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
- ACTIVE (requires)
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
- Author: Krisoula Zahariou