Blood Pressure secondary to Temp. Pacing

Specialties Cardiac

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I work at a CVICU and we temp pace a lot of our patient after surgery for cardiac output. However, we have been using lately to increase blood pressure. Does anyone now the physiological mechanisms involved? If the body naturally increased heart rate its due to SNS fight or flight and there is a catecholamine response involved, but if it artificially done?

Cardiac output equals HEART RATE times stroke volume.

I know that already! I was asking for physiological mechanisms not definitions. You need sympathetic stimulation which increases heart rate, contractility, stroke volume and cardiac output. End result higher blood pressure. The question I was eluding to was how using a temp pacer achieves this without the body natural response.

I work at a CVICU and we temp pace a lot of our patient after surgery for cardiac output. However, we have been using lately to increase blood pressure. Does anyone now the physiological mechanisms involved? If the body naturally increased heart rate its due to SNS fight or flight and there is a catecholamine response involved, but if it artificially done?

Just my simplistic mind I guess.. :chuckle ...didn't mean to insult you.

Specializes in Cardiothoracic nursing.

Hi there!

First of all - what kind of generators do you usually use? Single chamber or sequential pacing? Remember - if you have a ventricular pace you lose about 30% of CO (you lose the atrial systole) in a patient with poor ventricular function .... it's important!

At the other hand, you can produce electrical stimuli but for many reasons they probably don't produce mechanical contraction (try to increase the mV output - avoiding phrenic stiumulation!)

If after all the settings (output, sensing, rate) you can't increase the BP .... you have to assess the volemic status of the pt. and maybe his contractility it's not the best....

Hope this help.

Bruno M

Pacing after Cardiac Surgery is basically done for a target heart rate.

Basically if the heart rate is too high, ie 100, then the filling time of the ventricles are decreased, thereby reducing the preload for that ventricle, hence a reduced, CO, Blood pressure, etc. If I remember correctly, filling of the ventricles is passive, happening during dystole.

Ideally a heart rate ranging from 70-85, however, all this being said, this does nothing for the contractility of the ventricle, just another way to control the preload and finding the optimal point on the Starling curve for that patient.

this is how it was explained to me: we put bi-v-icd's in our heart failure pt's to increase cardiac output by synchronizing the chambers of the heart. a 100% A-V paced rhythm at a rate of 60-80 produces an improved stroke volume=better CO. what you may see is a higher blood pressure. notice how end stage chf-ers have sbp's in the 70's-80's? often even after the device is in. it is an uphill battle trying to increase co in these people and maintain some quality of life.

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