cardiac physiology · pdf file · 2017-03-28who had no prenatal care and ... •...

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Cardiac Physiology Cardiac Physiology

Gia Marzano, AC PNP Pediatric Cardiac SurgeryRush Center for Congenital Heart Disease

Rush University Medical Center

Objectives Part 1

• Fetal Circulation

• Transition to Postnatal Circulation

• Normal Cardiac Anatomy

• Ductal Dependence and use of PGE1

Objectives Part 2

• Basic principles of cardiac physiology

• Basic categories of congenital heart disease based on pathophysiology

• Application of physiology to your bedside management

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Fetal CirculationFew Concepts

• Fetal heart starts developing during the 3rd week of life

• By the 3rd month of development, all major blood vessels are present and functioning.

• Pulmonary Blood Flow is Low

• Gas Exchange (Oxygen) occurs in placenta

More Concepts

• Pulmonary Resistance is High– Lungs are still underdeveloped

– Small pulmonary arteries have a thicker smooth muscle layer than similar arteries in adults.

Fetal Circulation Overview

• Umbilical Circulation:– Pair of umbilical arteries

carry deoxygenated blood & wastes to placenta.

– Umbilical vein carries oxygenated blood and nutrients from the placenta.

• Placenta facilitates gas and nutrient exchange between maternal and fetal blood.

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• Oxygenated blood from placenta is transported to the fetus through the Umbilical Vein


• Most of the oxygenated blood bypasses the liver through the Ductus Venosus and mixes with De-Ox Blood from IVC


• Blood travels from the IVC and enters the RA

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• 40 % of oxygenated blood from the IVC bypasses the RV and is shunted to the LA via the Foramen Ovale

• The rest mixes with De-ox blood from the SVC and enters the RV


• Blood then travels to the LV and is distributed through the aorta mainly to the coronaries and upper body (carotid and subclavian arteries)

• Only 1/3 of this volume goes to the lower body

Fetal Circulation Overview• Most blood from the IVC

(60%) mixes with SVC blood and enters the RV from the RA

• Because the lungs are non-functional, most (90%) will be shunted away from the pulmonary arteries through the Ductus Arteriosus to the Descending Aorta and Placenta for oxygenation

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• Blood circulates to the body and returns to the placenta via the umbilical arteries


• Placenta re-oxygenates blood returning from the umbilical arteries

• New fetal cardiac cycle…


• Parallel circulation with shunts (PFO and PDA) allows various lesions to provide adequate transport of blood to placenta for oxygenation and deliver it to the tissues

• RV performs ~ 2/3 cardiac work RV larger and thicker at birth

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Transitional and Post-Natal Circulation

• What happens at birth ??

• The change from fetal to postnatal circulation happens very quickly.

• 2 major events:– Changes initiated by baby’s first breath.

– Elimination of the placenta

Transitional Circulation

• Clamping of the umbilical cord:– Eliminates the low

resistance placental circulation

peripheral vascular resistance increases

– decreases blood volume returning to the heart from IVC


• With initiation of pulmonary ventilation:– Increased alveolar O2 pressure

vasodilates the pulmonary arteries

– Pulmonary vascular resistance decreases significantly

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Pulm Blood flow increases 8-10 X

Drop in

pulmonary Vascularresistance

Increase in

systemic Vascularresistance

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Transitional Circulation• Increased pulmonary

blood flowincreased pulmonary venous return into LA LAP >RAP the greater LAP (and lower IVC flow) closes the valve of the foramen ovale, preventing right-to-left shunting.

Transitional Circulation• PDA: changes from

R2L conduit of blood to the descending aorta to a L2R conduit of blood to the lungs

• Ductus arteriosus constricts and closes functionally within several hours after birth, largely in response to the increase in oxygen tension.

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• PFO closure• Ductus arteriosus

closure • These events result

in the effective separation of the systemic and pulmonary circulations after birth.

Ductal DependenceThe Ductus Arteriosus

• In fetus: – large channel that allows

blood to bypass the lung circulation to the Dao and placenta for oxygenation

– as big as the Dao ! (10mm)

– allows equalization of Ao and pulm arterial P

The Ductus ArteriosusRole of O2

• Thick muscular layer• Towards late gestation, the muscle layer

thickens and the lumen becomes smaller• After birth, increased arterial O2 causes

more constriction of the ductus• Constriction decreases PO2 in the muscle severe hypoxia cell destruction and fibrosis

• Functional closure within 10-15 hrs after birth

• Complete closure within 5-7 days, can be up to 21 days

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Ductus ArteriosusRole of Prostaglandins

• Produced by the wall of the ductus and placenta

• 2 types: PGI2 and PGE2

• Relax the ductus arteriosus smooth muscle

• Metabolized in the lungs

• After birth, ↓↓ PG ductal closure

Ductus Arteriosusin Congenital Heart Disease

• In many CHD cases (mainly cyanotic), ductus does not close normally after birth:– TA/PA/TGA: arterial O2 remains low

after birth lower stimulus for constriction

– Left-sided lesisons (Ao atreasia, coarctation): arterial O2 increases after birth but the high PAP/flow keeps ductus patent


Ductal Dependency

• Normally, ductus carries ~ 60 % of combined C.O from the PA to the DAo

• If LV outflow tract is obstructed (e.g. aortic valve atresia, coarctation, interruption):– larger portion of combined C.O crosses

the ductus (~90%) larger Ductus

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Ductus Arteriosusin Lt sided lesions

Ductal Dependency

– After birth: need the ductus to provide most of systemic blood flow (from PA to Ao)


• If RV outflow is narrow (e.g. pulmonary atresia, tricuspid atresia)– minimal blood from RV to ductus

small ductus

Ductus Arteriosusin Rt sided lesions

Ductal Dependency

• After Birth: Need the ductus to maintain pulmonary blood flow

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Prostaglandin Therapy

• Indomethacin: inhibits PG production

• PGE1:– relaxes the ductus arteriosus

smooth muscle cells.

– Effective within the first 7-10 days after birth

– Dose: 0.05-0.1 mcg/kg/min

– IV/PO

Prostaglandin TherapySide Effects

• Apnea

• Fever

• Flushing

• Hypotension

• Thrombocytopenia

• Seizure

• Pyloric gastric outlet obstruction

Questions?

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Part 2

• Basic principles of cardiac physiology including

Flow and pressure relationships

Oxygen delivery

Determinants of blood pressure and cardiac output

Let’s start with a case…

• You are admitting a 4 day old female who had no prenatal care and presented to the ED with poor feeding, respiratory distress, lethargy and poor urine output. PGE infusion was started in the ED.

• On exam, she is floppy with grunting respirations and her skin appears gray.


• VS:T 97 P 190 R 70 BP 40/P SpO2 92%

• PE:

Chest: coarse BS with retractions

Heart: tachycardic, no murmur

Abd: soft, liver 4cm below RCM

Ext: gray, cool, cap refill 5 sec, poor distal pulses

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• Labs: WBC 8.2 Hg 11 Hct 33 Plt 189

Lytes:Na132/K5/Cl103/CO8/BUN13/Cr0.9

ABG: 6.99/32/54/8/-16/85%

CXR: cardiomegaly, increased PVM

ECHO: critical CoA

Questions…

• A nursing student asks “why is that baby gray?” How will you answer?

• Then she asks why the baby is so hypotensive. You explain…

• The MD decides to transfuse prbc and asks you to get consent from the parents. What will you tell them is the reason for the transfusion?

Flow and Pressure Relationship

(all you really need to know to understand any concept in cardiac

critical care….seriously!)

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Ohm’s Law

Pressure change (dP) Flow (Q) = __________________

Resistance (R)

Increased P Increased QIncreased R Decreased Q

Cardiac Physiology

• What is the purpose of the heart?

O2

Cardiac Physiology

Delivery of oxygen (DO2) is a direct function of the cardiac output (CO) and the arterial oxygen content (CaO2)

DO2 = CO x CaO2

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Cardiac Physiology

Oxygen DeliveryDO2 = CO x CaO2

Cardiac Output (CO)art Rate (HR) x Stroke Volume (SV)

Arterial Oxygen Content (CaO2(Hgb x 1.39 x SaO2) + (0.003 x PaO

roke Volume is directly related to:Preload

AfterloadContractility

Cardiac Physiology

• What are we trying to achieve?

Maximize O2 delivery

Provide adequate end organ perfusion

Maintain BP

Determinants of blood pressure

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Ohm’s Law

BP = Flow(Q) x Resistance(R)

What is Blood Pressure?BP

CO SVR (Afterload)

Heart rate Stroke Volume

Intravascular Volume(Preload)

Contractility

Maintaining Blood Pressure• Derrangement in:

– Volume status

– Cardiac function

– Vascular tone

– Heart rate

BP

CO SVR

HR SV

Preload Contractility

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Preload• Derrangement in:

– Volume status


– Vascular tone

– Heart rate

BP

CO SVR

HR SV


Determinants of Cardiac Output

• Preload-“Resting fiber length before contraction”

-End diastolic ventricular volume

-If preload is increased, SV and capability for pressure generation are increased.

• Frank-Starling Mechanism

-Compliance dependent

CVP

• CVP: Central venous pressure– Transduced via RA lines or CVL

– Reflects the intravascular volume status of the patient and the filling pressure of the ventricle

– Relationship between CVP and BP is important

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Afterload (SVR)• Derrangement in:

– Volume status


– Vascular tone

– Heart rate

BP

CO SVR

HR SV


Afterload

• Any factor that resists the ejection of blood from the heart (SVR or obstruction)

• With increasing afterload, shortening is decreased and slowed.

• Afterload reduction increases fiber shortening.

• Decreasing afterload helps the heart contract

Afterload

• Afterload (SVR) increased by– Acidosis, hypoxemia, pain, hypothermia– Aggressively treat/avoid these things

• Afterload reducers– Milrinone, dobutamine, nitroprusside, NO

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Contractility• Derrangement in:

– Volume status


– Vascular tone

– Heart rate

BP

CO SVR

HR SV


Contractility

• Often impaired

• Requires treatment with inotropes– Milrinone, epinephrine, dobutamine,

dopamine

– Calcium is an important component

Putting it all together…

• Decreased Cardiac Output can be caused by:– Decreased preload

– Increased (or decreased) afterload

– Impaired contractility

• All therapies aimed at maximizing these parameters

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Categories of CHD

Epidemiology of CHD

• Incidence estimated to be 8 to 10 cases per 1000 live births (0.8% - 1%)

• Increased to 5% - 15% in parents with CHD

• Prevalence increases as better treatments are available

• Age at presentation varies greatly and depends on type of lesion and severity

Age at Presentation

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Epidemiology of CHD

Categories of CHD

• Patients with too much PBF CHF

• Patients with too little PBF Blue

• Patients with too little systemic blood flow Gray

Categories of CHD

• Acyanotic Congenital Heart Disease– L R Shunt (Volume load)

– Obstructive (Pressure load)

• Cyanotic Congenital Heart Disease– Decreased PBF

– Mixing lesions

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Acyanotic CHD

• LR Shunt lesions (Volume load)– VSD, ASD, PDA, AV Canal

– Common denominator is communication between systemic and pulmonary circulations

– Magnitude of shunt depends on size of defect and relative SVR and PVR which will change over time

Acyanotic CHD

• Obstructive lesions (Pressure load)– CoA, AS, IAA

– Common denominator is obstruction of blood flow/ventricular outflow

– Lead to left heart failure (pulmonary edema)circulatory collapse

Cyanotic CHD

• Decreased PBF– TOF, PS with PFO, tricuspid atresia,

pulmonary atresia

– Common denominator is obstruction to pulmonary blood flow and a means of shunting RL

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Cyanotic CHD

• Mixing Lesions– TGA, TAPVR, truncus arteriosus, HLHS

– Common denominator is that there is complete mixing of systemic and pulmonary venous return without obstruction to PBF

Acyanotic CHD

• LR Shunt lesions (Volume load)– Most common lesions are ventricular

septal defect (VSD) 20-25%, atrial septal defect (ASD) 5-10%, patent ductus arteriosus (PDA) 5-10, AV Canal 2%

– Common denominator is communication between systemic and pulmonary circulations

– Magnitude of shunt depends on size of defect and relative SVR and PVR which will change over time

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Pathophysiology of VSD

• Qp:Qs is increased

• Increased PBF leads to decreased lung compliance, increased WOB, pulmonary edema

• Chronic increased PBF leads to increased PVR (Eisenmenger’s physiology)PHTN

Clinical Presentation - VSD

• History: poor feeding, diaphoresis with feeds, delayed growth and development, repeated pulmonary infections

• Will present at 6 to 8 weeks of age

• Exam: tachypnea, holosystolic murmur at LLSB, hepatomegaly

• CXR: cardiomegaly, increased PVM

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CXR - VSD

Management - VSD

• Diuresis

• Inotropy with digoxin

• Surgical repair when optimal

Acyanotic CHD

• Obstructive lesions (Pressure load)– Most common are coarctation of the aorta

(CoA) 8-10%, aortic stenosis (AS) 5%, interrupted aortic arch (IAA) 1%

– Common denominator is obstruction of blood flow/ventricular outflow

– Lead to left heart failure (pulmonary edema) circulatory collapse

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Ductal Dependence

• To provide pulmonary blood flow (PBF) – Critical PS

• To provide systemic blood flow (SBF) – Critical CoA

• To allow mixing - TGV

Pathophysiology of Critical CoA

• In fetal life, the descending aorta is supplied by the PDA

• With closure of the duct, systemic circulation is impaired which leads to poor perfusion, acidosis and circulatory collapse

Clinical Manifestations – Critical CoA

• History: CHF symptoms (poor feeding, diaphoresis), poor urine output

• Will present in first few days to weeks of life

• Exam: tachypnea, poor perfusion, decreased femoral pulses, shock, often NO MURMUR, usually gallop present

• CXR: cardiomegaly, pulmonary edema

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Management – Critical CoA

• Diuresis

• Inotropy with dopamine or dobutamine

• Prostaglandin (PGE1) infusion to re-open ductus arteriosus and restore systemic blood flow

• Balloon angioplasty vs. surgical repair

Cyanotic CHD

• Decreased PBF– Most common lesions are Tetralogy of

Fallot (TOF) 10%, pulmonic stenosis with PFO (PS) 5-8%, tricuspid atresia 1-2%, pulmonary atresia (PA) <1%

– Common denominator is obstruction to pulmonary blood flow and a means of shunting RL

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Tetralogy of Fallot

• Consists of four components– Large VSD

– Right ventricular outflow tract obstruction

– Right ventricular hypertrophy

– Overriding Aorta

• Only two components are important– VSD large enough to equalize pressure (R=L)

– RVOT obstruction – how severe determines if patient shunts RL (“Blue Tet”) or LR (“Pink Tet”)

Clinical Presentation of TOF

• History: cyanosis or hypoxic spells, dyspnea on exertion, squatting

• Exam: cyanotic (“Blue Tet”), murmur variable – usually loud (grade III-IV) systolic ejection murmur with thrill

• CXR: boot shaped heart, decreased PVM

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CXR - TOF

Cyanotic CHD• Mixing Lesions

– Most common lesions are transposition of the great arteries (TGA) 5%, total anomolous pulmonary venous return (TAPVR) 1%, truncus arteriosus <1%, hypoplastic left heart syndrome (HLHS) <1%

– Common denominator is that there is complete mixing of systemic and pulmonary venous return without obstruction to PBF

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Pathophysiology of TGA

• Pulmonary and systemic circulations are parallel

• Defects permitting mixing are essential for survival – ASD, VSD, PDA

• Poor mixing results in hypoxia, acidosis and death

Clinical Presentation of TGA

• History: cyanosis, poor feeding, dyspnea

• Presents in the first few days of life

• Exam: systolic murmur of VSD may be present, may have no murmur

• CXR: cardiomegaly, egg-shaped cardiac silhouette

Management of TGA

• Treat acidosis

• Administer O2 to decrease PVR and increase PBF (increase mixing)

• PGE1 to reopen ductus and increase mixing

• Balloon atrial septostomy

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Summary

• All congenital heart lesions can be categorized based on flow and pressure relationships

• Caring for these patients entails maximizing oxygen delivery and maintaining adequate blood pressure

Back to our case…

• You are admitting a 4 day old female who had no prenatal care and presented to the ED with poor feeding, respiratory distress, lethargy and poor urine output. PGE infusion was started in the ED.

• On exam, she is floppy with grunting respirations and her skin appears gray.

Questions…

• A nursing student asks “why is that baby gray?” How will you answer?

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Categories of CHD

• Patients with too much PBF CHF

• Patients with too little PBF Blue

• Patients with too little systemic blood flow Gray

Questions…

• Then she asks why the baby is so hypotensive. You explain…

Contractility• Derrangement in:

– Volume status


– Vascular tone

– Heart rate

BP

CO SVR

HR SV


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Questions…

• The MD decides to transfuse prbc and asks you to get consent from the parents. What will you tell them is the reason for the transfusion?

Cardiac Physiology

Oxygen DeliveryDO2 = CO x CaO2

Cardiac Output (CO)art Rate (HR) x Stroke Volume (SV)

Arterial Oxygen Content (CaO2)(Hgb x 1.39 x SaO2) + (0.003 x PaO

cardiac physiology · pdf file · 2017-03-28who had no prenatal care and ... •...

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