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Cardiology - Coggle Diagram
Cardiology
Preoperative risk assessement
Mitigation: Prehab, optimise fluid and inotropes, staff, facilities
Counsel, document, consider risk benefit
Goldman
Lee
History
Prescence, symptoms, severity, stability, prior treatment
Clincal
Major
REecnt MI
decompensated CCF
unstable angina
Signiificant arryhtmias
severe valvular heart disease
Intermediate
Stable angina
MI >6/12
Treated MI
DM
Minor
old age
Uncontrolled HPT
abnormal ECG
Non sinus rhythm
Functeional Capacity: METS
Type of surgery
High Risk: Aortic , vascular, prolonged, fluid shifts and haemorrhage
Intermediate: Carotid endartectomy, head and neck, ab, chest, orthos
Low: supereficial, cataract, breast.
IHD
Pathophkysiology
Atheroma
SUPPLY DEMAND make this left to right
Rupture/emboli/thrombi
Increased risk during surgery
Sympathethic surge-> I+ platelet adhesions
Increased coahualtion,
Blood supply
mechanical
Vessel calibre
Extensive capillary network
Proximal Epicardial arterires: elastic/ conductance
Precapillary: Muscle sphincters, regulate to local metabolic Adenosine and NO
Capillary: Endothelial NO and ET-1
atheroma, spasm, tone
**
occlusion
decrease in flow and pressure drop post obstruction
r^4
symptoms at 90% occlusion
Atherosclerosis: mechanical, chemical and elastic limitation
Heart rate: time in diastole compensated by metabolic
Systolic compression
endocardial flow
Coronary VENOUS flow also
CPP
dBP - LVEDP
Metabolic flow coupling
60% Fatty acids
40% CHO, glucose= lactate
Hypoxia: some anerobic glycolysis, then death
DO2
Hb concentration
pA02
1.34Hb.SPO2 + Pa02x 0.003
Autoregulation: 60-180
rest 80ml/min/100g to 400
low PO2
adenosine
NO, lactate, H, CO2
Neural
Effects on vessels is countered by metabolic effects of myocytes
Systemic adrenaline
beta2, vasodilatation
Demand
Contractilty
myocardial force independent of preload and afterload
force and velocity
SNS, inotropes
Wall tension T= Pr/2h
Laplace
T= Transmural P x Radiuis/ 2thickness
Preload and afterload increase wall tension
If extramural pressure ( intra thoracic or diastolic aortic pressure) must lead to a an increased Intramural pressure
Pressure volume curve area = work= oxygen reqd
Heart rate
increases amount of contractions per min
but decreases tension by reducing filling, smaller; radiuis;less tension
Bowditch effect: more intracystolic Ca with higher rate
Tutorial: S Moodley
Ischaemia
Hypoxia from Supply vs Demand
Metabolite accumulation, then symptoms
Obligate Aerobic, diastole and systole is active
Abnormally high intra-cytosolic Ca causes necrosis
Reuptake is active
Infarction: 10min, moves from endocardium to epicardium
Stunning
initial dysfunction after reperfusion
slow return, when myofibrils are resynthesized
from: Oxygen free radicals and intracystolic Ca overload
Hibernation
Protective
Chronic low MDO2
Preconditioning
Protective
after short episodes of ischaemia
becomes tolerant of Ca overload
Volatiles: protective
Circulation
5% of total CO
ml/100g/min
RCA has similar flow in systole and diastole vs LCA ( diastole mainly)
Intraoperative considerations
avoid tachycardia and BP extremes
supply vs demand
sympathetic activation mitigation
maintain CPP: diastolic BP, coronary diameter
Prevent hypoxia: maintain normoxia, Hb >10
Minmise ventricular wall tension: normal LVEDP
Premed
Anxioloysis
Beta blocker: reduce heart rate
alpha 2 agonist: sedation. analgesia
Induction
Avoid hypotension (titrate)
Avoid ketamine: indirect stimulation SNS
Intubation
Blunt response: opiod, IV local, MgSO4, induction agent
Mainatenance
IAA-> vasodilation, min effect on cardiac output
Halothane: vagal stimulation, D- cardiac output
Isoflurane: coronary steal syndrome
Bradycardia ok if BP normal
Analgesia
MMA: minimise SNS
opiods: D- PVR
NSAIDS: antithrombotic
Neuraxial for postop in abdominal surgery
Pre-op regional for NOF preop complications
Monitoring
ASA
TOE
IABP
CVC
HCT > 30%
Hb> 8
ECG: resting, Halter, stress
Imaging: PET, MUGA<
Clinical: METS 6min walk
Direct
Ventriculography: Angiography
Fick:
Kety-Schidmt: Nitrous oxide or FFA
Microcirculatory resistance
Endothelial Fxn: occlusion and reperfusion
Reversal and recovery
Anticholinergics: braycardia
Antimuscarinic: tachycardia
Extubation response
Avoid hypothermia, hypoxia, hypotension, tachycardia, shivering, pain, anaemia
Regional
Epidural: decreases preload, afterload, coagulation responses
Analgesia
ESC ACS
#
Injury
CTn > 99th percentile, acute if rises/falls
Infarction
CTn elevation
Setting: Clinical or ECG changes
10min only
Inside to out , subendo to sub epi
Biomarkers
Troponin I > TnT > CKMB
Release can be n, permeability, death
Mutiple reasons
COpeptin
Rulin in/out ( use o and 1 or 2 hours)
PPV is 60% for rule in, butr still need ICA
TYPEs
1: Atheroscelrotic plaque rupture
symtoms, ECG ischaemia, pathological Q waves, imaging of loss or new RWMA suggestive of ischaemia, angiography thrombus
Type 2: Supply demand
may be present in CAD or develop into type 1
Spasm, dissection
NSTEMI management
Clinical Scores
GRACE
Hypertension
Intraoperative management
Ischaemia, arrhythmias, haemodynamic instability more common if preop BP high
Titrate volatiles and vasoactive drugs
?continue vs stop ACEI
Altered cerebral autoregulation
20% deviation only
Mointoring
IABP: if swings/haemorrhage anticipated
ECG
watch fluid admin and Ventricular compliance
Induction
Hypotension then HPT
Often volume depleted
any agent ok
Ketamine with BZA/propofol
Blunt intubattion with opiod: fentanyl 2.5-5mcg/kg
remifentanil 0.5l-1mcg/kg
lignocaine 1.5 mg/kg
Esmolol: 0.3-1.5mg/kg or labetalol 5-20mg
MgSO4
Maintenance: titrate to BP
Vasopressors
Antihypertensive Drugs
CIEDS
Pacemakers
Set a time interval for sensing and action, inhibition or triggering of an impulse, and where that action is carried out.
Coding
Rate-responsive Pacing
Rate modulation in response to a certain monitored condition, exercise,
Accelerometer, thoracic impendence, blended to minute volume
Sensing
Multisite
(more than one lead in a chamber, or biventricular pacing)
Cardiac resynchronisation therapy
*
Pacing
Multisite Pacing
ICDS
Radioopaque thick coils
Perioperative management
Check device in preceding 6-12 months
Check with CIED team
Electromagnetic Interference
0-10nine Hz can interfere
Xrays, Infrared, UV unlikely
Inhibition of pacing most common effect
Asynchronous pacing
Defibrillatory shock (watch for changes in pacing and unrecognised EMI
EC monopolar>>>>>bipolar
Evoked potential monitors
Nerve stimulators
External defibrillators
Fasciculations
Shivering
Large Vt
MRI
ECT
EC shock wave lithotripsy
unipolar ICED are at higher risk ( pulse generator =anode, circuit= antenna
Noise disregarders
Filters and shields
Intraop
Adverse outcomes to avoid
Damage to device, leads, site
Failed pacing/defib
Inappropriate defib
Changes in Pacing
Inadvertent reset
Preop
cardiac autonomic neuropathy
Tests (normal)
Deep breathing HRV
HRV with standing
Valsalva
BP changes with standing
Handgrip
DIBP increases by > 16mmHg
Cold pressor response
Investigations
ECG
altered ANS innervation
dysrryhtmias
undiagnosed /subclincal ischaemia
Echo
Dliation
dyskiesia
Valvular Heart Disease
Mitral Regurgitation
Haemodynamic
Goals : FULL, FAST FORWARD
adequate preload
high normal HR (>90 reduces systolic regurgitiant time, and diastolic filling t4 LV overload)
Low PVR
Low SVR
Pathophysiology
occurs before aortic valve opens (LVEDV low EF is supranormal)
H
Complex Cardiac lesion
R to L shunt, PDA, Eisenmengers
Consider mass effect
RVH: dominant R wave
VSD: Paradoxical embolism
GOALS
Reduce Shunt
Maintain Afterload
Minimize PVR
Protect Preload
Avoid Tachycardia
Anaesthesia
Physiology
Microcirculation
Arterioles
Major resistors, increase in number< decrease in radius
metarterioles: bypass and control
vasomotion
Lymphatics
Blind ends
Absent in skin, CNS, Cartilage and Bone
Actin/Myosin, Valves, Muscle Pump
Protein flow varies
Returns the 4l cap filtrate
Capillaries
Local beds
Q=A.V
T= P.r/2h thin and narrow, low tension, higher pressures 35mmHg tolerated
Dilate:
Ach, ATP, bradykinin, serotonin, Substance P, histamine
Causes
NO
formation from L arginine
increased CGMP
Decreases cytosolic Ca
vasodilation
Prostacyclin
from AA
inhibits platelet agg and vasoconstriction
Glycocalyx
continuous, intraluminal, covers gaps
subglycocalyx space Onc determines NFP
Damaged by: Shear, Inflammation (ANP, DM, hi GM, TNF bradykinin, CRP, Tryptase)
Protected by: Hydrocortisone, Sevoflurane, ATIII, NAC
Starling Forces
NFP = ( Pcap-Pif) - (Onc cap- Onc if)
Subglycocalyx onc pressure more important
Capillary hydrostatic most important
proporional to Postcap resistance/precap resistance
POST cap resistance more NB
Pharmacology
Inotropes and pressors
Sympathometics
Beta
alpha
Non catecholamines
PD3i
Ca sensitisers:Levosimendan
Vasopressors
alpha
Vasopressin
