemoreceptor reflexes. Mention of normal conduction and pacing as well as blood supply limited by diastole scored additional marks.

G3iii / 18B18: Describe the factors affecting LV function (12%)

Any physiology qn:

  • Define
  • Quantify
  • Classify +/- Equations

Definition

LV function =   Ejection of blood into aorta during systole

                        Relaxation and filling of ventricle during diastole

Quantification

Normal LV Function = EjF 55-65%

(most common clinical measure)

Classification

Systole

  • PRELOAD – sarcomere length just prior to contraction ≅2nm
  • AFTERLOAD – the sum of all factors required to overcome so that blood may be ejected from the H to the arterial circulation
  • CONTRACTILITY – the calcium dependant mechanisms that increase contractile force, independent of loading factors

Diastole

  • RELAXATION
    • ACTIVE (requires)
      • ATP
      • O2
      • substrate (glucose)
      • CPP {CPP = (MAP-RAP)/Resistance}
    • PASSIVE = LV compliance

Regulation of Cardiac Performance

Intrinsic

Pacemaker Activity

H can initiate its own beat in absence of neural/hormonal control

Intrinsic rate of discharge of SA Node @100bpm

(in absence of autonomic influences, this is KA Intrinsic HR)

Frank-Starling Mechanism

States:  the ability of cardiac muscle fibre to contract is dependant upon and proportional to its initial fibre length

Important intrinsic adaption allow CO to match VR of ventricles

Insert diagram FS Curve

(CO v LVEDP) in A1013

LV mass = ­mass = ­FoC

 Age = ­age = replacement of myocytes w scar tissue

 Ventricular Interdependence

The response of one ventricle to the changes in pressure and volume in the remaining other

Extrinsic

Neural – ANS

NT

Parasympathetic

ACh

Sympathetic

Ach & NA

Rec

Parasympathetic

M2

Sympathetic

b1

Intrac

Response

Parasympathetic

Gq

­↑K

Membrane hyperpolarisatn

Sympathetic

Gs

­↑cAMP

­↑Ca++

Outcome

Parasympathetic

↓HR

↓transmission through AV node

↓contractility

Slows relaxation in diastole

Sympathetic

­↑inotropy

­↑chronotropy

↑↓automaticity

↑Coronary VD

­↑dP/dt

Cardiac Reflexes

BaroR

ChemoR

Bainbridge

Bezold-Jarisch

Cushings

Oculocardiac

Anrep effect -↑ ­afterload ->↑ ­contractility

­↑ESV -> myocardial stretch ->↑ ­Ca++ release ->↑ ­FoC ->↑ ­SV -> ­↑CO

Treppe effect – a stepwise ­↑myocardiac contraction due to ­↑Ca++ intrac

(treppe = steps, German)

Hormonal

Catecholamines – NA & Adr -↑ ­symp

Thyroid hormones -↑ ­FoC, ↑­symp stiml, ↑­BMR

Insulin – direct +inotropy of H

Temperature

­↑temp = ­↑HR

 Chemical/Metabolic

O2 – hypoxia = myocardial pedpression

pH – hypercapnia = ↓Ca++ releave from myocyte, ↓sensitivity of myofilamients to C++

Ca++  – required for myocardial contraction

K+ – responsible for RMP

 Drugs ( don’t regulate = influence)

Ie inotropes, b-blockers, Ca++ sensitizers