The document discusses cardiovascular physiology, specifically describing the cardiac cycle and regulation of blood pressure. It contains the following key points: 1. The cardiac cycle consists of ventricular systole and diastole. Systole includes isovolumic contraction, rapid ejection, and slow ejection phases. Diastole includes isovolumic relaxation and three filling phases. 2. Blood pressure is regulated rapidly by baroreceptor and chemoreceptor reflexes, and over longer periods by the renin-angiotensin-aldosterone system. 3. Factors like preload, contractility, and afterload influence stroke volume and thus cardiac output according to Frank-Starling's law.

1. CARDIOVASCULAR
PHYSIOLOGY

4. INTERCALATED DISC

9. Cardiovascular system
Physiology

23. • Ventricular systole (0.3 s)
• 1. Isovolumic (isometric) contraction phase (0.05 s) and
• 2. Phase of ventricular ejection
• rapid ejection phase (0.1 s) and
• slow ejection phase (0.15s)

24. Ventricular diastole (0.5 s) consisting of:
• 1. Protodiastole (0.04 s),
• 2. Isovolumic (isometric) relaxation phase (0.06 s),
• 3. Rapid passive filling phase (0.11 s),
• 4. Reduced filling phase or diastasis (0.19 s) and
• 5. Last rapid filling phase which coincides with the atrial systole (0.1 s).

29. VENTRICULAR SYSTOLE

30. ISOVOLUMETRIC CONTRACTION
• closure of AV valves(S1)  opening of semilunar valve
• 0.05 seconds
• This phase lasts for 0.05 s, until the pressure in the left and right
ventricles exceeds the pressure in the aorta (80 mm Hg) and
pulmonary artery (10 mm Hg) and the aortic and pulmonary
valves open
• pressure inside the ventricles rises rapidly to a high level
• bulging of AV valves into the atria producing a small but sharp rise
in the intra-atrial pressure called c-wave in JVP
• Volume remains same (d/t closed semilunar & AV valves )

31. Phase of ventricular ejection
• begins with the opening of semilunar valves and lasts for about 0.25 s
Rapid ejection (0.10sec) Slow ejection (0.15sec)
• 2/3rd of blood ejected
• Contraction of ventricles AV ring
pulled down Stretching of atrial
muscles  dilation of ventricle  X
DESCENT IN JVP
• 1/3rd of blood ejected

32. Phase of ventricular ejection
• The right ventricular ejection begins before that of left and continued
even after left ventricular ejection is complete.
• Aortic valve closes before pulmonary valve
• As both the ventricles almost eject same volume of blood, the
velocity of right ventricular ejection is less than that of the left
ventricle

33. Volume changes in systole
• At the end of each diastole, the ventricular volume is about 130 mL.
This is called end-diastolic volume.
• About 80 mL of blood is ejected out by each ventricle during each
systole. This is called stroke volume.
• Thus, about 50 mL of the blood is left in each ventricle at the end of
systole. This is called end-systolic volume.

34. Ventricular diastole

35. Protodiastole
• ventricles start relaxing and
intraventricular pressure falls rapidly
• the elevated pressure in the distended
arteries (aorta and pulmonary artery)
immediately pushes the blood back
towards ventricles closure of
semilunar valves (S2)
• dicrotic notch in the down slope of aortic
pressure curve called the incisura
• AORTIC VALVE CLOSES BEFORE
PULMONARY VALVE

36. Isovolumetric relaxation
• closure of the semilunar valves AV
valves opening
• 0.06 sec
• causes rapid fall of pressure inside the
ventricles (from 80 mm Hg to about
2−3 mm Hg in the left ventricle)
• AV valves open peak of v-wave on
the atrial pressure tracing

37. Rapid passive filling phase (0.11 s)
• AV valves open, the high atrial pressure rapid, initial flow of blood
into the ventricles.
• rapid passive filling phase third heart sound (S3)
•  Y WAVE IN JVP

38. Reduced filling and diastasis (0.19 s)
• DIASTASIS
• pressure in the atria and ventricles reduces slowly and remains little
above zero.
• This decreases the rate of blood flow from the atria to ventricle
causing a very slow filling called diastasis

39. Last rapid filling phase (0.1 s)
• Coincides with the atrial systole
• SHARP RISE IN JVP D/T ATRIAL SYSTOLE  A WAVE

44. CARDIAC INDICES
• ELECTROMECHANICAL QS2
• LEFT VENTRICULAR EJECTION TIME
(LVET)
• PRE EJECTION SYSTOLE (PEP)

45. ELECTROMECHANICAL QS2
• TIME INTERVAL B/W ONSET OF QRS
COMPLEX (ventricular activation ) &
CLOSURE OF AORTIC VALVE(S2)
• CALCULATED BY ECG &
PHONOCARDIOGRAM

46. LVET
• time interval b/w opening &
closure of aortic valve
• REQUIRES ONLY CAROTID
PULSE RECORDING

47. PRE EJECTION SYSTOLE
• DIFFERENCE B/W QS2 & LVET
• EVENTS PRECEDING SYSTOLIC EJECTION
• REQUIRES ALL 3 RECORDING
• ECG
• PHONOCARDIOGRAM
• CAROTID PULSE

48. • NORMAL PEP/ LVET = 0.35

49. AORTIC PRESSURE CURVE

50. AORTIC PRESSURE CURVE
• PRESSURE IN AORTA
VARIES B/W 80mmHg to
120 mmHg
• NOTCH IN EARLY PART
OF DOWNSTROKE 
INCISURA
• D/T CLOSURE OF AORTIC
VALVE

53. PRESSURE VOLUME LOOP

58. Loop is shifted to left contractility is increased &
compliance is decreased
Loop is shifted to right  volume overload
• Sympathetic stimulation
• Pressure overload
• Concentric hypertrophy
• MR
• AR

59. JVP

60. Right IJV is used for measuring JVP

68. duration Frequency Relation with
ECG
RELATION WITH
JVP
S1 0.15 24-45 Hz Closure of AV
valve @
beginning of
ventricular
systole
Lateral half of R
wave of QRS
S2 0.12 50 Hz Closure of
semilunar valve
@ end of
ventricular
systole
lateral half of T
wave
S3 0.1 Low pitched Vibration in
ventricles d/t
rapid filling
Between T & P
wave
Y WAVE
S4 0.1 <20 Hz Last rapid filling
phase by atrial
systole
Following P
wave

73. Cardiac output

74. • Cardiac output = stroke volume * HR

76. Measurement of CO
• Methods based on Fick’s principle
• Indicator or dye dilution method
• Thermodilution method
• Doppler technique echocardiography

77. • Pulmonary blood flow/min= right ventricular output.
• Right ventricular output = left ventricular output (cardiac output).

78. Ficks principle

80. Dye indicator method
• Based on stewart Hamilton principle

82. Cardiac reserve
• Maximum percentage above which CO can increase above normal
• 300-400 percent

85. Factors affecting stroke volume
Preload Contractility Afterload

86. preload
• Frank starling law
• “energy of contraction is proportional to the initial length of the cardiac
muscle fber” (Starling’s law of the heart or the Frank-Starling law).

87. • CO regulated by changes in changes
in cardiac muscle fber length
• Frank starling law
Heterometric
regulation
• regulation due to changes in
contractility independent of lengthHomometric
regulation

88. Increased stroke volume Decreased stroke volume
• Increased total blood volume
• Increased venous tone
• Increased pumping action of skeletal muscle
• Increased negative intrathoracic P
• Sympathetic discharge causing decrease in venous
capacitance by decreasing venous compliance
• Lying down
• Decreased total blood volume
• Decreased venous tone
• Decreased pumping action of skeletal muscle
• Less negative or positive intrathoracic P
• Sitting or standing

89. Contractility of ventricle
Increased contractility Decreased contractility
• Catecholamine's
• Digoxin
• Xanthine
• Hypoxia
• Hypercapnia
• Heart failure
• MI

90. Increased contractility  shift to left

91. decreased contractility  shift to left

92. Frank
starling law
&
contractility

93. postextrasystolic potentiation
• independent of ventricular filling, since it occurs in isolated cardiac
muscle and is due to increased availability of intracellular Ca2+

94. Afterload
• Depends on MAP which depends on TPR
• Decreased peripheral resistance
• Wet beri beri
• Thyrotoxicosis
• Exercise
• AV fistula
• Severe anemia

95. BP

96. Auscultatory gap

100. • Length :width ratio = 2:1

101. Riva rocci cuff

103. MAP 
mean
arterial
pressure

105. • Intraarterial P is always higher than sphygmomanometer

106. Regulation of blood pressure
Rapidly acting (seconds to
minutes)
Intermediate acting (few minutes
to hours)
Long term mechanism (3-10 days)
• Baroreceptor (BP is b/w 70-170
mmHg)
• Chemoreceptor (<80mmHg)
• CNS ishemic response (when
BP<40mmHg)
• Hormonal release
 ADH
 Angiotensin II
• Capillary fluid shift mechanism
• Stress relaxation & reverse
stress relaxation
• Renin fluid conservation
mechanism
• RAAS sytem

107. • Most rapidly acting
• Baroreceptor reflex >> chemoreceptor reflex

108. Baroreceptor reflex
• carotid sinus and aortic arch
receptors

112. Baroreceptor reflex Chemoreceptor refelx
Receptor location Carotid sinus & aortic arch wall Carotid body and aortic body
Stimulated by Increased stretch Hypoxia hypercapnia acidosis
Afferent • IX
• X
• IX
• X
Efferent Sympathetic & parsympathetic Sympathetic & parsympathetic
Main response • Decrease in BP when
stimulated
• Increase ventilation

114. Regional circulation

117. Cerebral circualtion

118. Cerebral circulation
• No reserve fuels in brain
• Glucose continuously supplied through blood
• During starvation brain uses ketone bodies

119. Brain circulation
• 750ml /min
• 54ml/100g/min

120. • Autoregulation present.
• Factors regulating cerebral blood flow (CBF):
• a.Inc. pCO_2 & dec. pO_2 cause vasodilatation & vice versa
• b.Cerebral metabolism rate
• c.Cerebral perfusion pressure: Mean arterial pressure – intracranial pressure
• d.Blood viscosity
• e.Temperature: Fall in temp. by 1^o C decrease CBF by 5-7%

121. Autoregulation of cerebral blood flow

122. Autoregulation
• autoregulation maintains a normal cerebral blood flow at arterial
pressures of 65–140 mm Hg.

123. Metabolic regulation of cerebral blood flow