Univentricular circulation

Mar 6, 2018Download as pptx, pdf

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This document discusses cardiovascular physiology concepts related to cardiac output, blood flow distribution, and oxygen delivery and utilization in the body. It covers topics like the factors that affect cardiac output, regional resistance factors, blood flow redistribution, and the relationships between cardiac output, blood flow ratios in the pulmonary and systemic circulations, oxygen saturation levels, and oxygen delivery. The key ideas are that optimal oxygen delivery occurs at a pulmonary to systemic flow ratio of 1, with the lowest total cardiac output, and that subtle imbalances can significantly impact oxygen saturation and delivery levels.

Healthcare

 Cardiac output affected by
 Preload
 Afterload
 Rate
 Rhythm
 Contractility
 AP shunts
 Regional Resistance
 Neurohumoral Factors (Inflammation, sympathetic
nervous system)
 Local Factors (Autoregulation)

 Redistribute Blood flow to brain and heart
 Mesentric and splanchnic circulation- silent ischemia during
compensated shock
 Baroreflex - Contractility, HR, SVR & decreases venous
capacitance
 Often body impairs systemic flow in face of myocardial
dysfunction (regional ischaemia due to high SVR)
 Ischaemic organ damage can occur even in presence of normal
global oxygen economy
 Regional Ischaemia →MODS→Death

 In series/ Normal circulation Qp=Qs=Qt
 In parallel circulation Qt= Qp+Qs
 At same Qt if Qp increases, Qs Decreases and vice a versa
 Pulmonary artery = Systemic artery= SaO2
 If Qs low = Sa-vO2 is high
 If Qs High = Sa-vO2 is low

200
At Increased Qs
At decreased Qs
150
2070
50
50
100
50
50
SvO2 decreases
SvO2 increases
O2 delivered = Qs*O2 content of blood
At fixed O2 content and
at fixed O2 Extraction (suppose 50)
Oxygen delivered will depend on Qs

 Increased O2 demand:
 SvO2 reduces
 SaO2 will reduce
▪ (Vicious Cycle)
 SVR depends on many
factors

 Optimal systemic oxygen delivery occurs at
 Qp:Qs = 1 with
 lowest Qt (total cardiac output)
Fick Principle:
Equality of systemic
oxygen consumption
and pulmonary
oxygen uptake

 At Normal
extraction =25% &
SpvO2 = 100%
(No lung issue)
 Pulse ox (SaO2)=
75%
 SvO2 = 50%
 Qp:Qs = 1
75%
75%
75%
50%
100%

 At same saturation (75%)
 Any Qp:Qs is possible depending on Qt (PARRCA)
 Sa-vO2 (Extraction) = <25% : Qs high, Qp low,
Qp:Qs low at high Qt
 Sa-vO2 (Extraction) = >25% : Qs low, Qp high
Qp:Qs high at low Qt

 At same Sa-vO2: (Systemic flow is fixed)
 Any SpO2 is possible depending on Qt (PARRCA)
 If SaO2 High: Qp is high and Qp:Qs = 2 at high Qt
 If SaO2 Low: Qp is low and Qp:Qs = 0.5 at low Qt

 At same Qt (Total cardiac output)
 Any Qp: Qs can exist
 At Qp: Qs = 2
▪ Qp increases: SaO2 increases
▪ Qs reduces: Sa-vO2 increases
 At Qp:Qs = 0.5
▪ Qp decreases : SaO2 decreases
▪ Qs increases: Sa-vO2 decreases

 At same Qp:Qs = 1
 Many SpO2 are possible depending on Qt
(PARRCA)
 At high Qt :
▪ both systemic and pulmonary blood flow is high
▪ SpO2 high, SvO2 high & Sv-aO2 < 25%
 At low Qt :
▪ Both systemic and pulmonary blood flow is low
▪ SpO2 low, SvO2 low & Sv-aO2 > 25%
▪ Tissue oxygen utilization is impaired if SvO2<50%

 At constant Qt moderate alteration in Qp:Qs balance will have minimal effect on SaO2
 At fixed Qp:Qs, Increase in Qt can deliver more oxygen to tissue
 As tissue cannot utilize oxygen if SvO2<50%, so body has very less O2 reserve to maintain
increased O2 demand in parallel circulation.
 Body has more oxygen reserves at high Qt but at an expense of myocardial oxygen demand
 Another way to increase O2 delivery is by Increasing Hb

 Optimization of SaO2 alone will result in acute hemodynamic
collapse unexpectedly in an apparently stable child.

 Gas manipulation of PVR
 Inspired CO2: Increased PVR, decreased SVR, Increased O2 delivery
(esp. brain)
 Subatmospheric FiO2: Raises PVR
 Controlled PPV while avoiding hypervenilation (PEEP)
 O2 can be used if:
 Respiratory pathology is present
 Restrictive communications
 Control of elevated SVR was more effective than increasing PVR
 Inotropes increase SVR at high doses
 Inodilators preferred (while preventing significant hypotension)
 Morphine reduces Sympathetic outflow
 Regional saturations of brain, liver, kidney, gut and muscle can be
measured to rule out regional ischaemia
 Increase Hct > 50% increases O2 carrying capacity

 Pulmonary venous SpvO2 = 100%
 Variablity in Arteriovenous saturation
difference
 Not possible to obtain true sytemic venous
mixed venous saturation

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Revision Total Hip Replacement (THR) is among the most demanding procedures in orthopedic surgery. Unlike primary THR, it involves addressing pre-existing complications such as implant failure, dislocation, bone loss, or infection, often in the presence of compromised soft tissues and bone quality. While primary THR offers high success rates and reproducible outcomes, revision THR requires greater surgical expertise, meticulous planning, and personalized execution to restore function and minimize complications. This presentation by Dr. Prabhat Pandey is designed as a comprehensive resource for orthopedic surgeons, residents, and joint reconstruction teams who seek to understand and master the essential principles, decision-making algorithms, and advanced techniques used in revision THR. Revision hip arthroplasty is associated with: Increased operative time and blood loss Higher complication rates: infection, dislocation, thromboembolism, nerve injury, and periprosthetic fracture The need to manage weakened bone stock and soft tissue envelope Difficulty in removing failed implants, including intramedullary components. Revision surgery is warranted in cases of: Prosthetic dislocation or instability Mechanical loosening of components Implant wear or breakage Periprosthetic fracture Deep infection Osteolysis or bone resorption Painful loosening without overt signs of mechanical failure Each case demands tailored intervention based on the severity and combination of these factors. 3. Principles of Successful Revision THR Safe removal of loose or failed components Preservation of host bone and soft tissue integrity Effective reconstruction of bone defects using bone grafts or metal augments Achieving stability of the revision components Restoration of biomechanics, particularly the anatomical center of rotation. Dislocation rates: 0.3–10% in primary THR Up to 28% in revision THR Influencing Factors: Surgical approach Abductor muscle function Component malpositioning Patient compliance Prosthesis longevity Underlying diagnosis (e.g., hip fracture, neuromuscular disorder Revision Total Hip Replacement is not merely a technical endeavor—it is a test of surgical judgment, experience, and adaptability. Successful outcomes hinge on: Thorough preoperative assessment Judicious use of classification systems like Paprosky Proficiency in implant removal Skillful reconstruction of defects Meticulous postoperative care This presentation distills the complex decision-making process into an organized, practical guide for any surgeon facing the challenge of revision THR. Understanding Surgical Approaches and Their Risks Dislocation Types and Management Preoperative Planning Essentials Surgical Options for Instability and Revision Operative Exposure and Implant Removal Techniques for Removing Cemented Implants Cementless Implant Removal Managing Bone Deficiency in the Acetabulum Paprosky Classification: Detailed Breakdown

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Univentricular circulation

1. Dr.AbhinavAgarwal

2.  Cardiac output affected by  Preload  Afterload  Rate  Rhythm  Contractility  AP shunts  Regional Resistance  Neurohumoral Factors (Inflammation, sympathetic nervous system)  Local Factors (Autoregulation)

3.  Redistribute Blood flow to brain and heart  Mesentric and splanchnic circulation- silent ischemia during compensated shock  Baroreflex - Contractility, HR, SVR & decreases venous capacitance  Often body impairs systemic flow in face of myocardial dysfunction (regional ischaemia due to high SVR)  Ischaemic organ damage can occur even in presence of normal global oxygen economy  Regional Ischaemia →MODS→Death

4.  In series/ Normal circulation Qp=Qs=Qt  In parallel circulation Qt= Qp+Qs  At same Qt if Qp increases, Qs Decreases and vice a versa  Pulmonary artery = Systemic artery= SaO2  If Qs low = Sa-vO2 is high  If Qs High = Sa-vO2 is low

5. 200 At Increased Qs At decreased Qs 150 2070 50 50 100 50 50 SvO2 decreases SvO2 increases O2 delivered = Qs*O2 content of blood At fixed O2 content and at fixed O2 Extraction (suppose 50) Oxygen delivered will depend on Qs

6.  Increased O2 demand:  SvO2 reduces  SaO2 will reduce ▪ (Vicious Cycle)  SVR depends on many factors

7.  Optimal systemic oxygen delivery occurs at  Qp:Qs = 1 with  lowest Qt (total cardiac output) Fick Principle: Equality of systemic oxygen consumption and pulmonary oxygen uptake

8.  At Normal extraction =25% & SpvO2 = 100% (No lung issue)  Pulse ox (SaO2)= 75%  SvO2 = 50%  Qp:Qs = 1 75% 75% 75% 50% 100%

9.  At same saturation (75%)  Any Qp:Qs is possible depending on Qt (PARRCA)  Sa-vO2 (Extraction) = <25% : Qs high, Qp low, Qp:Qs low at high Qt  Sa-vO2 (Extraction) = >25% : Qs low, Qp high Qp:Qs high at low Qt

10.  At same Sa-vO2: (Systemic flow is fixed)  Any SpO2 is possible depending on Qt (PARRCA)  If SaO2 High: Qp is high and Qp:Qs = 2 at high Qt  If SaO2 Low: Qp is low and Qp:Qs = 0.5 at low Qt

11.  At same Qt (Total cardiac output)  Any Qp: Qs can exist  At Qp: Qs = 2 ▪ Qp increases: SaO2 increases ▪ Qs reduces: Sa-vO2 increases  At Qp:Qs = 0.5 ▪ Qp decreases : SaO2 decreases ▪ Qs increases: Sa-vO2 decreases

12.  At same Qp:Qs = 1  Many SpO2 are possible depending on Qt (PARRCA)  At high Qt : ▪ both systemic and pulmonary blood flow is high ▪ SpO2 high, SvO2 high & Sv-aO2 < 25%  At low Qt : ▪ Both systemic and pulmonary blood flow is low ▪ SpO2 low, SvO2 low & Sv-aO2 > 25% ▪ Tissue oxygen utilization is impaired if SvO2<50%

13.  At constant Qt moderate alteration in Qp:Qs balance will have minimal effect on SaO2  At fixed Qp:Qs, Increase in Qt can deliver more oxygen to tissue  As tissue cannot utilize oxygen if SvO2<50%, so body has very less O2 reserve to maintain increased O2 demand in parallel circulation.  Body has more oxygen reserves at high Qt but at an expense of myocardial oxygen demand  Another way to increase O2 delivery is by Increasing Hb

15.  Optimization of SaO2 alone will result in acute hemodynamic collapse unexpectedly in an apparently stable child.

16.  Gas manipulation of PVR  Inspired CO2: Increased PVR, decreased SVR, Increased O2 delivery (esp. brain)  Subatmospheric FiO2: Raises PVR  Controlled PPV while avoiding hypervenilation (PEEP)  O2 can be used if:  Respiratory pathology is present  Restrictive communications  Control of elevated SVR was more effective than increasing PVR  Inotropes increase SVR at high doses  Inodilators preferred (while preventing significant hypotension)  Morphine reduces Sympathetic outflow  Regional saturations of brain, liver, kidney, gut and muscle can be measured to rule out regional ischaemia  Increase Hct > 50% increases O2 carrying capacity

17.  Pulmonary venous SpvO2 = 100%  Variablity in Arteriovenous saturation difference  Not possible to obtain true sytemic venous mixed venous saturation

18.  Thank you

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Univentricular circulation

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