Determinants of Cardiac Output

JL Radcilffe, EMS 410/510, 14 January 2002

 

Heart Rate

Neural control of chronotropic response

Sympathetic activity: Norepi causes ‘positive’ chronotropic response (beta andrenergic)

Parasympathetic activity: Vagus N. release of Acetylcholine causes negative chrono.

 

Regulation of chronotropic response: Via central command and feedback from numerous receptors

Chronotropic response before and after transplantation ->

After transplantation, direct autonomic control is removed. Note higher resting HR (no vagal suppression) and lower exercise HR (no direct sympathetic stimulation). Blood-born catecholamines can still facilitate an increase in HR and contractility.

 

Stroke volume and ejection fraction... (again)

Stroke volume
SV = EDV-ESV

Ejection fraction:

EF = [(EDV-ESV)/EDV] x 100

or…

EF = (SV/EDV) x 100

 

Preload, afterload, Frank-Starling law

Preload: End diastolic pressure (filling!)

Afterload: Systemic arterial pressure against which the heart must pump. Systemic hypertension or aortic valve dysfunction can increase afterload.

Frank-Starling Law: Heart contracts more forcefully during systole when filled to a greater degree during diastole.

 

Contractility:

SNS stimulation increases contractility of individual cardiac cells.

Result: Upward shift in isometric length/tension curve. This is called a positive INOTROPIC response!

Determinants of Cardiac Output

Determinants of MVO2

Muscle contraction accounts for 75% of myocardial ATP use.

Isovolumetric contraction phase is particularly ‘expensive’.

Both preload and afterload affect this!!!

Increasing heart rate is costly!

Less oxygen used at a given Q if HR is lower and SV higher.

Rate-pressure product as an index of MVO2: HR x SBP x 10-2

Angina pectoris may occur at a specific RPP

Imaging -- Echocardiography and Angiography

Click here to visit the Medscape Cardiology Echo Page and look at many echo case studies

Click here to the team learning angiogram activty link!