Cardiology Flashcards
Cardiogenic shock definition
Acute circulatory failure causing inadequate oxygen utilisation by cells, caused by cardiac dysfunction
hypo perfusion with or without hypotension
phenotypes - commonest cold and wet
usually characterised by SBP < 90, HR > 60, oliguria, congestion
Ventricular assist devices
Type of mechanical circulatory support, which can be short or longterm which provides flow in order to maintain cardiac output
LVAD
RVAD
BiVAD
Total artificial heart
Minimally invasive - impella
Indications for VAD
Bridge to recovery - CS
Bridge to candidacy - improve organ perfusion and assess for transplant
Bridge to transplant
Destination therapy (international)
VAD components
- inflow cannula (to pump)
- outflow cannula
- pump
- electrical controller
- cable connecting device to controller
- power supply
VAD mechanisms
Pneumatic, hydraulic, mechanical pusher plate - pulsatile
continuous non-pulsatile - rotor, centrifugal
Contraindications to VAD insertion
General - age > 65 with biventricular failure
Resp - severe dysfunction fixed pulmonary HTN
CVS - severe valve lesions
CNS - severe stroke, inadequate psychosocial support
Renal - longterm RRT
Liver - cirrhosis, high BMI
Haem- contraindication to anticoagulant
VAD complications
Early:
Bleeding
Tamponade
RV failure
Haempdynamic instability
Late
LVAD failure
arrhythmias
pump thrombosis
embolic stroke
anticoagulation related e.g. ICH
Collapsed patient with LVAD
- signs of life and breathing (pulse may be absent)
- if no signs of life, auscultate for humming sound. if absent, LVAD failure
- ventilate and try to restart
- ensure power source working
if device not failed likely pathologies - ventricular rrhythmias - defib
- hypovolaemia
CPR controversial - likely to dislodge cannula, disrupt anastomosis. maybe if all other failed
Causes of bradycardia
Intrinsic
- idiopathic (degenerative)
- ischaemia
- cardiomyopathy
- infiltrative - sarcoid
- infective - paravalvular abscess, myocarditis
- psot cardiac surgery
extrinsic
- training
- drugs
- hyothermia
- metabolic abnormalities
- electrolyte abnormalities
- high icp
Types of pacing
percussion
transcutaneous
epicardial
endocardial (temp / perm)
How does pacing work?
delivery of electrical stimulus to the myocardium resulting in wave of depolarisation and contraction of the cardiac chambers.
relies on intact myocardial and or conducting tissue.
Generic PM classification
I - chamber paced O, A, V, D
II - chamber sense O, A, V, D
III - Response to sensing O, I, T, D
IV - Rate modulation O, R
V - multisite pacing O, A, V, D
Inhibition means that if there is spontaneous cardiac activity, the pacemaker is inhibited
Examples of atrial pacemaker modes
AOO - asynchronous atrial pacing (no sensing, no modulation). usually response to AAI with magnet. If SA node intact, will compete. If fast enough then SA node signal will fall on refractory period.
AAI - atrial demand pacing. senses atrial activity. if above threshold then pacemaker doesn’t;t do anything. if atrial firing too slow, pacemaker takes over. relies on intact AVN
Examples of ventricular pacemaker modes
If AVN doesn’t work or fibrillating atria
downside is poor a-v synchrony and poor rv-lv synchrony (RV ejection reduced, LV and atria contracting simultaneously)
limited to people in outpatient setting who are fairly stationary or in icu when atria and AVN have failed
VOO - magnet applied to VVI. Spread from right –> left –> LBBB. risk of r on t.
VVI - ventricle sensed, if QRS complex generated pacemaker does nothing. will fire if no ventricular activity
Dual chamber pacing benefits
- add atrial systolic volume to ventricular ejection
- prevents retrograde atrial contraction
- Better QOL
- lower risk of AF
Dual chamber modes
VAT - broken AVN. atria sensed, then paces ventricle. AVN becomes large pacemaker loop. Ventricular pacing broad
DDD
- if normal A and V contraction PM does nothing
- if one chamber doesn’t;t contract PM takes over
- if both don’t contract atrial then ventricle zapped, pre-determined interval
CRT-D / CRT-P
cardiac resynchronisation therapy - improve cardiac function, symptoms, morbidity in chronic HF
If ICD indicated then CRT-D
Pacemaker check in patient with temporary wires
every day
1. underlying rhythm - reduce PM rate to see native rhythm
2. sensitivity - minimum current the PM can sense, lower number = greater sensitivity. leave sensitivity at half the pacing threshold (sensitivity at which sense indicator flashes during each endogenous depolarisation)
3. Capture threshold - minimum output required to stimulate action potential - confirmed with QRS complex after each spike. reduce energy output until QRS no longer follows each spike. leave output at twice the capture threshold
4. rate - optimum 80-90. may wean to backup e.g. 40.
pacemaker problems
output failure - failure to produce a pacing spike
failure to capture - spikes don’t lead to qrs
over sensing - inappropriate inhibition of pacing in response to non-cardiac signal
undersensing - continues to pace, ignoring intrinsic cardiac activity
cross talk - DDD, ventricular wire senses atrial contraction and interprets as ventricular activity, therefore not pacing ventricle . if no AV conduction then no ventricular output
endless loop tachycardia - atrial wire internets ventricular contraction as atrial, leading to another ventricular contraction and so on.
overdrive pacing
Slow VT
pace above rate to take over myocardial activity and convert to sinus rhythm
OOHCA epidemiology
55 per 100,000
most at home
98% adults
50% witnessed
80% cardiac in origin
25% shockable initially
70% bystander cpr
< 10% survive to hospital discharge
In hospital
- PEA 52% asystole 20% shockable 17%
53% ROSC 23.6% survival to discharge
Key concepts in cardiac arrest management
- early recognition
- early cpr to buy time
- early defibrillation to restart heart
- post-resucitation care to restore qol
priorities
- competence at practical skills - CPR, defibrillation, simple airway management
- recognise shockable / non-shockable
- Hs and Ts
Drugs in cardiac arrest
- adrenaline - non-shockable 3-5 mins. shockable after 3rd shock
- amiodarone - refractory VT/VF after 3rd shock
- calcium chloride - hyperkalaemia or calcium channel blocker OD
- alteplase - PE
- sodium bicarb. hyperkalaemia, TCA OD
Post-cardiac arrest syndrome
- brain injury
- myocardial dysfunction
- systemic ischaemia-reperfusion injury
management priorities in cardiac cause
PPCI within 120 mins
- prolonged door to balloon time in STEMI associated with increased mortality
secure airway and IV access
NG and antiplatelets
cardio and neuroprotective maintaining MAP, temperature
delays - scan, cvc, art line
CT pre angio
if signs of cerebral or PE pre arrest
- headache
- seizures
- focal neurological deficit
- SOB / hypoxaemia
TOMAHAWK trial
delayed / selective PCI vs immediate PCI in OHCA NSTEMI - if haemodynamically and electrically stable appears no benefit to immediate PCI.
2021 ERC guideline - consider emergent angiography if high suspicion of occlusion e.g. shockable
Post-resuscitation care
RESP - LPV PO2 10-13 sats 94-98 PCO2 4.5-6
CVS - MAP > 65
RENAL ; UO > 0.5ml/kg/hr
GLUCOSE 6-10
TEMP < 37.8
AVOID SEIZURES
Neuroprognostication
M < 3 at 72 hrs without confounders
Two + of following = likely poor outcome
- CT / MRI showing hypoxic injury
- SSEPs absent
- Absent pupillary response
- NSE > 60 at 48 or 72 hr
- malignant EEG > 24hr
- status myoclonus < 72hr
e-CPR
VA ECMO - bridge to specific intervention
inclusion may be
- known reversible cause
- prolonged resuscitation anticipated
- signs of life during cpr
- short no flow and low flow times
ARREST trial - benefit
Cardiac arrest in CICU
Hypovolaemia
- bleeding - medical (coaguloapthy, platelets)/ surgical (drain output e.g. 400ml 1st hr, 200ml in consecutive hours)
- vasodialtroy shock / capillary leak - vasoplegia rewarming, sepsis, anaphylaxis
Low CO
- myocardial stunning, metabolic dysfunction, reperfusion injury, ischaemia
Hypoxia
- pulmonary oedema
- misplaced ETT
Electrolytes
- hypo / hyperkalaemia
- hypomagnesaemia
hypothermia
- failure to warm from bypass
tension
- kinked drain
tamponade
toxin
- e.g. protamine reaction
thrombosis
- coronary artery occlsion / PE
dysrthyhmias - AF, VT
Cardiac advance life support
management of cardiac arrest in post-op cardiac patient
cardiac arrest may present unconventionally - absence of pulsatile arterial trace, reduction in ETCO2
questionable benefit to CPR / Adrenaline - surgical complications high, may be worsened by mechanical injury
CALS protocolr
VF / VT - 3 x shocks / BLS / amiodarone
Asystole / bradycardia - pace if wires / BLS / external pacing
PEA - BLS / turn off pacing to exclude VF
Resternortomy
shock every 2 mins
FiO2 1.0, o PEEP
Exclude PTX / HTX
Adrenaline only by senior
restternotomy
full scrub sacrificed in interest of time
decontamination, sterile drape and gloves
scalpel to reopen
assistant hold wires while operator cuts
assistant pulls wires out
internal cardiac massage / drainage of tamponade
cardiac tamponade
condition whereby compression of the heart leads to increased intrapericardial pressure, impaired right ventricular filling, ultimately leading to obstructive shock and cardiac arrest
Causes
- neoplastic - primary cardiac, lung, lymphoma
- infective - EBV, CMB, HIV, TB, pneumococcal
- iatrogenic - PCI, TAVI, ICD
- Trauma
- vascular - type a dissection
- renal failure
causes of effusion unlikely to progress to tamponase
- autoimmune
- thyroid
- dressers syndrome
diagnosis of cardiac tamponade
clinical
- becks triad muffled heart sounds, hypotension, raised JVP
- pulsus paradoxical - pressure drop 10mmhg on inspiration
others
- electrical alternans, low voltage qrs
- cxr - large cardia shadow
- echo - effusion / ra / rv diastolic collapse
- diastolic rv collapse - 90% sensitivity
- systolic ra collapse - earliest sign
- plethoric ivc (> 20mm and < 50% reduction)
tamponade depends on compliance of pericardium and time rather than size
constrictive pericarditis vs cardiac tamponade
similariites
- diastolic dysfunction nad prserverd EF
- increased ventricular interdependence
- increased respiratory variation of vent inflow / outflow
timing
- constrictive - filling impaired by reaching elastic limit of pericardium. early diastole not affected
- tamponade - impaired filling throughout
pressure
- constrictive pericarditis prevents transmission of -ve intrathoracic pressures in inspiration chambers - RA pressure remains constant
- ra pressure decrease during inspiration in tamponade
pericardial drainage
if stabile - 12-24hr
- if shock - immediate
indications
for surgical drainage
- trauma
- ventricular rupture
- type a dissection
- purulent effusion in septic patient
contraindication to immediate
- uncrectte coagulaopathy
- pet < 50
- incr > 1.5
supportive measures in tamponade
- avoid surges in catecholamines - pain etc
- fluid bluses
- tertiary centre if possible
Hypertensive emergency
severe hypertension in association with acute hypertension mediated organ dysfunction
- malignant hypertension - HTN + fundoycopic changes, microangiopathy, DIC (fibrinoid necrosis)
- sudden severe phaeochromocytoma
- severe PET
- acute hypertension with other conditions - dissection, acute MI, acute HF
- hypertensive encephalopathy
- SAH, ICH
symptoms of hypertensive emergency
hypertensive encephalopathy
- headache, visual disturbance, lethargy, seizure, LOC
others
- chest pain, duponoea, dizziness
PRES - clinics-radiological diagnosis - hypertensive encephalopathy with white matter vasogenic oedema in occipital lobe
IX HTN emergency
All - fundiscotm ECG, bloods, ACR, pregnancy test in women
Specifics - echo, CT/MRI brain, CT aorta, CXR, US renal
BP targets
malignancy / encephalopathy - 25% reduction MAP
ACS / Pulm oedema - sBP < 140
Dissection - sBP < 120
Stroke < 185/110 if thrombolysis otherwise none
Infective endocarditis
infection of the endocardium - valves, walls
haematogenous spread of organisms
may gain access to blood stream due to IVDU / dental / immunosuppression
seed onto cardiac structure - non-native
sterile thrombotic vegetation - mass in heart, organisms adhere during bacteraemia - facilitated by platelets and fibrin
clinical features of IE
insidious presentations
- fever
- weight loss, anorexia
- murmur
- thromboembolic / immune phenomonen
acute / complications
- heart failure
- cariogenic shock
- septic shock
- myocarditis
- abscess
- pervalvular extension
- conduction disorders
- septic emboli
diagnosis of IE
clinical suspicion
Dukes criteria
- 2 major / 1 major 3 minor / 5 minor
major
- intracardiac mass on echo
- +ve micro - 2 separate isolates of typical organism
minor
- fever
- patient risk - ivdi or prosthetic
- vascular phenomena - arterial emboli, septic pulmonary infarcts, ICH, conjunctival haemorrhage, Janewy lesion
- immune phenomena - osler node, Roth spot, GN
- micro not meeting major
organisms in IE
- strep viridans / bovis and staph aureus
- HACEK
- haemophilus, actinobacillus, cardiobacterium, eikenalla, kingella
Indications for surgical management in IE
Hear failure - severe regurgitation obstruction, refractory pulmonary oedema, cariogenic shock
uncontrolled infection - abscess, MDR organism, fungi
prevention of emboli - very large vegetation
ACS
STEMI
NSTEMI
UA (no biomarker change)
In addition
- cardiac arrest
- electrical or haemodynamic instability with CS
MI diagnosis
- raised biomarker
- at least 1 of
- symptom of ischaemia
- new ST/T/LBBB
- new loss of viable myocardium / rwma
- intracoronary thrombus on angiography
STEMI ECG changes
2mm STE in V2-3
1mm STE in 2 contiguous other leads
New LBBB
Old LBBB and sgarbossa
MI classification
Type 1 - acute thrombus / plaque rupture
Type 2 - O2 supply / demand mismatch, normal coronaries
Type 3 - death
Type 4 - related to PCI
Type 5 - related to CABG
definitive management of STEMI
- STEMI presenting within 12 hrs of onset of symptoms and within 120 mins of time thrombolysis could be given
- fibrinolysis if PPCI cannot be delivered within 120mins. repeat ECG / rescue PCI
Antithrombotic managaement STEMI
DAPT aspirin / prasugrel. ticagrelor if not for PPCI
PPCI - GP IIb/IIIa inhibitor
anticoguatlion - UFH, enoxparin
Mx NSTEMI
- aspirin loading
- fondaparinux
- DAPT
- GRACE score for risk
immediate invasive management if unstable shock, arrhythmias - invasive < 24h if high risk established NSTEMI, dynamic hcnages
secondary prevention
ACEi, beta blocker, stain
DAPT 12mo
Causes of AF in critical illness
- pre-existing AF
- sepsis / infection - greater catecholamines
- hypovolaemia
- PE
- Electrolyte abnormalities
- vasoactive substances
- atrial stretch - volume overload
chronic structural / electrical remodelling - age. daiebets, HF
arrhythmogenic atrial subtrate and trigger
Mx new AF
adverse features (shock, syncope, chest pain, pulmonary oedema) - DCCV
correct reversible
- electrolytes
- ischaemia
- oxygenation
- volume status
- infection
manage instability
- rate related -b eta blockers
- rhythm related magnesium ,amiodarone
anticoagulation
DDX broad complex tachycardia
Regualar
- VT
- SVT with BBB
Irregular
- AF with BBB
- Pre-excited AF
Long QT
Start of QRS to end of T wave
affected by HR
QTc = Qt / square root of RR
430ms men 450ms women
Long QT syndrome - long QT is absence of secondary cause - inherited
Long QT in critical care
- Drugs
- Antipsychotics - haloperidol
- antiarrhtyhmics - amidoarone, sotalol
- TCA,
- others - maclroides, fluconazole
electrolytes - K, Mg, ca
Hypthermia
Raised ICP
Torsades de Pointe
polymorphic VT
multiple ventricular foci resulting in variable QRS amplitude, axis, duration
associated with prolonged QT. leads to VF
address precipitating cause
2G MgSo4
overdrive pacing
DCCV if unstable
defibrillation if arrest
Cardiomyopathy
structurally and functionally abnormal heart muscle
in absence of coronary artery disease, hypertension, valvular, congenital heart disease
Types of cardiomyopathy
Primary
- Dilated
- enlargement leads to deficient actin/myosin cross linking. systolic failure, embolic. familial = various. non-familial = prgancny, Kawasaki, myocarditis, alocohol
- Hypertrophic
- myocardial hypertrophy in absence of haemodynamic stress. Familial = glycogen storage disease. non familial = athletic training
- Restrictive
- stiff ventricles, impaired diastolic filling and dysfunction. hazardous anaesthesia (-ve inotropy, IPPV, vasodilation all problematic). familial = haemochromatosis non-familial = amyloid, scleroderma, radiation
- ARVC
- myocardial cells replaced by adipose or fibrous tissue.
Each phenotype - familial and non-familial forms
Secondary
- Toxins : alcohol
- Ischaemia
- Inflammatory : viral myocarditis
- Metabolic : amyloidosis
- Peripartum
Takutsubo cardiomyopathy
potentially reversible cause of acute HF
transient regional LV apical or mid-apical dysfunction without obstructive coronary disease
may mimic ACS - T wave, cardiac enzymes, chest pain
elevated NA concentrations - emotional or physical stress. apical ballooning
stress induced cardiomyopathy may also occur in neurogenic myocardial stunning
complications - acute HF LVOTO, MR, LV thrombus
Mx
- acute HF - vasoactive, MCS, ECMO
- LVOTO - fluid, beta blocker
- palm oedema - diuretics
- thromboembolism
- dyshythmias
peripartum cardiomyopathy
rare idiopathic CM
systolic dysfunction LVEF < 45% 3rd trimester or month postpartum
heart failure definition
clinical syndrome
structural / functional abnormality of the heart
leading to elevated intracardiac pressures and or inadequate cardiac output
at rest and / or during exercise
acute / chronic / acute on chronic
preserved EF / mild / mod / severe
Mx chronic heart failure
- beta blockers
- spironolactone
- ACEi
- SGLT-2
others - loop diuretics
- ARB
Non-pharm - smoking cessation, weight loss, cardiac rehab
- underlying disease
- cardiac reynchornisation
- MCS/transplantA
Advanced heart failure
persistence of HF symptoms despite maximal therapy
- NYHA III / IV
- Severe cardiac dysfunction (EF < 30% / isolated RV / non-operable severe valve / persistently high BNP)
- decompensation - episodes of pulmonary or systemic congestion, or low output, or malignant arrhythmias
- severe exervice impairment
causes of acute Heart failure
CHAMPIT
C - coronary ACS
H - Hypertensive emegrency
A - Arrhythmia
M - mechanical - rupture, trauma, valve
P - PE
I - Infection - myocarditis, sepsis
T - tamponade
(+ drugs)
presentation of acute HF
congestion
- SOB, cough, orthopnoea, PND, raised JVP, gut congestion, hepatomegaly, ascites
hypoperfusion
- cold, sweaty, oliguria, altered consciousness
- lactate, acidosis, creatinine
cariogenic shock
syndrome of life threatening tissue hypo perfusion due to inadequate cardiac output from primary cardiac dysfunction
- SBP < 90
- despite adequate filling
- signs of ypoperfusion
A - at risk - no signs or symptoms
B - Beginning - relationship time hypotension
C - classic CS - hypo perfusion beyond volume resuscitation
D - deteriorating - failing to respond despite vasoactive, MCS
E - extremis - cardiac arrest ongoing CPR / ECMO
INTERMACS - 1-4 micht be suitable for short term MCS. 5-7 stable ambulatory
MX acute left HF
myocardial hypperfusion - increae O2 delivery - high flow O2, cpap, IPPV, increase perfusion - inopressor, IABP, inodialtor
reduce myocardial O2 demand
- beta blocker, reduce afterload (vasodilator
improve myocardial function
- inotrope, revascularisation, alternative pump - VAD< ECMO
specialis input, transfer, relief of symptoms - opiates
HFpEF
HF symptoms / signs with EF > 50%
diastolic HF
passive and active filling of ventricle
cardiorenal syndromes
- acute decompensated HF –> AKI
- Chronic HF –> CKD
- AKI –> acute HF
- CKD –> chronic HF
- codevelopment of HF and CKD
Pulmonary hypertension
mPAP > 20 on right heart cath
1 - PAH - idiopathic. PAWP < 15 and PVR > 3 wood units ‘pre-capillary’
2 - due to LVF
3 - due to CLD
4 - due to chronic thromboembolic
5 - due to systemic disease
pathophysiology of pulmonary HTN
1 - vascular smooth muscle hyper troy
2 - diastolic dysfunction, ball up of pressure, MR
3 - HPVC
4 - obstruction of pulmonary vascular bed
Chronic pulmonary HTN Mx
- General - rehab, infection prevention
- ca channel blockers
- endothelia receptor blockers - bosentan
- PDE5 ihinitors
- supplemental O2
- lung transplant
Pulmonary HTN implications for critical care
admission
- RHF and supportive care
prognosis
- under 50 PAH 80% 5yr survival
- pulm HTN needing ICU - 40% mortality (esienmengers may be better as chronic RV remodelling
- intubation - haemodynamic collapse
worse outcomes
- low systemic BP
- low sodium
- high creatinine
morbidity and mortality with surgery
right heart failure
clinical signs and symptoms
- dyspnoea, reduced exercise, fatigue, dizziness
- decompensation - JVP, hepatomegaly, a ascites, peripheral oedema
echo - TAPSE > 17, P/V overload - RV:LV EDD > 1
rising lactate, low SCVO2 and anuria
PAC
right heart failure mx
general
-underlying cause
- O2
- avoid hypoxia, hypercarbia, acidosis
- avoid pain, hypothermia
- advanced monitoring - IBP, CVP, CO, PAC
- fluid assessment, may benefit from fluid or diuretics
specific treatments
- increase forward flow - milrinone
- reduce PAP - milrinone, epoprostonel,
- sildenafil
- maintain systemic BP (vasopressin less effect on PVR than NA)
- liaise with tertiary centre / ecmo
aortic dissection
creation of false lumen between layers of the aortic wall after creation of defect
high pressure blood flow extends the tear
intimal tear implicated occurring at regions of high stress and pressure
predisposing factors are high BP and integrity of vessel wall
risk factors
- BP related - HTN, stimulant drugs, pregnancy
- wall related - connective tissue disease, dyslipidaemia / plaques, aneurysm, iatrogenic
classification of aortic dissection
acute < 2 w chronic > 2 week
stanford
A - proximal - ascending aorta
B - distal - distal to left SCA
DeBakey
I - ascending tear, dissection involves all of thoracic aorta
II - ascending tear, dissection in ascending only
III descending, usually descrninfin only
a extends to diaphrgam
b beyond diaphragm
presentation dissection
severe pain, loss of pulse volume
sudden chest pain - ripping, tearing, stabbing
back pain (more in type b)
associated with tachycardia hyper/hypotension, sweating, breathlessness, stroke, syncope, differential pulses
air leak syndrome
movement of air from air containing cavity to one which doesn’t usual contain air
- tracheobronchail tree
- sinuses
- GI tract
- can compromise function and compress important striations
- PTX, pnuemomediastinum, pneumoperitoneum, pneumocephalus, pneumopericardium, subcutaenous emphysema
pneumothorax classificatio
spontaneous
- primary - no underlying lung disease
- secondary - underlying lung disease
traumatic
iatrogenic (ventilator, CVC, bronchoscopy, pleurocentesis, tacheostomy
bronchopleural fistual
connection between pleural space and major bronchus
air leak - persisten = more than 4 days post ip
mx PTX
unstable = drain
Primary spontaensou
- < 2cm conservative
- breathless or > 2cm needle aspration.
- if remain breathless or > 2cm - drain
secondary spontaensou
- breathless or > 2cm - drain
traumatic and iatrogenic generally need drain
PPV - drain
suction on chest drain
not routine
persistent air leak / incomplete re-expansion
high volume low pressure
management of large air leak
airway - check position
ventilation - luv, spont, differential / single lung / ecmo
monitoringserial
definitive - conservative, surgical or bronchoscpic repairs
urgical review in sponaenous
- persistent air leak 5 days
seconda ipsilateral ptx
1st contraleteral
Cardiac output monitoring
clinical
- vital signs / GCS / UO / CRT
non-invasive
- tran-thoracic bioimpendence
- TTE
minimally invasive
- PICCO
- LIDCO
- ODM
Invasive
- PAC
PAC
8Fr 110cm
- distal lumen - measure PCWP / SVO2
- Proximal lumen - 30cm RA - inject ate +/- 2nd for infusions (blue)
- Balloon port - red - 1.5ml
- thermistor 3.7cm from end
- monitoring connection
PAC waveforms
- CVP - 3-8mmhg
- RV - systolic 25 diastolic 0-10
- PA - Systolic 25 diastolic rise 10-20 + dicrotic notcg
- PCWP - 4-12
Landmarks - RA 20cm RV 30cm PA 40cm
PA measurements
Measured
- CVP
- RAP
- RVP
- PAP
- PCWP
- SVO2
- core temperature
- CO
Derived
- mean - mPAP / mRVP
- CI
- SV / SVI
- SVR / PVR / SVR / PVRI
SVRI (MAP – CVP)/CI x 79.92
1900-2400 dyn/sec/cm5/m2
PVRI (mPAP - PCWP) / CI x 79.92
SVO2 vs SCVO2
SCVO2 = central O2 sat (SVC)
SVO2 = mixed (PA)
In health
- SVO2 > SVCO2 (SVC from brain -greter O2 extraction)
Conditions when SVCO2 > SVO2
- Anaesthesia (reduced cerebral O2 extraction)
- Shock - blood returning via IVC lower O2
PACman
- PAC no improvement in mortality, LOS
- 10% complication rate
- alternatives available
Oesophageal doppler
Doppler effect - when a sound wave is reflected off a moving object, the frequency shift is proportional to the velocity of the object
ultrasound frequency, reflects of RBCs in descending aorta
velocity-time curve of blood flow
stroke disstance - distance travelled by blood in one heart beat multiple by aortic CSA = SV
90cm, trace at 40cm
assumptions
- angle of prove to direction of blood flow constant
- aortic CSA constant
- laminar flow
- 70% CO via descending aorta
ODM interpretation
- Low SV - fluid
- Low FTc - fluid (330-360)
- Low PV - inotrope
- low PV and low FTc - reduce afterload
PICCO
thermistor tipped femoral a line + cvc
transpulmonary thermodilution
pulse contour analysis (AUC systolic arterial pressure waveform is proportional to SV) - SVV / CO / SVR
GEDV / EVLW / CI / ITBV
PICCO inaccurate
Significant shunt
Significant PE
Significant AS
IABP
Pneumonectomy
PICCO interpretation
CI < 3
- Low preload (low GEDV / ITBV)
- low EVLW - give fluid
- high EVLW - give fluid cautiously
- high preload
- low EVLW - catecholamine
- high EVLOW - catecholamine and fluid removal
CI > 3
- low preload GEDV/ITBV - fluid
- high preload
- high preload, low EVLW - good
Lidco
standard arterial line, CVC not needed
interference if on lithium, shunts, NMBD
transpulmnonary lithium dilution - measures lithium on arterial side via change in voltage - generates blood flow
