Cardiomyopathy Flashcards
A 53-year-old male patient is listed for an emergency laparotomy for small bowel obstruction. He has a history of hypertension and alcohol excess and is a smoker. He has a dilated cardiomyopathy but has not been reviewed for this since his diagnosis 2 years ago.
What is a cardiomyopathy?
- A contemporary definition (2007) from the European Society of Cardiology (ESC) Working Group on myocardial and pericardial diseases states that a cardiomyopathy is “a myocardial disorder in which the heart muscle is structurally and functionally abnormal, in the absence of CAD, HTN, valvular disease and congenital heart disease sufficient to cause the observed myocardial abnormality”.
- The ESC Working Group classifies cardiomyopathies into the following categories:
- Hypertrophic cardiomyopathy.
- Dilated cardiomyopathy.
- Arrhythmogenic right ventricular cardiomyopathy.
- Restrictive cardiomyopathy.
- Unclassified (such as Takotsubo cardiomyopathy).
What are the risk factors for the development of a dilated cardiomyopathy?
- Family history.
- Male gender.
- Afro-Caribbean ethnicity.
- Sickle cell disease.
- Alcohol excess/substance misuse.
- Muscular dystrophy.
- Hypothyroidism.
- Exposure to cardiotoxic chemotherapy agents.
What signs and symptoms associated with dilated cardiomyopathies would you explore in this patient?
Evidence of heart failure:
- Dyspnoea.
- Reduced exercise tolerance.
- Orthopnoea.
- Paroxysmal nocturnal dyspnoea.
- Peripheral oedema.
- Ascites.
- Dysrhythmias
/palpitations. - Evidence of thromboembolic events or complications.
How does a dilated cardiomyopathy lead to cardiac failure?
- Ventricular enlargement and dilatation cause systolic dysfunction and reduced stroke volume due to overstretching of the actin and myosin filaments.
- Given the increase in ventricular radius increases wall tension (through the Law of Laplace), the afterload (as defined by the ventricular wall tension in systole) increases, leading to the increased myocardial oxygen demand.
- Compensatory mechanisms occur. Sympathetic stimulation increases heart rate and contractility to initially help maintain cardiac output. Activation of the renin-angiotensin-aldosterone system and ADH secretion raises systemic vascular resistance (angiotensin II, ADH) to maintain mean arterial pressure, and increases intravascular volume (aldosterone, ADH) and therefore preload (if on the ascending part of the Frank-Starling curve).
- Although these compensatory mechanisms initially help to preserve cardiac output, they ultimately worsen the ventricular dilatation, wall tension, and oxygen demand, which further perpetuates systolic dysfunction and cardiac failure.
How would you assess this patient preoperatively?
History:
- The preoperative assessment should include a review by a consultant surgeon and anaesthetist, assessing the need for surgery and risk stratifying the patient using an appropriate tool e.g. P-POSSUM score. This should be discussed with the patient prior to surgery.
- The patient should be discussed with the ICU team preoperatively, for consideration of optimisation prior to surgery and for management postoperatively. Ensure ongoing resuscitation if appropriate.
History:
* Ensure a thorough CVS history focusing on the patient’s current symptoms, as described above to ascertain the degree of systolic dysfunction, cardiac failure if present and any evidence of end-organ dysfunction or thromboembolic events. Conduct a review of the patient’s previous notes and any discussions with the cardiology team regarding the patient’s diagnosis and any initiated treatment.
- Take a history of the patient’s other comorbidities including their smoking and alcohol history and current intake/medical conditions associated with either.
- Discuss previous anaesthetics, the airway and drug history.
- Explore the time course of the patient’s current illness, oral intake and treatment so far including antimicrobial therapy.
How would you assess this patient preoperatively?
Examination & Investigations:
Examination:
* Bedside observations.
* Cardiovascular and respiratory examinations.
* Airway assessment.
Investigations:
* Routine baseline bloods for evidence of coagulopathy, hepatic or renal dysfunction, evidence of anaemia, and biomarkers of heart failure. Measure an arterial blood gas to determine the patient’s resting efficiency of gas exchange and lactate.
- Chest X-ray for assessment of pulmonary oedema, or co-existent infection.
- ECG in particular for atrial dysrhythmias, conduction defects, or ST segment/T wave abnormalities.
- Echo for left and right ventricular size and function, the presence of valvular dysfunction (such as mitral regurgitation caused by stretching of the mitral annulus from ventricular dilatation), atrial size, estimated pulmonary artery systemic pressure, and the presence of sluggish intracardiac blood flow or an intracardiac thrombus.
NB The degree of investigations or preoperative optimisation should be balanced against the urgency for surgery. TTE would be very useful!
What are the priorities for the anaesthetic management of this patient?
Pre-op:
- Ensure a thorough work-up, as described above.
- Optimise cardiac medication if evidence of heart failure and control
dysrhythmias.
What are the priorities for the anaesthetic management of this patient?
Intra-op:
- Ensure a cardiostable anaesthetic led by an experienced team.
- Monitoring: ensure large bore IV access and intra-arterial, central venous pressure and cardiac output monitoring to guide
treatment. - Avoid tachycardia.
- Aim to maintain sinus rhythm. Dysrhythmias will be poorly tolerated. Ensure electrolytes are optimised (including Mg2+) and treat dysrhythmias early with anti-arrhythmic drugs or cardioversion as appropriate.
- Maintain an appropriate preload; both hypovolaemia and fluid overload will be poorly tolerated. Use fluids or diuretics carefully.
- A high afterload (that increases myocardial work and reduces cardiac
output) or an excessively low afterload (that compromises coronary perfusion or end-organ perfusion) will be poorly tolerated. Avoid both of these situations. - Beware of anaesthetic agents that cause myocardial depression and drugs that cause either a significant increase in SVR or tachycardia (e.g. ketamine), or those that can precipitously drop SVR and compromise coronary perfusion (e.g. propofol). Depth of anaesthesia monitors should be considered to assist with agent titration and mitigate the cardiovascular effects of excessively deep anaesthesia.
What are the priorities for the anaesthetic management of this patient?
Intra-op continued…
- Inotropic support may be required, depending on the degree of ventricular impairment. A systemic infammatory response from the surgery may also precipitate a degree of vasoplegia-induced hypotension, which may need vasopressor support. Note that pure vasopressor or high alpha-mediated vasoconstriction, leading to a high afterload, may be poorly tolerated if the afterload is increased without complementary inotropic support. This highlights the utility of considering cardiac output monitoring or intraoperative/bedside echo to optimise vasoactive support.
- Avoid excessive PEEP or high airway ventilatory pressures that would compromise ventricular filling.
- Beware of fluid shifts, insensible fluid loss, and blood loss during the laparotomy, as these will effect the above.
- Maintain normothermia.
- If blood products are administered, ensure Ca2+ is maintained/
replaced (as Ca2+ is chelated by citrated blood products). A low Ca2+ level will be negatively inotropic, which will be poorly tolerated in this instance.
What are the priorities for the anaesthetic management of this patient?
Postoperative:
- Close monitoring and supportive treatment in cardiac intensive care.
