3. Introduction
HEART DISEASE IN PREGNANCY
• The incidence of cardiac lesion is less than 1% amongst hospital deliveries. The
commonest cardiac lesion is of rheumatic origin followed by the congenital ones.
• Rheumatic valvular lesion predominantly includes mitral stenosis (80%). Predominant
congenital lesions include patent ductus arteriosus, atrial or ventricular septal defect,
pulmonary stenosis, coarctation of aorta and Fallot’s tetralogy.
4. Rare causes of heart diseases in pregnancy are
hypertensive,
thyrotoxic,
coronary cardiac diseases
During pregnancy there is progressive anatomical, physiological and biochemical
change not only confined to the genital organs but also to all systems of the body.
This is due to of maternal adaptation to the increasing demands of the growing
fetus.
5. Classification of Cardiac Diseases Seen in
Pregnancy
1.Valvular lesions due to rheumatic heart disease
• Mitral stenosis, Mitral insufficiency, Aortic insufficiency, Aortic stenosis (AS
2.Congenital heart disease
a. Congenital heart disease without shunt (Cardiomyopathy
b. Congenital heart disease with shunt
i. Acyanotic (left → right) with increased pulmonary blood flow: (Atrial septal defect (ASD)
ii. Cyanotic (right → left) – Tetralogy of Fallot
iii. I. Eisenmenger’s syndrome of PDA, ASD, VSD
7. PHYSIOLOGICAL CHANGES IN PREGNANCY
By the 20th week of gestation, cardiac output increases by 40% due to increased stroke
volume and heart rate.
Blood volume increases by up to 50% while systemic vascular resistance (SVR) falls.
This will place additional strain on a failing heart and in those with a significant shunt.
As SVR falls there will be increased right to left shunting which may reduce pulmonary
perfusion. Coupled with the increased oxygen demand of pregnancy this can lead to
increasing hypoxia.
8. SIGNS AND SYMPTOMS OF SEVERE HEART DISEASE
Severe or progressive dyspnea,
Progressive orthopnea,
Paroxysmal nocturnal dyspnea,
Hemoptysis, Exertional syncope,
Chest pain related to effort or emotion
Progressive or generalized edema indicate the presence of heart disease.
10. General Principles of Anesthetic Management of the
Parturient with Heart Disease
• Hemodynamic changes that occur in pregnancy represent a significant stress test. Hence,
women with cardiac disease who remain asymptomatic throughout pregnancy tolerate
labor and delivery well. unlike, symptomatic patients usually tolerate pregnancy, labor,
and delivery poorly.
• The goals of anesthetic management during labor and delivery in pregnant women with
heart disease include: Analgesia, hemodynamic monitoring, Optimizing cardiovascular
and respiratory functions by manipulating various hemodynamic factors and tailoring
anesthetic technique for maternal and fetal well-being.
11. The concept of producing cardiac grid” for each patient with cardiac lesions has five hemodynamic
factors that include;
1. preload, (2)
2. pulmonary vascular resistance (PVR),
3. systemic vascular resistance (SVR),
4. heart rate, and
5. myocardial contractility.
The cardiac grid will determine the desirable hemodynamic requirements for a particular lesion.
For this, the evaluation of the patient should be complete, and diagnosis of the type of cardiac
lesion should not only be based on clinical findings but also should be confirmed by diagnostic aids
such as echocardiography.
13. Factors poorly tolerated by parturients with congenital heart disease
regardless of functional status
14. Valvular lesions
• The most important functional consequence of rheumatic heart disease is
valvular stenosis and regurgitation.
• Valvular disease may result in stenosis, insufficiency (regurgitation or
incompetence), or both.
• Stenosis is the failure of a valve to open completely, obstructing forward
flow. .insufficiency is failure of valves to completely or perfectly close
resulting in backwards flow.
• Mitral stenosis is the commonest heart lesion associated with rheumatic heart
disease met during pregnancy.
15. SPECIFIC CARDIAC CONDITION AND MANAGEMENT
1. MITRAL STENOSIS
Mitral valve serves to ensure one way blood flow from the left atrium to the left
ventricle of the heart. It opens when the left l.A pressure is higher than the l.V
pressure allowing blood to full in the l.V and closes when the left ventricle contract
to prevent back flow. Has two flops supported by fibrous rings , mitral stenosis
occurs when The valves thicken and becomes funnel shaped . calcium can
accumulate on the cusps , leaflets and annulus, has a result blood volume increases
in the left atrium , there is an impaired L.A emptying and L.A filling.
16. ANESTHETIC MANAGEMENT;
The goals are :
Maintain a slow heart rate
Maintain a sinus rhythm if present . aggressively treat acute atrial fibrillation.
Avoid precipitating events of tachycardia by preventing pain ,hypoxemia, hypercarbia and
acidosis .
To prevent rapid ventricular rate , digoxin therapy should be started prior to pregnancy and
should be continued to maintain ventricular rate less than 110 beats per minute.
Regional anesthesia is preferred as induced sympathectomy reduces both preload and after
load.
17. • Both RA or GA can be used
• Epidural anesthesia is an option (e.g., 5 ml boluses of bupivacaine 0.1% with fentanyl
2 μg ml−1)
• IV fluid administration should be avoided; if necessary, it should be given in small
(100–200 ml) boluses
• Vasopressors low dose of phenylephrine
• GA also provide stable hemodynamics
• Etomidate is best used as an induction agent
• Beta blockers such as esmolol and moderate dose of opioids should be administered
before induction
18. 2.MITRAL REGURGITATION
Mitral regurgitation (MR) is a commonly encountered valve lesion. MR can either involve
structural abnormalities in the valve or in its sub valvar components, or functional
abnormalities due to annular or left ventricular dilation causing maladaptation of the mitral
valve leaflets. Mitral valve regurgitation leads to incomplete closure of the valve leading to
the blood from the left atrium to be regurgitate back wards. Thereby compromising the
emptying and filling.
19. Anesthetic management
The primary goal in patients with chronic MR is maintaining forward
systemic flow. The heart rate should be maintained in the high-normal
range, i.e., 80 to 100 beats/minute.
Tachycardia decreases the regurgitant volume by shortening systole.
Bradycardia has dual detrimental effects MR: it increases the systolic period
duration, thus prolonging regurgitation, and it increases the diastolic filling
interval, which can lead to LV distention.
20. Management
• Epidural anesthesia can prevent an increase in systemic vascular resistance (SVR)
associated with pain and prevent pulmonary congestion
• The main consideration is maintaining slight increase in SVR and central blood volume
• Invasive blood pressure monitoring (severe cases)
• Prevent hypoxemia, hypercarbia, acidosis that will lead to an increase in PVR
• Avoiding Aortocaval compression and myocardial depression
• Vasopressors may be a benefits to this patient due to its chronotropic effects if required
• If is GA required; ketamine and pancuronium may produce desirable effects
21. 3.AORTIC STENOSIS/ AORTIC REGURGITATION
The Aortic valve serves to ensure one way of oxygen rich blood from the left
ventricle into the aorta and to the body . The aortic valve consists of three
leaflets , a defect valve is one that fails to close open properly . Aortic
stenosis happens when the aortic valve does not fully open . Aortic
regurgitation on the other hand happens when the valve fails to close fully,
both conditions may result in the heart not pumping enough blood to the
body and this may result in left sided heart failure.
22. AORTIC STENOSIS MANAGMENT
GOALS
Maintain sinus rhythm , our goal heart rate is between 60-80 B/M.
Prevent tachycardia, this is because its poorly tolerated because it does not
allow enough time in diastole to perfuse coronary arteries.
Avoid hypotension because these patients have an increased left ventricular
end diastolic .
23. Anesthetic management;
Maintain heart rate and Maintain sinus rhythm (patient have a fixed SV, a slow HR decreases CO
and severe tachycardia increases myocardia oxygen demand and decreases time for the diastolic
perfusion of the hypertrophic LV )
Avoid myocardial depression during anesthesia and Prevent pain.
GA: combination of etomidate and mid dose opioids with succinylcholine for rapid sequence
intubation and adequate analgesia is needed. Avoiding induction drugs like propofol is essential
to prevent hypotension.
Epidural or spinal anesthesia is contraindicated
Vasopressors like neosynephrine because does not increase heart rate but improves blood
pressure.
24. Anesthetic management for aortic regurgitation
Maintaining a relatively fast heart rate (approximately 90 beats/min) will
minimize the time spent in diastole and leads to a decreased regurgitant
fraction.
Tachycardia is well tolerated in these patients
reducing afterload (maintaining a relatively low systemic vascular resistance
[SVR])will minimize the pressure gradient back across the aortic valve during
diastole, improving forward flow and decreasing LVEDP.
25. cont
In considering the choice of drugs for general anesthesia ;
Drugs that cause bradycardia should be avoided
inotropic agents such as β-agonists may be needed to improve left
ventricular function.
26. Cardiomyopathies
1.Dilated cardiomyopathy
Dilated cardiomyopathy (DCM) is a disease of the myocardium characterized
by impaired systolic function and dilatation of the left and right ventricles
Pathogenesis-DCM is predominantly characterized by systolic dysfunction.
There is a progressive enlargement of one or both ventricles to the stage that
the interaction between actin and myosin filaments becomes inefficient,
leading to a reduction in stroke volume and systolic impairment. The severely
dilated ventricles have a low wall thickness to diameter ratio leading to a
remarkable increase in the ventricular wall stress and oxygen demand and
further systolic function impairment
27. Anesthetic management:
1. The goals of anesthesia management in patients with DCM
are:
• Avoid myocardial depression.
• Maintain adequate preload and prevent increases in afterload.
• Avoid tachycardia.
• Prevent sudden hypotension by careful titration of anesthetic agents.
28. • Peripheral nerve blocks offer minimal hemodynamic changes.
• Central neuraxial blockade reduces afterload and improves cardiac output.
• The accompanying hypotension resulting in myocardial hypoperfusion
must be prevented
Local and regional anesthesia techniques
29. • Avoid overdose of induction agents since the circulation time is impaired.
• Etomidate causes least hemodynamic changes.
• Ketamine should be avoided, as it increases the systemic vascular
resistance (SVR).
• Although propofol has a negative inotropic effect, it is useful in reducing
the SVR.
• All volatile anesthetic agents cause myocardial depression in high
concentration.
• Opioids have minimal cardiovascular effect and reduce the requirement of
anesthetic agents
General Anesthesia:
30. 2.Hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy (HCM) is defined as a primary cardiac muscle
hypertrophy of the left ventricle in the absence of other structural or
functional abnormality.
Pathophysiology
Hypertrophy in HCM can be asymmetrical, concentric, midventricular, and
apical. It can also involve the right ventricle. Hypertrophic obstructive
cardiomyopathy (HOCM) occurs in 70% of these cases.
31. Diastolic impairment of the left ventricle is the major pathophysiological
abnormality in HCM. Extracellular fibrosis results in increasing hypertrophy,
ventricular stiffness, shape distortion, and further diastolic impairment. On the
other hand, the systolic function remains normal with high ejection fraction
until the later stages of the disease when patients develop biventricular systolic
dysfunction due to myocardial fibrosis (end-stage HCM)
32. The aims of perioperative care are:
• Adequate preload and afterload
• Maintain SVR and Avoid sympathetic activation
• Reduce contractility and Avoid tachycardia and maintain sinus rhythm
• I.V. fluid bolus and alpha-adrenergic agonist (phenylephrine) are the preferred first
line of treatment for hypotension in patients with left ventricular outflow
obstruction Regional anesthesia should be used with caution: general anesthesia is
considered safer in obstructive HCM, as spinal anesthesia-related sympathetic
blockade and
• decreased preload and afterload are dangerous in these patients.
33. Peripartum Cardiomyopathy
Pathophysiological changes during pregnancy and labor (reduced SVR;
increased blood volume; aortocaval compression; and increased heart rate
and contractility due to pain, stress, and blood loss during labor) can have
detrimental effects on pregnant women with cardiomyopathy. The mortality
in this group of patients is as high as 30–60% due to pulmonary oedema and
systemic embolization.
34. Management
• Neuraxial anesthesia reduces afterload, promoting forward flow and avoids the use
of general anesthetic agents that reduce myocardial contractility
• Maintain myocardial perfusion by avoiding: Arrhythmias episodes of hypotension
or tachycardia
• Optimize cardiac output maintain preload but prevent fluid overload maintain /
increase myocardial contractility prevent increased afterload
• Titrated neuraxial anesthesia, by incremental top-up of an epidural or a combined
epidural and low-dose spinal anesthetic technique, may achieve these aims
35. • If general anesthesia is undertaken, induction should be as smooth as possible
to minimize both hypotension and hypertension.
• The pressor response to laryngoscopy and intubation should be attenuated by
administration of an appropriate dose of a rapid-acting opioid, e.g. alfentanil
or remifentanil.
• Inotropes, such as dobutamine, may be necessary to offset the myocardial
depression of intravenous and volatile anesthetic agent
36. Cyanotic heart lesions
• A congenital heart lesion characterized by right-to-left shunt is associated
with recirculation of desaturated blood. Cyanosis varies directly with
hematocrit level. An anemic parturient woman with poor oxygen
saturation may not manifest cyanosis, whereas a woman with
polycythemia may appear even cyanotic at higher oxygen saturations.
37. In Tetralogy of Fallot, and similar lesions with obstructed pulmonary
outflow tracts, a reduction in SVR and BP is best treated with a pure
α-agonist such as phenylephrine. If there is obstruction of the RV
outflow tract, catecholamines release from inadequate pain relief, light
GA, and/or exogenous catecholamines release associated with stress or
anxiety should be avoided.
38. Eisenmenger syndrome
This is any condition in which there is a large communication between the
systemic and pulmonary circulations with pulmonary hypertension,
bi-directional shunt, and cyanosis. Over time, those lesions with large
left-to-right shunts, high pulmonary blood flow, and normal PVR may
develop right-to-left or bi-directional flow (shunt reversal). Such lesions
include ASDs, VSDs and PDAs.
39. Anesthetic options
General and regional anesthetic techniques have been employed successfully in
parturient with congenital heart disease. GA, with endotracheal intubation,
provides airway protection. Mechanical ventilation eliminates the work of
breathing and may reduce oxygen consumption, thereby improving arterial
oxygen content. The complications of controlled mechanical ventilation include
decreased venous return as well as ventricular dysfunction, compression of
pulmonary vessels, hypoxemia, hypo- or hyper-carbia, and acidemia.
40. The choice of anesthetic drugs should be of primary importance, If the
hemodynamic effect of the lesion is worsened by tachycardia, anesthetic drugs
that are known to cause an increase in heart rate through vagolysis (e.g.,
pancuronium) should not be administered
Regional anesthesia allows spontaneous respiration with little disruption of
ventilation and perfusion relationships, which may be critical in parturient
women with complex heart lesions.
41. Conclusion
An understanding of the hemodynamics associated with the structural lesion
and the appropriate use of invasive monitors are most important in providing
optimal conditions for labor and delivery for both anesthesiologist and
surgeons.
42. References
BowdleTA, HoritaA, Kharasch ED, editors. The Pharmacologic Basis of Anaesthesiology:
Basic Science and Practical Applications. New York: Churchill Livingstone; 2004.
Keith G.Allman (2011) Oxford handbook of anaesthesia ;3rd edition ,oxford university press
inc,New York. USA
Kumar .V (2013) Robbins Basic Pathology ,9th edition, Saunders Elsevier Inc, Philadelphia,
USA
