basics

1. Cardiac anatomy
and
physiology
by
Kamal raj kumar
pg-1

2.  Normally located in the middle and slightly to the left side of the thoracic
cavity on the diaphragm between 3rd and 5th ribs.
 Weighs about 325 gm is males and about 275 gm in females.

4. Heart has ….
 Base
 Apex
 Anterior
 Posterior

5. Right Atrium
 Receives venous blood from whole of
the body via the superior vena cava
(SVC) at its upper end and inferior
vena cava (IVC) at its lower end.
 It pumps into Right ventricle (RV)
through the tricuspid valve during
the ventricular diastole.
 Right atrial appendage – arises from
the antero superior part of the right
atrium. It is to the left of the
ascending aorta.
 Sulcus terminalis – shallow
vertical groove along the right
heart border between SVC and
IVC.
 RA and SVC junction – Sino atrial
node.

6. Right ventricle
 Triangular shaped or
crescent shaped
 Opens into pulmonaryartery
through pulmonaryvalve
 Most anteriorchamber
 RV wall measures 4-5 mmin
thickness.
 Three portions – inflow ,
outflow and apical trabecular
portion or body of RV.

7. Left atrium
 Posterior most chamber
 Receives oxygenated
blood from pulmonary
veins
 Pulmonary veins open
into LA from the
posteriorwall
 Left atrial appendage
is anterior.

8. Left ventricle
 Bullet shaped
 Blunt tip forms the
apex of the heart
 LVwall is 8-15 mm in
thickness.

9. Layers of Heart Wall
 Pericardium - membrane (sac) that surrounds and protects theheart,
 it has two layers:
 ( a ) Fibrous pericardium - superficial layer, tough,inelastic, prevents
overstretching, provides protection, and anchors the heart in place
 ( b ) Serous pericardium - deeper layer,thin;
 (i) parietal layer - fused to the fibrous pericardium, and
 (ii) visceral layer (or epicardium) adheres to the heart itself
 Pericardial cavity (between the two layers) is filled with
pericardial fluid which reduces friction.

10. Layers of Heart
Wall
11

11. FIBROUS:THIN INELASTIC, DENSE
IRREGULAR CONNECTIVE TISSUE
---HELPS IN PROTECTION, ANCHORS
HEART TO MEDIASTINUM
SEROUS: THINNER, MORE DELICATE
DIVIDED INTOPARIETAL AND VISCERAL
13

12. MYOCARDIUM:RESPONSIBLE FOR PUMPING
 ENDOCARDIUM: THIN LAYER OF ENDOTHELIUM WHICH
IS CONTINOUS WITH THE LINING OF THE LARGE BLOOD
VESSELS ATTACHED TO THE HEART.
1
EPICARDIUM: COMPOSED OF MESOTHELIUM AND
DELICATE CONNECTIVE TISSUE (IMPARTS A SLIPPERY
TEXTURE TO THE OUTER SURFACE OF THE HEART).

13. Coronary Circulation
• Def: Blood flow to heart through coronary arteries is coronary
circulation
• Normal value: 250 mL/min at rest or
70 ml / 100 gm / min
• This may increase upto to 2000 ml / min

14. Coronary circulation
• Consist of
1) Arterial supply
2) Venous drainage
3) Lymphatic drainage

15. Arterial supply
• The cardiac muscle is supplied by two coronary
arteries the right and left coronary arteries.
• Both arteries arises from the sinuses behind the
cusps of the aortic valves at the root of the aorta.

17. Rt. Coronary artery
• Smaller than left coronary artery
• Arises from anterior coronary sinus
• Emerges from the surface of heart between
pulmonary trunk and right auricle.
• Winds round the inferior border to
diaphragmatic surface to reach the posterior
inter-ventricular groove.
• Terminates by anastomising with left
coronary artery
EKG: lead II, III & AVF

18. Branches
• Large Branches
– Acute marginal
– Post-interventricular
• Small branches:
– Right atrial
– Infundibular
– Nodal – in 60% cases
– Terminal

19. Anterior schematic diagram of heart shows course of dominant right coronary artery
and its tributaries. AV = atrioventricular, PDA = posterior descending artery, RCA = right
coronary artery, RV = right ventricular, SA = sinoatrial

20. AREAS OF DISTRIBUTION
• Right atrium
• Ventricles
– Greater part of right ventricle, except the area
adjoining the anterior inter-ventricular groove.
– A small part of the left ventricle adjoining the
posterior interventricular groove.
• Posterior part or the inter-ventricular septum
• Whole of the conducting system of the heart except a part of the
left branch of AV bundle. The SA node is supplied by left coronary
artery in 40% cases

21. LEFT CORONARY ARTERY
• Arises from left posterior aortic sinus
• Runs forward and to the left and emerges between
the pulmonary trunk and the left auricle.
• Here the anterior inter-ventricular branch is given
• After giving off the anterior interventricular branch it
runs into the left anterior coronary sulcus as the
circumflex artery.
• It winds around the left border and near posterior
interventriular groove it terminates by anastomosing
with the right coronary artery.
EKG: lead V3 &V5

22. BRANCHES:
• Large Branches:
– Left anterior desending arteryEKG: Lead V5
– Left circumflex branch EKG: lead 1& AVL
• Small Branches:
― Left atrial
― Pulmonary
― Terminal

23. Dominant left coronary artery anatomy. Left anterior oblique schematic diagram of
dominant left coronary artery anatomy, including left anterior descending artery and
left circumflex artery tributaries, is shown. AVGA = atrioventricular groove artery, PDA =
posterior descending artery.

24. Areas of distribution
• Left atrium
• Ventricles:
 Greater part of left ventricle, except the area
adjoing the posterior interventricular groove.
 A small part of right ventricle adjoining the
anterior interventricular groove.
• Anterior part of interventricular septum.
• Part of left branch of AV bundle

25. Collateral circulation
• These channels open up in the emergencies when the coronary
arteries are blocked.
• Cardiac anatomosis: The two coronary arteries anastomose in the
myocardium
• Extra cardiac anastomosis: The coronary arteries anastomose with
the
• Vasa vasorum of the aorta,
• Vasa vasorum of pulmonary arteries,
• Internal thoracic arteries
• The bronchial arteries
• Phrenic arteries.

26. CORONARY ARTERY DOMINANCE
• Artery that gives the posterior interventricular artery determines
the coronary dominance
• If Posterior interventricular artery is supplied by right coronary
artery (RCA), “right-dominant”(70%)
• Posterior interventricular artery is supplied by the circumflex artery
(CX), a branch of the left artery, “left-dominant”(10%)
• Posterior interventricular artery is supplied by both the right
coronary artery (RCA) and the circumflex artery, then “co-
dominant”(20%)

27. VENOUS DRAINAGE OF THE HEART
• The venous drainage of the heart is by
three means:
– Coronary sinus
– Anterior cardiac veins
– Venae Cordis minimae

28. CORONARY SINUS
• This is the largest of vein of heart situated in the left posterior
coronary sulcus. It is about 3 cm long and ends by opening into the
posterior wall of the right atrium
• Its tributaries are:
− Great cardiac vein: It accompanies LAD enters the left end of
the coronary sinus
− Middle cardiac vein: It accompanies the posterior
interventricular artery and joins the right end of the
coronary sinus
− Small cardiac vein: It accompanies the right coronary artery
and joins the right end of the coronary sinus

29. − Posterior vein of left ventricle: It runs on the
diaphragmatic surface of the left ventricle and ends in the
middle of the coronary sinus.
− Oblique vein of left atrium ( of Marshall): It runs on the
posterior surface of the left atrium, joins the left end of
coronary sinus and develops from the left common
cardinal vein.
− The right marginal vein: It accompanies the marginal
branch of the right coronary artery.

30. ANTERIOR CARDIAC VEIN
3 to 4 small veins run on the anterior wall of the right ventricle, open
directly into the right atrium.
VENAE CORDIS MINIMAE
(also called smallest cardiac veins, venae cardiacae minimae, or Thebesian
veins)
• Numerous small veins present in all 4 chambers of heart which open
directly into the cavities.
• The Thebesian venous network is considered an alternative
(secondary) pathway of venous drainage of the myocardium.

31. Lymphatics of heart
• Lymphatics of the heart accompany the coronary arteries and
form 2 trunks.
• Right trunk ends in brachiocephalic nodes and the left trunk
into the tracheobronchial lymph nodes at the bifurcation of
the trachea.

32. PECULIARITIES OF COR.CIRCULATION
• BF during diastole
• End arteries
• Anatomical anastomosis
• High capillary density
• High 02 extraction
• Regulation is mainly by metabolites
• The coronary vessels are susceptible to degeneration and
atherosclerosis.
• There is evident regional distribution: The subendocardial
layer in the left ventricle receives less blood, due to more
myocardial compression (but this is normally compensated
during diastoles by V.D). However, this renders this area more
liable to ischemia and infarction

33. Myocardial Oxygen Supply
Determined by:
Coronary Blood Flow & O2 Carrying Capacity
 Oxygen saturation of the
blood
 Hemoglobin content of the
blood
(CorBF = CorPP /CorVasRes)
 Coronary perfusion pressure
(pressure gradient across the
myocardium)
 Coronary vascular
resistance

34. CORONARY BLOOD FLOW (CBF):
• The resting coronary blood flow is about 250 ml/min., which is
about 0.7 – 0.8 ml/gm of heart muscle, or 4- 5 % of the total
cardiac output
• In severe muscular exercise, the work of the heart increased
and the CBF may be increased up to 2 liters/ minute

35. Physiology of the coronary flow
• C.B.F. occurs mainly during diastole due to compression of coronary blood
vessels in systole by the contracted muscle fibers .
• Coronary perfusion pressure :
• Driving force for blood flow in coronary arteries
• Pressure gradient across the myocardium (diff between aortic pressure
and intraventricular pressure)
• It varies throughout the cardiac cycle being greater during diastole than in
systole (phasic).
Dependent on:
• Arterial pressure
• Intraventricular pressure
• Coronary sinus / RAP
• CorPP changes during sysole and diastole
Left Ventricle Right Ventricle
Systole CorPP = aortic systolic P –
LV systolic P
=120 – 120
= 0mmHg
= aortic sys P – RV
sys P
= 120 – 25
= 75mmHg
Diastole CorPP aortic dias P – LV
dias P
= 80 – 5
= 75mmHg
aortic dias P – RV
dias P
= 80 – 5
= 75mmHg

36. Perfusion time (diastolic time)
• Most of coronary flow occurs during diastole
• Flow is rate dependent → i.e. ↑HR → ↓diastolic
time → ↓CorBF
Coronary Vascular resistance
 External compression
Calibre of vessels ↓with ↑intraventricular pressure which
compresses the vessels overlying it → interrupt flow
 Intrinsic regulation
 Local metabolites
 Endothelial factors
 Neural factors (esp. sympathetic nervous system)

37. Coronary autoregulation
• Ability of the organ to regulate their own blood supply as per
metabolic need by constricting or dilatation of blood vessels
using vasoactive substance
• If there is sudden change in aortic pressure, coronary vascular
resistance will adjust itself proportionally within few seconds;
so that a constant blood flow is maintained.
• Range of autoregulation: 60 – 140 mmHg of MAP.
• The myocardial oxygen tension and presence of
vasoconstrictors or vasodilators influence the range of coronary
autoregulation

38. Coronary Autoregulation
• Myocardial muscle cell - produces byproducts of aerobic
metabolism (lactate,adenosine, etc)
• Vascular endothelial cell (arteriole) - reacts to metabolic
byproducts
• Vascular smooth muscle cell (arteriole) - signaled by endothelial
cell to contract (vessel constriction) or relax (vessel dilation)
Involves 3 different cells

39. Mechanism:
Myogenic response: an increase in passive stretch, caused by
increased perfusion pressure, causes active smooth muscle
contraction.
Chemical theory:
• ↑metabolite production (↑pCO2, ↑K+, ↑H+, ↓pH, ↓pO2,
adenosine ) → vasodilation of coronary vessels via release of
vasoactive substances (1° NO, prostacyclin)
o This is most important controlling factor of vessel size

40. Endothelium derived relaxation factor (EDRF):
• Hypoxia, ADP, VIP, muscular exercise (increase distention
force), stimulate vascular endothelium to secrete EDRF, which
is a potent vasodilator, that causes coronary dilatation and
increase CBF.

41. Autoregulators
• Other endothelial- derived factors
contribute to autoregulation
 Dilators include:
EDRF (NO)
Prostacyclin
Bradykinin
 Constrictors include:
Endothelin-1
thromboxane A2

42. Other factors influencing the
vascular resistance
Myocardial metabolism
• Vasomotor tone is almost exclusively determined by local metabolic oxygen
demand.
• Pre-capillary sphincters are relaxed and more capillaries recruited.
Hypoxia
Release
adenosine
Coronary
vasodilatation
opens ATP-
sensitive
potassium
channels

43. Neural control:
Direct effect:
• Parasympathetic: vagus has very slight distribution to coronary, so its
stimulation has slight dilator effect.
• Sympathetic: Both alpha and Beta receptors exist in the coronary vessels.
Sympathetic stimulation causes slight direct coronary constriction.
Indirect effect:
• Plays a far more important role in normal control of coronary blood flow than
the direct. Sympathetic stimulation increase both heart rate and myocardial
contractility, as well as its rate of metabolism leading to dilatation of coronary
blood vessels. The blood flow increase proportional to the metabolic need of
heart muscle

44. Humoral control
• Peptide hormones like antidiuretic hormone, atrial natriuretic
peptide, vasoactive intestinal peptide, and calcitonin gene-
related peptide require an intact vascular endothelium.
• Antidiuretic hormone in physiological concentration has little
effect on the coronary circulation but causes vasoconstriction
in stressed patients.
• Other peptides cause endothelium-mediated vasodilatation.
• Angiotensin II causes coronary vasoconstriction by releasing
endothelin, the strongest vasoconstrictor peptide in humans
• Angiotensin-converting enzyme inactivates bradykinin, a

45. Vascular endothelium
• Final common pathway regulating vasomotor tone.
• It modulates the contractile activity of the underlying smooth
muscle through synthesis and secretion of vasoactive
substances in response to blood flow, circulating hormones
and chemical substances.
• Vasorelaxants are endothelium-derived relaxing factor, nitric
oxide, prostacyclin and bradykinin.
• Vasoconstrictors include endothelin and thromboxane A2. The
net response depends on the balance between the two
opposing groups

46. REFLEX CONTROL
• Anrep’s reflex: Increased venous return causes increased
pressure in right atrium, leading to reflex increase in CBF e.g.
during muscular exercise.
• Gastro-coronary reflex: Distention of the stomach with heavy
meal causes reflex vasoconstriction of coronary blood vessels
decreasing CBF.

47. Intrinsic Cardiac Conduction System
Approximately 1% of cardiac muscle cells are autorhythmic
rather than contractile
70-80/min
40-60/min
20-40/min

48. Electrical Signal Flow - Conduction Pathway
• Cardiac impulse originates at SA
node
• Action potential spreads throughout
right and left atria
• Impulse passes from atria into
ventricles through AV node (only point
of electrical contact between
chambers)
• Action potential briefly delayed at AV
node (ensures atrial contraction
precedes ventricular contraction to
allow complete ventricular filling)
• Impulse travels rapidly down
interventricular septum by means of
bundle of His
• Impulse rapidly disperses throughout
myocardium by means of Purkinje
fibers
• Rest of ventricular cells activated by cell-
to-cell spread of impulse through gap
junctions

49. Electrical Conduction in Heart
•
THE CONDUCTING SYSTEM
OF THE HEART
AV node
Purkinje
fibers
Bundle branches
A-V bundle
AV node
SA node
Internodal
pathways
SA node depolarizes.
Depolarization spreads
more slowly across
atria. Conduction slows
through AV node.
Depolarization wave
spreads upward from
the apex.
4 Depolarization moves
rapidly through ventricular
conducting system to the
apex of the heart.
5
3
2 Electrical activity goes
rapidly to AV node via
internodal pathways.
1
4
5
3
2
Atria contract as single unit followed after brief delay
by a synchronized ventricular contraction
1
SA node
Purple shading in steps 2–5 represents depolarization.

50. Electrical Conduction
• SA node - 75 bpm
– Sets the pace of the heartbeat
• AV node - 50 bpm
– Delays the transmission of action
potentials
• Purkinje fibers - 30 bpm
– Can act as pacemakers under some
conditions

51. Intrinsic Conduction System
• Autorhythmiccells:
–
–
–
–
Initiate action potentials
Have “drifting” resting potentials called pacemaker potentials
Pacemaker potential - membrane slowly depolarizes “drifts” to
threshold, initiates action potential, membrane repolarizes to -60
mV.
Use calcium influx (rather than sodium) for rising phase of the
action potential

52. Pacemaker Potential
•
•
•
•
•
•
Decreased efflux of K+, membrane permeability decreases between APs, they slowly close at
negative potentials
Constant influx of Na+, no voltage-gated Na + channels
Gradual depolarization because K+ builds up and Na+ flows inward
As depolarization proceeds Ca++ channels (Ca2+ T) open influx of Ca++ further depolarizes to
threshold (-40mV)
At threshold sharp depolarization due to activation of Ca2+ L channels allow large influx of
Ca++
• Falling phase at about +20 mV the Ca-L channels close, voltage-gated K channels open,
repolarization due to normal K+ efflux
At -60mV K+ channels close

53. AP of Contractile Cardiac cells
– Rapid depolarization
– Rapid, partial early
repolarization,
prolonged period of
slow repolarization
which is plateau phase
– Rapid final
repolarization phase
PX = Permeability to ionX
+20
-20
-40
-60
-80
-100
Membranepotential
(mV)
0
0 100 200 300
Time (msec)
PK and PCa
PNa
PK and PCa
PNa
Membrane channels
Na+ channels open
Na+ channelsclose
Ca2+ channels open; fast K+ channelsclose
Ca2+ channels close; slow K+ channels open
Resting potential
1
2
30
4 4
Phase
0
1
2
3
4

54. AP of Contractile Cardiac cells
• Action potentials of
cardiac contractile cells
exhibit prolonged
positive phase (plateau)
accompanied by
prolonged period of
contraction
– Ensuresadequate
ejection time
– Plateau primarily due to
activation of slow L-type
Ca2+channels

55. Why A Longer AP In Cardiac Contractile Fibers?
•
•
•
We don’t want Summation and tetanus in our myocardium.
Because long refractory period occurs in conjunction with
prolonged plateau phase, summation and tetanus of cardiac
muscle is impossible
Ensures alternate periods of contraction and relaxation which are
essential for pumping blood

56. Refractory period

57. Membrane Potentials in SA Node and Ventricle

58. Action Potentials

59. Excitation-Contraction Coupling in Cardiac Contractile
Cells
• Ca2+entry through L-type channels in T
tubules triggers larger release of Ca2+from
sarcoplasmic reticulum
– Ca2+induced Ca2+release leads to cross-bridge
cycling and contraction

60. Cardiac cycle

61. CarlJohn
Wiggers
Sir Thomas
Lewis
Otto
Frank
Ernest H

62. Introduction
Principal function of cardiovascular system is to deliver oxygen
and nutrients to and remove carbon dioxide and wastes from
metabolizing tissues.
It is by two specialized circulations in series
1.a low resistance pulmonary driven by right heart
2.a high resistance systemic driven by left heart
Systolic pressure in the vascular system refers to the
peak pressure reached during the systole,not the mean
pressure.
The diastolic pressure refers to the lowest pressure during
diastole.

64. Normal values
PRESSURES (mm Hg)
Right atrium mean 0-5
a wave 1-7
v wave 1-7
Right ventricle peak systolic/end diastolic 17-32/1-7
Pulmonary artery peak systolic/end diastolic 17-32/1-7
mean 9-19
PCWP 4-12
LA mean 4-12
a wave 4-15
v wave 4-15
LV peak systolic/end diastolic 90-140/5-12
Aorta peak systolic/end diastolic 90-140 /60-90
mean 70-105
Resistance (dynes/cm2) SVR 900-1400
PVR 40-120
Oxygen consumption index (L-min/m2) 115-140
Cardiac index (L-min/m2) 2.8-4.2

65. Wiggers diagram
The X axis is used to plot time,
The Y axis contains all of the following on a single grid:
Blood pressure
Aortic pressure
Ventricular pressure
Atrial pressure
Ventricular volume
Electrocardiogram
Arterial flow (optional)
Heart sounds (optional)
JVP
Illustration of the coordinated events makes it easier to correlate
the changes during the cardiac cycle.

70. Cardiaccycle
• The cardiac cycle describes pressure,volume and flow
phenomena in the ventricles as a function of time.
• Similar for both LV and RV except for the timing,levels of
pressure.

72. Mechanical events in Cardiac cycle
• Systole
• Isovolumic contraction
• Maximal ejection
• Reduced ejection
• Diastole
• Isovolumic relaxation
• Rapid filling phase
• Slow filling phase /diastasis
• Atrial systole

73. • The letters are arbitrarily allocated so that atrial systole(a) coinicides with the a wave and (c ) with the c wave of JVP.
• Isovolumic
contraction(b)
• Maximal
Ejection( c)
LV
CONTRACTION
• Isovolumic
relaxation(e)
• Start of relaxation and
reduced ejection (d)
LV
RELAXATION
• Rapid phase(f)
• Slow filling
(diastasis)(g)
• Atrial systole or
booster(a)
LVFILLING

74. LVcontraction
• Actin myosin contraction triggered by arrival of Calcium ions at
contractile proteins.
• ECG – peak of R wave
• LVpressure >LA pressure (10-15mm Hg)
• Followed approx. 50msec by M1.
• Delay of M1 – inertia of the blood flow – valve is kept open.
• Isovolumic contraction as volume is fixed.
• Increased pressure as more fibers enter contractile state.
• LVpressure >Aorta – Aortic valve opens – silentevent
clinically.

76. • Phase of rapid ejection:
• Pressure gradient across the aortic valve
• Elastic properties of aorta,arterial tree (systolic expansion)
• LVpressure rises to peak and then falls.

78. LVrelaxation
• Activated phospholamban causes calcium transfer into SR.
• Decreases contractile apparatus function – phase of reduced ejection –
blood flow from LVto aorta decreases but maintained by aortic recoil
– WINDKESSEL EFFECT*.
• Aortic valve closes as LVpressure drops
• Isovolumic relaxation
• Mitral valve opens – clinically silent event.
† Giovanni Borelli,Stephen Hales,Fick(mathematical foundation).
†WINDKESSEL in german AIRCHAMBER or elastic resorvoir.

79. LVfilling
• Rapid filling phase – active diastolic relaxation of LV.
• LA- LV pressures equalize - diastasis.
• LA booster atrial systole – important in exercise and LVH.
• First phase of diastole –isovolumic phase – no ventricular
filling.
• Most of ventricular filling –rapid filling phase.
• Diastasis -5%
• Final atrial booster phase -15%.
• The sucking effect of ventricle – myosin is pulled into the
space between the two anchoring segments of titin.
• Dominant backward pressure wave –diastolic coronary
filling.

82. Physiologicsystole,diastole
• It is related to the events occuring at the cellular level ,by
change of pressure and the electrical events.
• Physiological systole –start of isovolumic contraction to the
peak of ejection phase.
• Physiological diastole – commences as pressure falls.
• Fits well in pressure volume curve .

83. Cardiological systole,diastole
• It is related to the valve closures.
• Systole – M1-A2
• Thereby starts later than physiological systole and ends later.
• Diastole –A2-M1

85. Protodiastole
• Proto –means original,first
• The period of start of ventricular relaxation.
• Lasts until the semilunar valves are closed.
• It is 0.04 sec.

88. Pressure volumeloop
• Best of the current approaches to the assessment of the
contractile behaviour of the intact heart.
• Es,the pressure – volume relationship .
• Changes in the slope of this line joining the different Es points
are generally good load independent index of the contractile
performance of the heart.
• Enhanced inotropic effect, Es shifted upward and to the left.
• Lusitropic effect shifted Es downward and to right.
• The P-V relationship is linear in smooth muscle,curvilinear in
cardiac muscle(exponential).

90. Determinants of Ventricular Performance
• Cardiac output (CO) is the product of heart rate
(HR) and stroke volume (SV):
CO = HR x SV
• Stroke volume is determined by three main
factors: preload, afterload and contractility.
• Preload is the ventricular volume at the end of
diastole.

91. Starling's law of the heart.
• The relationship
between ventricular
end-diastolic volume
and stroke volume is
known as Starling's
law of the heart.
• An increase in
preload (end-diastolic
volume) increases
stroke volume.

92. Determinants of Ventricular Performance
• Afterload is the resistance to ventricular ejection.
This is caused by the resistance to flow in the
systemic circulation and is the systemic vascular
resistance.
– Is affected mainly by:
• ventricular volume (size)
• arterial vasomotor tone (arterial resistance)
• ventricular wall thickness
– Afterload is increased by:
• increase in ventricular volume
• increase in arterial vasomotor tone
• decrease in ventricular wall thickness
– Afterload is decreased by the opposite changes

93. Determinants of Ventricular Performance
• Contractility describes the ability of the myocardium to
contract in the absence of any changes in preload or
afterload.
• In the sympathetic nervous system, Beta-adrenergic
receptors are stimulated by noradrenaline released from
nerve endings, and contractility increases.
• A similar effect is seen with circulating adrenaline and
drugs such as ephedrine, digoxin and calcium.
• Contractility is reduced by acidosis, myocardial ischemia,
and the use of beta-blocking and anti-arrhythmic agents.