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Post operative management of the patient with cardiac disease

Cardiac physiology

Myocardial oxygen supply

Specific cardiac disorders

Non-cardiac surgery

Cardiac surgery

Further reading

Cardiac physiology


Starling’s law. Now thought that the relationship between stroke volume and end-diastolic volume may be a linear one


  • 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


  • inherent property of ventricle to perform work, independent of preload and afterload
  • cannot be measured directly

Myocardial oxygen supply and demand


  • 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


  • 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


  • 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



  • 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


  • 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


  • 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


  • 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


  • 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


  • 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


  • 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


  • uncomplicated cases can usually be extubated within 2-6h
  • more complex cases should be ventilated until cardiovascular support has been weaned


  • 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


  • 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


  • 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).


  • 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


  • 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)


  • 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


  • 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


©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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