7. 7
Carotid sinus
senses BP
Parasympathetic
Sympathetic
2
Baroreceptor Reflexes
in BP Control BP1
8. 8
Carotid sinus
senses BP
Parasympathetic
Sympathetic
Vasomotor Center responds
with Symp. NS activity
and Parasymp. activity
2
3
Baroreceptor Reflexes
in BP Control BP1
9. 9
Carotid sinus
senses BP
Parasympathetic
Sympathetic
PVR
Heart rate
and contractility
Vasomotor Center responds
with Symp. NS activity
and Parasymp. activity
2
3
4
4
Baroreceptor Reflexes
in BP Control BP1
10. 10
Carotid sinus
senses BP
Parasympathetic
Sympathetic
PVR
Heart rate
and contractility
Vasomotor Centre responds
with Symp. NS activity
and Parasymp. activity
Baroreceptor Reflexes
in BP Control
BP
2
3
4
4 5
BP1
11. 11
• Cardiac Output (Output of Pump)
– heart rate x stroke volume
• Caliber of Arteries & Arterioles (Flow
Resistance)
– Neural
• sympathetic & parasympathetic NS
– Hormonal
• Renin-angiotensin-aldosterone system
– Local transmitters
• Nitric Oxide (NO)
Blood Pressure Control:
Control of Stroke Volume
12. 12
Stroke volume (SV)
• Stroke volume (SV) is volume of
blood pumped by right/left
ventricle of heart in one
contraction
• Specifically, it is volume of blood
ejected from ventricles during
systole
• SV is not all of blood
contained in left ventricle
• Normally, only about two-
thirds of blood in ventricle is
put out with each beat
• What blood is actually
pumped from left ventricle
is stroke volume and it,
together with heart rate,
determines the cardiac
output
Calculation
Its value is obtained by subtracting end-systolic
volume (ESV) from end-diastolic volume (EDV)
for a given ventricle:
SV = EDV − ESV
In a healthy 70-kg man, the left ventricular EDV
is 120 ml and the corresponding ESV is 50 ml,
giving a stroke volume of 70 ml.
14. 14
Venous filling pressure and
stroke volume
• The Frank-Starling relationship
StrokeVolume
End diastolic volume (filling pressure)
Output increases with
increased filling pressure
Overdistended,
output falls
Blood Pressure Control:
Control of Stroke Volume
15. 15
What determines venous filling pressure?
• Blood volume, mostly contained in a distensible
venous circulation!
Blood Pressure Control:
Control of Stroke Volume
16. 16
• Cardiac Output (Output of Pump)
– heart rate x stroke volume
• Caliber of Arteries & Arterioles (Flow
Resistance)
– Neural
• sympathetic & parasympathetic NS
– Hormonal
• Renin-angiotensin-aldosterone system
– Local transmitters
• Nitric Oxide (NO)
Blood Pressure Control:
Renin-Angiotensin
39. 39
Volume Reduction
• Reduces cardiac filling pressure (LVEDV/P)
• Thus reduces stroke volume and cardiac
output
• Independent vascular relaxation with long
term use
See Diuretics eNotes
40. 40
Clinical Use of
Antihypertensives
• Consequences of chronic high blood pressure
– heart failure
– arterial disease
• kidney failure
• strokes
• myocardial infarction (heart attack)
• Aim of treatment
– prevent consequences of high BP
42. 42
• Oxygen demand depends on heart work
• Coronary artery partial obstruction (due to
atherosclerosis) limits blood supply to part of the
myocardium
• Coronary circulation can meet oxygen demands of
myocardium at rest, but not when heart work increased
by exercise, etc.
– Ischemia (O2 deficiency) causes pain: “angina”
What is Angina and Why Does it
Happen?
43. 43
Determinants of Heart Work
• Heart work determined by:
1. Heart rate
2. Cardiac contractility
3. Peripheral resistance
See: Antihypertensive Agents
Physiological Factors Influencing Arterial Pressure for full discussion
44. 44
• Reduce heart rate and contractility
– adrenoceptor blockers
– Ca2+ channel blockers (verapamil and diltiazem)
• Dilate resistance vessels
– Ca2+ channel blockers (nifedipine, felodipine,
amlodipine)
– Nitrates
Drug Treatment of Angina:
Limiting Heart Work
47. 47
Nitric Oxide and Vasodilation
After receptor stimulation, L-
arginine-dependent metabolic
pathway produces nitric oxide
(NO) or thiol derivative (R-NO).
NO causes increase in cyclic
guanosine monophosphate
(cGMP), which causes relaxation
of vascular smooth muscle.
EDRF=endothelium-derived
relaxing factor.
From: Inhaled Nitric Oxide Therapy
ROBERT J. LUNN, M.D.
http://www.mayoclinicproceedings.com/inside.
asp?ref=7003sc
48. 48
Use of Nitrates
• Very fast, short-lived vascular dilatation (Greater
in venules than arterioles)
• lower vascular resistance means less heart work
• less heart work means less need for coronary
artery blood flow
– therefore, nitrates help chest pain (angina) that
happens during exercise when there is coronary artery
obstruction.
• Not used for managing chronic high blood pressure
49. 49
Digitalis purpurea (Foxglove)
Cardiostimulatory
Medicines from foxgloves are called "Digitalin". The use of Digitalis purpurea extract
containing cardiac glycosides for the treatment of heart conditions was first described
in the English speaking medical literature by William Withering, in 1785. It is used to
increase cardiac contractility (it is a positive inotrop) and as an antiarrhythmic agent to
control the heart rate, particularly in the irregular (and often fast) atrial fibrillation. It is
therefore often prescribed for patients in atrial fibrillation, especially if they have been
diagnosed with heart failure. From: http://en.wikipedia.org/wiki/Digitalis