16A13: Exam Report

Describe the cardiovascular effects of a sudden increase in afterload.

21% of candidates passed this question.

It was expected the answer would start with a definition of afterload and then proceeded to indicate what effects this increase in afterload would have on ventricular end-systolic pressure, ventricular end-diastolic pressure, left atrial pressure, cardiac output, myocardial oxygen demand and myocardial work, coronary blood flow and systemic blood pressure.

Most candidates who failed to pass this question submitted answers that were just too brief, only including a small subset of the material required. Very few candidates included any mention of myocardial oxygen demand or myocardial work or the impact upon the cardiac output. A number of candidates included a detailed description of the Sympathetic Nervous System and the Renin-Angiotensin system, material which was not asked for. There were quite a number of incorrect perceptions about what effect a sudden increase in afterload would have on the systemic blood pressure. Candidates who mentioned the baroreceptor response and the stretch receptor response where rewarded with additional credit.

G3ii / 16A13: Describe the cardiovascular effects of a sudden increase in afterload

Definition

  • AfterL = sum of all factors required to overcome so that blood may be ejected from heart to the arterial circulation

AfterL gives rise to Wall Tension in the ventricle → ∴afterL can be thought of as the wall tension required to overcome impedance to eject blood into the arterial circulation

Consequences of ↑ Afterload

↑ Ventricle End Systolic Pressure

  • ↑ Ventricle End Systolic Pressure
    • ↑ESP at the expense of ejection
    • ∴↓SV

↑LV End Diastolic Pressure

  • Shifts F – S curve down & right
  • ↑LVEDP
  • Due to ↓velocity of fibre shortening
  • ↓SV
  • ↑LV End Diastolic Vol
  • ∴↑P

↑Lap

  • End diastolic vol has implications for LAP
  • ↓gradient for blood to move from LA → LV
  • ∴LA required ↑pressures to move blood

↓CO

  • ↓SV
  • CO = HR x SV
  • ∴↓CO
  • PV loop is taller & thinner

BP

  • ↓SV because heart takes longer to develop enough pressure to eject blood, but it has a short period
  • ∴↓SV
  • BP = CO x SVR
  • ∴↓CO = ↓BP

Myocardial O2 Demand & Work

  • AfterL (wall tension) is related to the tension that individual myocytes must develop in order to generate a pressure during contraction
  • At a given radius & thickness, a myocyte must generate ↑contractile force (wall stress) to develop a higher pressure (to overcome ↑afterL
  • i.e. ↑Aortic P 50% = wall stress myocytes must generate are 50% more
  • ∴Myocyte O2 consumption ↑50% because myocardial O2 consumption is very closely related to wall stress

Coronary Blood Flow

  • Hypertrophy due to ↑afterL
  • Myofibril growth > cap network
  • ∴↓capillary density
  • ↑intramyocardial P load = ↑work & O2 demand
  • Hypertrophied tissue has impaired vasomotor response to hypoxia

Baroreceptor Response

  • ↓arterial BP 2° ↑afterL
  • ↓afferent firing by BaroR
  • NTs release symp inhibition → ↑ & ↓ parasymp. Outflow
    • Heart = ↑HR, SV
    • Resistance Vessels = VC
    • Capacitance Vessels = VC = ↑VR