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PICU > Cardiac > Flashcards

Cardiac Flashcards

1
Q

How do you differentiate the R and L ventricle on echo?

A

L Ventricle: MV, two leaflets, no septal attachment, only attaches to the free wall of ventricle.

R Ventricle: TV, three leaflets, attaches to septum, anterior and posterior free wall. Trabeculation also seen on septum.

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2
Q

Definition Malposition vs Transposition

A

Malposition = 1 vessel comes off wrong ventricle

Transposition = 2 vessels (both) come off wrong ventricle.

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3
Q

Determinants of Cardiac Output on Heartware VAD

A

RPM: faster rate increases suction and propells more blood, only variable that can be set/changed on device.

Preload: unobstructed circuit, volume status

Afterload: BP, vasodilatation/constriction

Non-pulsatile: if no native ejection may need to oversew aortic valve to ensure adequate retrograde perfusion to coronaries.

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4
Q

Post operative monitoring Heartware VAD

A

LAP: how well is the LV being offloaded by device

Watts: how much work is the device doing to achieve cardiac output? rising watts may indicate changing haemodynamics or clot formation.

Volume status of LV: serial echo, expect decreased LV volume, decreased MR, improved RV function/pressures.

CXR: resolution of pulmonary oedema

Anticoagulation parameters:

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5
Q

ECG: ventricular rate > atrial rate

A

Wide complex = VT until proven otherwise

Usual complex = JET

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6
Q

Causes Mechanical Valve dysfunction

A

Thrombosis
Endocarditis - sticky leaflets
Pannas/scar tissue on valve
Residual Lesions - VSD changes haemodynamics
Malposition - usually seen immediately post operatively

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7
Q

Post Op LCOS - mechanisms

A

Reperfusion injury after removal of XClamp

  • translocation of O2 to endothelial space results in profound endothelial dysfunction
  • sheer stress/injury as blood reperfuses

Endothelial tone/reactivity
- NO depleted during XClamp, less reactive

Residual lesions/Restrictive Physiology
- esp if ventriculostomy

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8
Q

DORV phsyiology

A

To understand physiology need to know

  • location VSD
  • relationship of the great vessels

Remote VSD

  • complete mixing
  • single ventricle physiology

Subaortic VSD

  • VSD flow to aorta “pink”
  • VSD physiology
  • if concurrent PS - tetralolgy physiology

Subpulmonic VSD

  • VSD flow to PV “blue”
  • TGA physiology (taussig bing)

Doubly committed

  • VSD flow to aorta and PA
  • complete mixing lesion
  • large VSD physiology
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9
Q

Blood mixing - TGA

A

Mixing occurs best at atrial level

  • low pressure system - bidirectional flow, better mixing
  • VSD/PDA - high to low pressure - unidirectional flow

Role of PDA - shunts blood from aorta to PA

  • increased pulmonary blood flow
  • increased venous return to LA
  • increased LAP
  • increased flow across ASD
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10
Q

Restrictive RV physiology

A

Antegrade flow into PA during diastole
- atrial contraction, RV diastolic pressure > PA so PV opens

Thickened poorly compliant RV

  • elevated EDP, low EDV, poor filling
  • R to L shunt at level of ASD, cyanosis
  • systolic function usually preserved
  • often large PD/chest drain losses
Volume resuscitation
Avoid epinephrine
Decrease PVR
Ventilate to low MAP
Maintain A-V synchrony
Open chest
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11
Q

Post cardiac transplant - graft dysfunction

A

Both ventricles susceptible to ischaemic injury

RV particularly vulnerable

  • unprepared, previously healthy donor
  • exposed to increased PVR post op - bypass, recipient high PVR, transient LV failure with high LAP
  • RV harder to preserve cold temperature when grafting, located in anterior chest, exposed to heating from surgical lights/less contact with icy slurry
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12
Q

Restrictive Cardiomyopathy Physiology

A

Good systolic function
Small ventricles with MR/TR
Huge atrial with increased filling pressures

PRELOAD DEPENDANT
- PPV effects are marked, often results in clinical deterioration
VADs don’t work - inadequate ventricular filling

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13
Q

Dilated Cardiomyopathy Physiology

A

Poor systolic function with large ventricles

PPV/afterload reduction

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14
Q

RV failure management

A

Cautious volume administration
- Increased RAP results in decreased VR and CO

Reduce intrathoracic pressure - avoid PPV

Norepinephrine - move septum back to optimal position, improve RV perfusion

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15
Q

Blue BCPS - causes

A

Decreased Pulmonary Blood Flow

  • decreased cerebral blood flow/low pCO2
  • obstruction to flow - mechanical/clot
  • increased PVR
  • veno-venous collaterals

Pulmonary Venous Desaturation
- lung pathology

Mixed Venous Desaturation (ratio red:blue blood)

  • decreased oxygen delivery - anaemia, LCOS
  • increased oxygen extraction - sepsis, metabolic state
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16
Q

Ventilation strategies to improve pulmonary blood flow

A

Goal: reduce mean airway pressure

TV 8-10ml/kg
Long IT
Low PEEP
Low rate

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17
Q

BT shunt with raised CO2

A

Rising CO2

  • marker of dead space ventilation (zone 1 conditions)
  • increasing ventilation wont help, need to increased PBF

CO2 retention secondary to low PBF alone equates to PaO2 < 25-30

Differentiating low PBF vs lung pathology

  • if PaO2 > 60 blood is able to oxygenate, therefore should be able to ventilate off CO2, indicates lung pathology
  • PaO2 25 - poor oxygenation and increased CO2 - indicates poor BPF
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18
Q

PA Banding - physiology

A

Increased RV afterload post op
Decreased shunt volume - improved cardiac output
Decreased pulmonary venous return to LV - improved LV function
If patient dependant on mixing - must have unrestrictive atrial connection or PA band will not be tolerated

Proximal MPA band - can obstruct circumflex artery or PV anatomy (incompetent valve)

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19
Q

Rejection post Cardiac Transplant

A

High index of suspicion
Suspect if: New arrhythmia, new ECHO change

Hyperacute
- within mins, usually ABO incompatibility

Acute Cell Mediated
- host T-lymphocyte mediated against allograft tissue

Antibody Mediated
- activation of complement system, typically occurs months to years post transplant

Cardiac allograft vasculopathy
- accelerated graft atherosclerosis, occurs months to years post Tx, likely antibody mediated process

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20
Q

Blue TGA

A

Needs transfer for urgent BAS

Intubate and muscle relax
- improved lung dynamics, decreased O2 consumption
High FIO2
Optomise cardiac output - volume, inotropes
PGE’s - maintain duct, no advantage to high dose (risk hypotension)
Trial iNO - stop if no improvement in 15mins

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21
Q

Increased WOB post ccTGA repair (double switch)

A 
Pulmonary venous obstruction (baffle)
LV dysfunction (deconditioned LV, CHF)
Coronary ischaemia
PA band - semi lunar valve insufficiency
Recurrent laryngeal N palsy
Phrenic N palsy
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22
Q

Critical PS - blue post balloon dilatation

A

Non compliant RV - remains stiff post balloon
Increased PVR (neonate, open duct) - Increased RV afterload
Poor RV compliance leads to TR

All contribute to increased R to L shunt at atrial level
Improves with age as PVR falls and ventricle remodels

23
Q

TET spell - physiology

A

Vicious cycle

  • hypoxia - stimulates respiratory center - increased RR and adrenergic tone
  • catecholamines increase contractility, increase RVOTO
  • increased RR with large neg ITP swings - increased VR which shunts R to L, increasing cyanosis/hypoxia
24
Q

Management TET spells

A 
Knees to chest - increase SVR, decrease systemic venous return
Oxygen - decrease PVR
Remove precipitants
Morphine - relieve distress, slow RR
Fluid bolus 
B blockers - reduce infundibular spasm, decrease HR
Vasopressors - increase SVR
Correct Acidosis - consider ventilating
PGE if newborn
Surgical repair
25
Q

Reduced pulmonary blood flow post Norwood

A

Low PBF - respiratory acidosis

  • need to fix PBF to clear CO2
  • increasing ventilation will take a long time (dead space)
  • as PBF improves, CO2 will start to clear, decreasing PRV and improving PBF further

Trial iNO

Increase BP to force more blood through shunt (risk myocardial dysfunction secondary to increased afterload)

Consider upsizing shunt
ECMO

26
Q

Components Circular Shunt

A
  • Free PI/ incompetent PV
  • TV regurg
  • Atrial communication - R to L shunt, blood to LV
  • PDA - LV sends blood to PA which then enters RV via incompetent PV

Management

  • Promote systemic blood flow (milrinone, inotropes)
  • Ventilate to respiratory acidosis - decrease PVR
  • Urgent PDA ligation
27
Q

Atrial ECG

A

Unipolar atrial wire study

  • Atrial wires in RA
  • leads I & II intracardiac ecg (atrial ecg)
  • lead III surface ecg

Bipolar atrial wire study

  • Atrial wires into RA and LA
  • lead I pure intracardiac ecg, superaugmented atrial activity
  • leads II & III unipolar ecg
28
Q

Ischaemia on ECG

A

LAD - V4-V6, I, avL

circumflex - II, III, aVF (inferior septum)

R coronary - V1, anterior leads, V3R, V4R, reciprocal change V6

ALCAPA - q waves I, aVL, V5, V6

deep q waves = established infarct

29
Q

SVT Management

A

Fastest sinus rate 220-225
Consider diagnosis in all > 200/min

Stable: adenosine
Unstable: synchronised cardioversion
Post-op: rapid atrial pace - set rate 10% above atrial rate

30
Q

Complete Heart Block - with pacemaker failure

A

Haemodynamic assessment

Isoprenolin 0.01mcg/kg/min

Transcutaneous pacing

Trouble shoot pacemaker leads:

  • Skin lead to ground
  • Reversal of ventricular polarity
  • Atrial wire in + pole to ground, ventricular wire in - pole

Transvenous/oesophageal pacing wire placement
Urgent open sternum and epicardial wire placement

31
Q

Pulmonary Hypertension - intubation

A

Fentanyl - ablate catecholamine response

Ketamine - bronchodilator and good haemodynamic stability

Isoprenolin 10mcg/kg bolus

  • pulmonary vasodilator + chronotropy
  • may relieve PHT crisis

Rescue epinephrine on standby
ECMO back up

32
Q

Fick Equation - Single Ventricle

A 
Qp = VO2/(CpvO2 - CpaO2)
Qs = VO2/ (CaO2 - CmvO2)
CxO2 = (1.32 x Hb x SxO2) + 0.003 x PxO2

O2 added to Qp = O2 consumed by Qs
Arterial Hb = Venous Hb
Single ventricle SaO2 = SpaO2

Qp/Qs = (SaO2 - SmvO2) / (SpvO2 - Spa)2)

Assumptions:

  • CO/oxygen extraction normal (Sa)2 - SmvO2 = 25%)
  • normal SpvO2 >95%
33
Q

Single Ventricle Physiology: Manipulating the circulation

A

Pre Op:

  • no restriction to PBF
  • manipulations targeting Qp and Qs both effective
  • avoid supplemental O2

Post Op:

  • fixed anatomical restriction to PBF
  • ventilatory changes have minimal effect on BPF
  • focus on improving CO/SVR
  • transient myocardial dysfunction (increased ventricular afterload post shunt, post CPB)
  • BP is not a good marker of CO (may indicate high SVR with low CO)
  • pulmonary venous desaturation common - don’t be afraid to give O2
34
Q

BT shunt vs RV-PA conduit vs hybrid

A

BT shunt:

  • continuous pulmonary blood flow
  • no ventriculotomy
  • higher risk clot
  • diastolic run off - risk of coronary/end organ ischaemia

RV-PA conduit:

  • pulsatile pulmonary blood flow
  • PBF only in systole
  • no diastolic run off
  • larger diameter (to compensate for increased length), less risk thrombosis
  • ventriculotomy - restrictive physiology
  • more distortion to PA’s

Hybrid:

  • arch remains hypoplastic - poor brain perfusion
  • continuous pulmonary blood flow
  • defers arch repair (DHCA) to stage 2
35
Q

Post Op Norwood management

A

Ultimate Goals:

  • SmvO2 50, MAP 50, Sat 75
  • Hb 140

Increased CO improves O2 delivery more than manipulating Qp:Qs

Increase Cardiac Output

  • inotropy
  • afterload reduction

Coronary issues

  • MS/AA highest risk
  • watch for low diastolic BP combined with high EDP
  • estimate by RA pressure/CVP
  • CPP = DBP - CVP (risk ischaemia < 20)
36
Q

Decompensated Heart Failure - physiology

A

Increased lung water
- decreased pulmonary compliance

Respiratory Compensation

  • increased RR and tidal volume
  • results in increased neg pressure swings - overall decreased ITP
  • worsens LV failure

PPV

  • increases ITP - afterload reduction
  • decreased metabolic demands, decreased CO needs
37
Q

Open Sternum Physiology

A

Uncouples Pra from increased ITP

  • restores venous return and RV preload
  • allows time to treat increased ITP (diuresis, ventilation)
38
Q

Cardiac contribution to pulmonary dysfunction

A

Shunt lesions
- increased PBF (oedema with reduced compliance)

Increased PVR - longstanding high PBF lesions

Airway compression

  • LA and PA’s close to airway
  • vascular rings/slings - malacia
39
Q

Mixed Venous Saturations

A

SvO2 ~ SmvO2 - percentage of oxygen bound to Hb returning to R heart

ScvO2 - surrogate for SvO2

SvO2 = SaO2 - (VO2/CaO2)

CaO2 = SaO2 x Hb x 1.32 + 0.003 x PaO2

Normal SvO2 60-80

Normal extraction:

  • heart 37%
  • brain 69%
  • liver 66%
  • kidneys 92%
  • gut 66%
  • SVC 72%
  • IVC 80%
40
Q

Causes low SvO2

A

low SvOw

  • inadequate cardiac output
  • low Hb
  • low saturations
  • increased O2 needs (sepsis, fever, seizures)
41
Q

Restrictive LV physiology

A

Restrictive LV physiology

  • decreased EDV
  • increased EDP

Poor tolerance of volume loading

Risk impaired coronary perfusion

  • CPP = diastolic BP - LVEDP
  • increased HR worsens ischaemia

High LA pressures

  • pulmonary oedema
  • pulmonary hypertension
  • increased RV afterload

LAP > 16 usually predictive of failure

42
Q

Pulmonary Hypertension - risk factors

A

Increased pulmonary blood flow
- L to R shunts

L sided obstruction

High PaO2 (TGA)

43
Q

ECMO - eCPR physiology

A

rapid rise in BP as ecmo flows increase

  • transfusion of blood from venous capacitance to constricted arterial system
  • rapid wean of vasopressors
  • slow increase flows to avoid intracranial haemorrhage

Increasing flows after ecmo established has less effect on BP as arterial circulation now relaxed - need to add volume or vasopressors

44
Q

How does increasing systemic BP help in pulmonary hypertension?

A

Improved coronary perfusion to failing RV
- perfusion during systole lost in PHT

Improved interventricular interdependance
- septum moves back, improves ventricular contraction

45
Q

Single ventricle physiology - restrictive ASD

A

Increased LA pressures

  • pulmonary hypertension
  • results in reduced PBF
    • cyanosis
    • pulmonary oedema - WOB

Decreased blood return to ventricle
- decreased cardiac output

46
Q

Re-entrant Tachicardia

A

Sudden onset/offset
Fixed RR interval
Narrow or usual complex QRS

Treatment:

  • pace termination - rapid atrial pacing or overdrive pacing
  • ablate track - adenosine, cardioversion, cath lab

NB adenosine will not work in atrial flutter - pathway does not include AV node.

47
Q

Automaticity arrhythmia

A

Atrial - AET, MAT
AV node - JET, junctional
Ventricular

Warm up / cool down
Beat to beat variability
Narrow QRS unless from ventricle

Management:

  • remove stimulus - sedate, analgesia, reduce catecholamines, muscle relax
  • cool
  • drugs - B blockers, amioderone
  • overdrive pacing - will capture but not change underlying rhythm

Defibrillation does not work

48
Q

TAPVD physiology

A

Unobstructed:

  • behaves like large ASD
  • increased pulmonary blood flow
  • minimal desaturation - sats 85-90

Obstructed:

  • early presentation - sick hypoxic baby
  • pulmonary hypertension
  • pulmonary oedema
49
Q

Obstructed TAPVD

A

Supracardiac:

  • vertical vein travels between LPA and L bronchus or aorta/bronchus
  • occasionally see stenosis at oriface of vertical vein

Cardiac:

  • obstruction is rare
  • occurs at connection of venous channel to coronary sinus

Infracardiac:

  • obstruction at level of diaphragm
  • long draining vessels - increased resistance secondary to length
  • stenosis at point of intersection with systemic venous system
50
Q

LVAD vs ECMO

A

LVAD vs ECMO

  • better decompression of heart
  • increased longevity of circuit - no oxygenator
  • smaller circuit, minimal exposure to foreign plastic, less SIRS
  • allows rehabilitation and normalisation of life
51
Q

Berlin Heart Prerequisites

A

Requires competent aortic valve

No MS - inhibits ventricular filling. MR is permissible, should improve post LVAD

Minimal TR - severe TR results in poor PBF and reduced preload to LVAD

Intracardiac shunts must be closed

Good RV function - offloading LV should improve RV function

52
Q

VAD anticoagulation protocol

A

Unfractionated heparin
- start 12-24hrs post op

Dipyridamol
- begin day 3-5

Aspirin
- when drains removed

Omega 3 fatty acids

  • decreases plt aggregation
  • anti-inflammatory effects

Targets:

  • heparin level 0.35 to 0.5
  • ATIII > 75%

Longterm
> 12mths - warfarin, INR 3-4
< 12mths - enoxaparin

53
Q

DORV repair

A

Anatomy determines repair

VSD needs to be baffled to an outflow tract to septate the heart

  • remote/non committed - single ventricle repair
  • doubly committed - usually biventricular repair

Baffle - risk of OTO

PICU (2 decks)

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