Cardiovascular monitoring is the essential monitoring required.

1. CARDIAC
MONITORING
Presentor : Dr. Madhu Priya V
Moderator : Prof Abhiruchi

2. Cardiac monitoring
◦ Pulmonary artery catheter
◦ Trans esophageal echocardiography
◦ Coagulation monitoring.
◦ Cardiac output monitoring

3. Pulmonary artery catheter
◦ The standard PAC has a 7.0 to 9.0 Fr
circumference, is 110 cm in length
marked at 10-cm intervals and contains
four internal lumens.

4. ◦ The yellow port if the most distal port and
is placed in the pulmonary artery, its tip is
used for PAP monitoring.
◦ The red port leads to a balloon near the
tip which is used to float the catheter
through the cardiac chambers and is
attached with a syringe to inflate it with a
capacity of 1.5ml.
◦ The port with a temperature thermistor,
the end of which lies just proximal to the
balloon.
◦ The blue or the proximal port is at 30 cm
distance from the distal port and is used
for CVP monitoring.
◦ The white port opens just near the
proximal port and can be used to connect
intra venous solutions

5. Indications
◦ Major procedures involving large fluid shifts or blood loss in patients:
◦ Right sided failure, pulmonary hypertension
◦ Severe left sided heart failure nor responsive to therapy
◦ Cardiogenic or septic shock or with multiple organ failure
◦ Orthotopic heart transplantation
◦ Left ventricular assist device implantation

6. Contra indications
◦ Absolute Contraindications
1. Severe tricuspid or pulmonic valvular stenosis.
2. Friable right atrial or right ventricular masses ( tumours/thrombus )
◦ Relative Contraindications
1. Severe arrhythmias
2. Coagulopathy
3. Newly inserted pacemaker wires

7. Insertion technique
◦ PACs can be placed from any of the central venous cannulation sites, but the right
internal jugular vein provides the most direct route to the right heart chambers.
◦ The balloon at the tip of the catheter is inflated with air, and the catheter is
advanced into the right atrium, through the tricuspid valve, the right ventricle, the
pulmonic valve, into the pulmonary artery, and finally into the wedge position.
◦ Waveform monitoring is the most common technique for perioperative right-sided
heart catheterization in the surgical unit.

8. ◦ The right atrial waveform is seen until the
catheter tip crosses the TV and enters the RV.
◦ In the RV, there is a sudden increase in SBP
but little change in DBP, compared with the
right atrial tracing.
◦ The catheter is advanced through the RV
toward the PA. As the catheter crosses the
pulmonary valve, a dicrotic notch appears in
the pressure waveform.
◦ The PCWP (also termed pulmonary capillary
occlusion pressure) tracing is obtained by
advancing the catheter approximately 3 to 5
cm farther until a change in the waveform
associated with a drop in the measured mean
pressure occurs.

9. Right atrium
◦ The waveforms are similar to CVP waveforms
◦ A wave – atrial contraction pressure. Corresponds
with compliance and volume. Small a wave with
reduced volume and compliance.
◦ C wave – tv rebound, isovolumetric contraction
during ventricular systole
◦ X descent – atrial relaxation
◦ V wave – passive venous filling of atrium, depends
on compliance and volume. Large v wave – TR
◦ Y descent – rapid emptying of RA after TV opens

10. Changes in waveforms
◦ Elevated V waves – filling of ventricles
◦ Tricuspid regurgitation
◦ LV-RA shunt
◦ Loss of y descent
◦ Cardiac tamponade
◦ Rapid y descent – rapid filling of RV
◦ Constrictive pericarditis
◦ Constrictive cardio myopathy
◦ Severe TR
◦ Elevated a wave – due to increased
pressure with atrial contraction.
◦ Tricuspid stenosis
◦ Pulmonary stenosis
◦ Thick non complaint RV
◦ RV dysfunction
◦ Cannon a waves
◦ AV dissociation
◦ V tach
◦ V pacing
◦ TS
◦ Absent A waves
◦ Atrial fibrillation/flutter

11. Right ventricle
◦ Isnt typically seen when PA cath is in
place.
◦ Can be seen :
◦ Malposition
◦ Migration of PA cath tip
◦ Cardiomegaly
Measurement :
◦ Systolic : the highest point of the
wave
◦ Diastolic : the lowest point of the
wave

12. Pulmonary artery pressure
◦ Systolic pressure = RV pressure
◦ Dichrotic notch = closure of pulmonary
valve
◦ Steepness of diastolic run off is due to PA
compliance. Inversely proportional to the
PVR.
◦ Diastolic step up is seen as the PA
pressure decreases during systole.
Measurement :
◦ Systolic : the highest point of the wave
◦ Diastolic : the lowest point of the wave

13. Pulmonary artery pressure
◦ Increased
1. Pulmonary artery hypertension
2. PH due to left heart failure
3. PH due to lung pathology like
emphysema
4. PH due to chronic PE
◦ Decreased
1. Hypovolemia
2. Pulmonary vasodilators
3. Right HF

14. • Due to pullback from PA to RV
• Reposition
• Inflate balloon
• Due to measurement of PCWP
• Do not flush
• Deflate balloon
• Reposition by deep breaths or cough
• Bundle branch blocks
• Arterial due to contraction of Left heart
• PA pressure due to contraction of Right
heart

15. RV vs PA waveform
◦ RV pressure increases during diastole
due to the filling of RV.
◦ PA Pressure decreases with diastole.
◦ Dichrotic notch is nonspecific.

16. Pulmonary capillary wedge pressure
◦ When the balloon is inflated, the backflow
on the PA is measured.
◦ LA -> PV -> Pulmonary capillaries -> PA
◦ Resembles RAP but with C absent. As
pressure is transmitted through capillaries
and hence dampened.
◦ A wave delayed – circulation through
capillary bed.
◦ Measurement – peak of A wave = LAP
pressure

17. PCWP
◦ Reflection of PV pressure/ LAP as there is
no valve in between
◦ When MV open, reflection of LVEDP
Increased wedge pressure :
◦ Increased LVEDP – LV hypertrophy
◦ PV stenosis
◦ MS/MR
◦ Due to vessel damage/ balloon rupture
◦ To fix : slowly inflate until PAO waveform
appears

18. PAC in chest Xray

19. Normal intra cardiac pressures

20. Measuring cardiac output from PAC
◦ Newer technologies applied to PAC monitoring allow nearly continuous cardiac
output monitoring using warm thermal indicator.
◦ Small quantities of heat are released from a 10-cm thermal filament incorporated
into the RV portion of a PAC, approximately 15 to 25 cm from the catheter tip.
◦ The resulting thermal signal is measured by the thermistor at the tip of the catheter
in the pulmonary artery. The heating filament is cycled on and off in a
pseudorandom binary sequence, and the cardiac output is derived.
◦ Typically, the displayed value for cardiac output is updated every 30 to 60 seconds
and represents the average value for the cardiac output measured over the
previous 3 to 6 minutes.

22. Complications
During catheterization
◦ Arrythmias, ventricular fibrillation
◦ RBBB, complete heart block ( if persisting LBBB )
Due to catheter residence
◦ Mechanical : catheter knots, entangling with or dislodgement of pacing wires
◦ Thromboembolism
◦ Pulmonary infarction
◦ Infection, endocarditis
◦ Endocardial damage, cardiac valve injury
◦ Pulmonary artery rupture/pseudo aneurysm

23. Echocardiography

25. Trans-esophageal echocardiography
• TEE is a safe and relatively minimally invasive procedure, although
echocardiographers should be aware of potential complications resulting from
probe insertion and manipulation

26. Probe positions

28. 11 basic views
Esophageal views
1. 4 chamber view
2. 2 chamber view
3. Long axis view at ME
4. Aortic valve Long axis view
5. Aortic valve short axis view
6. Ascending aorta Long axis view
7. Bicaval TV view
8. RV inflow outflow view
Aortic views
1. Descending aorta Long axis
view
2. Descending aorta short axis
view
Trans gastric view
1. Trans gastric mid pulmonary
view

29. 1. Upper esophagus
◦ Structures viewed :
1. Ascending aorta
2. Pulmonary artery and its branches
3. Trachea and bronchi
◦ Identifies :
1. Aortic dissection
2. Pulmonary embolism
3. Incorrect placement of pulmonary artery
catheter

30. 2. Mid esophagus
• 4 chamber view
• 2 chamber view
• Mid esophageal long axis view
• Aortic valve short axis view
• Rv inflow outflow view
• Bicaval view

31. Four chamber view
Structures viewed :
1. Left and right atria and ventricles
2. Aortic valve
3. Mitral valve
4. Tricuspid valves
Identifes :
◦ Asd presence/absence
◦ Chamber enlargement
◦ Mitral valve pathology
◦ Tricuspid valve pathology

33. Two chamber view
Structures viewed :
◦ Left atrial appendange
◦ Mitral valve
◦ Left ventricular apex
Identifies :
◦ LV systolic function
◦ LAA interrogation for clot or sluggish flow
◦ LV apex pathology

35. Long axis view
Structures viewed :
◦ LVOT 1 cm from the aortic valve
◦ Ascending aorta
◦ Aortic valve
◦ Mitral valve
◦ LV chamber size and function
Identifies :
◦ Aortic root pathology
◦ Aortic insufficiency
◦ Mitral valve insufficiency and pathology

38. Aortic valve short axis view
Structures viewed :
◦ Pulmonary valve
◦ Main pulmonary artery
◦ Right ventricle
◦ Tricuspid valve
◦ Aortic valve
Identifies :
◦ Pulmonary valve pathology
◦ Right ventricle pathology
◦ Aortic stenosis

40. Bicaval view
Structures viewed :
◦ Right atrium
◦ Left atrium
◦ Superior vena cava
◦ Inter artrial septum
Identifies :
◦ Atrial septal defect
◦ Metastatic tumour
◦ Fluid assessment from SVC
◦ Guiding central/pac placement

42. 3. Trans gastric
Structures viewed :
◦ Left and right ventricles
◦ Aortic valve
◦ Mitral valve
◦ Tricuspid valve
Identifies :
◦ Hemodynamic assessment
◦ LV hypertrophy/ enlargement
◦ LV systolic function
◦ MV pathology
◦ Cardiac output and stroke volume

43. Transgastric basal short axis view
Structures viewed :
◦ Basal left ventricle
◦ Mitral valve leaflets
Identifies :
◦ Basal left ventricular function
◦ Mitral valve – fish mouth appearance
◦ colour mode – mitral regurgitation

44. Transgastric mid short axis view
Structures viewed :
◦ Mid walls of left ventricle
◦ Antero lateral and postero medial papillary
muscles
◦ Part of Right ventricle
Identifies :
◦ Volume status - LVED diameter
◦ Wall motion – whether walla thickened/
contracting

46. Trans-gastric long axis view
Structures viewed :
◦ Anterior and inferior LV walls
◦ Mitral valve
◦ Papillary muscles
◦ Aortic valve
Helpful in :
◦ Prosthetic valve assessment ( artefacts in
mid esophageal )

48. Coagulation monitoring
◦ Cardiac surgery is an area in which coagulation monitoring has vital applications.
Cardiopulmonary bypass (CPB) procedures could not be performed without an
effective method of preventing blood from clotting in the extracorporeal circuit.
◦ An ideal anticoagulant agent should be easy to administer, rapid in onset, titratable,
predictable, measurable in a timely fashion, and reversible.
◦ Heparin use during CPB has continued until the present time, most likely because
of the drug’s rapid onset, ease of measurement, and ease of reversibility.

49. Heparin & ACT
◦ Heparin acts as an antithrombin III (AT III) agonist and accelerates AT III binding to
thrombin.
◦ Whole blood is added to a test tube containing an activator, either diatomaceous
earth (celite) or kaolin. The presence of activator augments the contact activation
phase of coagulation, which stimulates the intrinsic coagulation pathway.
◦ More commonly, the ACT is automated, In the automated systems, the test tube is
placed in a device that warms the sample to 37°C. The Hemochron device rotates
the test tube, which contains celite activator and a small iron cylinder, to which 2 mL
of whole blood is added. Before clot forms, the cylinder rolls along the bottom of
the rotating test tube. When clot forms, the cylinder is pulled away from a magnetic
detector, interrupts a magnetic field, and signals the end of the clotting time.
◦ Normal 80-120
◦ Safe limits 400-480.

50. Heparin resistance
◦ Heparin resistance is documented by an inability to increase the ACT of blood to
expected levels despite an adequate dose and plasma concentration of heparin.
◦ It is primarily caused by antithrombin III deficiency in pediatric patients.
◦ It is multifactorial in adult cardiac surgical patients.
◦ Patients receiving preoperative heparin therapy traditionally require larger heparin
doses to achieve a given level of anticoagulation.
◦ Heparin resistance also can be a sign of heparin-induced thrombocytopenia. Other
possible causes include enhanced factor VIII activity and platelet dysfunction
leading to a decrease in ACT response to heparin.

51. Heparin induced thrombocytopenia
◦ Heparin-induced thrombocytopenia (HIT) is a potentially life-threatening disorder
that occurs in patients receiving unfractionated heparin (UFH) and, less commonly,
low-molecular-weight heparin (LMWH).
◦ The immunologic form is mediated by an antibody to the heparin–platelet factor 4
complex.
◦ Diagnosis of HIT requires both clinical evidence (thrombocytopenia and thrombosis)
and laboratory findings. Laboratory tests include a functional assay or antibody-
based assay. The most used antibody-based assay is the enzyme-linked
immunosorbent assay, which measures immunoglobulin G (IgG), IgM, or IgA
antibodies that bind to the heparin-PF4 complex.
◦ Plasmapheresis may be used to reduce antibody levels. The use of heparin could
be avoided altogether through anticoagulation with direct thrombin inhibitors such
as argatroban or bivalirudin. These thrombin inhibitors have become the standard of

52. Heparin neutralisation
◦ Reversal of heparin-induced anticoagulation is most frequently performed with
protamine.
◦ The recommended dose of protamine for heparin reversal is 1 to 1.3 mg protamine
per 100 IU heparin.
◦ Protamine-heparin complexes activate AT III in vitro and result in complement
activation. The anticoagulant effect of protamine also may be caused by inhibition of
platelet aggregation, alteration in the platelet surface membrane, or depression of
the platelet response to various agonists.
◦ Protamine reactions have been classified into three types.
◦ Type 1 – hypotension
◦ Type 2 – immunological
◦ Type 3 – catastrophic pulm hypertension leading to RHF.

53. Heparin rebound
◦ The phenomenon referred to as heparin rebound describes the re-establishment of
a heparinized state after heparin has been neutralized with protamine.
◦ The most postulated explanation is that rapid distribution and clearance of
protamine occur shortly after protamine administration, thus leaving unbound
heparin remaining after protamine clearance.
◦ Residual low levels of heparin can be detected by sensitive heparin concentration
monitoring in the first hour after protamine reversal.

54. Thrombin inhibitors
◦ These anticoagulant drugs are superior to heparin.
◦ They inhibit both clot-bound and soluble thrombin. They do not require a cofactor,
activate platelets, or cause immunogenicity.
◦ These drugs include hirudin, argatroban, and bivalirudin.
◦ Heparin remains an attractive drug because of its long history of safe use and the
presence of a specific drug antidote, protamine.

55. Monitoring for platelet function.
◦ Bedside Coagulation and Platelet Function Testing can be done with :
Viscoelastic Tests:
1. Thromboelastography,
2. Thromboelastometry
3. Sonoclot

56. THANK YOU