I wonder if anyone can help me. I am doing an essay and the patient is having a severe asthma attack. Can anyone predict what his preload, afterload, stroke volume , contractility would be like? His pulse is 150, bp 140/88, sats 90% with o2, he is 44 , has hx of childhood asthma and long term steriods. He is receiving iv salbutamol, iv hydrocortisone, nebulised adrenaline and nebulised vent/atrovent. His abg shows resp acidosis with metabolic compensation.

I'll help you begin to think through it. First look up the meds and their cardiovascular effects. Now his hr is up. CO= HR X stroke volume. there is no info that his stroke volume is affected so work with the HR. Now think about afterload with these types of meds.

reply back, lets see if you're on track.

I'm assuming an acute attack... can't understand how it's compensated metabolically when the renal fix takes a bit to kick in.?? Was there more info? Do you have the ABG #'s ? I'm wondering if your reading it wrong... usually a bit alkalotic at first with the rapid resp. rate. This sound more long term with gas trapping.

Thankyou for responding. My answer so far is: Lung hyperinflation increases afterload of r)ventricle by increasing the length of the pulmonary vessels and by effects of alveolar cap. compression. Increasing intrathoracic pressure during forced exp. decreases venous return & R) vent. filling increases. Increase may cause intraventricular septum shift toward L) vent. resulting in diastolic dysfunction of L)ventricular filling (preload).Total effect of events is insp. increase in stroke volume and exp. decrease in stroke volume. Contractility is enhanced by circulating catacholamines and nebulised adrenaline etc. Bld gases are Ph: 7.25, PaO2: 55, PaCo2:65, HCO3:30, BE:-4. Hope to hear from you again. Thanks

after frequent violent episodes and a hx of bad asthma you will starte to develop phtn "pulmonary htn"... this will primarily affect the rt side of the heart first. once you start having rt sided heart failure you'll get all the increased pa/cvp readings that typically correspond with rt side failure. eventually it'll back up to start bothering the lt side, and then your really going to notice the large wedges,svr but decreased co and ci d/t most likley from systolic failure. but obviously this is a extreme case but one you might see, but for the most part asthma flare-ups will cause some sort of phtn, along with copd,emphysema and fibrosis.

Originally Posted by RN1980

after frequent violent episodes and a hx of bad asthma you will starte to develop phtn "pulmonary htn"... this will primarily affect the rt side of the heart first. once you start having rt sided heart failure you'll get all the increased pa/cvp readings that typically correspond with rt side failure. eventually it'll back up to start bothering the lt side, and then your really going to notice the large wedges,svr but decreased co and ci d/t most likley from systolic failure. but obviously this is a extreme case but one you might see, but for the most part asthma flare-ups will cause some sort of phtn, along with copd,emphysema and fibrosis.

Ditto this, except the LEFT sided effect. Often times with severe COPD, Pulm HTN, the Left side of the heart is without any major problems, but you may start seeing Rt BBB due to the enlargement of the RV, then the RA also becomes enlarged. Sometimes also resulting in Tricuspid regurg, even to the point of requiring replacement, but rare. Fortunately, the L side is usually not very greatly affected, because then along with the lung issues you'd be combatting pulmonary edema as well.