Cardiac Flashcards
How do you differentiate the R and L ventricle on echo?
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.
Definition Malposition vs Transposition
Malposition = 1 vessel comes off wrong ventricle
Transposition = 2 vessels (both) come off wrong ventricle.
Determinants of Cardiac Output on Heartware VAD
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.
Post operative monitoring Heartware VAD
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:
ECG: ventricular rate > atrial rate
Wide complex = VT until proven otherwise
Usual complex = JET
Causes Mechanical Valve dysfunction
Thrombosis
Endocarditis - sticky leaflets
Pannas/scar tissue on valve
Residual Lesions - VSD changes haemodynamics
Malposition - usually seen immediately post operatively
Post Op LCOS - mechanisms
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
DORV phsyiology
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
Blood mixing - TGA
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
Restrictive RV physiology
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
Post cardiac transplant - graft dysfunction
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
Restrictive Cardiomyopathy Physiology
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
Dilated Cardiomyopathy Physiology
Poor systolic function with large ventricles
PPV/afterload reduction
RV failure management
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
Blue BCPS - causes
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
Ventilation strategies to improve pulmonary blood flow
Goal: reduce mean airway pressure
TV 8-10ml/kg
Long IT
Low PEEP
Low rate
BT shunt with raised CO2
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
PA Banding - physiology
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)
Rejection post Cardiac Transplant
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
Blue TGA
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
Increased WOB post ccTGA repair (double switch)
Pulmonary venous obstruction (baffle) LV dysfunction (deconditioned LV, CHF) Coronary ischaemia PA band - semi lunar valve insufficiency Recurrent laryngeal N palsy Phrenic N palsy
Critical PS - blue post balloon dilatation
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
TET spell - physiology
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
Management TET spells
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
Reduced pulmonary blood flow post Norwood
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
Components Circular Shunt
- 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
Atrial ECG
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
Ischaemia on ECG
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
SVT Management
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
Complete Heart Block - with pacemaker failure
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
Pulmonary Hypertension - intubation
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
Fick Equation - Single Ventricle
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%
Single Ventricle Physiology: Manipulating the circulation
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
BT shunt vs RV-PA conduit vs hybrid
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
Post Op Norwood management
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)
Decompensated Heart Failure - physiology
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
Open Sternum Physiology
Uncouples Pra from increased ITP
- restores venous return and RV preload
- allows time to treat increased ITP (diuresis, ventilation)
Cardiac contribution to pulmonary dysfunction
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
Mixed Venous Saturations
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%
Causes low SvO2
low SvOw
- inadequate cardiac output
- low Hb
- low saturations
- increased O2 needs (sepsis, fever, seizures)
Restrictive LV physiology
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
Pulmonary Hypertension - risk factors
Increased pulmonary blood flow
- L to R shunts
L sided obstruction
High PaO2 (TGA)
ECMO - eCPR physiology
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
How does increasing systemic BP help in pulmonary hypertension?
Improved coronary perfusion to failing RV
- perfusion during systole lost in PHT
Improved interventricular interdependance
- septum moves back, improves ventricular contraction
Single ventricle physiology - restrictive ASD
Increased LA pressures
- pulmonary hypertension
- results in reduced PBF
- cyanosis
- pulmonary oedema - WOB
Decreased blood return to ventricle
- decreased cardiac output
Re-entrant Tachicardia
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.
Automaticity arrhythmia
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
TAPVD physiology
Unobstructed:
- behaves like large ASD
- increased pulmonary blood flow
- minimal desaturation - sats 85-90
Obstructed:
- early presentation - sick hypoxic baby
- pulmonary hypertension
- pulmonary oedema
Obstructed TAPVD
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
LVAD vs ECMO
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
Berlin Heart Prerequisites
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
VAD anticoagulation protocol
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
DORV repair
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
