The document explains cardiac output as the volume of blood pumped by the heart each minute, influenced by heart rate and stroke volume. It discusses concepts such as preload, afterload, contractility, and factors affecting stroke volume, while also addressing the heart's response to changes in venous return. Additionally, it mentions the effects of anesthetic drugs on the cardiovascular system, including their vasodilatory actions and negative impact on contractility.

2.  Definition
It is the volume of blood pumped
systematically by the ventricle of the heart
each minute
Cardiac output depends on 2 variables
Heart rate and Stroke volume
CO = HR x SV

3. CO = HR x SV
72 x 70
= 5 Litres approx
Cardiac index
= CO
BSA

5.  Autonomic nervous system controls
automaticity and rate of spontaneous
depolarization of SA Node
Sympathetic system increases heart rate
Parasympathetic system decreases heart rate

6.  It is the difference between the ventricular
End Diastolic Volume (EDV) and the End
Systolic Volume (ESV)
SV = EDV – ESV
= 120 – 50ml
=70 ml of blood
EDV is the volume of blood in the ventricle at
the beginning of contraction and
ESV is the volume of blood in the ventricle at
the end of contraction

7. Increase:
-Stronger atrial contraction.
-Increased total blood volume
-Increased venous tone.
-Increased sk m pump.
-Increased negative intrathoracic pressure.
Decrease:
Standing
Increased intrapericardial pressure.
Decreased ventricular compliance

8.  Pre load
 After load
 Contractility
 Wall motion abnormalities

11.  Ability of the heart to change its force of
contraction and therefore stroke volume
in response to changes in venous return .
 Also defined as the ability of the heart to
pump all blood coming to it without
allowing systemic stasis, within limits.

12. Mechanism of Starling Law:
An increase in preload lead to an increase
in the sarcomere length and increases
troponin C calcium sensitivity, which
increases the rate of cross-bridge
attachment and detachment, and the
amount of tension developed by the
muscle fiber. This increases SV.

14. Afterload can be defined as the
"load" that the heart must eject
blood against.
 The afterload is closely related to
the aortic pressure.

15.  When arterial
pressure is reduced,
the ventricle can
eject blood more
rapidly, which
increases the stroke
volume and thereby
decreases the end-
systolic volume.

16.  An increase in afterload, lead
to an increase in end-systolic
volume and a decrease in
stroke volume. An increase in
afterload shifts the Frank-
Starling curve down and to
the right (from A to B).
Explanation:, an increase in
afterload decreases the
velocity of fiber shortening.
This reduces the rate of
volume ejection so that more
blood is left within the
ventricle at the end of systole
(increase end-systolic
volume)
.A decrease in afterload shifts
the Frank-Starling curve up
and to the left (A to C).

17. Vascular tone (and therefore blood
pressure)
Aortic stiffness
Myocardial tension (affected by
hypoxia, volume overload)
Preload
Valvular regurgitation

18.  Aortic stenosis.
 Arterial hypertension

19.  Almost all anaesthetic drugs have actions on
cardiovascular system
 They act as vasodialators and decrease both
pre load and afterload
 They are negatively inotropic , reduce
contractility
 This is the reason for a fall in Blood pressure
during induction and maintenance of
anesthesia
 Management?