Hypertension in the cardiac surgical patient

Controlling the blood pressure, whether high or low, is a part of the "management encompassing resuscitation, initial and ongoing monitoring and supportive treatment" for "Cardiac surgery: including sternotomy for bypass grafting, valve surgery and aortic surgery", a Level 1 topic from Section 2.1.18 in the second edition of the CICM Syllabus for the Second Part Examination. This issue was explored in Question 10 from the first paper of 2008, which had an extremely ordinary college answer associated with it, and which did not go into the management options.

How high is too high?

The discussion of circulatory endpoints in the routine management chapter specifies the other  haemodynamic variables we could use as goals or boundaries, if such a thing is interesting to the reader. The main reason to bring these up here is to point out that, like with MAP and virtually all the other variables, there is no agreement on the upper threshold of blood pressure in this population, or at least nothing based on any sort of evidence or observational data. Venerable textbooks from thirty years ago (Glenn's Thoracic and Cardiovascular Surgery, 6th ed from 1996) are still listed on the RACS reading for cardiothoracic surgery final exams and they give a MAP of 70-105 mm Hg as the normal set of values for cardiac post op patients, which implies an upper systolic range of around 120-150. Estafanous & Tarazi (1980) are probably the most widely quoted authority on the subject and they propose the following definitions, on the basis of their own historical data:

• SBP > 160 in previously normotensive patients, or
• An increase in more than 30 mmHg of SBP or DBP from whatever the baseline pressure is.

Consequences of hypertension in the cardiac surgical patient

"You'll blow the grafts", senior ICU nurses will threaten if you leave the hypertension unaddressed. This fear is transmitted from the Gothic horror written by Fawzy Estefanous during the dawn ages of cardiac surgery. He was the first to describe and define (as SBP >160), although he could not in all honesty ascribe any problems to this discovery:

"There were no serious complications related to these hypertensive episodes in this series of patients; only occasional premature ventricular contractions were noticed in the more persistent cases."

The specific concerns that the anastomotic sites of the coronary artery grafts will somehow become compromised by arterial hypertension can be traced back to Viljoen & Estefanous et al (1976), whose report - "leakage at suture lines occurs particularly at the aortic cannulation site (2 cases in our series)"-  seemed to be referring to unpublished experience with cardiac surgical patients prior to 1973. Subsequent papers, such as Vuylsteke et al (2000), mostly reference this same paper when they mention bleeding risk from hypertension, which suggests that our experience of this phenomenon may be very limited.  Australia's own McIlroy et al (2019) found that there was no association with the rate of blood loss via drains and peak systolic blood pressure, and in actual fact the patients with more bleeding were (unsurprisingly) those with the lower MAP. So, perhaps the idea that with enough pressure the coronary grafts will pop off their targets and flail around hosing blood is probably somewhat farfetched; but one could point to several other less dramatic consequences which are probably more realistic and still undesirable:

• High afterload, and therefore lower cardiac output
• Increased subendocardial pressure, and so lower cardiac perfusion (thus poorer contractility)
• Theoretically, myocardial ischaemia as the result of these
• Arrhythmias, following from the poor perfusion narrative
• Increased MR and AR
• Heart failure, in the sense that 
• Increased need for sedation, as propofol is occasionally misused as an antihypertensive
• Extension of a dissection, if one was not noticed at the end of the case

Causes of hypertension in the the cardiac surgical patient

Why are they like this, you ask yourself. Fully 60% of patients end up on noradrenaline; why can't you be more like those people? From Estefanous, the following are possible causes:

• Pain
• Anxiety
• Inadequate sedation in a partially paralysed patient
• Pre-existing hypertension, and the perioperative cessation or regular medications
• Rebound phenomenon from ceased antihypertensives
• Hypercapnia
• Shivering due to hypothermia
• The sudden improvement of aortic flow following the repair of a stenotic aortic valve, which exposes the systemic circulation to being bullied by a massively hypertrophied left ventricle.

To this list, one might add stroke and intracranial haemorrhage, however rare. Artifactual hypertension (measurement error) and the unintelligent use of vasopressors is listed by the college examiners in their answer to Question 10, but those were 2008 examiners, and the current crop appear more inclined to expect these to already be excluded by the mature trainee, i.e mentioning these possibilities in a written answer is unlikely to score a large amount of points.

Management of hypertension in the cardiac surgical patient

From the above causes, the following list of solutions presents itself:

• Analgesia should be first line, for humanitarian reasons but also because it would be shameful to miss this easy solution
• Adequate sedation (without overreliance on propofol as an antihypertensive)
• Co-analgesia with clonidine, which may have a salutary effect on all three among blood pressure, pain and anxiety
• β-blockers, which will inevitably also be required for the prevention of AF, and so seem like an elegant solution
• Vasodilators, if the low heart rate of the clearly calm and pain-free patient does not permit the use of clonidine or β-blockers

Of the vasodilators, there are many, and the classical texts hold forth on the use of such monstrous substances as sodium nitroprusside and diazoxide, but the modern trainee would be rather less likely to resort to these. The choice of vasodilator will depend largely on which class would be the most optimally synergistic with the patient's individual situation. For example:

• Calcium channel blockers such as amlodipine could be offered to patients whose radial arteries have been grafted, on the grounds that these may have some protective effect against graft spasm.
  • If titratability is required, clevidipine may be a better choice, or GTN infusion if the SVG was the graft, as veins respond very well to the dilating effects
• Hydralazine may be helpful if the vasodilating effect needs to be short-lived, and prazocin could be beneficial if longer activity is requred