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59 Cards in this Set

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Shunts

Abnormal pathway that leads to an increase or decrease in pulmonary or systemic blood flow*




flow direction is pressure dependent

Shunts and pulmonary blood flow

Increased blood flow resulting in a volume or pressure overload to the pulmonary circulation (VSD, ASD, PDA, AVC, Truncus)




Decreased blood flow - resulting in relative inability to oxygenate blood (HLHS, TOF, Tricuspid Atresia)

Shunts QP/QS=

Sat (aorta) - Sat (SVC) / Sat (pulm venous) - Sat (PA)

Obstructive lesions

Obstruction to blood flow due to a supravalvar, subvalvar, or primary valvular abnormality.




increased ventricular workload and relative reduced circulation distal to obstruction - NO FLOW NO GROW

4 Main Problems associated with CHD

Chronic Hypoxemia, CHF, Arrhythmias, Pulmonary Disease

Cyanosis

Cyanosis occurs most commonly in lesions where




pulmonary blood flow it anatomically decreased (TOF)




mixing of systemic and pulmonary blood flow (single ventricle)

chronic Hypoxemia different from acute hypoxia

Chronic - Disrupts all major organ systems. CVS, polycythemia, decrease cardiac reserve, myocardium replaced by fibrotic tissue, increased epi levels and sympathetic tone

Chronic Hypoxemia

Polycythemia- viscosity - think - stroke




limits blood flow- fatigue, headache


Rx- Short NPO, IV rehydration, Phlebotomy (>Hct 65%)


Abnormal Hemostasis

Chronic Hypoxemia

Growth - nl 1/3 metabolism devoted to growth - need increase caloric intake




CNS - delayed neurologic development, brain abscess, DHCA

CHF

Common with shunts lesion resulting in increased pulmonary blood flow (VSD)




Obstructive lesions that stress the ventricle past its capacity to pump effectively (AS)

CHF symptoms

Diaphoresis, Tachypnea, Poor feeding, Failure to thrive, and Recurrent Resp infection

Ohm's law

I (current) = V (electromotive force) / R (resistance)




CV physiology


Q (blood flow) = P (Pressure drop across vascular bed) / R (resistance in vascular bed)

Poiseuille Relationship

Small radius higher resistance - less blood flow

Flow Cardiac Output increase vs decrease

Increase - Volume loading, Chronotropic agents, inotropic agents




Decrease- inhalation anesthetics, hypovolemia, dysrhythmias, ischemia, high mean airway pressures

Systemic Resistance Increase vs Decrease

Increase - Sympathetic simulation (pain), a-Adrenegric agonists




Decrease - Various anesthetic agents, vasodilators, a-Adrenergic antagonists, B-adrenergic Agonists

Pulmonary resistance increase vs decrease ****

Increase - hypoxemia, hypercarbia, acidosis, high mean airway pressure, sympathetic stimulation, a-Adrenergic agonists, Hypervolemia *




Decrease- Oxygen, Hypocarbia, alkalosis, Prostagladin E1, a-Adrenegric antagonists, vasodilators, cGMP - Viagra *

Atrial Septal Defect

Allows blood to shunt from atrium to atrium




>8mm likely require intervention




Ostium Secundum - Central and Most common

Atrial Septal Defect degree of shunting depends on what

1. the compliance of the two chambers


2.The larger the defect , the greater the volume of shunted blood




usually left to right shunt

Atrial Septal Defects

Rarely close spontaneously, Paradoxical embolization at risk, can cause CHF with large shunts, and can cause pulmonary vascular resistance changes over time

Atrial Septal Defect Repair?

Truly curable.




can be closed with:


surgery - patch or suture closure


Cath lab- catheter device closure

Atrioventricular Canal Defects

Partial AV canal - primum ASD and Cleft in MV




Complete AV canal - failed fusion of endocardial cushions. Large amount of shunting - CHF




NEEDS EARLY SURGICAL INTERVENTION

Ventricular Septal Defects

L to R shunt. - CHF and Pulmonary HTN




size of shunt and magnitude of the shunt.




May close spontaneously by age 5




Rarely symptomatic and require closure.

Tetralogy Of Fallot

Narrowing of the RV ifundibulum or Pulmonary Stenosis


VSD


Overriding Aorta


RVH

TOF

Wide spectrum




right to left shunting at the VSD and thus systemic desaturation presenting as cyanosis*

Primary therapy to tx

surgical - closure of VSD and relief of any RVOT obstruction

TOF Tet spells

Hypercyanotic episode- due to increased right to left shunting from decreased systemic blood pressure and increased RVOT obstruction.

Treatment of TET spells

increase intravascular volume


100% of FiO2 adequate ventilation


Phenylephrine increase SVR


Beta blockade (minimize spasms)


Narcotics

Total Anomalous Pulmonary Venous Return

Left to right shunt


0.6% percent see on autopsy


Obstructed TAPVR requires emergent surgery.


pulmonary HTN- occurs 50% patient preoperatively



Transposition of Great Arteries - mortality

Without intervention, mortality is 45% in first month to 90% at one year.


Patients with TGA rarely have other extra cardiac defects

Transposition of Great Arteries Patho

In simple TGA- the aorta arises from the Right ventricle and the pulmonary artery arises from the left ventricle




Incompatible with life unless other inter-circulatory mixing.




systemic circulation unoxygenated, pulmonary circulation - oxygenated blood circulation

Early tx of TOGA

PGE1 to keep PDA OPEN*** or need ASD or VSD


balloon atrial septostomy




sx- arterial switch operation/procedures

Truncus Arteriosus

NEED VSD***


septation between the aorta and pulmonary artery that occurs 4-5 weeks after conception




The basic defect is a large VSD and the pulmonary arteries arise directly from th aorta.

Truncus Arteriosus results in

mixing of systemic and pulmonary blood b/c of the absence of a separation between circulations



in neonate the streaming and increased PVR direct blood flow to the systemic circulation

Truncus Arteriosus causes what systemic disease

as the PVR decreases in the young infant, pulmonary over circulation rapidly occurs and CHF develops


IRREVERSIBLE VASCULAR DISEASE- if left untreated***


mortality high if untreated

Tx of Truncus Arteriosus

Early tx of CHF and alteration of pulmonary blood flow




surgical correction is undertaken after stabilization and involves closure of the VSD and placement of an RV to PA conduit

Patent Ductus Arteriosus

10% isolated finding usually with complex CHD




in fetus right to left


After birth left to right




Typically closes over first 72 hours

PDA

The risk of endocarditis generally mandates closure of the PDA.


L to R shunt.


Large PDAS steal from systemic circulation lowering diastolic B/P and putting coronary circulation at risk

PDA ligation closure options

Surgical Ligation


Trans-Catheter coil embolization or device.

Coarctation of the Aorta

Untreated - cardiac failure, aortic rupture, endocarditis, CVA.




Rigid-like thickening originating from the aortic media and protruding from the lateral and posterior walls of the aorta. - as the child grows the lumen is further comprised.

Coarctation of the Aorta Major Patho effect**

Increased Afterload on the systemic ventricle. **


Results in LVH**


Hypertension proximal to the coarctation and hypotension distal to the coarctation is common**


Feeding hard

Coarctation of the Aorta **

Tx Surgical and Ballon dilatation




HTN requiring antihypertensive therapy may persist in spite of early repair*****

Hypoplastic Left Heart Syndrome

Aortic valve atresia with resultant hypoplasia of the ascending aorta. **




LV non functional **




NEED PDA OPEN. **




Transverse and ascending aorta are supplied retrograde through a PDA and the descending aorta ante grade from the PDA

Hypoplastic Left Heart Syndrome MUST HAVE

PDA


Atrial Mixing


Q;Q close to 1


PBF and SBF are dependent on the ratio of PVR:SVR




AS PVR decrease systemic perfusion deteriorates


Compensatory increase in SVR worsens the problem**

Single Ventricle Physiology

systemic venous blood mixes with oxygenated blood form the lungs.




after birth PVR Drops and PBF increases relative to systemic flow. causing a rise in O2 sats and drop in systemic BP***

Single Ventricle O2 estimate

Useful to use O2 sats to estimate ratio of pulmonary to systemic blood flow




balanced systemic artery sat is 75-85%




Excessive PBF >85%- overcirculation and ventricular dilation, decrease systemic b/p




Decreased PBF <75%- cyanosis, myocardial ischemia, and low cardiac output

Single Ventricle clinical presentation

Cyanosis - avoid supplemental o2 with Large PDAs




Resp distress within first 24-48 hours of life. ductus arteriosus begins to close or ASD restrictive.




Lethargy, poor feeding, shock, seizures, renal failure

Hypoplastic Left Heart Syndrome

PVR decrease PBF increase causing overload- systemic circulation poor .


results in acidosis, chf and death despite increase arterial oxygenation

Tx hypo plastic left heart syndrome

Early medical - stabilizes hemodynamic, decrease PaO2 and raise PaCO2 to raise PVR


correct acidosis


vasodilators to decrease SVR


PGE1 to keep PDA open.

Hypoplastic left heart syndrome Norwood surgery

Norwood stage 1- Aortic arch reconstruction by anastomosis of main PA to ascending and transverse aortic arch with patch aterioplasty


systemic to PA shunt


Atrial septectomy

Hypoplastic left heart syndrome norwood stage 2 at 4 months

bidirectional glenn shunt stage 2 at 4 months


removal of systemic to PA shunt


anastomosis of SVC to PA




decreased PVR 3-6 months will have normal filling

Stage 3 fontan

at 2 years


Redirect IVC blood to PA- near complete systemic venous return to the lungs for oxygenation




RA and RV now almost fully oxygenated for systemic via neo-aorta

Long term implications with fontan

arrhythmias aflutter or intra-atrial reentry tachycardia




protein-losing enteropathy




Thrombosis

Anesthetic implications of Adults with completed fontan

CVP (pulmonary venous pressure)- dictates pulmonary blood flow.




Avoid hypoxemia, hypercarbia, metabolic acidosis, increased catech, and myocardial depressants to prevent increase in pulmonary vascular resistance

Antibiotic prophylaxis who gets it

Prosthetic cardiac valve, cardiac transplant, endocarditis




CHD- unrepaired or incompletely repaired (Cyantoic blue heart


Completely repaired in the last 6 months with prosthetic material.


repaired CHD residual defects at the site or adjacent to prosthetic patch or device

Procedures that need antibiotic prophylaxis

Dental procedures (with gums),

Respiratory Procedures (tonsils/adeno) incision or biopsy


Infected tissue such as I/D of infected tissue


When to give antibiotic

give 30-60 minutes prior to procedure




if dose missed given within 2 hours after procedure.

Ventilation Hypercarbia vs Hypocarbia

hypercarbia - increase PVR, decrease SVR, shunts




Hypocarbia - decrease PVR and increase SV, shunts




Positive pressure- CO, PEEP, and Lung vol.

Specifics of surgery

Almost never B blockers or Ca Antagonists




R-L delayed induction- air emboli


L-R increased induction



good tricks

maintain HR, Contractility and preload to maintain cardiac output.




Always think - preload, rate, rhythm, contractility, and after load.