Cpb surgical&clinical orientation

CP Bypass: Surgical &Clinical orientation 1

Cardio Pulmonary Bypass:
Surgical & Clinical Orientation

for
Students
of

Perfusion Technology, Anesthesiology
& Cardiac surgery

By

Dr. Anil G. Tendolkar


TO

MY REVERED TEACHER

DR. GURUKUMAR B. PARULKAR

Sir,
surgery
more I practiced cardiac surgery

more I realised the importance of your teachings.

Sincerely,

Anil


Introduction
The art of planning & conducting perfusion based on patient’s pre-operative condition, state of
the heart, surgical step and etcetera, is fast disappearing. Today, perfusionists are becoming more
‘monitor oriented’, may be, more technically smart but poorer in clinical orientation.

I was fortunate to work under Dr. G.B. Parulkar, the then head of the department of cardiac
surgery, KEM Hospital Mumbai, India, initially as a resident in cardiac surgery and later as a junior
colleague. Dr. Parulkar taught us (his students) planning of CPB based on patient’s clinical condition,
CPB implications of every surgical step, different surgical checks and counter checks as to ensure a safe
CPB. This book is an attempt to archive the knowledge I acquired from Dr. Parulkar through years.

To understand clinical implications of a disease, understanding of pathophysiology of heart
diseases is essential. Hence, I have described pathophysiology of every disease before describing the
relevant CPB management.

Today, anesthesiologists & perfusionists are integral part of a cardiac surgical team. The three
work differently but simultaneously and share the same space. This, many a times, produces conflicting
situations. Hence it has become imperative for all the members of the team to know implications and
pitfalls of every surgical step.

I sincerely hope this book helps perfusionists, anesthesiologists and surgeons in improving their
understanding of cardiopulmonary perfusion and help them in achieving a successful outcome.


Preface

Dear All,

It is my proud pleasure to offer this book to you.

This book is not a text book and it is not intended to replace detail reading of cardio-pulmonary perfusion,
cardiac physiology or cardiac pathology. This book is meant only for improving the understanding of
cardiopulmonary perfusion from a clinical & surgical point of view.

I sincerely hope that this book helps you in achieving this goal.

Sincerely,

agt


Contents
1. Preoperative Assessment…………………………………………… 06
2. Relevant Pictorial Anatomy………………………………………… 09
3. Surgical Aspect of CPB ……………………………………………... 19
4. Mitral Stenosis ……………………………………………………….. 33
5. Mitral Regurgitation …………………………………………………. 40
6. Aortic Stenosis ……………………………………………………… 44
7. Aortic Regurgitation ………………………………………………… 49
8. Tricuspid Valve Disease ……………………………………………… 53
9. Multivalvar Affections ……………………………………………….. 56
10. Artificial Valves …………………………………………………….. 57
11. Atrial Septal Defect …………………………………………………... 59
12. Ventricular Septal Defect ……………………………………………. 68
13. Tetralogy of Fallot………………………..…………………………..... 74
14. Functional Single Ventricle …………………………………………… 81
15. Total Anomalous Pulmonary Venous Connection …………………… 89
16. Transposition of Great Arteries ……………………………………… 93
17. Coronary Artery Disease ………………………………………… 101
18. Mechanical Complications of CAD ………………………………… 117
19. Rupture of Aneurysm of Sinus of Valsalva …………………………. 120
20. LA Myxoma ………………………………………………………… 123


1. Preoperative Assessment
The importance of noting the following points in a preoperative assessment is,
1. Age: At extremes of ages tolerance of patients to artificial circulation is poor. Hence, for neonates,
infants and elderly, all the pharmacological and hardware interventions to reduce the inflammatory
response should be attempted.

2. Weight and Height: for calculation of body surface area (BSA) and hence, the flows.

3. Body Volume assessment: A cardiac patient could be in congestive cardiac failure with excessive
volume in the intravascular compartment. Conversely, some cardiac patients are vasoconstricted and in
these patients going on CPB yields a very low venous return. Thus, instead of going by a fixed formula
for body volume calculation, knowing the actual body volume status will help a perfusionist in
appropriate priming.

Body volume can be assessed by:

a) Clinical: raised JVP, edema feet, enlarged liver are associated with higher body volumes.
b) Mean CVP (Normal = 5-6mm of Hg) Higher pressure values are associated with higher
intravascular volumes.
c) Chest X-ray: Cardio-Thoracic (CT) ratio: (Normal < 50%) Higher ratio is associated with more
blood in the heart and or in the pulmonary circulation. Details of volume distribution will be
discussed with individual cases.
Prominent right heart border is associated with increased volume in systemic venous circuit.
d) 2D Echocardiography: This can estimate actual cardiac chamber size .Normal chamber
dimensions ( approximately) are
LV Internal Diameter (LVID): 2.0 cm in systole and 3.0 cm in diastole
LA: < 2.0 cm
RVID: < 1.0 cm
Remember that the above figures are of diameter (d = 2 r) of the chambers and volume of the
chamber would be 4/3 π r3.

Other descriptive terms in an echo report which indicate volume overload are,

a) IVC not collapsing during inspiration, b) dilated coronary sinus (in the absence of LSVC)
c) Volume Overload (VO) as RVVO/RAVO/ LAVO

4. Hemoglobin/ PCV: Any patient with liver congestion (as in CCF), frequent episodes of lower
respiratory tract infection (LRTI) (as in VSD) has low hemoglobin.

All patients with cyanotic heart disease have higher hemoglobin (polycythemia) as a
compensation for the decreased oxygen carrying capacity. The hemoglobin increases proportionate to the
arterial saturation.

5. Plasma Volume: Plasma volume is in inverse proportion with the Hb/ PCV value. Patients with low
hemoglobin (i.e. anemia) or CCF though have a proportionately large plasma volume; the serum protein
values are low due to poor nutrition as a result of heart disease (cardiac cachexia)

6. Systemic Vascular Resistance (SVR): In patients with a stenotic disease (e.g. mitral stenosis) SVR is
increased as a body compensatory mechanism. The rise in SVR is usually in proportionate with the
severity of stenosis.


SVR is low in patients with regurgitant or incompetent lesions (e.g. mitral regurgitation)

Preoperative and intraoperative medication can change the SVR.

Patients with high SVR have collapsed veins (inspect saphenous vein at the ankle- anterior to medial
malleolus) low volume pulse and a high diastolic pressure.
Patients with low SVR have a dilated vein, good or high volume pulse, and normal or low diastolic
pressure.

7.Organ Function : inadequate perfusion due to acute or chronic heart failure , atherosclerotic arterial
disease causing narrowing or occlusion of the arteries, cardio-arterial embolism, chronic venous
congestion affect the function of various vital organs like brain, liver and kidneys.

8. Arterial Tree: Artery may be blocked or significantly narrowed due to atherosclerosis or embolism.
As a result, CPB however well conducted, will not benefit the organ with vascular obstruction.

9. Arterial Cannulation: For median sternotomy aorta is the site of choice for arterial cannulation.
Other sites are

Site For Advantage Disadvantage

Cannulation

( Skin incision site)

Ascending Aorta 1.Performed through surgical incision 1.cerebral embolism
2.Clean area
( Sternotomy) 3.Size of cannula is not a limitation
4.complications related to cannulation
can be easily detected
Femoral Artery 1.used for quick cannulation 1. in a potentially infected area
2.percutaneous cannulation possible 2. lymph collection possible
( Groin) 3. can be performed prior to surgical 3. retroperitoneal dissection
incision
4.scar can be concealed
Iliac Artery 1.can be performed prior to surgical 1.deeper dissection than femoral
incision cannulation required
( Lumbar- 2.size of the cannula could be larger than 2. possibility of injury to ureter
retroperitoneal incision) in femoral cannulation 3. retroperitoneal dissection due to
3. cannulation in a cleaner area cannulation

Axillary Artery 1.For cerebral perfusion
2.Used in combination with the above
( Axilla) mentioned sites

Venous cannulation: Apart from commonly used sites like RA appendage, SVC & IVC other used sites
are right ventricular outflow (RVOT), and femoral veins.

These sites will be discussed as per different situations.

Cardioplegia Delivery: Antegrade: 1) root 2) coronary ostial 3) through grafts


Retrograde: 1) RA 2) coronary sinus

Left Heart return: Normally, approximately 1% of the cardiac output (i.e. 1% of 5000 ml = 50 ml per
minute) returns back to heart via bronchial veins which open into pulmonary veins (PV). This is called
‘left heart return’. From PV, the blood eventually enters LA & LV. In a cardioplegically arrested heart,
accumulation of this blood in LA/LV obstructs the operative field, distends the heart and rewarms the
heart. In certain conditions the amount of left heart return could be more.

To prevent the above mentioned problems, the LH return is sucked away through a LH vent. Various sites
for LH venting are shown below.

LH Venting Operation Vent type
Site

RSPV AVR, Ascending aortic operation sump, curved multiperforated
corrections through RA/RV
LA body MV surgery , MV+ other valve surgery Sump

VSD corrections through RA/RV long stiff

IAS Only TV surgery, corrections through Sump
RA/RV

PA TOF correction through RV, LA myxoma Sump
excision

LA appendage Only TV surgery, corrections through Sump
RA/RV

LV apex AVR, any operation on aorta curved multi-perforated

ASD Any operation involving ASD closure Long stiff, sump

Aortic Root CABG Root cardioplegia cannula

Preoperative Medications: Patient is on oral or intravenous medications prior to surgery. These
medications alter SVR, blood volume, electrolytes or clotting status.

Prior Treatment: Prior operation or intervention changes the plan for surgical approach, surgical steps,
cannulation, cooling status, cardioplegia delivery.

Special Considerations: like early cross clamping may be required in some cases


2. Relevant Pictorial anatomy
Figure 2.1: Parts of heart and blood vessels that can be seen through a median sternotomy incision

Parts shaded gray are covered by pericardial fold or thymus or mediastinal fat. Hence require
dissection to visualise them. The rest are seen after opening the pericardium. (Parts shown with dotted
lines are posterior to the heart but in the pericardium)

Right sided structures are anterior and left sided structures are posterior. Thus, RA, aorta and right
superior pulmonary vein (RSPV) are anterior structures and are easy to cannulate.

For operating on a part beyond or distal to the structures shown above; pleura or thoracic cavity has to
be opened.

Fig 2.2: Surfaces of heart

Heart is a conical structure and with the surfaces as shown below. Coronary arteries located on
anterior surface are the easily seen and those on the posterior surface are the most difficult to see.


.

Figure 2.3: .The space between the medial surfaces of the two lungs is called Mediastinum

Mediastinum is divided into anterior mediastinum (shaded bluish-green in fig 2.4), containing heart
and thymus; and posterior mediastinum, containing trachea, esophagus and descending thoracic aorta.

Fig 2.4: Approaches to mediastinum

The mediastinal structures can be approached through the following incisions:
1. Median sternotomy 2.Right anterior thoracotomy
3. Left anterior thoracotomy 4.Left posterior thoracotomy


Figure 2.5: Arrangement of Cardiac Chambers

The right side chambers are anterior also, while the left sided chambers are posterior.
The arrangement of various chambers in relation to each other is shown below.
Note: LA is the posterior most chamber.

Anterior

Posterior


Figure 2.6: Anatomy of Inter Atrial septum (IAS)

SVC: Superior vena cava IVC: Inferior vena cava FO: Fossa Ovalis CS: coronary sinus
TV: Tricuspid Valve
Shaded area: Septum Primum. Nonshaded area: Septum Secundum (the line separating the two areas
is an imaginary line passing through coronary sinus and parallel to SVC & IVC

Figure 2.7: Parts of IVS: (The boundaries are not accurately defined)

m: membranous septum inlet: under the leaflets of tricuspid valve
outlet: below the pulmonary valve body: The remaining part of RV


Figure 2.8: Atrio-Ventricular Valve. The Tricuspid Valve and the Mitral valve are called right and left
AV valve, respectively. The basic plan of an A-V valve remains the same.

Annulus, cusps, chordae, papillary muscle and LV wall constitute MV apparatus. Chordae and
papillary muscles together are called ‘subvalvar structure/ apparatus’.

Figure 2.9: Mitral Valve (Close position) as seen during surgery through LA

1: Anterior commissure 2: Annulus 3: Anterior Mitral Leaflet (AML)
4: Posterior Mitral Leaflet (PML) 5: Common Annulus 6: posterior commissure


Figure 2.10: Tricuspid Valve (Close position) as seen during surgery through RA

1. Anterior Tricuspid Leaflet (ATL) 2 Septal Tricuspid Leaflet (STL)
3. AV Node 4. Annulus 5. Posterior Tricuspid Leaflet (PTL) 6. Coronary Sinus


Figure 2.11: Aortic valve (Close position) as seen during surgery through Aorta

1. Left Coronary Cusp (LCC) 2.Left Coronary artery (LCA)
3. Right Coronary artery (RCA) 4. AV Node
5. Right Coronary Cusp (RCC) 6.Non Coronary cusp (NCC)
7. Common (with MV) Annulus

Figure 2.12: Aorta (Longitudinal section)

1. Ascending aorta 2. Sinu-Tubular Junction 3.Sinus of Valsalva
4.Cusps or Leaflets 5. Annulus 6. Coronary artery


Figure 2.13: Coronary Artery Anatomy: (Arteries which are not accessible for surgical anastomosis
are shaded black).

The reasons some coronary arteries are not accessible for surgery are,
Left main (LM) & proximal LAD: posterior to MPA
Left Circumflex (LCx): deep in the left (i.e. posterior) AV groove & covered with great cardinal vein
Septal: deep in the IVS
Middle third of RCA: deep in the right AV groove, covered by fat

Figure 2.14: Coronary arteries and their related surfaces

Anterior Territory (Red) LAD and Diagonals
Posterolateral Territory (Creamy red): Ramus and OM
Inferior Territory (Green): PD & PLV


Figure 2.15: Drainage of Right SVC

.

Fig 2.16: Most common anatomy when L SVC is also present


Left SVC: Can be found as an associated anomaly with a number of congenital heart diseases.
Normally left subclavian vein (LSCV) and left internal jugular vein (LIJV) join to form left
innominate vein (L Inn V). The two innominate veins join to form right sided SVC. Left SVC is
formed by joining of LSCV and LIJV. The L Inn V is either absent or small in caliber. In fact, size of
L Inn V is inversely proportional to the size of LSVC. As blood from superior half of the body is
carried by an additional SVC, the size of right SVC is small.

The LSVC runs posterior to the heart, in the AV groove and, most commonly, opens into coronary
sinus. Rarely, as a rule in a complex congenital heart disease, LSVC opens into the roof of LA.

Bilateral SVC share the superior venous drainage, hence, does not impose any volume overload on
the heart.
Left SVC is managed by
ligation : if L Inn V is of significant in size
Drainage : a) by cannulation: b) with a cardiotomy sucker:


3. Surgical Aspect of CPB
Need for CPB:

For operating on a part of the body, the part has to steady, dry (blood free) and relaxed. The part should
be steady, so surgeon can dissect & place incisions accurately; the part should be dry, to allow surgeon to
view the operating area well and the part should be relaxed so that, it can be retracted to provide access.
Due to these requirements, cardiac surgery, initially, was considered an impossibility. This was because
heart continuously pumps blood to provide oxygen and nutrition to the entire body and stoppage of its
function results in anoxia and fatal damage to the tissues. The damage is seen maximum in organs which
are vulnerable to anoxia. Brain is one such organ and is the first to suffer damage. Hence a machine to
substitute the function of heart was devised.

Soon it was realised that far more number of cannulae and a much more complex circuit are required
when only heart is bypassed, rather than, when heart and lungs are bypassed together. The large number
of cannulae reduced the visibility of the operating field and complex circuit made conduct of bypass
difficult.

Thus, the help of heart lung machine maintains the perfusion primarily of brain and other organs while
heart is stopped and is being operated upon.

Basic Steps of OHS:

1) Sternotomy or Thoracotomy
2) Pericardiotomy and pericardial retraction
3) Placement of aortic & venous purse strings
4) Systemic heparinisation
5) Aortic and venous cannulation
6) Commencement of CPB, appropriate core cooling
7) Aortic crossclamping and delivery of cardioplegia
8) Cardiotomy and completing intracardiac procedure
9) Closing the cardiotomies and deairing the heart
10) Declamping the aorta & regaining of cardiac activity & contractility
11) Weaning off CPB
12) Decannulation & Protamine administration
13) Sternotomy / thoracotomy Closure

1) Incisions for OHS: (ref fig 3.1)
1) Median Sternotomy
2) Left posterior thoracotomy
3) Left anterior thoracotomy (left sub-mammary incision)
4) Right anterior thoracotomy (right sub-mammary incision)


Fig 3.1: Various incisions for CV operations

Operations that could be performed through the various incisions are:

1) Median Sternotomy: Any operation on the heart, pericardium, ascending aorta, arch of the aorta and
SVC can be performed through this incision. Importantly, any complication arising out of operation on
the heart can be managed. Arterial as well as venous cannulations can be performed through the same
incision and thus, a separate incision for cannulation is not required. Any complication arising out of
cannulation can be easily detected and rectified immediately.

2) Left Posterior Thoracotomy( Left Periscapular Incision): Operations on the distal aortic arch and
descending thoracic aorta are performed through this incision .Closed mitral valvotomy, pericardectomy ,
closure of PDA , repair of coarctation of aorta can also be performed through this incision.

3) Left Anterior Thoracotomy (Left Sub-mammary Incision): CABG to LAD, Diagonal system can be
performed. Closed mitral valvotomy and MPA banding can also be performed through this incision.

4) Right Anterior Thoracotomy (Right Sub-mammary Incision): Allows approach to RA and LA and
there by surgeries like ASD closure, TV surgery, Perimembranous VSD closure and MV surgeries can be
performed. CABG to RCA or PD can be performed. A separate incision for arterial cannulation may be
required


Fig 3.2: Transverse Section through thorax showing various approaches for CV
operations

Complications of Sternotomy: A) Accidental tear of the underlying structure is a dreaded complication of
median sternotomy (ref fig 3.3). The incidence is likely to happen,
a) in a redo cases where pericardium was not closed at the time of previous surgery. Following the first
operation, adhesions develop between sternum and the underlying structures.
b) if an underlying structure is dilated. Neck arteries or ascending aorta can be dilated due hypertension,
aneurysm or AR. While the venous side structures like left innominate vein, RA or RV is likely to be
damaged in patients with gross CCF or TV disease. In case of a tear, a hurried institution of CPB may be
required.


Fig 3.3: structures that can be damaged during median sternotomy
(Shown with a black line)

B) Opening of pleura: The inferior end of the right pleura can get opened if during sternotomy the lungs
are not properly deflated or remain inflated due to underlying lung disease. During bypass blood from the
pericardial well can seep into right pleural opening, resulting in a significant (3-4 liters) 4th space blood
loss. The heart being to the left of the midline left pleura is protected from accidental opening during
sternotomy. However, the left pleura can get opened during harvesting of pericardial patch, excising left
lobe of thymus, dissecting vertical vein in a case of TAPVC and harvesting of LIMA.

2) Pericardial Retraction: helps in a) lifting heart anteriorly to improve surgical visibility b) rotating the heart to
expose various parts of heart easily 3) create a pericardial well which helps in sump suction.


3) Placement of Purse-String Sutures: For preventing dislodgement, a cannula is placed through purse string
sutures. For aortic cannulation, two concentric purse string sutures are placed as on the ascending aorta
(ref fig 3.4)

Fig 3.4: Aortic purse string suture

Purse-strings are placed as distally as possible in cases where aortotomy is required (AVR, CABG). The
two ends of purse-string thread are passed through a hollow plastic tube called snugger or snare (ref. fig
3.5) with the help of a hook. This helps in tightening the purse-string around the cannula.

Fig 3.5: Snugger assembly

Purse-string for Venous Cannulation Sites: (ref fig 3.6)
a) SVC Purse-string: SVC Cannulation: straight or Pacifico cannula
b) RA appendage Purse-string:
i) SVC cannulation: straight or curved cannula
ii) IVC cannulation: straight cannula
iii) RA cannulation: straight cannula
iv) Two stage Cannulation: Cavo –Atrial cannula
c) IVC Purse-string: IVC Cannulation: straight or Pacifico cannula


Fig 3.6 : Venous purse string sites

4) Systemic Heparinisation: Adequate systemic hearinisation is essential prior to all further steps. At some
centers , a period of 3 minutes is allowed to elapse after heparin administration before cannulation is
begun; while at others, ACT of > 300seconds is necessary for cannulation.

5a) Aortic cannulation: Aortic or arterial cannulation is always performed first. This helps in managing blood
loss during cannulation and, in case of hypotension, allows commencement of CPB with a single venous
cannula or start a ‘suction bypass’.

Prior to cannulation, some surgeons loop aorta with a tape (called ‘go around’ or ‘taping’).Looping the
aorta helps in manipulation of aorta for purse string, cannulation and clamping. For looping the aorta,
dissection is carried on the left side of the aorta, in the areolar tissue between aorta and pulmonary artery,
and on the right side, between RPA and aorta (ref fig 3.7).

In cases with dilated aortae (systemic hypertension, poststenotic dilatation of AS, AR, aneurysm of
ascending aorta), tense MPA (due to PH) or with a previous surgery this looping could be difficult and
may result in injury to MPA, RPA or posterior surface of aorta.

The steps of aortic cannulation are,
a) both the cardiotomy suctions are put on
b) the aorta is incised within the purse-string and cannula is inserted
c) simultaneously, both the snuggers are tightened.
d) cannula & snuggers are tied together
e) aortic cannula is clamped and cap or a blocker over the connecting end of the cannula is removed
f) under controlled partial unclamping, surgeon checks the speed of at which blood gushes out
through the cannula. (to ensures that the tip of the cannula is in the lumen of the aorta.)
g) cannula is attached to the arterial line, without accidentally introducing any air bubble in the arterial
line.
h) cannula is fixed to the skin ( particularly if it is a straight tip cannula)*.


i) cannula and the arterial line are arranged in a smooth curve*.

Fig 3.7: looping of aorta prior to cannulation

Fig: 3.8: Direction of tip of the cannula

The tip of the cannula should be directed towards the arch of the aorta (indicated by the left shoulder of
the patient) and bevel directed inferiorly as to direct particulate emboli, if any, towards descending aorta.

Perfusionist should ensure that the cannula tip is in proper position at steps marked with asterisk (*), by
checking line resistance. During these steps cannula can dislodge.

Complications of aortic cannulation: a) dissection of aorta: (ref. fig. 3.9) likely with a thick atherosclerotic
aorta, short tip straight cannula and if a ‘blind’ or ‘close’ technique of cannulation is practiced. (In the
blind or close technique of aortic cannulation, the aorta is stabbed or scoured within the purse string and
the cannula is inserted without partially clamping the aorta)


b) selective cannulation of neck vessels : seen when aortic purse-string is too distal, with use of straight
cannula without a guard or a butt .
c) cannula tip abutting against posterior aortic wall: seen with small aorta ( ASD, VSD, tight MS) or due
to excessive insertion of a straight cannula.
d) breaking of purse-string suture.

Fig 3.9: Position of aortic cannula tip

Right Aortic Arch: In some congenital heart diseases like tetralogy of Fallot and truncus arteriosus, the
aorta arches over the right bronchus i.e. the transverse arch is directed towards the right. The descending
thoracic aorta crosses thoracic vertebrae at various levels to reach the diaphragmatic hiatus in the
diaphragm on left of spine.

(This is how a right aortic arch differs from aorta in situs inversus where the aorta passes through the
diaphragm on the right of spine.)

In right aortic arch or situs inversus, the tip of the arterial cannula should be directed to towards the
patient’s right shoulder

5b) Venous cannulation: SVC cannulation is always done first as this involves less retraction of heart and
hence, less chance of hypotension during cannulation. The sump suction is placed in the posterior
pericardial cavity and the stiff or metallic sucker is placed in the recess between SVC & the aorta.
Surgeon and the assistant hold corresponding sides of SVC or RA appendage, as the situation be, and
incision is placed within the purse-string suture to perform cannulation.


With the venous cannula appropriately placed, blood should rise in the cannula and the height of the
blood column should be equal to the central venous pressure. The blood column should move with
respiration. A continuously rising blood column indicates the cannula is fitting tightly into SVC or
wedging of the tip of the cannula into one of the tributaries. An absence of blood column in the cannula
indicates the tip of the cannula in periadventitial tissue.

Management of L SVC: The algorithm for managing LSVC is as follows

Left Innominate vein

(Bridging Innominate)

Lt Inno. Vein size > Lt Inno. Vein
LSVC
absent or very small

Ligate or snug during Manage by Manage by
CPB
sump suction Cannulation

in the coronary

Direct LSVC Through RA – CS Through CS
Pacifico cannula straight cannula straight cannula
(on partial CPB) (prior to CPB) ( after opening RA
on cross clamp)

6) Commencement of CPB: When a perfusionist informs a surgeon ‘full bypass’, surgeon checks the following
a) RA should be totally empty with CVP < 0 mm of Hg
b) MPA should be soft

Causes of RA remaining full even on full CPB are
a) IVC cannula wedged in the hepatic veins
b) presence of L SVC
c) IVC cannula displaced in to RA/RV: seen in patients in gross CCF with dilated RA/IVC

If MPA is full, surgeon vents the left heart through an appropriate route. In a case with CHD, MPA is
tense on ‘full CPB’, then PDA should be suspected.


Cooling: Target temperature for cooling is according to the intra cardiac procedure time, if surgeon
intends circulatory arrest (in CHD or arch aneurysm cases) and quality of myocardial preservation
required.

During cardioplegic arrest myocardium gets continuously rewarmed due to left heart return and through
the surrounding viscera (aorta, lungs, liver) which are at a higher temperature. If the CPB perfusate
temperature is low, then this rewarming is slowed down.

Some surgeons don’t cross-clamp the aorta unless a certain temperature is reached (e.g. 320C).

During cooling the LV distends in patients with AR and TOF with aorto-pulmonary collaterals. Though
cooling reduces the heart rate, distension of LV, actually, increases the myocardial oxygen consumption.
Hence surgeon keeps a watch on LV distension, MPA fullness, PA diastolic pressure (on the monitor) &
broadening of QRS complex of ECG to avoid myocardial damage.

Cooling on CPB is delayed and patient is kept actively warm,
a) during release of intrapericardial adhesion on CPB
b) in patient with AR (cooling is started only when surgeon is ready to cross clamp)
c) till a patent BT shunt, PDA or MAPCA is ligated

7) Aortic cross clamp and delivery of cardioplegia: Aortic cross clamping is a crucial event and the following
check list is observed prior to cross clamping
a) availability of all the sutures, valves, patches and special instruments, if any.
b) no resistance on arterial line, i.e. acceptable line pressure
c) venous reservoir level is adequate, RA is empty and MPA is soft.
d) cardioplegia is ready to be delivered. This is particularly important in cases where early crossclamping
is required.

Indications for early cross clamping: Early cross clamping is required when severe LV distension is likely
to occur when cooling begins. This is seen in patients with
a) significant AR
b) cyanotic heart disease with large number of collaterals
c) Aorto Pulmonary Window
d) Truncus Arteriosus

Complications of aortic clamping:
a) incomplete clamping of aorta: occurs mainly in a tense and or dilated aorta. Making the aorta soft by
reducing the flows during cross clamping helps to prevent this complication. Failure to arrest the
heart completely or early recovery of heart from cardioplegia results due to this complication.
b) accidental clamping of tip of the aortic cannula: seen with straight tip cannula or if the cannula tip is
wrongly directed towards the aortic valve . The complication will result in a sudden increase
in arterial line pressure.
c) accidental clamping of cardioplegia cannula: will result in sudden increase in cardioplegia delivery
pressure
d) partial clamping of MPA: occurs when aorta is cross-clamped without adequate dissection between
aorta and pulmonary artery.(described under ‘go around’ of aorta p.25, fig 3.2 ). Due to partial
clamping of MPA, deairing (described later) becomes difficult.
e) injury to RPA: tip of the clamp can puncture the RPA, particularly in redo cases


Cardioplegia delivery: Cardioplegia is just one aspect of myocardial protection. The other important
aspects of myocardial protection are – prevention of LV distension at all times, and prevention of
rewarming of heart.

During delivery of antegrade root cardioplegia, surgeon checks the following

a) aortic root should be distended and should not be too tense( coronary block) or too soft( AR)
b) absence of LV distension
c) distended , turgid coronaries on the anterior surface of the heart( RV branches of RCA branches
and distal LAD are visible without dislocating the heart )
d) veins should be distended and their colour should change from, initial, dark blue to, later, bright
red as the delivery of cardioplegia progresses.
e) quick diastolic arrest of heart.

Management of antegrade root cardioplegia in patients with grade I to II AR: This grade of AR does not
require aortic valve replacement hence the aorta is not opened and cardioplegia is delivered through root
injection. But due to AR, the cardioplegia leaks into LV. Hence to avoid leak-back into LV as well as to
provide sufficient pressure-head for cardioplegia delivery, surgeon compresses the subaortic region
externally, during the delivery of the cardioplegia.

Cardioplegia by ostial route is delivered in all cases where aorta is opened. These cases are

a) aortic valve replacement or repair
b) Aorto Pulmonary window closure
c) Repair of rupture of the aneurysm of sinus of Valsalva
d) Ascending aortic aneurysm repair
e) Arterial switch operation ( for second cardioplegia, if required)
f) Repair of truncus arteriosus

Cardioplegia can be delivered through one ostium at a time or through the two ostia simultaneously with
the help two cannulae attached to a Y connection. A perfusionist has to adjust the delivery of cardioplegia
accordingly.

Cardioplegia is delivered retrogradely when,
a) antegrade delivery is not feasible due to coronary ostial block, coronary artery disease, difficult to
visualise coronary ostium ( e.g. redo AVR)
b) surgeon does not want interruptions during a prolonged surgery

Insertion of retrograde coronary perfusion (RCP) cannula: This can be performed prior to starting the
CPB or on CPB.A purse string is placed on RA anterior and inferior to RA appendage purse-string.
Guided by the left index finger, which is placed on the coronary sinus, the RCP cannula is introduced and
placed in the coronary sinus. Retraction of heart during the placement of RCP cannula may result in
hypotension; hence, some surgeons place the cannula on CPB. While inserting the cannula on CPB, RA
should be kept slightly full as to avoid air locking of the venous cannula (when inserting RCP cannula)
and also, to keep the mouth of coronary sinus open. Keeping RA full results in distension of heart. Hence,
RCP cannula should be inserted before commencing cooling.

During retrograde cardioplegia delivery, the coronary veins are tense and red in colour and the blood
coming retrogradely through the coronary arteries or ostia is dark in colour. The Middle cardiac vein (the
vein accompanying PD) should be turgid during delivery of retrograde cardioplegia. The middle cardiac


vein opens just distal to coronary sinus and its ostium can get blocked easily by the balloon of a
malplaced RCP cannula.

Cardioplegia is repeated every 30 to 40 minutes, according to expected cross-clamp time and some times,
during AVR, prior to lowering of valve. After lowering of valve visualisation of ostia could be difficult.

While repeating cardioplegia

a) surgeon discards the initial 30-50 ml of cardioplegia which has warmed-up in the tubing
b) vents out air from the aortic root( air enters aortic root through cardiotomy)
c) prevents air embolism to RCA by initially clamping the RCA
d) loosens the IVC loop if RA is likely to distend

8) Cardiotomy: to minimise the interference with the pumping function of the heart, cardiotomies are
a) as small as possible
b) avoid opening of ventricles ( pumping chambers)
c) avoid damaging coronaries or conduction system

9) Deairing of the heart: After completing intra cardiac procedure, all the cardiotomies are closed and the heart
is deaired. The technique of deairing the heart varies from surgeon to surgeon but all the techniques are
based on the principle of,
a) passive filling followed by active filling of heart b) filling the chambers in a serial manner.
These principles are achieved by,
i) just prior to closing cardiotomy, surgeon stops all the intra cardiac vents except aortic root vent
( passive filling)
ii) perfusionist by partially clamping the venous line fills the right side of the heart ( passive filling)
iii) surgeon gently presses the RV as to push the blood across pulmonary circulation to the left side
(active filling)
iv) anesthetist start ventilating ( active filling).Distended alveoli compress the pulmonary capillaries
and squeeze the air to PV-LA
v) surgeon deairs LA through cardiotomy / vent purse string ( active filling)
vi) surgeon massages LV and deairs the heart through aortic root. Remember, aortic root is the
highest and the last chamber prior to cross clamp. (active filling).
Once the surgeon is satisfied about deairing of heart, aorta is declamped.

Variations of the above steps of deairing are: a) aortic root may be deaired without attaching suction to
the root cannula. Blood squeezed out of heart is allowed to pass freely into the pericardial well.
(perfusionist should increase cardiotomy sump suction).
b) following MVR , a balloon catheter may be passed across the MV into LV and catheter connected to a
suction for air removal. LV is not massaged (for the fear of LV rupture) in this technique.
c) root suction continued for a long time after declamping. Some partially clamp the aorta, just distal to
the root suction to provide resistance to the LV ejection and ensure a better air removal.
d) head is lowered during air removal so that air , if any, on ventricular ejection would enter descending
aorta. Head low position, falsely, increases CVP and decreases venous return.

10) Declamping: After complete deairing, aorta is declamped. During aortic clamping, the aortic root is empty
and the aortic cusps could be in an open position. Hence, it is possible that at the time of declamping a
sudden gush blood coming from aortic cannula can distend the LV. Hence, at the time of declamping,
perfusionist lowers the arterial flow, allowing the root to distend & enable the cusps to coapt.


After declamping, myocardium gets perfused by warm, low potassium blood which washes away the
cardioplegia. Depending upon the time since the last cardioplegia, quality of myocardial protection and
serum potassium levels, the myocardium recovers and starts beating. The initial contractions are not
powerful. Also, the rhythm may not be sinus. Hence it is essential to keep the heart, in general, and, LV in
particular, empty. To keep the heart empty, left heart vents may be started or LA may be openly vented by
keeping LA purse-string or the last stitches of left atriotomy loose. When the later technique is used blood
pools up in the pericardial cavity and may seep into pleural cavity, if pleura is open. It is important to note
that aortic root suction can never empty a heart.

When ever a < grade II AR is left alone, after declamping , surgeon checks for LV distension and if
required, massages the LV till myocardial contractility is regained. LV may be vented by a LV apical
vent.

11) Weaning off CPB: After declamping aorta, heart regains activity and contractility. With adequate
contractility, if patient has bicaval cannulation, surgeon may decide to remove one of the venous
cannulae. This increases venous filling of the heart and thereby helps in providing pulsatile flow. Usually,
SVC cannula (the smaller of the two venous cannulae) is removed first. SVC cannula is clamped
appropriately, prior to removal.

Perfusionist now increasingly fills the heart, guided by the CVP and PA diastolic pressures. While
weaning off CPB, surgeon keeps a close watch on cardiac contractility, RA and PA filling and on PA
diastolic pressure, if available. While filling the heart, a rise in blood pressure with little or no rise in CVP
indicates an excellent contractility of heart.

The usual prerequisites for going off CPB are,
a) rectal temperature > 350C or nasopharyngeal temperature >37.50C
b) sinus rhythm is most preferred. If patient is in nodal rhythm the rate should be > 100/ min. Patients
with chronic AF rarely get converted to sinus rhythm, however, the ventricular rate should be more >
100/min. Temporary external pacing may be required for heart blocks. ST segments on ECG should be as
far as possible, isoelectric.
c) cardiac contractility: If myocardium has recovered from anoxia, it should be red in colour . The heart
should start ejecting on providing slight volume load i.e., the monitor will show a pulse wave form and
systolic blood pressure will rise with minimal or no rise in the CVP.
d) anesthesiologists should be able to ventilate both the lungs, easily . Collected secretions due to
unventilated lungs, endotracheal tube displaced while turning the table to improve surgical visibility,
collected blood or trapped air in the pleural cavity prevent normal expansion of the lungs.
e) if blood products are likely to be required, they should be available readily .
f) serum potassium levels, pH of blood ( ‘blood chemistry’) should be normal

With heart full and beating vigorously, bleeding from cardiotomy sites is checked.

12) Decannulation & Protamine Administration: Once hemodynamic stability is established after going off
CPB, venous cannula is removed. In case of bicaval cannulation if SVC cannula was removed earlier,
IVC cannula is removed after going off CPB.

Through aortic cannula, the residual blood in the venous reservoir is returned back, depending upon the
CVP and or the PA diastolic pressures. Anesthesiologist at this stage may increase the dose of
vasodilators as to increase the venous capacitance. A five to ten degree head high position also helps in
accommodating volume. A rough guide to amount of volume to be returned is to keep CVP, atleast, at the
preop value.


Heparin is reversed with protamine injection. Heparin-Protamine complex produces hypotension &
vasodilatation, called protamine shock, through various mechanisms. This occurs, usually, within
5minutes of starting protamine administration. One of the methods of managing this hypotension is to
infuse patient quickly. Hence many surgeons don’t decannulate aorta till the possibility of protamine
shock is over. To avoid clot formation around the tip of the aortic cannula after protamine administration,
blood returning through cannula should not be stopped completely.

Check list prior to starting protamine administration is:
1) no significant ( requiring suturing, heart retraction) cardiotomy site bleeding
2) hemodynamic stability
3) ability to fill up the heart quickly, if required
4) cardiotomy suckers are put-off ( some put it off after delivering 50% dose of protamine)
5) drugs to treat protamine shock are available.

Aortic decannulation is the last step of CPB. Prerequisites for aortic decannulation are
1) surgeon is satisfied with the operative correction.
2) there is no need to go back on CPB for achieving hemodynamic stability
3) no surgical cause of bleeding, requiring CPB to control it
4) all the blood from the venous reservoir is returned back

For decannulation, all ties around the cannula are cut, snuggers are loosened, and while surgeon removes
the cannula, an assistant simultaneously tightens the snuggers. Keeping the purse string-suture strands
tight, the plastic snuggers are discarded and the purse-strings are tied.
Complication of decannulation: Bleeding can occur from the cannulation site due to break of the purse
string suture, cut-through of the purse-string or loose tying. Bleeding could be very severe and may
require re-cannulation through a separate site.

Pericardial Closure: After confirming hemostasis, pericardium is closed. The closure starts over the aorta
and proceeds inferiorly for varying lengths.

Drains are placed to drain out the collected blood. When pleura is not opened, two drains are placed - one
behind the sternum (retrosternal) and the other, inside the pericardium behind the LV (retrocardiac). If
pleura is opened, it may be drained separately.

Pericardial closure can lead to tamponading effect on the heart, resulting in hypotension. This occurs in
cases where the heart is already distended or has an external conduit. In such situations, keeping the
pericardium open corrects the hemodynamics.

Pericardium is not closed whenever pericardium is used as a patch, e.g. RVOT patching of TOF.

13) Sternal closure: Thoracic integrity is established by approximating the two halves of the sternum. This is
done by passing multiple wires or bands around or through sternum.

Sometimes, sternal closure can give rise to hypotension. This happens especially when an external
conduit is used or heart is distended. In such situation sternum is not approximated and skin also, may not
be closed. The wound is covered with antiseptic dressing (‘delayed sternal closure’)


4. Mitral Stenosis
Etiology: Rheumatic.
Congenital (This is a rare cause and is associated with hypoplastic LV, aorta, etc)
Pathology:

1. Fusion of AML and PML begins at commissures, near the annulus and extends to wards the center
of the orifice. The mitral valve area (MVA) becomes progressively narrowed.

Figure 4.1 Mitral Valve
A: Normal MV in close position B: Normal MV in open position
C: Stenotic MV in open position: 1.MV Orifice 2. Fused commissures

Severity of MS is classified according to the MVA.
Clinically undetectable MS: MVA > 2.5 cm2
Mild MS: MVA 1.5 cm2 to 2.5cm2
Moderate MS: MVA 1.0 cm to 1.5 cm2
Severe MS: MVA < 1.0cm2
Critical MS: MVA ≤ 0.7 cm2
Cases coming up for surgical or interventional treatment of MS are with severe or critical MS.
2. Annulus, cusps thicken and may get calcified. Chordae thicken & fuse with each other.
Papillary muscles too fuse.
3. Clot forms in the LA, usually, with the advent of atrial fibrillation.

Pathophysiology: Stenotic MV obstructs the flow of blood from LA to LV resulting in
a) Back Pressure Effect
b) Decreased Forward Flow

a) Back Pressure Effect: The chain of events is
Stenotic MV → incomplete emptying of LA→ LAVO→ LA enlargement till limit of compliance
of LA is reached → ↑LA pressure → ↑ PV pressure → ↑ pulmonary capillary pressure → ↑ PA
pressure → ↑ RV pressure → RV failure→ ↑ RVEDP→ ↑ RA pressure → ↑ SVC & IVC
pressure.

Back pressure effect results in accumulation of blood in the pulmonary circulation, RA, SVC/IVC
and liver (in that order). Liver congestion is called ‘chronic passive congestion’.
Back pressure effect is responsible for clinical features of dyspnoea, edema feet & ascitis.
Development of atrial fibrillation worsens the back pressure effect as LA emptying is incomplete.


b) Decreased Forward Flow: Flow (F) through any orifice is proportional to square of area (A) of
the orifice (F∝ A2). Rheumatic mitral stenosis is a progressive disease. As the MV orifice area
decreases, the flow throw MV progressively reduces.

Blood flows through MV during diastole. As the flow of blood through the stenotic MV decreases
significantly, duration of diastole becomes relatively short to fill the LV adequately. Reduced LV
filling leads to reduced forward flow, i.e. reduced cardiac output (CO). Initially, the
manifestations of reduced cardiac output are after exertion but later, manifestations are even at
rest.

Body Compensation:

a) ↑SVR: Pressure = CO x SVR, hence as the CO reduces, the SVR increases to maintain
systemic pressure. Atrial systole is responsible for approximately 25% of ventricular filling.
With the development of AF, atrial systole is lost and the ventricular filling is further
compromised.
b) Slowing of HR: Slowing of heart rate prolongs the duration of cardiac cycle and thereby
increases duration of diastole. This improves the ventricular filling as longer period for
ventricular filling is now available.
Treatment:

Medical: is indicated when the mitral stenosis is mild and when there are no complications.
Medical treatment is mainly directed at
a) slowing the heart rate and there by improving the ventricular filling, forward flow & CO
b) reducing the venous congestion by diuresis .
c) prevent repeated attacks of rheumatic fever.
Drugs used are
1) Digoxin: to control heart rate, particularly if the patient is in AF. Improves RV
contractility if the patient is in CCF
2) β Blockers: (the main stay of current treatment) to reduce heart rate.
3) Diuretics: to reduce congestion.
4) Injection Benzathine penicillin G: this is a long acting Penicillin for preventing
recurrence of Rheumatic fever. It has no effects on hemodynamics.
Balloon Mitral Valvotomy (BMV): Performed when a) the cusps are pliant b) there are no LA
clot c) there is no MR. This is an interventional procedure performed in the cardiac
catheterisation laboratory under local anesthesia.


Fig: 4.2: Technique of BMV

Complications: 1. Iatrogenic MR: occurs due to tear of the cusp or chorda during dilatation.
Patient requires emergency surgery if MR causes hemodynamic disturbance. Approach is
through median sternotomy with conventional CPB. As the approach to MV for BMV is trans-
septal, an ASD (septal perforation) would exist and hence, SVC and IVC should be tape –
snugged, to avoid venous airlock on opening the LA.
2. Perforation of cardiac chamber producing cardiac tamponade. Managing this complication
rarely requires CPB.

Close Mitral Valvotomy (CMV):

Fig4.3: Technique of CMV


CMV is performed when the cusps are pliant, and there is no LA clot or MR. CMV is
performed under GA without CPB, through left anterolateral thoracotomy incision. A
Tubb’s dilator is passed through LV apex and index finger is passed through LA
appendage. With the help of the index finger, the Tubb’s dilator is guided across the MV.
Dilator is opened once the tip of the Tubb’s dilator is across the mitral valve. (ref fig. 4.3)

Complications of CMV
1. Iatrogenic MR: Significant MR requires surgical correction.
2. LV apical or LA appendage tear.
3. Accidentally finding LA clot

Emergency surgery can be performed through left chest or through median sternotomy,
depending upon patient condition and surgeon’s choice.

For CPB through left chest, arterial return is by left femoral arterial cannulation and
venous drainage is through MPA or RVOT cannulation. If RA is dilated, RA can be
reached even through left chest also. (ref fig 4.4)

Fig. 4.4: View of the heart chambers through left chest after opening the
pericardium

Open Mitral Valvotomy: Performed through median sternotomy but can be performed through right
thoracotomy. The mitral valve is approached through a longitudinal paraseptal incision on the LA
body (ref. fig 4.5).


Fig.4.5 Incision for Open MV surgery

Other approaches to MV are shown below in fig 4.6

Fig.4.6 Approaches to MV

(FO= fossa ovalis)


Opening of LA and sucking of blood through cardiotomy suction yields a significant amount of blood
stagnant in LA and pulmonary circulation.

If LA Clot is present, declotting of LA is done first. Declotting involves washing of LA with saline
hence; cardiotomy sump suction should be stopped during the use of washing of LA.

Mitral valve is opened surgically using knife and scissors. Valve is tested for competence using
saline. Perfusionist should observe the same precautions as observed while washing of LA.

Complications & Accidents: 1. Accidental opening of RA: this occurs during atriotomy and results in
venous air lock and a sudden decrease in venous reservoir level. This is treated by temporarily closing
the rent in the RA with a side biting clamp (like a Cooley clamp), looping & snugging SVC- IVC &
then, suturing the rent in the RA

2. Breaking of LA suture while tying knot: this results in unknotting and opening of the left
atriotomy. This complication achieves a serious proportion if a surgeon ties the LA suture only when
the heart has regained its activity. Due to breakage of suture before knotting, the LA suture line
unwinds, and the atriotomy opens up. Opening up of left atriotomy suture line on a beating heart
results in sucking in of air into LA. If the heart has already started ejecting, patient can suffer from
systemic air embolism.

Perfusionist helps treating the problem by filling the heart (to make LA pressure positive) and by
keeping the aortic pressure high (as to prevent opening of aortic valve). Anesthesiologist helps by
keeping the lungs in a semi inflated state, which also makes the LA pressure positive. Depending
upon the extent of opening up of LA suture line, surgeon resutures the LA on a beating or on a cross
clamped heart or cardioplegically arrested heart.

3. Iatrogenic MR: is treated surgically if it is severe and is producing hemodynamic compromise

Mitral Valve Replacement: Performed if the mitral leaflets are severely calcified or if open valvotomy is
not satisfactory due to severe subvalvar fusion or indistinct commissures.
Approach, precautions & accidents are as mentioned for OMV.
MVR is performed with or without excising the AML and PML. If a leaflet is excised, it is excised
with its chordae and papillary muscles.
Complications and Accidents: 1. Accidental opening of RA: (see above, in OMV)
2. Breaking of LA suture: (see above, in OMV)
3. LV rupture: This is an early and dreaded complication of MVR. The rupture can occur at any level
from the level of mitral annulus to the base of papillary muscle. The repair of rupture requires a quick
resumption of CPB. LV rupture results in a significant blood loss. Perfusionists should assess patient
blood volume & hemoglobin, a fresh, and plan priming accordingly.
4. Stuck Valve: A mechanical valve leaflet/s can get stuck in an open or closed position. This is
usually due to subvalvar structures affecting the hinge mechanism of a valve. Management of this
complication requires early reinstitution of CPB.
5. Cardiogenic shock due to injury to Left Circumflex Artery will require emergency coronary
bypass.


Clinical assessment chart for MS

Parameter Findings comment

Age Around 30yrs

Body weight Low weight and height
&
Height
Body Volume First pulmonary circuit volume increases then PH status
the systemic venous circuit volume
CVP, liver enlargement, effusions

Hemoglobin Low nails, blood investigation

Plasma Volume Increased , but protein concentration is low as in body volume

LFT report

SVR Increased high diastolic BP, cold limbs, lower
limb veins are constricted,

Organ Function Liver: chronic passive congestion LFT: raised bilirubin and SGPT
Brain : infarction in patients with embolic Transient ischemic episodes,
episodes hemiplegia
Arterial Tree Embolus can block any artery Pulse is not palpable
Check vascular Doppler studies
Arterial Aorta
cannulation Femoral : for reopen heart cases

Venous Bicaval but tapes are not required unless
cannulation 1)trans septal approach
2)previous BMV
3)TV surgery
Cardioplegia Antegrade through root Check 2DE report for grade of AR
For associated grade I / II AR,
root compression will be required
Arterial Pressure Could be high ( > 60) on bypass Expect in patients with high SVR

Venous return Good if CVP raised, liver palpable

Left Heart Sump-sucker in LA
Return

Preop Digoxin, diuretics Check for potassium levels
medications Beta blockers

Previous CMV Left thoracotomy scar
interventions BMV
OMV Median sternotomy scar
MVR Median sternotomy scar


5.Mitral Regurgitation

The term incompetence and regurgitation are interchangeably used. When regurgitation of blood is
present, a valve is considered incompetent.
Classification of MR: There are different ways of classifying MR.

Etiological Classification: A disease can affect, simultaneously, different anatomical components of MV
Rheumatic
Infective endocarditis
Endomyocardial Fibrosis
Marfan’s syndrome
Secondary to LV dilatation
Myocardial infarction
Post procedural or post operative
Anatomical Classification: A change in configuration of any component of mitral valve apparatus will
result in MR . A component of MV apparatus can be affected by a number of etiologies.
Annulus: dilatation
Cusps: shrunken, destroyed, torn
Chordae: ruptured, shortened, lengthened (ref fig 5.1, 5.2 & 5.3)
Papillary Muscle: dysfunction, ruptured
LV: aneurysm resulting in relocation of the papillary muscle
Classification according to compensation:
Acute: where body compensation for MR is absent as in myocardial infarction
Chronic: where body has compensated for MR as in rheumatic heart disease

Pathology & Pathophysiology: In MR, LV has two outlets- aortic valve & incompetent mitral valve (fig 5.2).
Blood flows in inverse proportion to the resistance offered at each outlet.

The resistance at the aortic outlet is the resistance offered by the aortic valve plus the systemic vascular
resistance (SVR). Normal aortic valve offers no resistance to the flow but presence of aortic stenosis
increases the resistance. The resistance at the mitral valve depends upon the size of regurgitant area and
LA compliance (dilated thin walled LA is well compliant, while thick walled small LA is poorly
compliant).
The final hemodynamic problems produced by MR are similar to those produced due to MS, i.e. back
pressure effect and decreased forward flow

Figure 5.1: Competent MV Figure 5.2: Incompetence due to chordal shortening


Figure 5.3: Chordal lengthening and MV prolapse

a) Back Pressure Effect: LA is subjected to high pressure, for a brief period, during LV systole. Also,
the LA gets volume overloaded (LAVO) as it receives pulmonary venous blood as well as the
regurgitant blood from LV.
The LA is much thinner , as a result, more compliant in chronic MR than it is in MS, and hence, the
back pressure effects are delayed. In a chronic severe MR, LA size could be 7 to 8 cm when measured
on 2D-Echocardiogram.
b) Decreased Forward Flow: Depending upon the resistance at the two outlets of the LV, the blood
flows forward into systemic circulation.
Body Compensation:
a) ↓SVR: In order to increase forward flow the SVR falls. Also, patient could be on drugs like, ACE
inhibitors, which reduce SVR.
b) LV function compensation: LAVO produced due to MR is passed on to LV results in LVVO. As
per Frank – Starling law, the increased in the myocardial fiber length results in better contractility and
the LV is able to handle the LVVO by pumping out the extra blood. In a compensated case the LV is
able to maintain adequate forward flow. When LVVO results in myocardial stretching beyond
physiological limits, the LV function deteriorates and the patient decompensates.

Fig 5.4: Relation between LVEF & severity of MR

Treatment:
Medical: is indicated so far as the LV function is maintained and the PH has not developed.


Medical treatment is mainly directed at a) improving forward flow by reducing SVR and b) reducing
the venous congestion by diuresis.
Drugs used are
1) Digoxin: to control heart rate, particularly if the patient is in CCF or AF
2) After Load reducing agents: ACE inhibitors and Angiotensin receptor blockers are the main stay
of current treatment.
3) Diuretics: to reduce pulmonary congestion
4) Injection Benzathine penicillin G: this long acting Penicillin is for preventing repeat attacks of
rheumatic fever
Surgical:
A) Mitral Valve Repair: is the first treatment of choice. Repair is feasible if the AML is intact and is
mobile. Repair is performed according to the anatomical problem, as shown
MV component Pathology Surgery
Annulus: dilated Annuloplasty
Cusp: short Advancement
Chordae: short Lengthening
long Shortening
Pap Muscle: ischemic Revascularisation

The approach to mitral valve is as described for OMV. Due to associated LAVO and LVVO, opening
of LA yields large amount blood in the cardiotomy suction. Due to washing effect of MR jet, blood is
not stagnant in LA and hence LA clots are rare.
B) Mitral Valve Replacement: is performed when patient has severe MR and the valve is
irreparable.

MVR with leaflet preservation: MVR when performed without preservation of the leaflet results in
deterioration of LV function. Hence MVR is performed by preserving AML& PML or with atleast,
preserving PML. (‘preserving PML’ means preserving the annulus-PML-chordae-papillarymuscle-
LV link)

Clinical assessment chart for MR

Parameter Findings comment
Age Around 30yrs
Body weight low weight and height
&
Height
Body Volume of blood in the pulmonary circuit PH status, LA size, LV size
Volume increases initially, followed by a rise in CVP, liver enlargement, effusions
volume of blood in the systemic venous
circuit
Plasma increased , but protein concentration is low as in body volume
Volume LFT report
SVR Low : chronic, compensated cases Low diastolic BP, wide pulse pressure,
bounding pulse,

High: acute , uncompensated cases High diastolic pressure, narrow pulse
pressure, cold limbs, collapsed
peripheral veins


Brain : infarction in patients with embolic Transient ischemic episodes,
episodes hemiplegia
Arterial Tree Embolus can block any artery Pulse is not palpable
Check vascular Doppler studies
Arterial Aorta: small sized aorta
cannulation Femoral : for reopen heart cases

Venous Bicaval but tapes are not required unless
cannulation 1)trans septal approach
2)previous BMV
3)TV surgery
Cardioplegia Antegrade through root Check 2DE report for grade of AR
For associated grade I / II AR,
root compression will be required
Arterial Pressure Could be low ( <30) on bypass in chronic seen in patients with long acting
cases ACE inhibitors

Venous return Good if CVP raised, liver palpable

Left Heart Return Sump-sucker in LA

Preop medications Digoxin, diuretics Check for potassium levels
ACE inhibitors, AR inhibitors
Previous CMV Left thoracotomy scar
interventions BMV
OMV Median sternotomy scar
MVR Median sternotomy scar


6.Aortic Stenosis

Etiology: Congenital: subvalvar / valvar / supra valvar
Acquired: Rheumatic Heart Disease
Degenerative
Pathology: Various configurations of aortic stenosis are shown in figure 6.1. All acquired AS are valvar but, a
valvar AS could be congenital or acquired. Narrowing at annular level (annular stenosis) could always be
a co-existing pathology.

Fig. 6.1: Types of aortic stenosis


Fig.6.2: Opening of normal and stenotic aortic valve

Pathophysiology: In AS the aortic valve area gets reduced to les than 1cm2. Narrow orifice produces
resistance to ventricular emptying during systole. The LV now has to generate far greater pressure to
pump blood into aorta (pressure overload). This produces LV concentric hypertrophy as this hypertrophy
is towards cavity of the LV, making the LV cavity small.

Fig. 6.3: LV hypertrophy in AS


The heart is small in size and dilates only in the last stage. Cardiac Output is maintained in the
compensated phase. The LV is muscle bound, hence, is poorly compliant. A slight volume overload gives
rise to rise in LVEDP. Till the mitral valve is competent, back pressure effects producing pulmonary
congestion are absent.

Body Compensation:
Slowing of HR: due to AS, LV requires a longer time to eject blood through the aortic valve. Hence
slower heart rate helps in ejection. Drugs which slow down the heart rate help in compensation.
↑SVR: to maintain blood pressure, the SVR rises to compensate for the decreased cardiac output

Myocardial Perfusion: is critical in patients with aortic stenosis.

Myocardial Perfusion Pressure = Coronary Artery Pressure – Intramyocardial Pressure

In aortic stenosis due to myocardial hypertrophy intramyocardial pressure is high. Hence a higher aortic
pressure (i.e. coronary artery pressure) will be required to maintain myocardial perfusion during off cross
clamp period or while delivering cardioplegia.
Treatment: (of congenital AS will be described along with treatment for other congenital heart diseases)
Medical: has limited value in patient with aortic stenosis. Drugs which slowdown the heart rate without
affecting myocardial contractility are useful. After load reducing drugs should not be used. Diuretics are
required when patient is in CCF.
Balloon Aortic Valvotomy: This interventional procedure is performed in cardiac catheterization
laboratory. It is performed mainly in pediatric age group when the leaflets are pliant and there is no AR.
The access is retrograde through femoral artery – aorta -- aortic valve.
Complication: 1. Iatrogenic AR: managed surgically if hemodynamically significant.
Surgery:
A) Open Aortic Valvotomy: Prior to the balloon intervention era, this was the treatment of choice in a
patient with severe AS. The aortic valve was opened under vision using conventional CPB in a
cardioplegically arrested heart. The approach was through aorta.

B) Aortic Valve Replacement: is performed when the cusps are rigid, calcified and or there is an
associated AR. The aortic valve is approached through an oblique, J shaped incision on the ascending
aorta.
Fig.6.4: Aortotomy for Aortic Valve Replacement


Cardioplegia is delivered through coronary ostia. In the absence of AR, some surgeons deliver the first
cardioplegia through root injection. Retrograde cardioplegia is also used.
Aortic cusps are excised and an artificial valve is implanted.
C) Aortic Root Widening: In aortic stenosis the annulus does not dilate. Such an annulus would
accommodate a valve which is small as compared to the BSA of the patient. To accommodate an
appropriate sized valve (Effective Orifice Area of the valve, preferably = 1.3 x BSA), the undilated
annulus is widened by cutting across the annulus and inserting a patch. Valve replacement is then
performed in the widened annulus.
There are a number of operations / techniques to widen the narrow aortic root.

Fig 6.5: Sites for aortic root widening (marked with black circles)
(For legends ref to fig 4.8)

D) Percutaneous AVR: This an emerging technique in which a valve mounted on a catheter is deployed
across the aortic valve, through a percutaneous approach. Obviously, no incision or CPB is required.

Complications and Accidents: 1.Bleeding from aortic suture line: this complication is seen when aortic
wall is thin. The seriousness of complication is sometimes appreciated after coming off bypass when the
aortic pressure rises. If a ‘cut-through’ or a ‘dog ear’ is noted as a cause of bleeding then a surgeon may
go on bypass and take an additional stitch under low flows ( required for short period of less than 15
seconds) as to soften aorta.
2. Stuck Valve: A mechanical valve leaflet/s can get stuck, immediately following implantation, in an
open or closed position. This is usually due to subannular calcium or hypertrophied IVS preventing
adequate disc movements. Management of this complication requires early reinstitution of CPB.
3. Cardiogenic shock: Post-operative cardiogenic shock results from depressed myocardial contractility.
The cause of cardiogenic shock specific to AVR with mechanical valve is of prosthesis occluding a
coronary ostium, resulting in acute ischemia. The complication is managed with reinsertion of prosthesis
or with bypass grafting.


Clinical assessment chart for AS

Parameter Findings Method of assessment/ comments
Age Around 30yrs if RHD
> 50yrs if of degenerative etiology
Body weight low weight and height for RHD
&
Height Normally built for degenerative etiology
Body Volume Normal. CCF only in terminal cases
Hemoglobin Normal
Plasma Volume Normal
SVR Normal to increased high diastolic BP, cold limbs, lower
limb veins are constricted,
Organ Function Brain : infarction in patients with embolic Transient ischemic episodes,
episodes hemiplegia

Liver : chronic passive congestion
LFT: raised bilirubin and SGPT
Arterial Tree Atherosclerotic changes may be present in Check vessels patency clinically and
patients with degenerative etiology who with vascular Doppler studies
present late
Arterial Aorta
cannulation
Venous Single venous, two stage
cannulation
1) all ostial
Cardioplegia 2) first through root, subsequent ostial Check 2DE report for grade of AR
3) retrograde for maintenance
Arterial Pressure Should be high ( > 60)
Venous return Normal to Low
Left Heart Through RSPV vent passed to LA// LV
Return
Preop Digoxin, diuretics Check for potassium levels
medications Beta blockers
Previous BAV
interventions


7. Aortic Regurgitation
Etiology: Rheumatic Heart Disease
Syphilitic Heart Disease
Marfan’s Syndrome
Ventricular Septal Defect
Infective Endocarditis (Gives rise to acute AR)
Dissection of aorta (Gives rise to acute AR)
Pathology: Aortic regurgitation is due incomplete coaptation of leaflets. The incomplete coaptation may be due
to dilated annulus (with normal leaflets) or due to defective leaflets failing to coapt. The leaflets could fail
to coapt due to thickening and shrinkage (RHD), destruction (IE), prolapse & deformity (VSD), detached
attachment (dissection). Due to large volume of blood passing through the aorta, the aortic annulus is
dilated.
Pathophysiology: Blood ejected by the LV (called stroke volume –SV) into aorta during systole has, as if, two
outlets.

Fig 7.1: Pathophysiology of AR

One is the forward flow, i.e. towards the body, and this flow is controlled by the SVR; and the other, is
the regurgitant flow and is controlled by the compliance of the LV (LVEDP) and duration of diastole.
Lower SVR helps in improving forward flow while a lower LVEDP & a longer diastole increases the
regurgitant flow. Thus, out of each LV stroke volume a part (a major part in the compensated stage)
moves forward and a (minor) part regurgitates back into LV (ref fig 7.1)

The regurgitant flow adds up to the volume of blood the LV receives from LA through MV, resulting in
LVVO. The compliant LV dilates to accommodate the LVVO. As per Frank – Starling law, the LV
ejection is also increased till a physiological limit of LV fiber stretching is reached. At this stage the
LVEF starts decreasing (ref fig 5.4). The failing LV dilates, which dilates the MV annulus also. Due to
dilated annulus the mitral leaflets don’t coapt. This type of MR where only the annulus is dilated and the
leaflets are normal, is called functional MR.


The problems are summarised as
a) Decreased Forward Flow: This occurs only in the late stage of chronic compensated
AR. Due LVVO, the LV is ejecting more and the cardiac output (CO) is adequate for the patient’s
activities so far as LVEF is normal
b) Back Pressure Effects: Mitral valve remains competent till late. This prevents any back pressure
effects But when the ejection fraction starts falling, LVEDP increases, LV dilates and patient develops
functional MR ( due to dilated MV annulus) and pulmonary congestion.

Body Compensation: (is absent in patients with acute AR)
↓SVR: helps in forward flow
Increase LVEF: helps in handling the LVVO and in maintaining adequate forward flow inspite of
regurgitation.
Tachycardia: as aortic regurgitation occurs during diastole, slowing of heart rate increases the diastolic
period and hence, the total regurgitant volume.
Treatment:
Medical: With preserved LV function patients are treated with after load reducing drugs.
Diuretics are required only when the LVEF fails.
Surgical:
A) Aortic valve repair: Usually performed in children with VSD and when the AR is less than severe.
Details of perfusion are as described for aortic valve replacement.
B) Aortic Valve Replacement: is performed for severe AR with deteriorating LV function.
The aortic valve is approached through an oblique, J shaped incision on the ascending aorta (ref fig 6.4)

Cardioplegia is delivered through coronary ostia. If retrograde cardioplegia is used, usually it is for
maintenance of arrest.
Aortic cusps are excised and an artificial valve is implanted by suturing the artificial valve to the aortic
annulus.
C) Aortic root Replacement (Bental’s Procedure): In patients with syphilis or in patients with Marfan’s
syndrome, the root is aneurysmal with gross AR. The root is replaced with a valved conduit with
implantation of the coronary buttons & replacement of the ascending aorta. Root can be replaced by
retaining the patient’s valve (valve saving operation)

Fig. 7.2: Diagrammatic presentation of Bental’s operation


The procedure is also required in patients with aortic dissection.
D) Ross Operation: This is Aortic valve replacement with autologous pulmonary artery and replacing
the pulmonary valve with a homograft (aorta or pulmonary artery).
This operation is performed for AS as well as for AR.

Fig. 7.3: Ross operation

Complications and Accidents: a) VF prior to aortic cross clamping:
Patients who have severely depressed LV function or dilated LV, when are connected to CPB, due to low
perfusate temperature or ‘faster’ cooling develop bradycardia leading to severe LV distension and VF.
The arterial return from the aortic cannula keeps flowing freely into LV and distends the LV. Hence, in
patients with severe AR, cardioplegia should be ready before instituting CPB; left heart vent should be
inserted before connecting to CPB & cooling should be done gradually. Surgeon should be ready for
massaging LV and early crossclamping.
b) bleeding from aortic suture line: seen in patients with a thin aortic wall. Reinstitution of CPB may be
required so as to control bleeding from a difficult spot (usually the inferior end of the incision)
c) Prosthetic valve complications: as mentioned before


Clinical assessment chart for AR

Parameter Findings comments
Age Around 30yrs if etiology is
RHD, Marfan’s Syndrome or syphilis

> 50yrs if AR is due to dissection
Body weight Well built.
& Marfan Syndrome patients are tall but slim External and bony features of
Height Marfan’s syndrome
Body Volume Normal . CCF only in terminal cases
Hemoglobin Normal
Plasma Volume Normal
SVR Decreased High volume brisk pulse, low (
zero) diastolic BP,
easily visible carotid, brachial and
radial pulses

Increased ( acute AR) cold limbs, absent pedal pulses
Organ Function Preserved in compensated cases
Arterial Tree Normal
Arterial Aorta
cannulation Femoral : for dissection extending into arch

Venous Single venous, two stage
cannulation Bicaval cannulation if has associated VSD or
if Ross procedure is planned
Cardioplegia all ostial
retrograde cardioplegia could be delivered for
maintenance of arrest
Arterial Pressure remains low due to low SVR
Venous return N
Left Heart Return Through RSPV in LA / LV
Preop medications ACE inhibitors, AT receptor inhibitors
Previous BAV
interventions


8.Tricuspid Valve Disease
Etiology : Rheumatic Heart Disease (TS as well as TR)
Infective endocarditis ( TR ) (common among drug addicts)
(Congenital anomalies of TV will be discussed along with other congenital heart diseases)

Functional TR: secondary to significant distal valvular lesions (like, MS &/or MR)
Development of functional TR: due to back pressure effects secondary to MV disease, PH
develops. Long standing severe PH results in RV failure and the RV dilates. RV dilatation
leads to dilatation of the RV annulus. Dilated annulus prevents TV leaflets from coapting,
resulting in TR. In functional TR, the leaflets are normal.

Pathology: Normally, RA is thin walled and hence is a compliant chamber. Due to volume and or pressure
overload of TS or TR, it distends. As there are no valves at the openings of SVC and IVC to prevent back
pressure effects, with rise in RA pressure, the systemic veins distend, liver gets congested and patient
develops edema of the feet, pleural effusion & ascitis ( usually in that order).
Treatment: 1.Leave alone: Functional TR subside as the distal lesion like, MS & or MR is relieved. Patients
with TV disease are on heavy diuretics like Frusemide, Torsemide and Spironolactones.
2. Balloon Tricuspid Valvotomy: performed in cardiac catheterization laboratory without CPB or
anesthesia, if patient has isolated TS.
3. DeVega’s annuloplasty: When the dilatation of the TV annulus is severe, or along with tricuspid
valvotomy, tricuspid annuloplasty is performed.

Fig.8.1: DeVega’s Annuloplasty

In DeVega’s annuloplasty, a 2-0 Ethibond suture is passed as shown above to purse string the annulus
corresponding to the ATL and the PTL. (ref. fig 8.1)
4. Tricuspid Valvotomy: Like open mitral valvotomy, the fused commissures are opened.
5. Tricuspid Valve Replacement: If significant TS and TR are present together, the TV valve is usually
replaced.

All tricuspid surgeries are performed through RA, on CPB.
Usually, tricuspid surgery is performed after completing mitral and aortic surgery& closing LA and aorta.
Some surgeons prefer to perform TV surgery before aortic valve replacement, as the open ‘unoccupied’
aorta offers a free access to delivery of ostial cardioplegia.
TV surgery can be performed by the following techniques


1) aorta cross-clamped & heart is cardioplegically arrested: this technique provides a dry , still field with
no cannula in the field. Left heart vent is through LA suture line (in multivalvular cases) or through IAS
(isolated TV cases). Disadvantage of this technique is that it prolongs the cross-clamp time.
2) declamped aorta with empty beating heart or fibrillating heart: after closing left atriotomy and
aortotomy, the heart is deaired and aortic cross clamp is released .Left heart vent is maintained according
to the beating status. Now the RA is opened and TV surgery is performed. For this technique cardiotomy
suction is required to suck away the blood coming through coronary sinus. By this technique, aortic cross-
clamp time is shortened and damaging stitch causing heart block can be immediately corrected.
For both the techniques the SVC and IVC should be looped and snugged

Clinical assessment chart for TV Disease

Parameter Findings comments
Age Around 30yrs
Body weight low weight and height
&
Height
Body Volume increased volume in systemic venous circuit PH status
CVP, liver enlargement,
effusions
Plasma Volume increased , but protein concentration is low as in body volume
LFT report
SVR according to proximal valve disease

S. Creatinine
Associated Renal dysfunction
Arterial Tree Normal
Arterial cannulation Aorta

Venous cannulation Bicaval & tapes are required
IVC purse string may have to be taken on
partial CPB
Large sized venous cannulae are required
Cardioplegia according to the proximal ( i.e. aortic/ mitral)
lesion
Arterial Pressure Could be high ( > 60) on bypass
Venous return Very good . venous reservoir could overflow CVP raised, liver palpable
Left Heart Return Sump-sucker in LA ( multivalvular cases)
trans septal ( isolated TV cases)
Pre op medications Digoxin , diuretics ( Frusemide as well as Check for potassium levels
Aldactone)
Previous as per proximal lesion Check for perforated IAS
interventions

Cpb surgical&clinical orientation

Cpb surgical&clinical orientation

Recomendados

Recomendados

Más contenido relacionado

La actualidad más candente

La actualidad más candente (20)

Destacado

Destacado (20)

Similar a Cpb surgical&clinical orientation

Similar a Cpb surgical&clinical orientation (20)

Último

Último (20)

Cpb surgical&clinical orientation