Physio Cardiac Performance Regulation/Clinical Case (20)

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  1. Left Ventricle Volume–Pressure Loop
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    1: mitral valve opening (beginning of ventricular filling aka diastole)

    1 → 2: period of ventricular filling (see volume increase & pressure increase slightly at the end when ventricular systole is occurring)

    2: mitral valve closes; end diastolic volume (EDV) & pressure (signals the very start of ventricular systole)

    2 → 3: isovolumic contraction (pressure JUMP w/out a volume change b/c both mitral & aortic valves are closed)

    3: aortic valve opening (pressure great enough to do so is achieved)

    3 → 4: ejection process (blood leaves ventricle, passes through to aorta)

    4: aortic valve closure

    4 → 1: isovolumic relaxation (both valves are closed, no volume change, but a PRECIPITOUS drop in pressure)

    1 & 4: end systolic volume (ESV)
  2. Ejection Fraction =
    • SV / EDV
    • (EDV – ESV) / EDV
    • the proportion of the end diastolic volume that's ejected from the heart in a beat
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    • same as the left, just with different valves (tricuspid & pulmonic) + much lower pressures
    • volumetric pressure curve is useful for looking at homeo & heterometric pressure changes
  4. What situation is depicted in this left ventricle volume–pressure loop graph?
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    • an increased preload (increased diastolic filling)
    • a heterometric change (dependent on sarcomere length @ the end of diastole)
    • increased preload can also be said as ↑ sarcomere length, end diastolic pressure (EDP), EDV, or venous return
    • results in an increased diastolic volume (seen from 1 → 2 with both the greater pressure & volume)
    • see a greater ejection pressure between 3 → 4 b/c more blood is exiting the L ventricle
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    • can also affect the R ventricle in a similar manner w/in the confines of lower pressure (could happen w/ a greater inflow of blood to the heart, eg. during exercise)
  5. What situation is depicted in this left ventricle volume–pressure loop graph?
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    • an uncompensated increased afterload (force ventricle sees after aortic valve opens - aortic pressure)
    • start with a higher than normal end diastolic volume, filling continues from 1 → 2
    • 3: aortic valve isn't opening until you get to a HIGHER pressure (ventricular pressure must be > than aortic pressure before valve opens)
    • 3 → 4: ejection is rather small (decreased velocity of contraction, stroke volume ↓)
    • could occur clinically w/ hypertension or aortic stenosis
  6. What situation is depicted in this left ventricle volume–pressure loop graph?
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    • the effect of positive ionotropic agents, eg. NE, causes increased force of contraction
    • 3 → 4: stroke volume ↑ b/c the heart pumps with greater force
    • 4: results in a lower ESV
    • 1: b/c you start at a lower volume, there is increased filling - 2 remains the same though
  7. What situation is depicted in this left ventricle volume–pressure loop graph?
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    • the effects of exercise: combines a positive ionotropic effect (contractility) w/ increased ventricular filling (EDV)
    • increase return of blood to the R ventricle → ↑ EDV
    • + ↑ emptying/ejection due to ionotropic effect (more powerful contraction)
  8. Systolic Murmur
    • occurs during systole (between S1 & S2) & could either be AV valve insufficiency or semilunar valve stenosis
    • aortic or pulmonic stenosis - aortic especially can be heard b/c the the pressure differences are large
    • mitral valve insufficiency (regurgitation, prolapse)
    • the direction of blood flow is out of the ventricle → the system
  9. Aortic Stenosis
    • there will be large pressure gradient between L ventricle & aorta b/c of the large resistance across the aortic valve
    • in this situation the PAo is lower than normal (due to the stiffened valve it's not getting as much blood as normal → lower pressure) & the PV is high, b/c not as much blood is leaving the L ventricle & it must contract harder against a stiff valve
  10. What is the eventual effect of high diastolic L ventricular pressure seen in aortic stenosis?
    • diastolic pressure is increased b/c an incomplete amount of blood is being ejected from the L ventricle → total EDV is greater
    • this elevates L atrial pressure → higher pressure in pulmonary veins → higher pulmonary capillary pressure
    • in this situation there is poor fluid/exchange in capillaries & EDEMA (fluid flooding alveoli)
    • this can cause Dyspnea (from pulmonary congestion due to a stenotic aortic valve)
  11. How could a high Left atrial pressure be picked up if such a situation as that aforementioned was thought to be occurring?
    using pulmonary wedge pressure
  12. Exertional Angina
    • results from inadequate O2 delivery for the level of physical activity
    • there is an imbalance of O2 supply & demand
    • to combat this situation O2 supply must increase or there must be a reduction in O2 demand
    • exertional angina is one of the 1st indicators that there's insufficient blood supply & the majority of angina pain comes from ATH plaques in coronary arteries, which can grow large enough to occlude the arteries 70-90%
  13. What is the only way to increase O2 supply to the heart?
    by increasing coronary blood flow – remember, O2 delivery is flow limited
  14. How can O2 demand be decreased?
    • by reducing myocardial work
    • W= P * (SV/beat) * (beats/min)
    • 1. reduce heart rate
    • 2. reduce stroke volume (by decreasing inotropy β via blockade or decrease EDV by lowering the venous return)
    • 3. reduce ventricular pressure (can do this by decreasing afterload, again decrease inotropy, or using vasodilators like nitroglycerin)
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  15. What is S–T elevation indicative of?
    a recent MI - more specifically, an elevated S–T signal is indicative of myocardial cell death
  16. S–T Changes
    • the ST segment represents the isoelectric period when the ventricle myocardiocytes are all depolarized
    • if a heart attack (MI) of certain severity has occurred, there's myocardiocyte death
    • in injured cells the Na/K pumps are not active → no depolarization occurs → the resting membrane potential is consistantly 0 mV
    • during this period where all alive cells are depolarized, there is a small dipole between normal cells which are at a negative potential outside & injured cells which are at 0 mV
    • this leads to displacement of the S-T segment from isoelectric (S remains elevated)
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  17. Left Axis Deviation (LAD)
    • a condition where the mean electrical axis of ventricular contraction (mean cardiac vector, ventricular axis) of the heart lies in a frontal plane direction between -30° → -90°
    • common causes of LAD include:
    • LEFT ventricular hypertrophy
    • left Anterior fascicular block (or hemiblock)
    • left bundle branch block
    • inferior myocardial infarction
    • reflected by a positive QRS complex in lead I & a negative one in leads aVF & II
  18. Right Axis Deviation (RAD)
    • a heart condition wherein the electrical conduction of the heart has an electrical axis greater than +90°
    • can be indicative of increased workload of the right ventricle (right ventricular hypertrophy), right bundle branch block, COPD, pulmonary arterial hypertension, a large pulmonary embolism (a clot in the pulmonary arteries requires the R ventricle to contract harder to push blood past it), loss of muscle power of the left ventricle (eg. in left sided MI), a left Posterior fascicular block, or Situs Inversus

Card Set Information

Physio Cardiac Performance Regulation/Clinical Case (20)
2014-02-16 21:02:49
MBS Physiology
Exam 2
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