ancillary factors venous pooling may significantly reduce …. cardiac output part...– venous...

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1 Ancillary Factors Ancillary Factors Affect the Venous System and Cardiac Output • Gravity – Venous pooling may significantly reduce CO Muscular Activity and Venous Valves Respiratory Activity 4/18/12 badri@GMC 79 4/18/12 badri@GMC 80 Venous return depends on how much blood returns to the heart, which is… affected by: blood volume, venous pressure and intrathoracic pressure What effect will increased venous return have on EDV? 4/18/12 badri@GMC 81 Gravity Gravity acts on vascular volume Mostly venous due to high compliance Preload decreases CO and arterial pressure fall Baroreceptor reflex HR increases Vasoconstriction 4/18/12 badri@GMC 82 Effects of Gravity on the Venous System and Cardiac Output • Gravity – Venous pooling may significantly reduce CO 4/18/12 badri@GMC 83

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Page 1: Ancillary Factors Venous pooling may significantly reduce …. cardiac output part...– Venous pooling may significantly reduce CO ... Mean Arterial Pressure . 9 ... • What#effect#will#hypertension#have#on#stroke#

1

Ancillary Factors

Ancillary Factors Affect the Venous System and Cardiac Output

•  Gravity – Venous pooling may significantly reduce CO

•  Muscular Activity and Venous Valves

•  Respiratory Activity

4/18/12 badri@GMC 79

4/18/12 badri@GMC 80

Venous  return  depends  on  how  much  blood  returns  to  the  heart,  which  is…  affected  by:  • blood  volume,  • venous  pressure  and    • intrathoracic  pressure  

•  What  effect  will  increased  venous  return  have  on  EDV?  

4/18/12   badri@GMC   81  

Gravity o  Gravity acts on vascular volume

n  Mostly venous due to high compliance n  Preload decreases n  CO and arterial pressure fall n  Baroreceptor reflex

o  HR increases o  Vasoconstriction

4/18/12 badri@GMC 82

Effects of Gravity on the Venous System and Cardiac Output

•  Gravity – Venous pooling may significantly reduce CO

4/18/12 badri@GMC 83

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2

Effect Of Gravity on Venous Pressure

4/18/12 badri@GMC 84 4/18/12 badri@GMC 85

4/18/12 badri@GMC 86

Skeletal Muscle Pump (Increase Venous Return)

4/18/12 badri@GMC 87

Muscular Activity and Venous Valves

4/18/12 badri@GMC 88

Effect of Venous Valves

4/18/12 badri@GMC 89

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3

Effects of Respiration •  Spontaneous respiration

–  Decreased intra-thoracic pressure results in a decreased right atrial pressure which enhances venous return

•  Mechanical ventilation –  Increased intra-thoracic pressure during positive-pressure lung

inflation causes increased right atrial pressure which decreases venous return

•  Valsalva Maneuver –  Causes a large increase in intra-thoracic pressure which impedes

venous return to the right atrium

4/18/12 badri@GMC 90

Increase Pleural Negative Pressure (Increase Venous Return)

4/18/12 badri@GMC 91

10

5

0

CA

RD

IAC

OU

TPU

T (L

/min

)

RIGHT ATRIAL PRESSURE (mmHg)

-4 0 4 8 12

15

IPP=

-4m

mH

g

IPP=

-2m

mH

g

IPP = INTRAPLEURAL PRESSURE

IPP=

-5.5

mm

Hg

IPP=

2m

mH

g

CARDIAC TAMPONADE

4/18/12 badri@GMC 92

•  Intrathoracic  pressure  (which  decreases  during  inspira;on  and  increases  during  expira;on)  inversely  affects  venous  return.  

•  What  effect  will  inhaling  more  deeply  have  on  venous  return?  

4/18/12   badri@GMC   93  

•  Blood  volume  and  venous    pressure  (which  increases  during  venoconstric;on  [constric;on  of  the  veins])  directly  affect  venous  return.  

•  What  effect  will  blood  loss  have  on  EDV?  

4/18/12   badri@GMC   94   4/18/12 badri@GMC 95

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4

Factors that Facilitate Venous Return

4/18/12 badri@GMC 96 4/18/12 badri@GMC 97

4/18/12 badri@GMC 98 4/18/12 badri@GMC 99

4/18/12 badri@GMC 100 4/18/12 badri@GMC 101

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5

4/18/12 badri@GMC 102

Plateau of CO curve determined by heart strength (contractility + ↑HR) ↑ Sympathetics ⇒ ↑ plateau

↓ Parasympathetics (HR↑) ⇒ (? plateau) ↑ Plateau Heart hypertrophy ⇒↑’s plateau Myocardial infarction ⇒ (? plateau) ↓ Plateau

The Cardiac Output Curve

4/18/12 badri@GMC 103

NORMAL

HYPEREFFECTIVE

-4 0 +4 +8

25

20

15

10

5

0

CA

RD

IAC

OU

TPU

T (L

/min

)

RIGHT ATRIAL PRESSURE (mmHg)

HYPOEFFECTIVE

CARDIAC OUTPUT CURVES

4/18/12 badri@GMC 104

•  Valvular disease ⇒ ↓ plateau (stenosis or regurgitation)

•  Myocarditis ⇒ ↓ plateau •  Cardiac tamponade ⇒ (? plateau) ↓ Plateau •  Metabolic damage ⇒ ↓ plateau

The Cardiac Output Curve (cont’d)

4/18/12 badri@GMC 105

4/18/12 badri@GMC 106

Cardiac and Vascular function curves o  Point of equilibrium à predicts cardiac

output and central venous pressure o  Steady state of this particular system

4/18/12 badri@GMC 107

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6

4/18/12 badri@GMC 108

25

20

15

10

5

0

CA

RD

IAC

OU

TPU

T A

ND

VE

NO

US

RE

TU

RN

(L/m

in/m

)

RIGHT ATRIAL PRESSURE (mmHg)

-4 0 4 8 12 16

NORMAL CARDIAC

VR CURVE NORMAL

SPINAL ANESTHESIA

SPINAL ANESTHESIA

MAXIMAL SYMPATHETIC STIMULATION

SYMPATHETIC STIMULATION

MAX

Copyright © 2006 by Elsevier, Inc. 4/18/12 badri@GMC 109

Changes in contractility o  Digoxin:

n  inhibits Na-K ATPase n  Ca++ builds up

Ejection fraction is an indicator of contractility

EF= SV/EDV

4/18/12 badri@GMC 110 4/18/12 badri@GMC 111

4/18/12 badri@GMC 112

Changes in volume: mean systemic pressure

o  Decreased blood volume o  Decreased venous compliance

4/18/12 badri@GMC 113

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4/18/12 badri@GMC 114 4/18/12 badri@GMC 115

Changes in Total Peripheral Resistance o  Constrict arterioles

n  Increased afterload n  Decreased venous return

4/18/12 badri@GMC 116 4/18/12 badri@GMC 117

4/18/12 badri@GMC 118

Pressure-Volume Loop o  ↑Preload o  ↑Afterload o  ↑Contractility

4/18/12 badri@GMC 119

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Pressure-Volume Loop o  ↑Preload o  ↑Afterload o  ↑Contractility

4/18/12 badri@GMC 120

Pressure-Volume Loop o  ↑Preload o  ↑Afterload o  ↑Contractility

4/18/12 badri@GMC 121

Pressure-Volume Loop o  ↑Preload o  ↑Afterload o  ↑Contractility

4/18/12 badri@GMC 122

Sympathetic and parasympathetic control o  Sympathetic

n  Stimulate: increase HR and increase vasoconstriction

n  Inhibit: decrease HR and decrease vasoconstriction

o  Parasympathetic (vagus) n  Stimulate: decreases HR

and causes vasodilation

4/18/12 badri@GMC 123

⇧ Stroke Volume = EDV-ESV

⇧ End Diastolic Volume

⇧ Preload

⇩ End Systolic Volume

⇩ Afterload

⇧ Contractility

4/18/12 badri@GMC 124

Summary of Factors That Influence

Cardiac Output and

Mean Arterial Pressure

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4/18/12 badri@GMC 126

Control of Cardiac Output

4/18/12 badri@GMC 127

Factors that affect the Cardiac Output

4/18/12 badri@GMC 128

Cardiac  Output  Concept  Map  

4/18/12   badri@GMC   129  

4/18/12   badri@GMC   130  

Myocardial Oxygen Consumption

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10

Myocardial Oxygen Consumption

•  Oxygen consumption is defined as the volume of oxygen consumed per minute (usually expressed per 100 grams of tissue weight)

4/18/12 badri@GMC 132

Myocardial Oxygen Demand is Related to Wall Stress

•  LaPlace’s Law

hPr

∝σ

Wall Stress

P

r

Wall Stress

h

4/18/12 badri@GMC 133

Factors Increasing Myocardial Oxygen Consumption

•  Increased Heart Rate •  Increased Inotropy (Contractility) •  Increased Afterload •  Increased Preload

–  Changes in preload affect myocardial oxygen consumption less than do changes in the other factors

4/18/12 badri@GMC 134

Magnitude & Distribution of CO at Rest & During Moderate Exercise

4/18/12 badri@GMC 135

In  Summary…  

•  Heart  rate  and  stroke  volume  are  the  two  factors  that  determine  cardiac  output.  

•  Each  of  these  is  affected  by  many  factors.  •  Chronotropic  agents  affect  heart  rate  while  inotropic  agents  affect  contrac;lity,  which  affects  stroke  volume.  

•  Some  factors  (e.g.,  epinephrine  and  norepinephrine)  affect  both.  

4/18/12   badri@GMC   136  

Shift to the right and downwards of the (Frank-Starling )curve

by heart failure

Normal stroke volume

Decrease in stroke volume

Stroke volume with uncompensated heart failure Normal end-diastolic volume

Normal heart

Failing heart

4/18/12   badri@GMC   137  

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11

Answers  to  Ques;ons  •  If  HR  increases,  what  will  happen  to  cardiac  output  -­‐Cardiac  output  increases.  •  If  SV  decreases,  what  will  happen  to  cardiac  output?  

-­‐Cardiac  output  is  expected  to  decrease  (note  that  heart  rate  can  be  increased  to  compensate).  •  What  effect  will  sympathe>c  nerve  impulses  have  on  heart  rate?  

-­‐The  norepinephrine  released  will  increase  heart  rate.  •  What  effect  will  parasympathe>c  nerve  impulses  have  on  heart  rate?    

-­‐The  ACh  released  will  decrease  heart  rate.  4/18/12   badri@GMC   138  

Answers  to  Ques;ons  

•  What  effect  will  increased  heart  rate  have  on  stroke  volume  (if  other  factors  stay  the  same)?  

 Stroke  volume  will  increase  to  some  extend  and  if  further  increases  will  lead  to  reduced  filling  ;me  and  SV  will  decrease  (note  that  SV  may  be  maintained  if  the  cause  of  the  increased  heart  rate  also  increases  contrac;lity).    •  What  effect  will  increased  venous  return  have  on  EDV?  EDV  will  increase.  •  What  effect  will  blood  loss  have  on  EDV?    EDV    will  decrease  (note  that  the  body  has  compensatory  mechanisms  to  ini;ally  maintain  SV  when  blood  is  lost).  

4/18/12   badri@GMC   139  

Answers  to  Ques;ons  

•  What  effect  will  inhaling  more  deeply  have  on  venous  return?  

 Venous  return  will  increase  because  deeper  inhala;on  lowers  thoracic  pressure  more  than  normal.  •  What  effect  will  epinephrine  have  on  stroke  volume?  

Stroke  volume  will  increase  due  to  the  increased  contrac;lity.  

4/18/12   badri@GMC   140  

Answers  to  Ques;ons  

•  What  effect  will  blocking  calcium  channels  have  on  stroke  volume?  

   Stroke  volume  will  decrease.  •  What  effect  will  hypertension  have  on  aGerload?      AQerload  will  increase.    •  What  effect  will  hypertension  have  on  stroke  volume?    

Stroke  volume  will  decrease  (and  the  heart  will  have  to  work  harder  to  eject  blood).  

4/18/12   badri@GMC   141  

The End