Cardiothoracic Anaesthesia

Cardiothoracic Anaesthesia Brief Overview

By Patrik Martner, Specialist Physician in Anesthesia & Intensive Care. Sahlgrenska university hospital.

Updated 2019-10-14


Anesthesia in aortic stenosis

  • Avoid tachycardia – aim for 60-80 beats / min
  • Maintain sinus rhythm
  • Maintain preload
  • Avoid hypotension – maintain SVR

Anesthesia in aortic insufficiency

  • Filled – Fast – Forward
  • High -> normal heart rate (90 / min) – possibly beta agonist
  • Maintain preload
  • Low SVR – anesthesia

Anesthesia in mitral stenosis

  • Like AS but with even more respect.
  • Avoid tachycardia & hypotension!
  • Cave hypoxia, hypercapnia & acidosis (aggravates pH)

Anesthesia in mitral insufficiency

  • Think AI -> high heart rate + adequate preload
  • Low SVR – anesthesia, milrinone, nitropress, IABP
  • Low PVR (cave hypoxia, hypercapnia & acidosis)

Cardiac tamponade

Clinical picture

  • Hypotension
  • CVP increased
  • Cold periphery
  • Muffled heart sounds
  • Tachycardia
  • Reduced SvO2
  • Jugular vein stasis
  • Pulsus paradoxus

Risk Factors

  • Coagulopathy
  • Platelet inhibition
  • Valvular Surgery

Ultrasound examination



Anaesthesia for CABG

Posted by Andreas Nygren Senior Physician in Anesthesia & Intensive Care.

Dep. of Cardiothoracic Anesthesia, Sahlgrenska University Hospital, Gothenburg, Sweden. Updated 2019-03-01


Coronary artery surgery (CABG) has been routinely performed in Sweden with great success since the early 70’s for the treatment of ischemic heart disease. In 2017, 2534 CABG operations were carried out in 8 different hospitals. Approximately 70% of patients are painless after 5 years and about 50% are painless after 10 years. The average age is 66, 75% are men. The number of patients being reoperated due to recurrence of stenosis is less than 10% but some are treated with additional PCI. The chance of coronary artery postoperative complications is 4.3% with a 30-day mortality of 1.1%, dialysis requirement 1.1%, stroke 0.6%, sternal infection 0.6%. Four percent (4%) is reoperated for bleeding. (Swedeheart.se).

Patients with coronary artery disease are usually treated with either percutaneous coronary intervention (PCI) or coronary by-pass surgery (CABG) due to coronary artery disease.

Number of coronary angiographies, percutaneous coronary intervention (PCI) and coronary surgery (CABG = coronary bypass surgery) during 1982–2009. (SwedeHearts annual report).

The European Society of Cardiology (ESC) and the European Association of Cardiac Surgery (EACTS) have in their guidelines divided the indication by prognosis and symptoms according to tables below.

Table 1: Categorization of ischemic coronary artery disease for prognosis and symptoms. Class I-III indicates the impact of anatomical changes on prognosis or presence of symptoms. Level A-C indicates the scientific degree of evidence.

Clinical indications for PCI and CABG, respectively, in coronary artery disease. I-III indicates the degree of recommendation for CABG and PCI, respectively. A-C indicates the scientific degree of evidence.

Cardiac surgery and Thoracic Anesthesia

Cardiac surgery mainly involves

  • Coronary by-pass surgery (CABG)
  • Heart valve surgery (aortic and mitral valve)
  • Combinations of coronary artery surgery and simultaneous valve operation
  • Thoracic aortic aneurysm and aortic dissection
  • Arrhythmia correction operation
  • Correction of congenital heart defects
  • Heart and lung transplants
  • Different types of lung resection

Coronary bypass surgery – CABG accounts for about 50% of all cardiac surgery. Indication for CABG is stable angina, unstable angina, ongoing myocardial infarction, or if the patient has had NSTEMI or previous STEMI with widespread coronary heart disease. The purpose is to alleviate symptoms and/or increase longevity.

Anesthesia for Coronary Surgery

Coronary artery surgery is performed by surgeons specialized in cardiothoracic surgery and anesthesia management by specialists in cardiothoracic anesthesia. Coronary artery surgery is usually performed on a standstill heart using extracorporeal circuit (ECC) and cardioplegia. The operation can be divided into three phases, one phase before one goes on the ECC, one phase with the extracorporeal circuit and one phase after the ECC is weaned off and the patient regains its own circulation and respiration.

The operation usually begins with a sternotomy where the chest is opened and the heart cannulated by the surgeon. A cannula is inserted in the aorta and one in the right atrium. The blood is drained (led out) from the patient’s veins or from the right atrium and collected in a venous reservoir. From the vein reservoir, the blood is then pumped through the heat exchanger, where the blood is cooled or heated depending on the desired temperature. Subsequently, the blood is pumped through an oxygenator for oxygenation and depletion of carbon dioxide. The oxygenated blood then returns to the patient through the aortic cannula to the aorta. After blood has been taken out into the ECC and the circulation is artificial, the heart is stopped by cardioplegia. Cardioplegia is a potassium-rich, usually ice-cold, solution that is delivered into the coronary artery when the aorta is clamped.

The Primary Extra Corporal Circuit (ECC) replaces the body’s heart function where the blood flow goes from normal pulsatile flow to a smooth laminar flow controlled by pumps in the ECC. The Extra Corporal Circuit consists of several parts such as oxygenator, heat exchanger, venous reservoir, cardiotomy reservoir, hemofilter and mechanical components such as pumps, vein clamp and cannulas. In the ECC, the gas exchange occurs and no longer via the lungs, the blood is oxygenated by an oxygenator and the carbon dioxide is eliminated in it. The ECC is operated peroperatively by a specialist trained perfusionist in collaboration with the surgeon and anesthesiologist. The venous reservoir serves as a buffer reservoir between a varying return flow and a relatively constant pump flow.

During the by-pass phase, the ventilator connected to the lungs by the endotracheal tube can be switched off. When the ventilator is disconnected, the lungs may collapse into atelectasis. At cardiovascular decommissioning, recruitment maneuvers may be needed to mobilize the collapsed lungs. Alternatively, breathing may continue during ECC to avoid pulmonary atelectasis, but usually only small volumes and low pressures are needed not to interfere with the surgery. Coronary by-pass surgery consists in that vein grafts are sewn in as by-passes of occluded or stenosed coronary vessels. Usually venous graft is taken from the patient’s own saphenous vein which is sewn over existing anastomoses, often 3-4 separate grafts (varies between 1-6). One may also use LIMA (Left Internal Mammary Artery) for LAD (Left Anterior Descending) to get cardiac revascularization. The aim of the surgery is complete revascularization, ie all vessels with > 50% stenosis and with a diameter of > 1.5 mm should be grafted. Normal operating time is 2 – 3.5 hours.

Cardiothoracic anesthesia demands the anaesthesiologist to be well versed in central hemodynamics and to be well acquainted with the pathophysiology of the sick heart. The anesthesiologist must also be quick and dexterous in the invasive technique involving the insertion of central venous accesses and monitoring of central hemodynamics associated with the initiation of anesthesia. One must also be well acquainted with the principles of anesthesia when using the ECC machine and cardioplegia, how to “start up the ECC” or discontinue the same (“going off the machine”). The anesthesiologist should be able to handle peroperative ultrasound of the heart (UCG), usually with a transesophageal probe.

Preoperative Assessment

The preoperative assessment should evaluate the patient’s cardiac status, general fitness and physiology prior to a forthcoming intervention. Preoperative stress can cause sympathetic-induced blood pressure and tachycardia, which increases oxygen consumption and should be avoided in unstable angina by good premedication.

Preoperative visit are routinely performed and premedication is given as needed in accordance with local routines, e.g. with analgesics, benzodiazepines and/or an opioid (Oxycodone 10 mg + Oxazepam 10 mg). The previously widely used heavy premedication in thoracic surgery is nowadays rare, earlier drugs such as morphine scopolamine in high dose was commonly used but this sometimes gave undesirable side effects with hallucinations, respiratory failure and pronounced somnolence. Any beta receptor blockade should be reduced, often in a halved dose on the day of surgery in order to avoid a drop in blood pressure peroperatively or bradycardia after ECC. Regarding coagulation inhibitors, acetylic acid (ASA) should be continued but ticagrelor and clopidogrel should be discontinued three respectively five days before the operation.

Preparation in the Operating Room

The setup on the operating table is controlled by the responsible anesthetist before the onset of anesthesia. ECG is applied with five leads (lead V5 and II provide the best ischemia and rhythm detection), pulse oximetry, possibly. BIS for measuring anesthetic depth and an arterial line for invasive blood pressure measurement. The arterial line is normally placed in the radial artery. At low ejection fraction (EF), a femoral artery line can also be provided because it shows a more central measurement of the arterial pressure (more reliable) and radial pressure can show lower pressure directly after cardiovascular depletion. Defibrillation plates are routinely set on the chest wall only during reoperation procedures.

After the anesthesia induction, a triple lumen-central venous line (CVC 16/20 cm long) is normally inserted for venous access and measurement of central hemodynamics. Anesthesia-induced sympathetic loss associated with anesthesia should be minimized as it may cause a significant drop in blood pressure due to anesthesia. reduced inotropy, vasodilation, lower preload, and bradycardia, and thus risks reducing the perfusion pressure over critical stenosis which can induce a vicious circle of ischemia. Therefore, one should assess how sensitive the patient is to blood pressure drop by noting changes in cardiac function, eg. cardiac hypertrophy, impaired wall motion, regional wall motion defects and the spread of coronary artery disease and possibly main stem stenosis (eg EF 40%, 3-vascular disease).

Ultrasound with transesophageal echo (TEE probe) for the detection of cardiac function and regional wall movement defects is always used. Note, take the history of swallowing dysfunction which contraindicates TEE as the TEE probe can damage the esophagus at the insertion. A pulmonary artery catheter (PA catheter/Swan-Ganz catheter) is not routinely used in coronary artery surgery but may be of value in intensive care afterwards, for instance in case of severe heart failure and pulmonary hypertension. Cardiac output measurement with pulse wave analysis has no place peroperatively due to major changes in afterload and vasopressor treatment, which are known sources of error for the method.

Induction and Maintenance Anesthesia

Several drugs are used for anesthesia induction, varying according to local practice and your own choice, but the principle is to maintain cardiac function stable and the coronary perfusion pressure. Opioids are usually given in high doses to avoid sympathetic stress and at the same time provide less need for hypnotic drugs which is vasodilatory and cardiodepressive. Common drugs in a standard induction may be fentanyl 500-800 µg, propofol 60-100 mg and rocuronium 40 mg, and then anesthetized with anesthetic gas, usually sevoflurane or isoflurane, for maintenance. In the case of lower ejection fraction or cardiogenic shock, a higher dose of fentanyl and a lower dose of propofol are given at the induction. Alternatively, ketamine is given 50-100 mg, midazolam, propofol, rocuronium and subsequently fentanyl. The onset of anesthesia must be individualized according to the patient’s condition and cardiac function.

Peroperative blood pressure control is maintained with vasopressor therapy primarily norepinephrine with bolus or continous infusion (0.05-0.5 µg/kg/min) or phenylephrine (0.1 mg), with concomitant bradycardia give ephedrine (5 mg) or adrenaline (0.01-0.1 mg) in incremental doses.

Blood pressure increases are treated with increased anesthetic doses, opioid bolus, or, if necessary, infusion of nitroprusside.

The anaesthesiologist must balance and stabilize the hemodynamics peroperatively, but the blood must also coagulate. Fibrinolysis inhibition is corrected by tranexamic acid that may be given peroperatively to avoid bleeding (eg 2 grams at induction and 2 g at end of operation). Antibiotic prophylaxis is routinely administered, e.g. cloxacillin 2 g x 3, clindamycin 600 mg x 3, or cefotaxime 2 g x 3.

Anesthesia for cardiac surgery must take into account the physiological changes that occur in the lack of oxygen in the heart and in the event of dramatic changes in heart rate and blood pressure. At myocardial infarction, ejection fraction (EF) and stroke volumes (SV) are often impaired, in some cases severely. In the case of ongoing coronary artery ischemia, “hibernation” or “stunning” in the heart can temporarily reduce the EF and SV, which can be improved during revascularization. The oxygenation of the heart (DO2) depends on the degree and extent of vascular stenosis and the perfusion pressure of the coronary arteries. When occluding a vascular area with concomitant stenosis of the collateral supplying vascular area, vasodilation can provide a “steal phenomenon” which redirects the blood flow from ischemic to already perfused (“luxury perfused”) areas. This phenomenon can lead to ischemia, ST changes, and impaired cardiac mobility.

The heart’s oxygen consumption increases with increasing heart rate and wall tension. Prolonged hypertension can cause hypertrophy in the left ventricle which can cause poorer oxygenation in the heart. Lowering of afterload and preload, a slower heart rhythm can reduce ongoing oxygen deficiency. At critical stenosis of the coronary arteries, the perfusion pressure in the coronary arteries is important for the flow, since the flow is essentially pressure dependent when the vessel is post-stenotic dilated.

Keep in mind that under cardiac anesthesia optimize the oxygen content and oxygen transport with good hemoglobin level and oxygen saturation, have enough but not too high perfusion pressure and “just right” heart rate. Peroperatively one should normally seek a heart rate in the patient around 70-100 beats per minute and a MAP between 70-90 mm Hg. Optimal physiology can vary for different cardiac conditions or other heart anomalies.

Maintenance Anesthesia

Inhalation anesthesia has in several studies shown lower cardiac injury biomarker levels and is generally considered to have a cardioprotective effect with reduced risk of mortality and complications compared to intravenous anesthesia (Uligh et al Anesthesiology 2016). EACTS guidelines 2017 routinely recommend the use of inhalation anesthetics for heart surgery. Normally, a MAC value is used peroperatively at 0.8-1.5. Adjustments to the anesthetic gas can also be used to control the blood pressure peroperatively.

Extracorporeal circulation

The operation usually begins with a sternotomy where the chest is opened and the heart cannulated by the surgeon. A cannula is inserted in the aorta and one in the right atrium. The blood is drained (led out) from the patient’s veins or from the right atrium and collected in a venous reservoir. From the vein reservoir, the blood is then pumped through the heat exchanger, where the blood is cooled or heated depending on the effect desired. Subsequently, the blood is pumped through an oxygenator for oxygenation and depletion of carbon dioxide. The oxygenated blood then returns to the patient through the aortic cannula to the aorta. After blood has been taken out in the extracorporeal circuit and the circulation is artificial, the heart is stopped by cardioplegia. Cardioplegia is a potassium-containing, usually cold, solution that is delivered into the coronary artery when the aorta is switched off.

Prior to that, heparin 350 U/kg is given intravenously as a bolus dose to achieve ACT over 470 sec, the heparin is given iv (in an entry where no ACT sample is drawn to avoid false elevated values). In case of insufficient effect of heparin, antithrombin III may need to be added.

With extracorporeal circulation, the physiology in the body changes fundamentally. During ECC, any circulation in the lungs decreases or ceases and inhalants can no longer be supplied by the anesthesia ventilator. However it is possible to connect a carburetor to the ECC to continue providing anesthetic gas, such as sevoflurane if desired. Alternatively, a total intravenous anesthesia is given during ECC, e.g. with a propofol  infusion. The depth of anesthesia can be monitored with BIS.

Cardioplegia, ice-cold crystalloid or hot blood cardioplegia, is given by the thoracic surgeon in the coronary arteries to stop the heart after cannulation and this is repeated about every twenty minutes during a stationary heart surgery.

Peroperative blood pressure targets during ECC are debated, lower pressures can cause blood pressure-dependent flow, and risk ischemia, at critical stenoses, known and unknown. MAP about 30 mm Hg during surgery increases the risk of kidney failure (Kanji et al JCTS 2010). The risk of stroke is increased both at low or high blood pressure (Vedel et al Circulation 2018). The extracorporeal machine flow is normally set to 2.4 l/m2 and provides a blood pressure independent but hematocrit dependent oxygen supply to the body. An oxygen supply below 270 ml/min/m2 has been reported to increase the risk of kidney damage. When the priming solution of the cardiovascular machine is about 1300 ml, dilution of the total blood volume occurs, which can give critically low hematocrit. One can counteract the hematocrit reduction by decreasing the priming volume or by transfusing blood.

ECC weaning

During closure of the Extra Corporal Circuit (ECC closure – “weaning ECC”), the ventilation is started first, if necessary with prior lung recruitment. The venous catheter of the ECC is squeezed successively so that the venous blood returns to the right ventricle instead of into the ECC. The heart chambers are gradually filled and gives increasing stroke volumes which are ultimately so large that the intracardiac pressure exceeds the aortic pressure and blood pumps out through the aortic valve and again a pulsatile artery curve is restored, the heart starts to pump functionally again. Often, the heart starts in a sinus rhythm but sometimes ventricular fibrillation occurs which needs to be defibrillated with internal defibrillation spatulas or alternatively a dose of about 10-20 mmol of potassium chloride is given which gives a transient asystole often followed by sinus rhythm.

The blood reservoir filling decreases and when the heart is filled and MAP is acceptable between 50 and 70 mm Hg, ECC is interspersed with simultaneous control that the heart’s filling and MAP are followed. One must observe movement of the heart visually and possibly any valve insufficiency. At increasing filling pressure and decreasing arterial pressure there is heart failure, and inotropic drugs may be given, e.g. calcium gluconate (100 mg/ml 10 ml), ephedrine 5 mg or milrinone 2-3 mg. Alternatively, the ECC is reinstituted and after an extra reperfusion time, a new weaning procedure is performed. During the reperfusion time, “stunning” of the heart muscle usually has decreased.

If ECC weaning does not succeed directly, the flow in the bypass grafts should be investigated with flow meters as well as ultrasound assessment of regional wall motion defects corresponding to the grafted areas. Ev. surgical measures may be necessary to sew new anastomosis or graft distally. With good flow but continued failure, inotropic infusion (eg milrinone 0.5 µg/kg/min, dopamine 2.5 µg/kg/min, or levosimendan) should be started. Consider insertion of an aortic balloon pump (IABP) that both relieves the heart and improves coronary perfusion pressure at severe heart failure.

The heparin effect is neutralized with Protamine 0.7-1 mg/100 U heparin and is followed by ACT measurement at <130 sec, or under original value if measured before.

Postoperatively

After surgery, the patient usually receives 2 drainage tubes in the thorax, one mediastinal and one in the left pleura if it is opened (often opens when removing LIMA). Acceptable drainage losses are initially 100-200 ml of blood the first hour but should then decrease. In the case of increased bleeding, coagulation substitution is administered according to coagulation samples, e.g. trombelastogram (ROTEM/TEG). Additional protamine, plasma, fibrinogen or platelets may be required. Extubation is performed according to local procedures, but normally body temperature should be > 36 degrees, no threatening reoperation due to increasing bleeding, FiO2 <40% with PEEP 5-10 cm H2O. Shivering (chills) is treated with heat blanket, and possibly an opioid (eg, meperidin 10-20 mg iv)

Pain relief regimens should contain paracetamol and opiate, eg paracetamol 1 g x 4 Oxycontin 5-10 mg x 2, oxynorm 5 mg as needed, NSAID’s should be avoided, especially in those who are at risk of renal failure but can be tested for residual pain in those with preserved renal function (eg Toradol 15-30 mg as needed)

PCA pump with morphine can be used for pain relief.

Antibiotic prophylaxis should be routinely administered for 1-2 days (eg cloxacillin 2 g x 3, clindamycin 600 mg x 3, or cefotaxime 2 g x 3).

Thoracic epidural anesthesia (TEDA)

Thoracic epidural block has been used for peroperative pain relief and sympathetic blockade. However, the risk exists for epidural bleeding as the patient group is elderly, generally vascular compromised, often having platelet inhibition and peroperatively full-heparinized. Pain relief in cardiac surgery with TEDA is comparable to pain relief with PCA. If anesthesia is used, it should be added well in advance of heparinization. Seek blockade over Th 2-10 for sympathetic blockade that provides protection against tachycardia and vasodilation.


Anesthesia for the heart disease patient

By Sven Erik Ricksten, Chief Physician, Professor of Anesthesia & Intensive Care.

Sahlgrenska University Hospital.

Updated 2020-09-02


The chapter can be divided into

  • Coronary artery disease (CAD)
  • Heart failure (systolic, diastolic)
  • Pulmonary hypertension
  • Right ventricular failure
  • Aortic regurgitation
  • Mitral valve disease

Surgical stress increases the myocardial O2 needs

  • Increased heart rate
  • Increased wall tension (P x r/w)
  • Increased blood pressure (P)
  • Increased radius (s) (due to increased LVEDFP)
  • Increased myocardial contractility
  • Increased sympathetic activity
  • Increased content of circulating catecholamines

Disruption of myocardial oxygen supply/demand ratio during surgery in coronary artery disease

Increased oxygen ”demand”

  • Tachycardia
  • Increased wall tension
    • LV radius
    • Arterial pressure
  • Increased contractility

Reduced “O2-supply”

  • Tachycardia
  • Hypotension
  • Reduced O2 content
  • Thrombosis (hypercoagulation, plaque rupture)
  • Vasoconstriction

Cardiac sympathetic activity and CAD

Efferent sympathetic trajectories (Th1-Th5)

  • Beta-receptors mediate:
    • Heart rate
    • Contractility
    • MVO2 elevation results in metabolic vasodilation
  • Alpha receptors:
    • Epicardial coronary arteries: stimulation produces vasoconstriction
    • Coronary vascular resistance: stimulation produces vasoconstriction

Increased sympathetic activity to the heart during stress in coronary heart disease

  • Increased MVO2
  • Constriction of stenotic coronary arteries
  • Plaque rupture – thrombus formation
  • Catecholamines increase platelet aggregation
  • Lowered arrhythmia threshold

Anesthesia and coronary artery disease (CAD)

  • Assessment of surgical risk (degree of surgical stress, duration, acute/elective)
  • Identify high-risk patients
  • Preoperative investigation and treatment
  • Perioperative treatment/prophylaxis
  • Choice of anesthesia technique

Preoperative risk factors for cardiac complications (Revised Cardiac Risk index)

  1. Age > 75 years
  2. Heart failure
  3. Ischemic heart disease
  4. Cerebrovascular disease
  5. Diabetes
  6. Kidney failure
  • 0 risk factors = low risk
  • 1-2 risk factors = intermediate risk
  • ≥ 3 risk factors = high risk

Investigation before high-risk surgery

  • About 1-2 risk factors no preoperative investigation
  • If ≥ 3 risk factors, a non-invasive stress test is recommended

Non-invasive stress test

  • If negative – no special action
  • If positive recommend coronary angiography
  • If this is positive it is recommended: coronary revascularization

Revascularized patients before elective surgery – “timing”

  • Delay elective surgery for at least 6 weeks, preferably 3 months after PCI with a stent
  • Delay elective surgery 12 months after PCI with drug stent (DES)
  • Former CABG within five years, no investigation

Coronary syndrome – unstable CAD

  • Rapid revascularization is prioritized before elective surgery
  • In acute surgical disease and at the same time unstable CAD, priority is given to surgery
  • Balloon dilation without stent before emergency surgery?

Perioperative myocardial infarction (PMI)

  • Patient with/or risk of arteriosclerosis (n = 8351)
    • Devereaux Ann Internal Med 2011; 154: 523
  • Criteria for PMI:
    • PAD or
    • Troponin/CK-MB increase and any of the following:
    • Ischemic symptoms, Q-wave, ischemic
    • ECG changes, coronary intervention
  • 5% PMI ≤ 30 days
  • 75% of these ≤ 2 days
  • 2/3 no clinical symptoms
  • 30-day mortality 11.6% vs. 2.2%

Perioperative ß-blockade and CAD

Effects of extended-release metoprolol succinate in patients undergoing non-cardiac surgery

POISE trial: a randomised controlled trial. Lancet 2008;31:1839-1847

  • 8351 patients with or at risk of arteriosclerosis undergoing general surgery were randomized to
    • Placebo (n = 4177)
    • Extended release metoprolol (n = 4174)
  • Dosage: 100 mg 2-4 h preop. + 100 mg < 6 h postop. 12 hours after the 1st dose of 200 mg daily for 30 days
  • If oral administration is not possible, 15 mg x 4 i.v
  • SAP > 100 and HR > 50/min before dose
  • Primary end-point: cardiovascular death, non-fatal myocardial infarction or cardiac arrest

Recommendations (Class I) for perioperative ß-blockade

  • ACC/AHA
    • Continue with ß-blockade per- and postoperatively in patient as preop. treated with ß-blockers
  • ESC/ESA
    • Known coronary heart disease
    • High-risk surgery
    • Continue with ß-blocker per- and postoperatively in patients as preop. treated with ß-blockers
    • When to start ß-blockade?
      • one month or at least one week before surgery, NOTE !! dose titration
    • Therapeutic target for HF ?: 60-70/min
    • How long to treat with ß-blockade? – month

Recommendation

  • Investigate noninvasive patients with ≥ 3 risk factors (work ECG, stress echo)
  • If pathological, coronary angiography
  • In case of significant coronary heart disease, revascularization before major general surgery
  • When preoperative treatment with ß-blockers, continue with ß-blockers perioperatively
  • ß-block perioperatively: patients undergoing high-risk surgery
    • patient with known CAD
    • high-risk patient (≥ 3 risk factors)
  • Avoid hypotension and bradycardia!
  • If contraindications to ß-blockade, consider clonidine

Other cardiac medications for surgery at CAD

  • Statins – start one month before surgery
  • Nitrates – no protective effect
  • ACE inhibitors – continue therapy postoperatively in patients with heart failure. NOTE hypotension risk!
  • Calcium antagonists – only for patients with Prinzmetal’s angina
  • ASA (?)

“Aspirin in Patients Undergoing Noncardiac Surgery”

Devereaux NEJM 2014;370:1494

  • Not aspirin treated (n = 5628)
    • Placebo
    • Aspirin, 200 mg preop., 100 mg/day for 30 days
  • Ongoing aspirin treatment (n = 4382)
    • Placebo
    • Aspirin, 200 mg preop., 100 mg/day for 7 days
  • Primary end-point: fatal or non-fatal infarction after 30 days

Premedication at CAD

  • Benzodiazepine (diazepam 0.1-0.15 mg/kg, flunitrazepam 0.5-1.0 mg)
  • Morphine 0.1 mg/kg
  • Scopolamine 0.2-0.4 mg

Monitoring in CAD and high-risk surgery

  • Invasive blood pressure
  • 2-3 lead ECG, ST trend
  • CVC
  • PA catheter – not indicated
  • TEE – in case of peroperative ischemia or in case of pronounced haemodynamic instability

Anesthesia induction and CAD

  • Hypnotics:
    • Midazolam
    • Ketamine
    • Propofol
  • Opiates (fentanyl)
  • Inhalants (sevoflurane, desflurane)

Maintenance of anesthesia at CAD

  • Isoflurane
  • Sevoflurane
  • Desflurane
  • TIVA (opiate + propofol)

Inhalation anesthetics, central and coronary hemodynamics

  • The inhalants have a negative inotropic effect
  • The inhalants are vasodilating (lowers SVR) opens ATP-dependent K+ channels

The inhalants are coronary vasodilators

Isoflurane and lactate production in patients with CAD

Nasal Sufentanil to children - 50 micrograms/ml

KiloMikrogramVolume (ml)
10200.4
13260.5
15300.6
18360.7
20400.8
23460.9
25501
28561.1
30601.2
35701.4
40801.6
45901.8
501002
551102.2
601202.4

Sevoflurane and coronary heart disease?

Do the inhalants have cardioprotective effects?

Mechanisms behind the cardioprotective effects of inhalants

  • Anti-ischemic effect
  • Preconditioning effect
  • Post-conditioning effect (reduces reperfusion damage after ischemia)

”Randomized Comparison of Sevoflurane Versus Propofol to Reduce Perioperative Myocardial Ischemia in Patients Undergoing Noncardiac Surgery”

Lurati Buse et al Circulation 2012;126:2696

Patients with known CAD or ≥ 2 risk factors for CAD and major surgery

  • Randomized to
    • Propofol (n = 201)
    • Sevoflurane (n = 184)
  • Primary end-point: myocardial ischemia (continuous ECG, troponin)

Cardioprotective effect of regional anesthesia in CAD?

Liu et al. Anesthesiology 1995;82:1474-1506

Can perioperative epidural (EDA) provide a heart-protecting effect?

Lumbar epidural anestesi (LEA) versus Thoracic epidural anesthesia (TEA)

Lumbar epidural anesthesia (LEA) vs Thoracic epidural anesthesia (TEA)

  • Lumbar epidural anesthesia? No!
  • Thoracic epidural anesthesia? Yes! (evidence Class IIa, level A)
    • If it is administered per and postoperatively !!!

Perioperative management of heart failure

By Sven Erik Ricksten, Chief Physician, Professor of Anesthesia & Intensive Care.

Sahlgrenska University Hospital.

Updated 2020-09-02


Chronic heart failure

  • Prevalence ≈ 2%
  • > 75 years, prevalence ≈ 8%
  • Within 10-20 years, the prevalence has increased 2-3 times
  • Increased age
  • Today, more and more people survive an acute infarction but experience heart failure

Chronic heart failure – clinical syndrome

  • Impaired cardiac ventricle function
  • Increased pressure in the pulmonary circulation
  • Impaired physical capacity
  • Neuroendocrine activation
  • Reduced survival

Pharmacological treatment

  • ACE inhibitors
  • Angiotensin-II receptor blockers
  • ß-blockers (metoprolol, bisoprolol, carvedilol)
  • Aldosterone receptor antagonists
  • Diuretics
  • Digoxin

ACE inhibitor, angiotensin II receptor blocker

  • Reduces angiotensin II, catecholamines, aldosterone
  • ADH. Increases bradykinin, NO, PGI2
  • Decreased production of tissue angiotensin II
  • Antiproliferative effect, reduces remodeling

ßblocker (metoprolol, bisoprolol, carvedilol)

    • Reduces MVO2
    • Increased glucose uptake
    • Improved energy utilization
    • Anti-arrhythmic effect
    • Reduced Ca2+ leakage from SR
    • Anti-apoptotic effect
    • Anti-oxidant

Aldosterone receptor antagonists

  • Decreases myocardial collagen
  • Lowers catecholamines
  • Improves baroreflex
  • Improves endothelial function (via NO)

Prognostic value of natriuretic peptides

Brain natriuretic peptide (B-type natriuretic peptide, BNP)

  • Formed in the left ventricle and released upon distension of the ventricular wall (increased preload)
  • Released together with NT-proBNP which is biologically inactive
  • Vaso-vendilation, increases GFR, natriures, inhibits RAAS

Prognostic value of natriuretic peptides (BNP, NT-proBNP)

  • Preop. increase in GDP/NT-proBNP increases risk of:
    • MACE (infarction, cardiac death) (OR: 19.8)
    • Mortality (OR: 9.3)
    • Cardiac death (OR: 23.9)
  • “Cut-off” level?
  • Method
  • GDP/NT-proBNP in relation to other methods?

NT-proBNP, limit values

  • < 400 ng/l heart failure unlikely
  • 400-900 ng/l possible heart failure
  • > 900 heart failure likely

Perioperative treatment

  • Identification of risk patient (EF, preoperative functional status, NT-proBNP, clinic)
  • Is the patient optimally treated for cardiac failure?
  • What do we do with the “failure medication” before surgery?

Pharmacological treatment

  • ACE inhibitor, angiotensin II rec. blockers
  • ß-blockers (metoprolol, bisoprolol, carvedilol)
  • Aldosterone receptor antagonists
  • Diuretics
  • Digoxin

Perioperative treatment

  • Identification of at-risk patient (EC, GDP, clinic)
  • Is the patient optimally treated for failure?
  • What do we do with the “failure medication” before surgery?
  • Choice of anesthesia technique (regional, general anesthesia?)

Case report

  • Pregnant week. 36
  • 190/100 mm Hg
  • HF 130 b/min
  • Dyspnoea
  • Systolic wheezing (MI?)
  • Pulmonary edema
  • Continuous spinal (Th6) for 14 hours
  • Regional anesthesia during surgery in the lower half of the body in a patient with heart failure

Case report

  • 37-year-old woman with twin pregnancy in w. 33. Looking for an emergency due to shortness of breath and bone swelling. Former heart healthy.
  • BP: 110/60 mm Hg
  • HF: 120 b/min
  • SpO2 90%
  • Slight increase of CK-MB. ECG: repol. interference.
  • Echo: biventricular failure. LVEF: 20% MI, TI grad 3/4
  • Treatment is started with furosemide and nitroglycerine infusion
  • Decision on acute caesarian section
  • Anesthesia drug technology?

Induction of anesthesia for heart failure

  • Hypnotics:
    • Midazolam
    • Ketamine
    • Propofol
  • Opiates (fentanyl)
DrugConcentrationStart up doseBolusContinuous infusionLockout timeLockout volume
Morphine1 mg/ml2-5 ml1-2 ml (1-2 mg)1-2 ml/hour6 min40 ml after 4 hours
Ketobemidone
1 mg/ml 2-5 ml1-2 ml (1-2 mg)1-2 ml/hour6 min40 ml after 4 hours
Ketamine

10 mg/ml
2-5 ml1-2 ml 1-4 ml/hour6 min40 ml after 4 hours

Maintenance of anesthesia

  • TIVA (propofol, opiate)
  • Inhalation anesthesia

Intraoperative monitoring of heart failure

  • Invasive blood pressure
  • 2-3 lead ECG, ST trend
  • PA catheter (SvO2, CCO)
  • CVL (ScvO2)
  • TEE – in case of pronounced hemodynamic instability

Recommendations

  • Identify high-risk patient
  • Arterial line, CVL (the day before)
  • Arterial pressure (MAP) central venous saturation before induction
  • Connect milrinone, norepinephrine (NA) to a CVL
  • Anesthesia technique you are used to
  • Control MAP (65-75 mm Hg) with NA
  • Control central venous saturation (≈ 60-70%) with milrinone
  • Control volume supply with CVP
  • Hemoglobin > 10 g /dl
  • Be two anesthesiologists at the start of anesthesia!

Diastolic heart failure

Diastole

  • Myocardial relaxation
    • Active, energy-intensive process
    • Affected by ischemia and
  • Inotropic drugs
    • Passive filling
    • Extracardiac factors
    • Structural factors

Diastolic dysfunction

  • Definition:
    • Normal filling pressure gives too low filling of LV
    • Elevated filling pressure is required for adequate filling of LV
  • 40-50% of heart failure patients have isolated Diastolic dysfunction

Isolated diastolic dysfunction

  • LVEF is normal, LVEDV low
  • Left ventricular hypertrophy
  • Abnormal mitral Doppler (E/A < 1)
  • Hypertension, aortic stenosis
  • Dynamic outflow obstruction of LV (functional aortic stenosis)

Treatment of outflow obstruction of LV with SAM

  • Increase preload (“volume challenge”)
  • Avoid tachycardia
  • Not inotropic agents
  • Not a vasodilator
  • In case of tachycardia, give ß-blockers
  • Control therapy with eco-Doppler !!!

Anesthesia for pulmonary hypertension

By Sven Erik Ricksten, Chief Physician, Professor of Anesthesia & Intensive Care.

Sahlgrenska University Hospital.

Updated 2020-09-02


Pulmonary hypertension and right ventricular failure

Pulmonary circulation and right ventricle

Interaction between RV and LV (”ventricular interdependence”)

  • Change in pressure/volume in one chamber directly affects pressure/volume in the other
  • Immediate power transmission between RV and LV
  • Joint muscle fibers, septum, pericardium
  • Diastolic and systolic interaction

Diastolic ventricular interaction at pressure/volume loading of RV

  • Increased volume / distension of RV during diastole, septum displaced to the left
  • Reduces LV volume, ie reduced LV preload
  • LV end-diastolic pressure (PCWP) increases
  • LV compliance decreases

 

Systolic ventricular interaction at pressure/volume loading of right ventricle

  • Under pressure/volume loading of the right ventricle, a flattened septum shifts from left to right in systole
  • LV-assist more efficient at a high system pressure
  • RV function deteriorates at a low system pressure (peripheral vasodilation)

Pulmonary hypertension

  • MPAP> 25 mm Hg or SPAP > 55 mm Hg
  • Right ventricular hypertrophy/failure

Classification:

  • Pulmonary arterial hypertension
    • Primary, idiopathic pulmonary hypertension (sporadic, familial)
    • Related to collagenous vascular diseases (scleroderma, lupus, RA)
    • Portopulmonary hypertension
  • Pulmonary venous hypertension (VK failure, MI / MS, AS)
  • Pulmonary hypertension assoc. with lung disease
  • Pulmonary hypertension caused by thromboembolism

Anesthesiological aspects of pulmonary hypertension

Anesthesia for primary / secondary pulmonary hypertension and RV failure

  • Retain chronic medication for pulmonary hypertension (Ca2+ antagonists, sildenafil, ET antagonists, i.v. PGI2)
  • Intravenous PGI2 is switched to inhalation
  • Light premedication
  • Insertion of PA catheter before induction (CVP, PA)

Anesthesia for primary / secondary pulmonary hypertension and RV failure

  • TIVA (propofol/opiate)
  • Avoid ketamine, N2O (increases PVR) and inhalants (negative inotropic effect)
  • TEE for monitoring RV function
  • Hypoxia and hypercapnia increase PVR
  • Regional anesthesia: may cause unwanted drop in blood pressure and RV failure
  • Noradrenaline for high SVR (MAP)
  • Inhalation NO, prostacyclin and / or milrinone (selective lowering of PVR)
  • In case of RV failure, i.v. milrinone + noradrenaline

Prevention / treatment of pulmonary hypertension and RV failure

  • Optimize RV preload (CVP 10-15 mmHg)
  • High system pressure improves the support from LV and improves RV perfusion
  • Selectively reduce pulmonary vascular resistance (inhalation NO, milrinone, prostacyclin)
  • Inotropic therapy for RV failure

Conclusions

  • The prevalence of chronic heart failure is constantly increasing
  • Understand the pathophysiology
  • Identify the risk patient
  • Anesthesia technique in itself less interesting
  • Adequate monitoring
  • Take the help of inotropic/vasoactive drugs
  • Do not forget the diagnosis of dynamic left ventricle with outflow obstruction in case of sudden and severe intraoperative cardiogenic shock
  • Noradrenaline + inhalation of vasodilators in pulmonary hypertension and RV failure

Mechanical ventilation in pulmonary hypertension and RV failure

  • Hypoxia and hypercapnia increase PVR and RV afterload
  • Increased respiratory rate increases intrinsic PEEP + “gas trapping”


Aortic valve stenosis

When is there an increased risk of giving anesthesia to patients with aortic stenosis?

Pronounced AS

  • Flap area ≤ 1 cm2
  • Mean gradient ≥ 50 mm Hg

Combined with

  • Impaired VK systolic function (EC < 40%)
  • Symptomatic AS (angina, syncope, dyspnoea)
  • Associated mitral regurgitation
  • CAD (25-50%)
  • High-risk surgery involves mortality between 2-10%

Pathophysiological aspects

  • Compensatory LV hypertrophy (concentric) normalizes the tension in LV afterload (P x r/2w)
  • Impaired diastolic function
  • Reduced chamber compliance
  • Impaired active relaxation
  • Normal end-diastolic volume (stretching of sarcomeres) requires high filling pressure (PCWP)
  • Intact atrial function is essential

Myocardial O2 ”supply/demand mismatch” in aortic stenosis

O2-demand

  • Increased LV mass
  • Increased wall tension
  • Heart rate
  • Contractility

O2-supply

  • High LVEDP
  • Increased tissue pressure
  • Reduced coronary perfusion pressure
  • Reduced coronary vascular reserve
  • Increased wall/lumen ratio
  • Decreased capillary density (20-30%)
  • CAD (25-50%)

Pathophysiological aspects

  • Hypotension/tachycardia -> supply-demand mismatch -> ischemia -> decreased SV -> hypotension ischemia
  • “Vicious circle” with rapid development of cardiogenic shock

Hemodynamic targets: Aortic stenosis

  • Heart rate: 65-80 b/min
  • Rhythm: Sinus
  • Preload: High
  • SVR: Normal/high
  • Inotropism: Normal/decreased

Anesthesia and aortic stenosis in general surgery

  • Identify patient. Cardiac murmur sounds?
  • No correlation m-n degree of wheezing o. Degree of aortic stenosis
  • Order eco-Doppler survey
  • Always consider valve surgery before elective surgery !!
  • Increased perioperative risk at gradient> 50 mm Hg or area ≤ 1 cm2

Anesthesia and aortic stenosis in general surgery

  • Avoid hypovolemia (give colloid)
  • Avoid vasodilation (phenylephrine, norepinephrine)
  • Maintain sinus rhythm
  • Avoid inotropic support
  • Be aware of the risk of myocardial ischemia !!
  • Heavy premedication, relaxed patient (ß-blockade)
  • High doses of fentanyl (5-10 mikrog/kg)
  • Low doses of hypnotics (propofol: 1-1.5 mg/kg)
  • TIVA, sevoflurane-fentanyl
  • Avoid regional anesthesia (relative contraindication)
  • Keep Serum hemoglobin > 10 g/dl

Monitoring

  • Standard 3-lead ECG, pulse oximetry
  • Arterial catheter
  • PAC with CCO and continuous SvO2 in pronounced symptomatic AS and high-risk surgery
  • CVK with measurement of CVP and continuous ScvO2
  • TEE: “Recommended if acute and severe haemodynamic instability develop perioperatively” (Class I)

Case report

  • Hypertension, hyperlipidemia
  • Dense aortic stenosis (area = 0.8 cm2, gradient 70 mm Hg, EF = 60%)
  • Coronary angioma: significant 2-vessel disease
  • Anemia
  • Investigation shows circumscript rectal cancer, risk of imminent ileus
  • Surgery of rectum with extirpation + sigmoidostomy!

Aortic valve insufficiency

Short film bicuspid flap

Short film bicuspid aortic valve in longitudinal section

Short film aortic valve with regurgitation

Short film mitral valve insufficiency

Short film mitral valve failure with color Doppler

Pathophysiological aspects

  • Volume load of LV
  • The degree of regurgitation is determined by:
    • Aortic valve defect
    • Aortoventricular pressure gradient
    • Diastolic duration
  • Chronic volume loading causes eccentric hypertrophy
  • Impaired contractility
  • High heart rate reduces regurgitation and increases “forward output”
  • Lowered SVR reduces regurgitation and increases “forward output”
  • Combine vasodilators (eg nitroprusside, nitroglycerin) with volume to avoid excessive reduction of preload

Hemodynamic targets in aortic insufficiency

”Faster, fuller and vasodilated

  • Heart rate – 85-100
  • Rhythm – Sinus
  • Preload – High
  • SVR – Lowered
  • Inotropism – Normal

Anesthesia and aortic insufficiency in non-cardiac surgery

  • Normal premedication and induction
  • “Vasodilatory anesthesia”
  • Opiate + isoflurane
  • Regional anesthesia
  • Use PA catheter for failure symptoms/low EF
  • At low CO/SVO2 inodilators (milrinone, levosimendan)

Mitral valve stenosis

Pathophysiological aspects

  • High atrioventricular pressure gradient for adequate filling of LV
  • Tachycardia increases the gradient
  • LA dilated, hypovolemic LV
  • Pulmonary hypertension, high PVR
  • Clinical symptoms when MVA < 2.5 cm2
  • Pronounced MS: MVA < 1.0 cm2
  • RV hypertrophy
  • RV failure + tricuspidal insufficiency
  • Atrial fibrillation common
  • Rarely CAD

Hemodynamic targets: Mitral valve stenosis

  • Heart rate: 65-80
  • Rhythm: Sinus
  • Preload: Normal/high
  • SVR: Normal/high
  • Normal Inotropism

Anesthesia and mitral stenosis in non-cardiac surgery

  • Strong premedication
  • Induction: High dose fentanyl
  • Low dose fentanyl + inhalant agent
  • Phenylephrine/norepinephrine in case of pressure drop

Anesthesia and mitral stenosis in non-cardiac surgery

  • Avoid tachycardia! Digoxin, ß-blockade
  • Maintain sinus rhythm!
  • TEE
  • PA catheter, monitor both CVP and PCWP Optimal intravascular volume
  • High CVP gives RV failure
  • “Low PCWP” gives hypovolemic LV
  • In case of RV failure, inodilators + inhaled NO or prostacyclin

Conclusion

  • The pathophysiology of heart disease
  • Identify the high-risk patient
  • Anesthetic / technology effects on cardiovascular
  • Monitoring
  • Vasoactive drugs

Minimize perioperative morbidity!


Mitral valve insufficiency

Common causes of mitral valve regurgitation

  • Prevalence 1-2%
  • Organic (primary)
  • Myxomatous degeneration
  • Fibroelastic deficiency
  • Calcification
  • Functional (secondary), CAD
  • LV failure (remodeling)
  • Papillary muscle rupture

Mitral valve insufficiency

Mitral valve insufficiency

When is there an increased risk of giving anesthesia to patients with mitral regurgitation?

Bajaj et al Am J Medicine 2013;126:529

  • EF < 35% (OR: 3.4)
  • Ischemic etiology to mitral regurgitation (OR: 4.4)
  • Asymptomatic patients with pronounced mitral regurgitation but with normal EF had no increased risk

Pathophysiological aspects

  • Similar pathophysiology as in AI
  • Volume load of LV
  • Impaired systolic function, overestimated by EF
  • Pulmonary hypertension with high PVR
  • LV hypertrophy
  • Clear v-wave (chamber systole) for PCWP measurement
  • Lowered SVR reduces regurgitation and increases “Forward output”
  • Avoid hypervolemia! Provides further dilation of the valve ring and more MI
  • Use PA catheter for preop monitoring. failure symptoms

Hemodynamic goals: Mitral valve regurgitation

”Faster, fuller and vasodilated

  • Heart rate: 80-95 b/min
  • Rhythm: Sinus
  • Preload: Normal
  • SVR: Lowered
  • Normal: Inotropism

Anesthesia in mitral valve regurgitation

  • Intubation and general anesthesia in acute mitral regurgitation (papillary muscle rupture)
  • Avoid surgical stress!
  • “Vasodilatory anesthesia”
  • Opiate + isoflurane
  • Regional anesthesia
  • Low EF inodilators (milrinone, levosimendan)
  • Morbidity postoperatively (pulmonary edema) !!

Monitoring

  • Standard 3-lead ECG
  • Pulse oximetry
  • Arterial catheter
  • PAC with CCO and continuous SvO2 in pronounced symptomatic MR/impaired EF and high-risk surgery
  • CVC with measurement of CVP and continuous ScvO2
  • TEE: “Recommended if acute and severe haemodynamic instability develop perioperatively” (Class I)

Anesthesia for Lung Surgery

Posted by Klaus Kirnö Senior Physician in Anesthesia & Intensive Care. Dep. of Cardiothoracic Anesthesia, Sahlgrenska University Hospital, Gothenburg, Sweden.

Updated 2019-03-01


Malignant suspected tumors in the lungs or already diagnosed lung cancer are the most common reasons for lung surgery. In these operations, a resection of a portion of the lung (lobectomy) or, in rare cases, the entire lung is performed (pulmectomy). Another frequent cause of surgical intervention in the lung is recurrent pneumothorax requiring repeated drainage treatments.

Lung surgery is performed by thoracoscopy or open thoracic surgery. The procedure almost always requires a ventilation separation of the lungs with single ventilation for a large part of the operation. The reason is that surgery requires the operated lung to be atelectic and lie still. For this, a double-lumen tube or a bronchial blocker is used.

Lung separation may also be relevant in conjunction with other intrathoracic procedures such as surgery on the descendant aorta or esophagus, surgical correction of thoracic deformities, and in certain cardiac surgery. The technique is then similar from the anesthetic point of view.

Preoperative assessment

The most important reason for perioperative morbidity and mortality associated with lung surgery is respiratory complications. Cardiac complications come in second place. Therefore, standard preop examination includes spirometry and work load ECG, preferably in the form of a complete Ergospirometry (respiration with gas exchange and ventilation analysis), of almost all elective lung surgery patients. CT-scan of thorax is also generally available and should be included in the assessment of trachea and bronchial anatomy.

Premedication

Here practice vary between clinics. Common medication is oral analgesia with, for example, paracetamol, usually in combination with other analgesics. An opioid can be given if the patient is not to receive a thoracic epidural (TEDA). However, routine oral sedation (benzodiazepines) is not recommended. Most importantly, the patient receives some of his usual medications (bronchodilators, anti-epileptics, beta-blockers (in half-dose), etc.).

Anesthesia

The anesthesia is routinely comprised of total intravenous anesthesia (TIVA) with propofol and remifentanil in TCI pumps in combination with thoracic epidural anesthesia (TEDA). For working environment reasons, one usually waives the use of inhalation anesthetics because of the risk of air leakage during the operation. A TEDA catheter is placed on level T4-T5 or T5-T6. The regional block is started preoperatively with bolus dose of both local anesthetic and opioid. At the same time, an infusion with Standard-epidural mixture (e.g. Breivik) or pure local anesthetic agent is initiated.

Lung separation

Ventilation separation of the lungs can theoretically be accomplished in three different ways: By single lumen tube, double lumen tube or single lumen tube with bronchial blocker.

The first option is rare and then used exclusively in an acute situation, where a heavy bleeding in one lung threatens to spread to the other lung with the subsequent risk of not being able to ventilate the patient. If, in this situation, one does not have immediate access to any of the other two alternatives, it can be lifesaving to intubate the main bronchus on the non-bleeding side with a single lumen tube. This is of course the easiest on the right side by pressing the tube far down. In intubation of the left main bronchus, a bronchoscope is used as a stylet.

In the normal case, double-lumen tube or single-lumen tube is used with a bronchial blocker. Both methods have their pros and cons. The type of surgery and, above all, the ability to intubate the patient is crucial.

Double-lumen tube (DLT)

Double-lumen tubes (DLT) are available in two variants, right and left curved (Fig. 1 and 2), depending on whether the bronchial part is towards the right or left side. In addition, the profile of the distal cuff differs (Figs. 3 and 4). A right deviated tube also has a hole on the side to secure ventilation to the upper lobe, which departs early in the right main bronchus. In the left main bronchus, the margin from carina to the upper lobe bronchus is 3-4 cm, so it is enough with a normal olive-shaped cuff.

Fig. 1. DLT left.

Fig. 2. DLT left mounted and ready for intubation. The picture shows the rigid stylet in the tube and the branching of the ventilation.

Fig. 3. DLT left, distal portion with olive shaped bronchial cuff.

Fig. 4. DLT right with the distal, more kidney-shaped cuff. The picture also shows the lateral hole which should secure the ventilation to the right bronchus.

Due to the anatomy around the right upper lobe bronchus, a DLT is more sensitive to small changes in position peroperatively. This is in contrast to a properly positioned DLT left that is rarely disturbed from its position. Therefore, the use of a right-deviated DLT is usually reserved for surgery which involves left-sided pulmectomy or where there are anatomical changes in the left main bronchus. For all other operations, DLT with left deviation is used.

The dual-lumen tubes are available in seven different sizes (Table 1) and are named according to French Size. The two smallest sizes are pediatric tubes. Size 32 to 41 is for adults. The table also shows the outer diameter in mm (divide F size by 3).

Table 1. DLT and sizes corresponding outer diameter

DLT French size (F)
F sizeOuter diameter (mm)
268.7
289.3
3210.7
3511.7
3712.3
3913.0
4113.7

Normally, size 35 is used for women and size 37 for men.

Intubation with DLT is done in the usual way using a laryngoscope. The included stylet allows the distal, bronchial portion of the tube to be easily flexed and begins by pointing this portion anteriorly to facilitate intubation. When the tracheal proximal cuff has passed the vocal cords, the tube must be rotated one quarter turn counterclockwise (left thumb) or clockwise (right thumb) before fully inserting the tube. Figures 5 and 6 shows intubation with a left tube. The stylet is now removed if not done before, the tubes are closed and the cuffs are insufflated. In connection with this, the depth of the tube is controlled by the distance numbers on the side of the tube. For the majority of patients, the distance to the front tooth row is around 29 cm. The patient’s body length is crucial, the tube is fixed further down on tall patients and vice versa.

 

Figure 5. Intubation with DLT left. When the distal portion has passed down into the trachea, the tube is rotated one-quarter turn counterclockwise to enter the left main bronchus.

Figure 6. Intubation DLT left. When the distal part has passed down into the trachea, the tube is rotated one-quarter turn counterclockwise to enter the left main bronchi (Benumof JL. Anesthesia for Thoracic Surgery. Saunders 1995).

The tube position is then checked with auscultation where at the same time the closure and lung separation is tested. If you turn off the ventilation to the left lung, it should be silent over the left lung field with continued ventilation sounds over the right side. Then you do the opposite. If all is cleared, it is advisable to wait for bronchoscopy until the patient is turned in side position, as the tube may change position during this procedure.

As an alternative to the above-described “blind” technique, one can use a fiberoptic bronchoscope earlier in the process. In this case one goes down with the bronchoscope in the distal bronchial section of the tube, identifies the carina, then goes down into the main bronchi and then uses the bronchoscope as a stylet (Fig. 7).

Figure 7. Intubation DLT left using fiberoptic bronchoscope (Benumof JL. Anesthesia for Thoracic Surgery. Saunders 1995).

With the patient in surgical mode (usually side position), a control bronchoscopy is then made before the start of operation for fine adjustment of the tube position. This is always done through the tracheal part of the tube. Carina is inspected and immediately distal, see the top of the bronchial blue cuff (Fig. 8).

Figure 8. Correct position of a double-lumen tube leftsided. Picture A shows carina and just distal to the left, the upper part of the distal blue cuff is seen (Campos JH. Curr Opin Anaesthesiol. 2009; 22: 4-10).

Bronchial blocker 

There are at least six different brands and/or variants of the bronchial blocker on the commercial market. In reality, all consist of a long catheter with an inflatable cuff at the end. By inflating the cuff in the right or left head bronchus, ventilation of the relevant lung is prevented (Fig. 9).

Figure 9. Inflated bronchial blocker in the right (A) and left (B) main bronchus (Campos JH. SAJAA 2008; 14: 22-6).

A bronchial blocker is placed through a single lumen tube and placed correctly using a fiber bronchoscope. Choose as large a tube as possible (8th or 9th) so you have enough space for both the catheter and the bronchoscope (Fig. 10).

Figure 10. Closure of bronchial blocker in the left main bronchus (Campos JH. SAJAA 2008; 14: 22-6).

Ventilation

Before closing the ventilation to one lung, so-called denitrogenation should be considered. This means that for 3-5 minutes, ventilation is done with 100% oxygen and 6-8 liters of fresh gas flow in order to remove all nitrogen gas from the airways and the circle on the anesthesia device. The effect is that any shunt problems are postponed and that the lung becomes atelectic faster, which pleases the surgeon.

The shutdown itself is performed by placing a forceps on the soft tube part to the side to be closed off (Fig. 11). Then, the tube cap is opened distally of the forceps to release the air allowing exsufflation.

Figure 11. DLT left. Switching off the ventilation to the right lung with forceps on the soft tube part. Note that the right tube is now open for evacuation of the air so that the lung becomes atelectic.

During shutdown, so-called protective ventilation is recommended with some form of pressure-controlled or pressure-controlled ventilation. Seek tidal volumes of 4-5 ml/kg corrected body weight. Peak pressure below 40 cm H2O and plateau pressure below 25 cm H2O. Usually PEEP 5 cm H2O on the ventilated lung. Permissive hypercapnia below 8 kPa if the patient does not suffer from right-sided heart failure. All this to reduce the risk of postoperative lung injury. Most patients cope with 50-70% O2 during the suspension of one lung ventilation.

In case of problems with shunting (SpO2 <90%) one can primarily try to increase FiO2. If it does not help it is most effective to ask for a small break in the surgery and temporarily inflate the closed lung with 100% O2. In addition, an O2 catheter for the suspended lung (2-5 liters/min) can often contribute positively. Selective CPAP to the suspended lung is also a possibility, but is rarely appreciated by the surgeon.

Closure of anesthesia

At the end of the operation, the suspended lung is re-expanded. This is most easily done manually using the APL valve of the anesthesia ventilation device and the ventilation balloon. Use a gas mixture with 40% O2 and a constant pressure of max 20 cm H2O and 5-10 cm PEEP. The procedure takes 20-60 seconds. The desired effect is observed directly by visual inspection of the lung at thoracotomy or via the thoracoscope at thoracic surgery. Then return to norm ventilation with 30-40% O2 and PEEP 5-10 cm H2O until awake. The patient is awakened from anesthesia in the usual way. If the patient remains in the respirator, the double-lumen tube is usually replaced with a single lumen tube before transport to the intensive care unit. A double-lumen tube should not remain in the trachea for more than a maximum of one day (recommendation).

Postoperative pain relief

Most effective is TEDA or paravertebral blockade in combination with paracetamol. However, with reduced coagulation capacity, these techniques are contraindicated. Intercostal blockade can then be considered but has a shorter duration and must almost always be combined with an opioid. Supplementation of ketamine, clonidine or NSAID may be necessary.

Ipsilateral shoulder pain

More than half of all patients with TEDA suffer from a troublesome shoulder pain on the same side as the surgical procedure. Everything indicates that it is a so-called “referred pain” mediated via sensory nerve pathways in the phrenic nerve and pain originating from the mediastinal and diaphragm part of the parietal pleura. The best effect on this pain is NSAIDs, eg inj ketorolac (Toradol) 15-30 mg iv, and paracetamol.

References

  1. Benumof JL. Anesthesia for Thoracic Surgery. Saunders 1995
  2. Slinger P (ed). Principles and Practice of Anesthesia for Thoracic Surgery. Springer 2011
  3. Lohser J. Evidence-based Management of One-Lung Ventilation. Anesthesiol Clin 2008;26:241-272.
  4. Campos JH. Curr Opin Anaesthesiol. 2009;22:4-10
  5. Campos JH. SAJAA 2008;14:22-6

Pacemaker

By Patrik Martner, Specialist Physician in Anesthesia & Intensive Care. Sahlgrenska University Hospital.

Updated 2019-10-14

A pacemaker consists of two parts. One is the pacemaker box, which is an encapsulated computer with battery. The other part is the electrodes, which sense the heart rhythm and, if necessary, emit electrical impulses that cause the heart to contract.

  • VOO = Fast frequency ventricular pace
  • VVI = Ventricular inhibited pace
  • AAI = Atrial Inhibited Pace
  • DDD = Atrial & ventricular initiated pace

Pace

  • Atrium
  • Ventricle
  • Dual (A+V)
  • O = None

Sense

  • Atrium
  • Ventricle
  • Dual (A+V)
  • O = None

Sense-svar

  • Triggered
  • Inhibited
  • Dual (T+I)
  • O = None

External temporary PM after cardiac surgery

Blue contact – atrium, white contact – chamber

Sc electrode to positive (+) pole

EMERGENCY – asynchronous high energy stimulation with VVO (unlock PM first!)

Stimulation

  • Atrial – normally 2-10 V (max range 0.1-18.0 V)
  • (output) Ventricle – normally 5-10 V (max range 0.1-18.0 V)
  • Guideline – 5 V above the capture threshold

Sensing

  • Atrial – normally 0.5-1mV (max range 0.2-20mV)
  • Ventricle – normally 2-3 mV (max range 1.0 – 20 mV)
  • AV interval Usually 150-180 m – compare with the patient’s PQ time