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CARDIAC OUTPUT

Cardiac output

# CO Amount of blood pumped out by each ventricle into circulation
/min.

# SV 70 90 ml
CO = HR X SV 5.5 L/min

Each ventricle pumps 5.5 L /min

# Cardiac Index 3.2L/m2/min


Measurement of Cardiac Output :

Direct Fick Method
# The Fick principle states that the amount of a substance taken up by
an organ (or by the whole body) per unit of time is equal to the
arterial level of the substance minus the venous level (A-V
difference) times the blood flow.







Conditions or Factors affecting CO

No change Sleep
Moderate changes Environmental temperature

Increase Anxiety and excitement (50-100%)
Eating (30%)
Exercise (up to 700%)
High environmental temperature
Pregnancy
Epinephrine

Decrease Sitting or Standing from lying position (20-30%)



Cardiac output product of HR & SV

Regulation of Stroke Volume

SV determined Inotropy & Ventricular preload


Ventricular preload .
VR
VR Results from
Blood volume
Respiratory activity
Muscle pump activity

# SV EDV(120ml)-ESV (50)=70 ml
- Any factor changing either one change SV

Control of HR
.HR determined by pacemaker activity SA node
.SA node exhibits automaticity determined by spontaneous
changes in Ca
2+
,Na
+
& K
+
conductance

. intrinsic automaticity if left unmodified by neurohumoral
factors exhibits a spontaneous firing rate of 100-
115 beats/min
. intrinsic firing rate with age

. HR below intrinsic rate primarily X nerve SA node
. normally at rest significant vagal tone on SA node
resting HR 60 - 80 beats/min
. HR above intrinsic rate both a withdrawal of vagal tone &
an activation sympathetic nerves SA node

- Reciprocal change in sympathetic and parasympathetic
activity permits HR during exercise

.HR modified by circulating catecholamines acting via
1
-
adrenoreceptors located on SA nodal cells

. HR also modified by changes in circulating thyroxin
(thyrotoxicosis causes tachycardia) & by changes in
body core temperature (hyperthermia HR)

. SA nodal dysfunction can lead to sinus bradycardia, sinus
tachycardia, or sick-sinus syndrome
Factors affecting EDV

Alteration in systolic & diastolic functions have different effects on
heart
. systolic contractions primary SV
.diastolic function also affects SV different way

. intrapericardial pressure limits extent ventricle filling

ventricular compliance [ ventricular stiffness due
to myocardial infarction ,infiltrative diseases and other
abnormalities]
.atrial contractions aid ventricular filling
.other factors affect amount of blood returning to heart so cardiac
filling during diastole
.an total blood volume VR
. Factors affecting VR
.constriction of veins size of venous reservoirs ing venous
pooling VR
. (a)thoracic pump or respiratory pump normal ITP [with in
chest but outside lungs] at end of expiration
subatmosphereic -2mmHg
.during inspiration ITP -5mmHg causing less P on larger
veins & arteries to right side of heart against gravity
And decent of diaphragm IAP to squeeze blood out of abdomen
these 2 factors VR during inspiration
.(b)Cardiac pump
.Vis A tergo force from behind drives blood forward
.VR mostly dependent on forward push from behind
propelling force imparted by
.contraction of heart to blood during its passage through heart & is
assisted by elastic recoil of arterial wall [windkessel effect]
blood enters venules with appreciable pressure higher than RA &
flow of blood in veins towards heart

Vis A Fronte force acting from front to attract blood in veins
towards heart
.exerted by contraction of ventricle & has 2 components

. Ventricular systolic suction ventricular systole causes
decent A-V junction & enlarges great venous reservoirs i.e. atria
& venae cavae piston like downward movement
attracts blood from veins to atria
.Ventricular diastole suction ventricular diastole cause
sudden atrial P V blood flow to atrium VR

( c ). Muscle pump rhythmic contraction of skeletal muscle
venous segments are squeezed P forces blood towards
heart out of each successive segment
.venous valves prevent back flow VR
.veins carry blood to heart
. Veins, particularly in extremities, contain one-way valves that
permit flow toward heart and prevent retrograde
flow

.Deep veins in lower limbs surrounded by large muscle
groups that compress deep veins when muscles
contract

. Venous compression pressure within vein, which
opens upstream valves and closes downstream valves,
there by acting as a pumping mechanism

. .External compression of veins, particularly when muscles in
extremities are contracted rhythmically as during exercise
propels blood toward heart VR

. pump important standing to help maintain central venous P &
VR & to venous & capillary pressure in feet and lower
limbs
. To prevent blood going backwards,veins have one-way
valves
(d). Total blood volume TBV VR
& TBV VR

(e). Capacity of venous system veins capacitance vessels
sympathetic activity venous tone VR
(f).Body position(effect of gravity) standing posture
peripheral pooling of blood VR
.body posture change from supine to standing gravity acts
upon vascular volume so that blood accumulates in lower
extremities
. as venous compliance [ ability of BV wall to expand or
contract passively with change in pressureimportant
function of large arteries & veins]is high, most of blood
volume shift occurs in veins
. venous volume & pressure feet & lower limbs when
standing
Myocardial contractility sympathetic stimulation
Mechanism of action :-
. catecholamines effect is mediated via
1
-adrenergic R & Gs
with activation of adenylcyclase & cAMP
.Xanthine such as caffeine & theophylin breakdown cAMP
+ve inotropic
.Glucagon cAMP formation +ve inotropic & is used to treat
some heart disease
.+ve inotropic effect of digitalis & related drugs due to inhibitory
effect on Na
+
-k
+
ATPase in myocardium
Myocardial contractility
Hypercapnia
Hypoxia
Acidosis
Quinidine
Procainamide & barbiturates depress myocardium contractility
.heart failure (intrinsic depression)
.During initial stages of exercise CO is due to an HR &
SV
. When level of exercise exceeds 40% to 60% of individual's capacity
SV has either plateaued or begun to at a much slower
rate
. Thus further CO are largely result of HR


* High CO
1. Beriberi
2. Arteriovenous fistula ( AV shunt )
3. Hyperthyroidism
4. Anaemia

Low CO
1. M I 5. Decrease TBV
2. Myocarditis 6. Acute venous dilatation
3. Cardiac tamponade 7. Obstruction to large veins
4. Valvular heart disease 8. Circulatory shock



#Pathologically High and Pathologically Low Cardiac Outputs