Cardiology basic science Flashcards
1
Q
What Anaerobic threshold is considered high risk in CPET?
A
<11ml/kg/min
2
Q
what is basal meta bolic rate?
A
3.5ml/kg/min
3
Q
What anaesthesia considerations should be kept in mind for a patient with aortic stenosis?
A
Avoid rapid drops in systemic vascular resistance (SVR): Maintain blood pressure, as patients have reduced cardiac output and rely on afterload to maintain perfusion.
Slow induction: Gradual induction helps prevent hypotension.
Maintenance: Use drugs that avoid further reduction of SVR, like phenylephrine if necessary.
Monitor: Close monitoring of heart rate, blood pressure, and rhythm is essential.
4
Q
Oxygen pulse is a term used to describe? the equation is?
A
oxygen uptake per heart beat
VO2/heart tare or SV x (CaO2-CvO2)
5
Q
Current guidance suggests when to do a pre-op ECG
A
If 1 or more risk factor and undergoing intermediate to high risk surgery
6
Q
Main indicators for pre-op ECHO? 2
A
Undiagnosed heart murmur
Evaluate LV function in pts with heart failure or dyspnoe of unknown origin
7
Q
When is pre-operative stress testing undertaken?
when to consider?
A
> or - to 3 risk factors and pts undergoing high risk surgery
consider in those with > or- 2 risk factors undergoing high risk or pts have intermediate risk surgery
8
Q
Stress radionucleotide myocardial perfusion imaging uses what?
A
dipyradimole-thallium imaging
9
Q
Clincal applications of stress echo? 4
A
diagnose CAD (inducible RWMA)
asses myocardial viability ptiot to revascularisation
identify a culprit lesion in pts with known CAD
risk stratification in pts with risk factors for cardiac disease prior to surgery
10
Q
When to do preop coronary angiography 3
A
acute MI, NSTEMI and unstable angina
refracotry angina not responsive to medical treatment
11
Q
Apfel and Koivuranta scores are used to predict?
A
PONV risk
12
Q
What scoring systems are available for pancreatitis?
Which one for ICU?
A
Glasgow and ranson
APACHE
13
Q
pre-operative optimisation with medication in coronary disease has 2 aims…
A
plaque stabilisation
reduction of ischaemia
14
Q
What did the POISE study demonstrate?
A
benefits of b-blockers lies ina small high risk group
give for 1 month pre-op and aim hr 60-80, systolic >100, use long acting B1 cardioselective if needed (bisoprolol or atenolol)
15
Q
What did the DECREASE 3 trial show for statins?
A
thos given statins in high risk group for 30days pre/post op had halved incidence of detectable ischemia and cardivasc. mortalitiy
16
Q
what do drug eluting stents release?
A
Paclitaxel or sirulimus
17
Q
what are the pleiotropic effects of statins? 6
A
increased endothelial production of NO synthas
Decreased endothelin 1 production
improved thrombogenic profile
decreased CRP/inflammation levels
plaque stabilization
reduced atherosclerosis
18
Q
Drug-eluting stent- what is mortality rate from stent thrombosis?
A
20%
19
Q
what to do with dual antiplatelet therapy?
A
continue aspirin,
if clopidogrel needs stopped 5-7 days pre op then restart asap
tirofiban has a short half life of 2hrs- good alternative
delay surgery 6-12 mnths after drug eluting stents or 6 weeks bare metal stents
20
Q
CVP- A wave represents
A
atrial contraction
21
Q
c wave in CVP_
A
unclear but possibly due to tricuspid bulging during ventricular contraction
22
Q
x- descent in cvp?
A
during ventricular systole- downward displacement of the ventricle and atrial relaxation
23
Q
v wave in CVP?
A
venous filing of the atria against a closed tricuspid valve
24
Q
Tricuspid regurgitations effect on v wave?
A
causes it to become more prominent
25
Y descent in CVP is?
Yawning opening of the tricuspid valve allowing passive ventricular filling
26
What does a rapid deep y descent potentially indiate
tricuspid regurgitation
27
what does a rapid short y descent potentially indicate
constrictive pericarditis, right sided diastolic failure- restrictive RV disease
28
what does a slow y descent indicate?
obstructive RV filling: tricuspid stenosis, right atrial myoxoma
29
What constitutes the largest single source of blood stream infection in hospitalized patients?
Central lines
30
Name ways to minimise infections with central lines
1. subclavian rather than jugular or femoral
2. totally implantable>tunnelled>untunnelled
3. PICC
transpartent dressing
no active infection prior to insertion
single lumen catheters
specialist nursing care to maintain cleanliness
31
4 pieces of data that can be gained from a PAC?
Pressure monitoring (PAC gives direct measurements of central venous, right sided intercardiac and PAP, PCWP
Mixed venous oxygen saturations
3. cardiac output with thermodilution, uses stewart hamilton equation to estimate CO
4. Vascular restistance- calculate by combing pressure and flow data
32
Assuming no valvular impedence- what 3 things impede flow in a arterial waveform?
1. Resistance (related to blood viscosity and valvular geometry)
2. Inertia- the volume of blood to be moved
3. compliance of the system( distensibility)
33
Where should transduce be placed within the PAC system?
mid point in a coronal plane and then transversely at junction og 4th intercostal space and the sternal margin
34
Normal RV pressures are?
Systolic 15-25 mmHg
Diastolic 3-12mmHg
35
36
what is usual PAOP
6-15 mmHg
37
causes of raised PAP with high PVR?
PE, pulmonary hypertension, hypoxic pulmonary vasoconstriciton
38
Raised PAP with normal PVR?
mitral valve disease, left to right shunt
39
Raised a wave in PCWP trace represents?
increased resistance to LV filling
Mitral stenosis, LV systolic or diastolic dysdfunction, volume overload, decreased LV compliance, (eg myocardial ischaemia, pr infarction)
40
Raised V wave in PCWP trace?
occurs when systole induces retrograde flow eg in mitral regurgitation or VSD complicating MI
41
when should PAOP be recorded- during which point of the breath cycle?
at end inspiration when intrathoracic pressure is equal to atmospheric pressure
42
pre-load in PAOP is represented by? and where (think west zones) must the tip of catheter lie and why?
LV end diastolic volume measurement- L atrial pressure
Weat zone 3 ( venous and arterial pressure is greater than alveolar pressure- so a continuous column of blood is created between tip of catheter and the left atrium)
43
Interpret preload estimations in PAOP with caution in 4 situations
1. lv diastolic failure
2. mitral valve disease
3. high levels of intrathoracic pressure- PEEP
4. raised PVR
44
what trial showed no benefit for icu patients CO monotioring with PAC as opposed to bedside/biochemical eg lactate/BP/Urine output or no monitoring
PAC-man
45
pulse contour analysis is reliant on what factors being in place?
Ventialted patient with stable intrathoracic pressure and >8ml/kg TV
46
How often does PiCCO system require calibration? what is needed for the system to work?
8 hourly cold water calibration
Art line with thermistor tip and a CVC line
47
temporal analysis of transpulmonary dilution curve allows what additional variables to be calculated? 2
Extrvascular lung water- cardiac or non in pulmonary oedema-a predictor of mortality in critically ill pts with acute lung injury
2. global end diastolic volume- volume based measure of preload (SV)
48
examples of uncalibrated monitors of CO ...2
PRAM pressure recording analytic method
Flotrac
49
assumptions made for Oesophageal doppler measurements? 4
constant aortic blood flow
radius of aorta based on either a direct measure or data variables
Angle between doppler beam and blood flow is within 30 degrees of axial flow
fixed ratio of blood flow between upper and lower limbs
50
Adrenaline admisnistration is less predictable than noradrenaline due to its actions on?
peripheral Beta 2 receptors which can lead to vasodilatation
51
Afrenaline exhibits positive dromotrophic and bathmotrophic effects which means?
increased AV conduction
increased myocyte excitability
52
How can adrenaline administration lead to elevated lactate levels?
Activation of the emden-meyerhoff pathway via pyruvate: makes interpretation of lactate levels potentially challenging
53
3 drawbacks to adrenaline infusion use?
1. significantly increased myocardial work and oxygen consumption (positive chronotropy and inotropy)
2.potential myocardial ischaemiafrom coronary vasoconstriction
-3. pro-arrythmogenic
-4. regional vasoconstriciton (splanchnic)
54
Dopamine is a natrually occuring precursor of?
Noradrenaline
55
In low doses (0.5-3mcg/kg/min) dopamine exerts its effects predominantly via?
DA1 and DA2 receptors
56
what effects does dopamine have at higher doses? (3-10mcg/kg/min)
Beta 1, some beta 2
57
when might dopamine be used in clinical practise?
in diuretic resistant hypotensive heart failure alongside furosemide infusion to improve haemodynamics and renal blood flow and facilitate diuresis
58
what is isoprenaline and when might it be used?
Synthetic form of dopamine
Used for its chronotropic effects in the treatment of bradycardia awaiting definitive pacing or in the presence of pulmonary hypertension behaving as an inodilator and inotrope
59
Dobutamine is?
Its uses may include?
A synthetic derivate of isoprenaline
B1 and B2 effects(vasodilatory)
so useful in low ouptu states without hypotension or alongside a pressor in refractory septic shock or cardiogenic and vasodilatory shock together
60
Milrinone and Enoximone are?
PDE 3 inhibitors that are inodilators- produce increased SV and CO, decrease in PAOP, PVR, SVR PA pressure
61
the effects of milrinone and enoximone are similar to dopamine with 2 important differences?
they have less effect on myocardial oxygen consumption and reduced tachycardia
more potent peripheral and pulmonary vasodilatation
62
Levosimendan is a ___________-sensitizer that exterts its effects in 4 ways
1. positive inotropy via?
2. vasodilatation of vascular smooth muscle
3. exerts cardioprotective effect via?
4. at high doses exerts what effect?
calcium-sensitizer
1. binds to calcium saturated troponin-c on cardiac myocytes to activate them causing positive inotropy
2. acts on ATP sensitive potassium channels on vascular smooth muscle
3. Via mitochondrial KATP channels
4. a mild PDEI
63
Levosimendan exerts what overall effects?
which patient group had positive results in recent studies?
increased CO/SV, reduced PAP and PCWP PVR and SVR
Critically ill as they cause increased CO/SV without increased myocardial oxygen demand
64
organic nitrates can have what effect in 50% of patients?
tolerance
65
nitroprusside contains what?
it mediates its effects through?
what may indicate toxicity? how to resolve this?
complex structure containing ferrous iron molecule bound to 5 cyanide molecules and nitric acid
mediates its effects by decomposition to nitrosothial on contact with red blood cells
suspected thiocyanate toxicity in confusion, lactic acidosis and seizures- may require haemofiltration
66
inhaled nitric oxide is effective to improve v/q mismatching because?
clinical applications of inhaled NO?
it is only absorbed into well ventialted areas of lung.
pulmonary htn of newborn
preventing RV failure due to pulm htn post heart transplant
supporting rv failure in critically ill
treatment in ARDS/COPD to improve oxygenation
treatment of ischaemia reperfusion injury after lung transplantation
67
potential complications of inhaled nitric oxide?
toxicity due to the formation of nitrogen dioxide (causing pulmonary oedema) or methaemoglobinamia (causing tissue hypoxia) though less likely at concentrations <80ppm
68
epoprostenol and iloprost are analogues of?
prostacyclin (pgi2) natrually occuring vasodilator
69
what are iloprost and eponoprostel licensed for use in?
treatment of NYHA class 3/4pulmonary hypertension via specialised aerosol or intravenous devices.
70
sildenafil is one of several ? it has been used successfully to treat?
phosphodiesterase 5 inhibitors- treats pulmonary hypertension following lung transplantation/rv dysfunction
also for weaning in pts on NO therapy
71
bosentan is?
an endothelin 1 inhibitor- pulmonary vasodilation in those with chronic thromboembolic pulm htn
72
conivaptan is?
a vasopressin receptor antagonist- reduces PCWP and right atrial pressure
73
neseritide is?
a recombiant DNA preparationof human ventricular BNP - binds to the guanylate cyclase recetor and converts GTP to cGMPresulting in smooth muscle relaxation- systemic hypotension limits its use
74
75
Mitral Stenosis (MS) - Anaesthesia Considerations
Q: What are the anaesthetic concerns for a patient with mitral stenosis?
1.Avoid tachycardia: Increases left atrial pressure and may worsen pulmonary congestion.
2. Maintain sinus rhythm: Avoid atrial fibrillation, which can exacerbate symptoms.
3. Optimize preload: Slight fluid loading may be beneficial, but excessive volume can increase pulmonary congestion.
4. Inhalational agents: Use cautiously as they can cause vasodilation and reduce preload.
76
Mitral Regurgitation (MR) - Anaesthesia Considerations
Q: What anaesthetic management is important for mitral regurgitation?
1.Maintain preload and afterload: To prevent a drop in stroke volume.
2.Avoid bradycardia: It can exacerbate regurgitation by prolonging the time the valve is open.
3.Inotropic support: Inotropes like dobutamine may be used if needed.
4.Minimize increases in systemic vascular resistance: As high SVR increases regurgitation.
77
Q: What should be considered in anaesthetic management for a patient with aortic regurgitation?
A:
1.Increase preload: This helps improve stroke volume and prevent further regurgitation.
2.Avoid vasoconstriction: This increases afterload, worsening regurgitation.
3.Maintain heart rate: A higher heart rate can reduce diastolic filling time and increase regurgitation.
4.Inotropes: May be needed to support left ventricular function.
78
What are the anaesthetic implications for a patient with tricuspid regurgitation?
What are the anaesthetic implications for a patient with tricuspid regurgitation?
A:
Increase venous return: Fluid boluses or careful positioning to enhance venous return to the heart.
Avoid increased pulmonary vascular resistance: Keep pulmonary pressures low.
Right-sided heart failure: Patients may have symptoms of right heart failure, and careful management of the airway and ventilation is essential.
79
How do stenotic lesions impact cardiac output in VHD
Stenotic lesions (like AS or MS) reduce the flow of blood through the valve, causing an increase in pressure in the chamber before the valve and a reduction in cardiac output
80
How do regurgitant lesions impact the CO
Regurgitant lesions (like AR or MR) result in backward flow, causing volume overload and eventually decreasing cardiac output due to reduced effective forward stroke volume.
81
What are the anaesthetic considerations for pregnant patients with valvular heart disease?
Cardiac output increases: Pregnancy causes an increase in blood volume and heart rate, which can exacerbate symptoms of VHD.
Vaginal delivery: A well-managed vaginal delivery with close monitoring is preferred over cesarean section unless obstetric complications arise.
Avoid excessive fluid administration: Increases the workload on the heart, particularly in patients with mitral or aortic regurgitation
82
Normal valve area in Mitral valve- what can it progress to and when do symptoms usually present?
4-6cm2
<1.5cm2
83
Describe the course of heart failure in MS?
There will initially be a low pressure in LV and underfilled, need for assisted filling in diastole from LA when heart rate is low (increased diastolic filling time needed) increasingly and this dilates to try and reduce PA pressures and RV will start to compensate and hypertrophy and eventually fail, PA pressures increase and eventually leads to chronic pulmonary hypertension
84
When is valave surgery required in MS for elective non-cardiac surgery?
<4 mets functional capacaity
85
How to avoid things that may worsen PH in MS?
hypercarbia, acidosis and hypoxia
86
What are the hazards associated with both regional techniques and cardiac valve replacement in MS
Take care with regional due to effects on haemodynamic stability and fluid/volume status
When valve is replaced the changes in preload (sudden increase) the chronically underfilled LV may fail to cope with the sudden increase in pressure
87
Which VHD may tolerate regional techniques well?
AR
88
Commonest causes of AR in adults?
rheumatic fever
Bacterial endocarditis
Aortic dissection (trauma)
Connective tissue disorders (marfans, ED, ankylosing spondylitis)
89
AR and MR like what features of heart rate and afterload/SVR?
Fast and loose SVR (minimise the time in diastole to decrease regurgitation. Lower afterload pressures mean more forward flo.
90
In AR the onset of dyspnoea usually signifies mortality within how many years?
2-4 years
91
Grading of aortic stenosis
1. mild>mean pressure across valve> valve area?
2.moderate
3.severe
4. critical
1. <25mmHg, <1.5cm2
2. 25-40, 1.5-1
3. >40, <1cm2
4.>70 <0.6cm2
92
in AS eventually there is a fixed________state and an inability to compensate for ___________
low cardiac output state
vasodilatation
93
In AS the onset of angina usually indicates a 5 yr mortality of?
Onset of syncope?
Onset of congestive cardiac failure?
5 years
3years
2years
94
Aetiology of MR?
chordae
papilliary
LV failure?
leaflet MR may occur due to?
Chordae MR- endocarditis or after MI
Papilliary may occur after ischaemia to pap muscles
LV failure- due to annular dilatation
Leaflet MR may occur due to Mitral prolapse, rheumatic fever or endocarditis related
95
MR fractions of >___% compromise cardiac output
60%
96
Which 2 trials have drawn attention to the pre-diabetic potential of beta blockers? and other potential adverse effects
ASCOT and VALUE
97
Which CCBs are contraindicated in patients on beta blockers?
Non-dihydromyridine (eg CCBs verapamil)
98
which electrolyte disturbance can be seen with ACEi/ARBs?
hyperkalaemia due to aldosterone blocking effects
99
in htn, prolonged hypotension of >____% is independantly associated with ?
Try to maintain blood pressure within what limits?
40%
cardiac events
20% of pts normal
100
systolic PAP can be estimated on ECHO by looking at?
the velocity of the tricuspid regurgitant jet
101
What drug treatment may be useful in patients with PH who showed vasodilator responsiveness at PAC testing
CCBs
102
What makes up 20% of cardiac malformations
VSD
103
What determines the significance of a VSD? 3
Size of the VSD
The PAP/SVR
104
VSD- describe what happens with regards to LA and LVEDF
VSD l-r shunt leads to an increase in LA volume due to attempt to have enough pre-load to maintain CO with the degree of volume being shunted. This can then lead to pulmonary congestion.
105
What can happen as a secondary effect in larger VSD with regards to the ventricles
The ventriclar pressures can equalise along with pulmonary vascular bed leading to a single chamber effect- if then the pressure in the aorta is less than PVR this can lead to r-l shunting
106
which measure can help distinguish an ASD from a vsd, what is this called?
pulmonary artery pressures
Eisenmengers syndrome
107
PDA is a communication in?
Usually closes when?
What happens in the shunting process?
Why might coronary and splanchnic circulations be affected?
Pulmonary artery and aorta
there is l-r shunting so la pressures can increase and also an increase in volumes to accomodate the loss of volume due to the shunted blood to maintain a normal co
There is shunting throughout the diastolic and systolic phasesand the diastolic flow may limit coronary/splanchnic perfusion
108
What 4 abnormalities in tetralogy of fallot?
Pulm stenosis
VSD
overriding aorta
rv hypertrophy
109
describe the process of a 'fallot spell' and the cause
Pulmonary infundibular spasm leads to complete r-l shunt so hypoxia, relieved by squatting or 100% oxygen
110
What conditions may predispose to supra valvular PS
Noonans, williams syndromes
Toxoplasmosis or rubella
111
ASD can lead to what shunt and what can happen to atria and ventricles
l-r shunt
biatrial enlargement
ventricular - RV overload
112
PFO affects how many people?
this can lead to?
what can happen in ventilated pts who are critically unwell?
20-25% of people
Paradoxical embolism
shunting may result in disproportionate hypoxaemia
113
Mechanisms of VTE? 4
venous stasis causing local hypoxia and endothelial activation
activation of innate and acquired immunity
Activation of platelets
microparticles ( these are submicron particles that are shed from white cells, platetlets and endothelial cells) they provide a membrane surface for assembly of clotting cascade products
114
main components of VTE
red cells and fibrin
115
name 3 congenital causes of VTE?
protein c and protein s deficiency, antithrombin 3 deficiency
116
what is dabigatran?
what property of it means consider what when needing reversed?
Direct thrombin (factor 2a) inhibitor
because it directly inhibits thrombin you may need factor 7 replacement along with prothrombin complex concentrated and ffp when major bleeding occurs
117
Rivaroxaban is?
it is superior to enoxaparin for use in what scenario?
What may be needed if bleeding as it is an upstream inhibitor of coagulation
A direct anti 10a inhibitor
superior in extended VTE prophylaxis following orthopaedic surgery
factor replacement needed in cases of overdose or major bleeding
118
Fondaparinux is what drug?
It is an indirect factor xa inhibitor
119
fondaparinux may be better than?
and is useful in what situation?
enoxaparin
Useful in HIT
120
how does aspirin work?
what have studies demonstrated in its use in primary and secondary prevention?
It causes the acetylation of cycloxygenase cox-1 enzyme that persists for the lifetime of the platelet
25% reduction in fatal vascular events
121
clopidogrel is part of what family? what receptor does it act on?
thienopyridines
the P2Y12 receptor irreversible binding on platelet surface
122
what are tirofiban and abciximab?
when are they used?
GP2b3a receptor antagonists
administered iv in acute setting of an ischaemic event
123
what scoring system is used to estimate stroke risk in AF?
CHADS2
congestive cardiac failure
Hypertension
Age >75
diabetes
prev stroke/tia (2)
124
high risk to use bridging with theraputic LMWH
Moderate risk to consider either proph or thera LMWH
Low risk to consider proph lmwh or nothing
mechincal metal valve
chads2 score 5-6 with AF
recent VTE
chads2 3-4
Bileaflet aortic valve
AF with chads2 1-2 or 1 previous episode of vte
125
PE - risk categories include- and features of each
High (>15% mortality- any hypotension or shock)
Intermediate (mortality 3-15%) no shock/hypotension but evidence of RV dysfunction or myocardial injury
Low risk (<1% early mortality) no adverse features or risk factors
126
