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
