Fig. 13.1
Pressure–volume curve of the left ventricle
In diastolic heart failure, there is a relaxation disorder of the left ventricle, which causes diastolic pressure increases during ventricle filling (d → a) disproportionally (d → a′).
Diastolic heart failure is seen in the echocardiography as [5]:
Slowed isovolumetric relaxation of the left ventricle, despite a normal ejection fraction (EF >45 %)
Normal or low end-diastolic ventricular volume with a decreased early diastolic filling phase and decreased diastolic elasticity (left ventricular end-diastolic pressure >16 mmHg)
Normal or decreased stroke volume
Increased filling pressures with increased left ventricular stiffness, often stress induced
Differentiating between diastolic dysfunction and diastolic heart failure is necessary. In symptomatic patients, there is said to be diastolic heart failure, whereas asymptomatic patients are referred to as having diastolic dysfunction. Another term, which is used for diastolic heart failure, is heart failure with normal left ventricular ejection fraction (HFNEF) [13]. HFNEF requires the following conditions to be satisfied:
Signs or symptoms of congestive heart failure such as pulmonary edema, ankle swelling, hepatomegaly, dyspnea on exertion, and fatigue
Normal or mildly abnormal systolic left ventricular function
Evidence of diastolic left ventricular dysfunction
Morphologically, there is a concentric hypertrophy of the left ventricle, as opposed to eccentric hypertrophy which is typical for systolic dysfunction.
Signs or symptoms of congestive heart failure in Mrs. Hill’s case are difficult to evaluate due to her debilitating spinal stenosis and inability to exercise. During the preoperative evaluation, she needs to be thoroughly evaluated to assess whether she is in optimal condition for the planned surgery, in addition to obtaining informed consent for anesthesia. In Mrs. Hill’s case, pulmonary edema needs to be ruled out by auscultation. In the chest X-ray, however, there are no signs of pulmonary congestion. If ordered, the lab values may show an increased proBNP level.
Risk factors of diastolic heart failure:
Geriatric age
Arterial hypertension
Obesity
Diabetes mellitus
Obstructive sleep apnea syndrome
Left ventricular hypertrophy
Aortic stenosis
Coronary artery disease
>> Dr. Baldwin now turned to Mrs. Hill. After he carefully checked all limbs and only got one small IV started in her left foot, he decided to place a CVC in the OR under local anesthesia prior to induction of anesthesia. Mrs. Hill gave informed consent. After taking Mrs. Hill to the OR, he made several unsuccessful puncture attempts of the internal jugular vein. Since he didn’t want to make additional attempts on her neck, he decided to go for the subclavian vein on the right. He was successful on the second try! The Seldinger wire was inserted gently; a few extrasystoles allowed Dr. Baldwin to be sure that he had landed at the right place. Mrs. Hill beamed up at him “That wasn’t bad at all!” she said.
Then Dr. Baldwin began the induction saying, “Sarah, please administer 150 μg of fentanyl, then 70 mg of propofol.” After Mrs. Hill was sufficiently anesthetized, she received 30 mg of atracurium. The next blood pressure was 68/35 mmHg. After a bolus of phenylephrine and 250 ml of a crystalloid infusion, the pressure increased to 87/54 mmHg, but then sagged again.
Anesthesia assistant Sarah pulled out the supplies for phenylephrine and vasopressin infusions and told the intern to prepare everything for invasive arterial blood pressure monitoring. Dr. Baldwin was having a hard time finding a pulse in the radial artery; he requested an ultrasound.
Finally, all invasive monitors were in place. The blood pressure, with the help of phenylephrine and vasopressin infusions, was 120/87 mmHg; the A–line was ready, the nasogastric tube in place, the eyes safely covered, and a urinary catheter placed. Anesthesia assistant Sarah had taken advantage of the vasodilation caused by the anesthetic agents to place a 16 g in the forearm. The anesthesia was maintained with 3.6 % end–tidal desflurane.
The orthopedic surgeon entered the OR: “Good morning; everything OK? Can we position the patient now? Did Mrs. Hill receive the antibiotic prophylaxis already?” The infusion with the antibiotic drip began, and Dr. Baldwin was happy that, despite the complicated induction, he was only 15 min late from the scheduled start of surgery.
13.1.3 Would You Have Chosen Another Procedure?
13.1.3.1 Invasive Blood Pressure Monitoring Before the Induction of General Anesthesia
Due to her comorbidities, Mrs. Hill should have received invasive arterial blood pressure monitoring prior to induction.
13.1.3.2 Placement of the CVC with Ultrasound Guidance
Since an ultrasound was available, it should have been used for the placement of the CVC. The ASA Practice Guidelines for Central Venous Access recommend use of ultrasound guidance for CVC insertion because it reduces complications and increases the success rate of internal jugular puncture [14].
13.1.3.3 Phenylephrine and Vasopressin Infusions Prepared Prior to Induction of General Anesthesia
Again, due to the Mrs. Hill’s preexisting conditions, it should have been assumed that continuous administration of vasopressors would be necessary. With this in mind, a phenylephrine infusion should have been set up before induction. Given Mrs. Hill was taking captopril, an angiotensin-converting enzyme inhibitor, a vasopressin infusion should also have been prepared in advance, as phenylephrine alone may not restore blood pressure with this class of drugs. Vasopressin is very effective in treating perioperative hypotension in patients on renin–angiotensin system antagonists preoperatively [16].
13.1.3.4 Etomidate?
Many anesthesiologists prefer etomidate as the induction anesthetic agent in patients with significant cardiac disease, since there is less negative inotropic effect than with propofol.
13.1.3.5 Timing of Prophylactic Antibiotic Administration
Administration of intravenous antibiotic was started shortly before Mrs. Hill was positioned prone. This was inappropriate timing. Mrs. Hill had to be disconnected from the monitors just as the drip began. Allergic reactions causing circulatory changes could therefore not be detected as quickly. In addition, perioperative antibiotic prophylaxis should not be given more than 30 min before skin incision, in order to work most effectively. An exception to this timing is vancomycin, which is given by slow infusion beginning within 60 min of skin incision. In prone spine surgery, especially when neuromonitoring is placed after prone positioning, it is best to wait to start the antibiotic after the patient is prone.
>> After the team turned Mrs. Hill to prone position, and after the monitoring cables were quickly reconnected, the blood pressure was 78/43 mmHg and heart rate 45/min, but it quickly increased to 95/min. The S P O 2 was 94 %.
Dr. Baldwin doubled the vasopressin infusion, and his assistant Sarah hooked up 500 ml of 5 % albumin infusion. The surgeon asked why the alarm was sounding and asked if he could help. “No, no,” said Dr. Baldwin, “the blood pressure will be better in a second.” And what do you know, the blood pressure increased to 105/65 mmHg. The student intern shyly asked Dr. Baldwin if Mrs. Hill might have just had a pulmonary embolus.
13.1.4 How Do You Explain to the Student What Just Happened?
The cardiopulmonary changes could have been caused by the following.
13.1.4.1 Relative Hypovolemia Due to Positioning
Relative hypovolemia due to the prone position is often seen. It is influenced by preoperative hypovolemia, the vasodilation effect of the anesthetic agents, and the simultaneous lowering of the legs, which is often done in this position. Patients need to receive adequate volume before induction, and there must be sufficient intravenous access available. Correction of hypovolemia is especially true for patients taking ACE inhibitors and angiotensin receptor antagonists, as hypovolemia severely exacerbates hypotension with these drugs. In addition, patients should only be disconnected from the monitor for the shortest amount of time possible. Vasoactive substances must be prepared and ready to administer.
13.1.4.2 Cardiac Event
Myocardial ischemia or infarction can’t be completely ruled out. The ECG and ST segments must be carefully monitored. The rapid response to the vasoactive substances and volume administration makes hypovolemia the most likely cause.
13.1.4.3 Pulmonary Embolus from a Preexisting Thrombosis
During the positioning, an embolus could have been dislodged from a thrombosis in the leg. In such an occurrence, a lowered end-tidal and relatively high arterial CO2 concentration would have occurred, due to the increase in dead space ventilation (see Sect. 11.1.7).
13.1.4.4 Vagal Reflex in Conscious Patients
The patient received relatively little anesthetic agents, and the end-tidal desflurane concentration was under the 0.7 MAC value. Therefore, the patient could have returned to consciousness during the positioning and reacted by fighting against the ventilator and suffered a vagal reflex. Fighting the ventilator is unlikely, however, since sufficient muscle relaxant was given.
13.1.4.5 Stimulation of the Carotid Sinus by Improper Positioning of the Head
Stimulation of the carotid sinus with the accompanying vagal reflex is possible and requires checking the head and neck positioning.
13.1.4.6 Allergic Reaction to the Antibiotic
An allergic reaction to the antibiotic is an important differential diagnosis. Allergic exanthema is not always the most predominant symptom [3], nor is bronchospasm always present.
The immediate therapy to stabilize the hemodynamics is identical to treating hypovolemia. If the symptoms persist, anaphylaxis must be considered in the differential diagnosis.
As a rule, antibiotic administration in anesthetized patients should always occur with simultaneous vital sign monitoring. The immediate actions in case of an allergic shock would be to remove the trigger (stop the antibiotic infusion), give 100 % oxygen, titrate IV epinephrine (50 μg boluses) to hemodynamic effect, and give a rapid fluid bolus of 500–1,000 ml. Antihistamines and steroids are second-line treatment in anaphylaxis.
>> Dr. Baldwin explained to the intern that the most likely cause was relative hypovolemia due to the prone position. Myocardial ischemia was very unlikely because there were no additional ST segment changes. He recommended that the intern take a blood gas in order to rule out pulmonary embolism.
The ABG showed:
Hb: 8.5 g/dl (reference 11.9–17.2 g/dl)
HCT: 26 % (reference 37–47 %)
P a O 2 : 272 mmHg (reference 70–100 mmHg)
P a CO 2 : 37 mmHg (reference 36–44 mmHg)
BE: –1 mEq/l (reference ±2 mEq/l)
Lactate: 1.1 mmol/l (reference 0.5–2.2 mmol/l)
Na +: 141 mEq/l (reference 135–150 mEq/l)
K +: 3.7 mEq/l (reference 3.5–5.0 mEq/l)
“Oh, Sarah,” said Dr. Baldwin, “Have you checked if the blood bank has crossmatched some bags for us?” His anesthesia assistant Sarah responded sheepishly that she had not yet had time to do so. “Then please call quickly,” said Dr. Baldwin. The bags of blood were not yet ready. The ward nurse had been unable to draw blood yesterday, due to Mrs. Hill’s bad veins. The blood would be ready in 25 min. “All right then,” said Dr. Baldwin.
The surgery began. At skin incision, Mrs. Hill was given fentanyl 250 μg IV. Her blood pressure had stabilized, and the vasopressin infusion was discontinued.
The next 2 h were unremarkable. Dr. Baldwin took some time to teach the student intern about differential diagnosis of sudden hypotension under anesthesia. In the meantime, his assistant Sarah had drawn a new ABG. The values were only slightly different from the first blood gas, and Dr. Baldwin was satisfied. He shot a glance at the suction container, which only had about 350 ml of bloody fluid. Mrs. Hill’s temperature was 35.8 °C.
“Oh,” asked the student intern, “shouldn’t we measure the CVP?” Dr. Baldwin replied “Yes, the absolute value won’t tell us much at this time, but we can still measure it. The CVP was 6 mmHg. A CRNA came in to give Dr. Baldwin a break. I’ll be right back; I just need a quick cup of coffee.” He disappeared around the corner.
13.1.5 What Does the CVP Indicate at This Time?
The CVP is an easily identified parameter. The CVP is defined as the pressure within the right atrium or within the vena cava as it enters the right atrium. Traditionally, CVP is measured with help from a central line, which is hooked up to a water column. The transition between the ventral to the middle third of the anterior posterior thorax diameter at the height of the sternum is used as a zero reference point (reflecting the right atrium/tricuspid valve). More information can be obtained with the help of a pressure transducer showing a central venous pressure curve (Fig. 13.2).
