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Post operative management of the patient with cardiac disease
Cardiac physiology
Preload
Starling’s law. Now thought that the relationship between stroke volume and
end-diastolic volume may be a linear one
Afterload
- def: load on a muscle after the commencement of contraction
- best equates with systolic myocardial wall tension. Not synonomous with SVR
- from Laplace’s law tension (T) if given by:
T= Ptm x R2/2H
where Ptm is the ventricular transmural pressure, R=ventricular
radius and H=ventricular wall thickness
- factors which increase afterload:
- increased ventricular radius
- increased intracavity pressure
- increased aortic impedance/SVR
- negative intrathoracic pressure
- factors which decrease LV afterload:
- increased wall thickness
- positive intrathoracic pressure
- decreased intracavity pressure
- decreased aortic impedance
Contractility
- inherent property of ventricle to perform work, independent of preload and
afterload
- cannot be measured directly
Myocardial oxygen supply and demand
Anatomy
- LCA divides into LAD and Cx arteries. Supplies anterior and lateral aspects
of LV, RBB, anterior fascicle of LBB and anterior 2/3 of septum
- flow in LCA occurs predominantly during diastole
- RCA supplies RA, RV, diaphragmatic and posterior walls of LV and lower 1/3
of septum. Also SAN in 55% and AVN in 90%. Flow occurs throughout cardiac cycle
- NB coronary dominance refers to which artery supplies posterior descending
artery. Flow in LCA is several times that in RCA
Physiology
oxygen extraction in coronary circulation is 60-70% so there is little scope
for increased extraction if demands increase. Therefore increased demand has
to be met by increased supply
LV perfusion occurs in diastole essentially and thus diastolic conditions
are of paramount importance
LCA blood flow = (Aortic diastolic pressure - LVEDP)/coronary artery
resistance
conventional belief is that perioperative myocardial ischaemia is due to
increased demand associated with tachycardia and hypertension or hypotension.
However recent data suggest that vasoconstriction and thrombotic occlusion may
also contribute
Specific cardiac disorders
Mitral stenosis
- severity can be assessed on basis of valve cross-sectional area:
- < 1 cm2 = severe
- 1 - 1.5 cm2 = moderate
- 1.5-2.5 cm2 = mild
- development of AF and loss of atrial contraction results in a marked
deterioration of haemodynamic function and may lead to an exacerbation of
pulmonary oedema
- LV compliance often reduced
- avoid:
- bradycardia because of relatively fixed stroke volume
- tachycardia because this reduces diastolic filling time and causes a large
increase in LAP which may precipitate pulmonary oedema and reduce cardiac
output
- hypovolaemia because this reduces LAP and therefore ventricular filling
(effect magnified by stenosed valve)
- vasodilatation, for the same reasons
More on mitral stenosis
Mitral regurgitation
Haemodynamics
- to and fro movement across valve
- regurgitant jet throughout systole
- forward flow through aorta decreased
- increased flow during diastole.
- increased LA and pulmonary venous pressures
- large V wave during ventricular systole
- left atrial pressure at the end of diastole similar to that in the ventricle
as valve not obstructed. Mean LAP usually not as high as in mitral stenosis
- LV dilatation and LVH
Management
Avoid:
- increased SVR; leads to increased regurgitation
- bradycardia; causes fall in cardiac output because ability to increase
stroke volume is lost. May also lead to over distension of LV
- myocardial depression; contractility progressively impaired in both acute
and chronic mitral regurgitation and therefore these patients are
particularly sensitive to myocardial depression
More on mitral
regurgitation
Aortic stenosis
Pathophysiology
- outflow obstruction results in relatively fixed stroke volume
- obstruction leads initially to LV hypertrophy and, if not relieved, to LV
failure and dilatation
- LV hypertrophy increases transmural pressure and decreases coronary perfusion
pressure
Problems
- LV hypertrophy and difficulty in oxygenating the subendocardium. The
vicious cycle that must be avoided is:
- high LV filling pressure
- decreased subendocardial perfusion pressure
- decreased subendocardial oxygen delivery
- subendocardial dysfunction
- decreased cardiac output
- decreased aortic and therefore coronary perfusion pressure
- further ischaemia
- dysrhythmias
- VF
Once in VF these patients are very difficult to resuscitate.
- LV dysfunction
- stroke volume relatively fixed and therefore falls in heart rate and in SVR
poorly tolerated. In the case of the latter, a fall also reduces coronary
perfusion pressure which may result in a reduction of cardiac output. Small
increase in SVR can usually be tolerated provided LV function has not
deteriorated
- tachycardia is also poorly tolerated because of the reduction in duration of
diastole
More on aortic stenosis
Aortic regurgitation
- associated with increased LV compliance and raised LVEDP
- avoid bradycardia and increased SVR as both increase regurgitant flow and may
precipitate cardiac failure.
- tachycardia and low aortic diastolic pressure result in decreased coronary
blood flow. Therefore the combination of ischaemic heart disease and AR
problematic
- associated with impaired contractility with chronic volume overload and
increased sensitivity to myocardial depressants
More on aortic regurgitation
Post-cardiac transplant patients
- transplanted heart denervated
- physiological changes:
- resting stroke volume and indices of myocardial contractility normal or
slightly reduced in the absence of rejection or significant pulmonary
hypertension
- under resting conditions intrinsic mechanisms (eg spontaneous
depolarization in pacemaker cells and Starling mechanism) can sustain
circulation
- demand for increased cardiac output met in short term by increase in
stroke volume rather than the normal response of increased heart rate. These
patients said to be "pre-load dependent"
- after some delay transplanted heart does increase its rate and development
of maximum heart rate is slower than in patients with innervated hearts.
Delay in achieving maximum heart rate seems to correspond to time required
for secretion and circulation of catecholamines
- return of heart rate to baseline also slower; probably related to absence
of vagal input
- note that while sympathetic stimulation can increase heart rate via
catecholamines there is no analogous mechanism for parasympathetic
stimulation to cause bradycardia
- denervation appears to have no significant effects on AV conduction time
or ventricular conduction
- note that remnant of native atria is left and that there are often 2 p
waves on ECG
- pharmacodynamic changes:
- drugs that act indirectly on heart fail to produce their effects eg
atropine, pancuronium, neostigmine
- even drugs that are directly acting may have unexpected effects eg digoxin
would seem to exert both parasympathetically mediated and direct effects on
cardiac conduction. Thus acute administration of IV digoxin has no effects
on AVN refractory period in cardiac transplant patients while it
significantly increases it in other patients. However studies of chronic
administration indicate a direct effect on the conduction system
- effects of norepinephrine also altered.
Norepinephrine infusion results in
an increase in BP which decreases in intrinsic rate of innervated atria as a
result of baroreceptor reflexes. In denervated hearts the intrinsic rate
rises due to a beta effect that is usually masked
- transplant recipients that were previously in severe heart failure have
reduced sensitivity to alpha1 agonists for as long as 32 months
after transplantation. Clinical significance unclear.
- by 3 yrs approx 30% of survivors have multi-vessel coronary stenoses.
Myocardial ischaemia is silent because of denervation and paroxysmal dyspnoea
may be the only symptom of ischaemia. Careful pre-operative assessment and peri-operative
ECG monitoring essential
Non cardiac surgery
- studies of post-operative period are few but data so far suggests that
post-operative factors may be at least as critical as intra-operative factors
- post-operative period can be stressful for several reasons:
- onset of pain during emergence from anaesthesia
- fluid shifts
- temperature changes
- hypoxia more likely
- changes in plasma catecholamine levels
- changes in haemodynamics
- changes in ventricular function
- changes in coagulation
- post operative myocardial ischaemia difficult to diagnose. Unexplained
hypotension, arrhythmia or pulmonary oedema may indicate ischaemia or MI
Management
- AVOID HYPOXIA. Supplementary oxygen should be continued for at least 24 hrs
and overnight for several days
Mechanical ventilation
- continue until patient warm, well oxygenated, haemodynamically stable
- negative intrathoracic pressure results in rise in afterload which may
precipitate cardiac failure
- respiratory and central stimulants (eg naloxone) may provoke massive
sympathetic stimulation and should be avoided
Circulation
- maintain BP & HR within 10% of patient's normal
- fluid shifts and continued blood loss are main causes of hypotension but
consider pneumothorax, myocardial ischaemia
- when considering causes of hypertension do not forget that urinary retention
can cause severe discomfort and hence hypertension
- dobutamine particularly useful in patients with AR as does not increase
afterload
Temperature
- shivering increases oxygen demand. Can be reduced by morphine but may
require temporary muscle paralysis
Cardiac surgery
Factors which influence post operative course
- pre-op factors
- surgical procedure and competence
- myocardial protection:
- cardioplegia
- hypothermia
- newer techniques such as addition of Ca channel blockers, substrates such
as aspartate or glutamate, adenosine regulating compounds; use of warm blood
cardioplegia before removal of aortic X-clamp and retrograde cardioplegia
via coronary sinus
- complications of cardioplegia include complete heart block due to K+
overload and infusion of contaminated fluid (rare)
- diffuse disease, myocardial hypertrophy and decreased myocardial reserves
shorten usual 20 min period of protection between doses
- anaesthetic technique
- cardiopulmonary bypass. Exposure of blood to non-endothelial surfaces and
shear stresses may cause:
- trauma to red cells
- diffuse inflammatory reaction via activation of WBCs and complement
- microembolism of air and microaggregates to cerebral and/or coronary
circulation. May lead to neurological deficits and myocardial dysfunction
- activation of and damage to platelets with resultant platelet dysfunction.
Loss of GPIb receptor from platelets leading to failure to form platelet
plug. Loss of receptor can be prevented by prophylactic use of aprotonin
- post operative complications
Management specific to post cardiac ICU
Fluids and circulation
- total body water and sodium expanded during CPB: restrict fluid and
sodium
- myocardial function after CPB impaired: nadir at about 4h
- may be risk of myocardial ischaemia despite revascularization
- requirements for K+ and Mg2+ may be large, depending on
amount and type of cardioplegia given, preoperative state and postoperative
diuresis. If K+ normal give 5 mmol/h initially, decrease when
diuresis settles. Give 20-40 mmol Mg SO4 in first 24h
Monitoring
- may be discrepancy between mean aortic and radial artery pressure of
10-30 mmHg for approx 60 min after CPB. If in doubt regarding BP measure femoral
artery pressure
- ST segment elevation is common. Usually due to pericarditis but the
possibility of ischaemia must be considered
Ventilation
- uncomplicated cases can usually be extubated within 2-6h
- more complex cases should be ventilated until cardiovascular support has been
weaned
Bleeding
- continuing major postoperative blood loss may be due to:
- difficult surgery or poor surgical haemostasis. Common sites of bleeding
are graft anastamoses, sternal wire insertion and internal mammary artery
pedicle
- reinfusion of retrieved pump blood containing heparin
- pre-existing liver disease secondary to heart failure
- preoperative therapy with aspirin,
warfarin or NSAIDs
- bypass-generated platelet or clotting factor problems due to the
activation of complement of kallikreins by plastic surfaces
- management includes: protamine to reverse heparin effect, FFP, platelets
and DDAVP 0.3 mcg/kg over 30 min to mobilize vWF from endothelial cells and
improve platelet function. Give platelets regardless of platelet count if the
patient has received aspirin within a week of surgery or has undergone
cardiopulmonary bypass
- re-operate if blood loss >200 ml/h for 3h or >400 ml for 1h
Hypertension
- common in immediate post-bypass period, especially patients on
beta-blockers, those with good LV function and those who have received large
doses of vasopressors during surgery
- pathophysiology not understood but thought to be related to stimulation of the
sympatho-adrenal system by a variety of stimuli including hypothermia and
haemodilution and increased activity of the renin-angiotensin system as a result
of non-pulsatile renal flow during bypass
- characterised by an increase in SVR with a normal cardiac output
- treatment is with vasodilators +/- beta blockers
Low output state
- clinically obvious if patient is hypotensive but may be manifestations may
be more subtle: persistent metabolic acidosis, obtundation, high core
temperature, oliguria and tachycardia
- management consists of treatment of reversible causes (eg tamponade and kinked
grafts), volume restoration, treatment of arrhythmias, pharmacological and
mechanical support and continued mechanical ventilation
- tamponade may be difficult to distinguish from LV dysfunction. Former can only
be definitively excluded by chest re-opening although in experienced hands TOE
may be as good
- if there is evidence of new ischaemia after CABG associated with circulatory
instability chest re-opening and inspection of grafts may be necessary
- NB appropriate manipulation of pre- and after-load essential
- often requires the use of catecholamines. Adrenaline,
isoprenaline, dopamine
and dobutamine most commonly used. Phosphodiesterase inhibitors have also been
used. Note that dobutamine may have almost exclusively alpha effects in patients
who beta blocked and that in these patients a phosphodiesterase inhibitor may be
more appropriate. However, while phosphodiesterase inhibitors do not usually
decrease BP, they occasionally produce catastrophic hypotension. Do not raise BP
- calcium can be used as a bolus to produce a moderate increase in cardiac
output for 15-30 min.
- glucagon:
- positive inotrope and chronotrope (independent of the sympathetic nervous
system)
- enhances automaticity of the SAN and AVN but not the ventricle
- coronary vaosdilator
- less potent than digoxin and catecholamines
- use limited by the development of excessive tachycardia and hypoglycaemia
- main indications are in treatment of acute heart failure and in patients
where it is necessary to overcome cardiac depression due to beta blockers
- ?? direct activation of adenyl cyclase (eg with forskolin) may prove useful
in the future
- intra-aortic balloon pump:
- occasionally required if pharmacological treatment fails (moderate
doses) or is not
tolerated, although increasingly used at an earlier stage.
- reduces after-load (thus reducing myocardial oxygen demand) while
increasing coronary diastolic perfusion
- risk of ischaemic complications in the leg
- damage to blood components, especially platelets
- continue mechanical ventilation until low output state resolves: may assist
failing LV by decreasing LVEDV and hence afterload, re-operation may be
necessary, and work of breathing may consume large fraction of oxygen delivery
in shock
- choice of vasodilators is between nitrates and nitroprusside. Although there
are theoretical advantages to the former this has not been demonstrated in
practice
Distributive shock
- occasional complication of cardiopulmonary bypass
- self limiting
- supportive therapy with vasopressors
Arrhythmias
- treat causes eg electrolyte abnormalities, hypoxia, hypercarbia,
tamponade and hypotension
- treat arrhythmias along conventional lines
- ventricular ectopics are common. Usually due to acidosis,
hypokalaemia, hypomagnesaemia, sympathetic stimulation, myocardial ischaemia or malplaced
intracardiac catheters. Correction of these factors will usually eliminate
ectopics but it may be necessary to raise K+ to 4.5-5 mmol/l and Mg2+
to > 2mmol/l. Treatment with anti-arrhythmics is not usally indicated unless
ectopics are frequent enough to cause haemodynamic disturbance. (However that
some advise suppression of ventricular ectopics with lignocaine).
Hypoxia
- respiratory failure may develop in patients with pre-existing lung
disease, tobacco abuse and general debility from heart failure
- surgical factors such as phrenic nerve palsy and left lower lobe atelectasis
during left IMA harvest compounded by postoperative pain and sputum retention
Hypothermia
- after CPB recooling occurs because of surgical exposure and perfusion
of cold fat layers
- may lead to hypertension, myocardial irritability, shivering
- shivering should be suppressed with narcotics and sedatives but short-acting
non-depolarizing muscle relaxants may also be needed if shivering is extreme
Renal failure
- may be due to pre-existing renal disease, haemolysis, hypoperfusion,
renal vasoconstriction, long CPB, nephrotoxic drug use or cholesterol emboli
- suspect renal failure if there is no postoperative diuresis
- suspect intravascular haemolysis if urine is opalescent pink without intact
RBCs (haematuria is cloudy pink)
Neurological
- post-op obtundation, focal deficits and confusion may occur
- macroemboli from surgical field cause most neuro complications. High risk
periods are during aortic cannulation, onset of bypass and weaning from bypass
- risk factors: atherosclerosis of ascending aorta, advanced age,
cerebrovascular disease, previous neurological event, duration of surgery, DM,
low cardiac output state
- long term problems rare
Miscellaneous
- other complications of cardiac surgery include wound infection, GI
haemorrhage and ischaemia, jaundice, cholecystitis, pancreatitis
- recent meta-analysis suggests that acadesine infusion starting 15 min before
induction of anaesthesia and continued for 7 h is associated with decreased
mortality due to decreased cardiac mortality and postoperative myocardial
infarction. No statistical decrease in stroke incidence. Acadesine is a purine
nucleotide analogue that selectively raises tissue adenosine levels during
ischaemic conditions
Further reading
Lee RP, Branch JM. Postoperative cardiac intensive care. In Oh TE. Intensive
Care Manual, 4th ed, 1997
Lisbon A, Vander Salm T, Visner MS. Management of the postoperative cardiac
surgical patient. In Rippe, 3rd ed., 1996
© Charles Gomersall July 1999
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