2 November 2011 Control of Cardiac Output Properties of Blood Vessels Announcements & Reminders Test 2 on Monday Photo-shoot Friday 1pm Biology Suite 1QQs & Moodle

1QQ # 24 for 8:30 1.What is the difference between a heart sound and a heart murmur? 2.What type of cell has “funny” Na+ channels and what is unusual about these channels? 3.In what situation might an ectopic pacemaker actually be beneficial?

1QQ # 24 for 9:30 1.How would heart rate be affected by an antagonist of beta adrenergic receptors? Explain your answer. 2.What type of cell has T-type Ca++ channels and what is the purpose of these channels in those cells? 3.Suppose your sinoatrial node pacemaker cells ceased working. Would your heart continue to beat, and if so, would it beat faster or slower than before? Explain.

CO = HR x SV 5L/min = 72 beat/min x 70 ml/beat 35 L/min = ? beat/min x ? ml/beat S 1 So far, we’ve dealt with the factors that control Cardiac Output by changing heart rate. + sympathetic - parasympathetic 2 1 3

Figure Stroke Volume Animation S 2

Frank-Starling Law of the Heart FS LoH = SV is proportional to EDV Ventricular Function Curve Does not depend on hormones or nerves Assures that the heart adjusts its output based on VENOUS RETURN Ways to enhance Venous Return: 1) muscle contractions 2) “respiratory pump” 3) venoconstriction S 3 ↑VR→ ↑EDV → ↑SV

Fig Low EDV High EDV Length-tension “curve” for Cardiac muscle Overinflation of ventricles leads to less effective pumping S 4

Overinflation of ventricles results in reduction in stroke volume S 5 Treatments? …..diuretics

Contractility NE from Symp postganglionics & EPI from Adrenal medulla Note: cardiac myofibers NOT innervated by parasympathetic division Increase Ejection Fraction S 6

3 Effects of Sympathetic Stimulation 1: Increase rate of contraction 2: Increase peak tension 3: Decrease twitch duration S 7 Why should the contraction be shorter?

Summary: Control of Stroke Volume End diastolic volume (preload) Contractility (strength of ventricular contraction due to adrenergic stimulation) Pressure in arteries that must be overcome = Afterload FS LoH S 8

Afterload is analogous to trying to pump more air into a tire that is already fully inflated (heart contracting to overcome diastolic pressure.) High blood pressure increases the workload of the heart….. Cardiac hypertrophy….increase chance of irregular conduction of AP through heart S 9 Hypertrophic cardiomyopathy

Figure Animation S 10

CO = HR x SV 5L/min = 72 beat/min x 70 ml/beat 35 L/min = ? beat/min x ? ml/beat S 11 Factors that control Cardiac Output by changing heart rate and stroke volume. + sympathetic - parasympathetic EDV (FSLoH) contractility Afterload (MAP)

Fig Even persons with heart transplants can adjust CO in the absence of innervation of heart. Summary of Factors that Regulate Cardiac Output Notice: No Parasymp innervation of Cardiac Myofibers, Parasymp to Conducting Cells only. S 12

End of material for Test # 2 Begin material for Test # 3

S 13 Heart is pump that generates pressure gradient. Blood flows through vessels, which have resistance. Arterioles have greatest resistance and create “backpressure” in the arteries and aorta. Mean Arterial Pressure = diastolic +1/3(systolic – diastolic) = /3(120-70) = = 87 mm Hg

MAP = CO x TPR Mean Arterial Pressure = Cardiac Output x Total Peripheral Resistance MAP = (HR x SV) x TPR S 14