UBP 4.5 (Long Form): Cardiovascular - CABG & Mitral Valve Replacement Flashcards Preview

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Flashcards in UBP 4.5 (Long Form): Cardiovascular - CABG & Mitral Valve Replacement Deck (18)
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1

Intra-operative Management:

How will you monitor temperature?

What are some acceptable methods of monitoring core temperature?

Why is there often a gradient between core and shell temperature on cardiopulmonary bypass?

(A 67-year-old, 128 kg, 5'8", male presents for quadruple CABG and mitral valve replacement. He complains of worsening chest pain.

PMHx: He is an insulin dependent diabetic, has chronic hypertension, and smokes cigarettes. He sleeps sitting up and takes prevacid due to his severe acid reflux.

Meds: Prevacid, Dobutamine, Lasix, NPH insulin

Allergies: NKDA

PE:

  • VS: P = 106, BP = 95/52, SpO2 = 89%, Temp = 36.6 C
  • Airway: Mallampati II, full cervical ROM
  • Pulmonary: bilateral crackles
  • CV: Regular rate; systolic ejection murmur

CXR: Left heart prominence; Kerley B lines and peribronchial cuffing are noted

EKG: ST-segment depression in the anterolateral leads; Q-waves in the inferior leads

Heart Cath: 4+ mitral regurgitation

ABG: pH = 7.43; paCO2 = 43; PaO2 = 71; SpO2 = 89% on 10L O2 by simple mask

Lab: Hgb = 11.3 gm/dL, GLucose = 174 mg/dL, Na+ = 140 mEq/L, K+ = 3.8 mEq/L)

It is important to measure both core and shell (peripheral) temperature when placing a patient on cardiopulmonary bypass, due to the temperature gradient that develops during cooling and rewarming.

This could be accomplished using a nasopharyngeal or tympanic membrane probe to monitor core temperature and a rectal or toe probe to monitor shell temperature.

Accurate monitoring of temperature is important to --

  • ensure adequate cerebral cooling following the initiation of bypass,
  • avoid large temperature gradients (greater than 10 C) that can lead to the formation of gas bubbles in the blood, and
  • ensure normothermia prior to the discontinuation of cardiopulmonary bypass.

2

Intra-operative Management:

How will you induce the patient?

(A 67-year-old, 128 kg, 5'8", male presents for quadruple CABG and mitral valve replacement. He complains of worsening chest pain.

PMHx: He is an insulin dependent diabetic, has chronic hypertension, and smokes cigarettes. He sleeps sitting up and takes prevacid due to his severe acid reflux.

Meds: Prevacid, Dobutamine, Lasix, NPH insulin

Allergies: NKDA

PE:

VS: P = 106, BP = 95/52, SpO2 = 89%, Temp = 36.6 C
Airway: Mallampati II, full cervical ROM
Pulmonary: bilateral crackles
CV: Regular rate; systolic ejection murmur

CXR: Left heart prominence; Kerley B lines and peribronchial cuffing are noted

EKG: ST-segment depression in the anterolateral leads; Q-waves in the inferior leads

Heart Cath: 4+ mitral regurgitation

ABG: pH = 7.43; paCO2 = 43; PaO2 = 71; SpO2 = 89% on 10L O2 by simple mask

Lab: Hgb = 11.3 gm/dL, GLucose = 174 mg/dL, Na+ = 140 mEq/L, K+ = 3.8 mEq/L)

Assuming this obese patient's airway exam was reassuring, I would move the difficult airway cart into the room, place the appropriate monitors, position the patient in reverse-trendelenburg, and apply cricoid pressure.

I would then utilize etomidate and fentanyl to achieve a sufficient depth of anesthesia to avoid stimulation during laryngoscopy, while at the same time, avoiding hypotension and bradycardia.

My goals in performing this induction include:

  1. safely securing the airway in this obese patient who may prove difficult to intubate and/or ventilate;
  2. avoid aspiration in this patient with severe gastroesophageal reflux;
  3. ensure an adequate depth of anesthesia to avoid a hypertensive or tachycardic response that could lead to worsening mitral regurgitation, cardiac ischemia, and/or pulmonary edema;
  4. avoid hypotension that could lead to inadequate coronary perfusion;
  5. avoid bradycardia that may worsen mitral regurgitation; and
  6. avoid bronchospasm secondary to smoking-induced airway hyperreactivity.

3

Intra-operative Management:

During laryngoscopy, the patient's blood pressure increases and he goes into atrial fibrillation. Why might this have happened?

(A 67-year-old, 128 kg, 5'8", male presents for quadruple CABG and mitral valve replacement. He complains of worsening chest pain.

PMHx: He is an insulin dependent diabetic, has chronic hypertension, and smokes cigarettes. He sleeps sitting up and takes prevacid due to his severe acid reflux.

Meds: Prevacid, Dobutamine, Lasix, NPH insulin

Allergies: NKDA

PE:

VS: P = 106, BP = 95/52, SpO2 = 89%, Temp = 36.6 C
Airway: Mallampati II, full cervical ROM
Pulmonary: bilateral crackles
CV: Regular rate; systolic ejection murmur

CXR: Left heart prominence; Kerley B lines and peribronchial cuffing are noted

EKG: ST-segment depression in the anterolateral leads; Q-waves in the inferior leads

Heart Cath: 4+ mitral regurgitation

ABG: pH = 7.43; paCO2 = 43; PaO2 = 71; SpO2 = 89% on 10L O2 by simple mask

Lab: Hgb = 11.3 gm/dL, GLucose = 174 mg/dL, Na+ = 140 mEq/L, K+ = 3.8 mEq/L)

  • The atrial fibrillation could be related to ischemia and/or atrial dilation resulting from worsening mitral regurgitation.
  • Inadequate anesthesia during larygnoscopy could lead to hypertension and tachycardia with worsening mitral regurgitation (secondary to hypertension) and increased myocardial oxygen demand (secondary to both the hypertension and the tachycardia).
  • An overaggressive induction dose of anesthesia could lead to bradycardia with worsening mitral regurgitation and/or hypotension with decreased coronary artery perfusion.

Any one of these conditions could result in additional myocardial ischemia and deteriorating cardiac function, leading to atrial dilation and fibrillation.

Atrial fibrillation should be aggressively treated in this situation, since it can lead to a further deterioration of cardiac function.

4

Intra-operative Management:

What would you do?

(Referring to patient's BP increasing and going into atrial fibrillation during laryngoscopy)

(A 67-year-old, 128 kg, 5'8", male presents for quadruple CABG and mitral valve replacement. He complains of worsening chest pain.

PMHx: He is an insulin dependent diabetic, has chronic hypertension, and smokes cigarettes. He sleeps sitting up and takes prevacid due to his severe acid reflux.

Meds: Prevacid, Dobutamine, Lasix, NPH insulin

Allergies: NKDA

PE:

VS: P = 106, BP = 95/52, SpO2 = 89%, Temp = 36.6 C
Airway: Mallampati II, full cervical ROM
Pulmonary: bilateral crackles
CV: Regular rate; systolic ejection murmur

CXR: Left heart prominence; Kerley B lines and peribronchial cuffing are noted

EKG: ST-segment depression in the anterolateral leads; Q-waves in the inferior leads

Heart Cath: 4+ mitral regurgitation

ABG: pH = 7.43; paCO2 = 43; PaO2 = 71; SpO2 = 89% on 10L O2 by simple mask

Lab: Hgb = 11.3 gm/dL, GLucose = 174 mg/dL, Na+ = 140 mEq/L, K+ = 3.8 mEq/L)

Since the atrial contribution to preload is less critical in patients with mitral regurgitation versus those with stenotic lesions,

I may just ensure control of ventricular rate (B-blocker, CCB, or digoxin) and monitor his blood pressure closely.

However, given this patient's coronary artery disease and the risk of worsening regurgitation and heart failure, I would have a low threshold for pharmacologic (amiodarone) or DC cardioversion should he develop signs of ischemia or persistent hypotension.

If all these interventions failed to stabilize the patient,
I would ask the surgeon to rapidly prepare for the institution of cardiopulmonary bypass.

5

Intra-operative Management:

Following the initiation of cardiopulmonary bypass, the perfusionist says that the venous reservoir level is decreasing.

What would you do?

(A 67-year-old, 128 kg, 5'8", male presents for quadruple CABG and mitral valve replacement. He complains of worsening chest pain.

PMHx: He is an insulin dependent diabetic, has chronic hypertension, and smokes cigarettes. He sleeps sitting up and takes prevacid due to his severe acid reflux.

Meds: Prevacid, Dobutamine, Lasix, NPH insulin

Allergies: NKDA

PE:

VS: P = 106, BP = 95/52, SpO2 = 89%, Temp = 36.6 C
Airway: Mallampati II, full cervical ROM
Pulmonary: bilateral crackles
CV: Regular rate; systolic ejection murmur

CXR: Left heart prominence; Kerley B lines and peribronchial cuffing are noted

EKG: ST-segment depression in the anterolateral leads; Q-waves in the inferior leads

Heart Cath: 4+ mitral regurgitation

ABG: pH = 7.43; paCO2 = 43; PaO2 = 71; SpO2 = 89% on 10L O2 by simple mask

Lab: Hgb = 11.3 gm/dL, GLucose = 174 mg/dL, Na+ = 140 mEq/L, K+ = 3.8 mEq/L)

I would immediately have the perfusionist reduce pump flows and

add fluid to the blood volume as necessary to prevent reservoir emptying with subsequent massive arterial air embolism.

At the same time, I would look for potential causes of decreased venous return, such as -- elevation of the heart by the surgeon or problems with the venous cannula, including -- air lock, inadequate diameter, kinking, malpositioning, or obstruction by thrombotic material.

6

Intra-operative Management:

Following surgical repair, the surgeon asks you to vigorously inflate the lungs.

Why? Is de-airing the heart important for this procedure?

(A 67-year-old, 128 kg, 5'8", male presents for quadruple CABG and mitral valve replacement. He complains of worsening chest pain.

PMHx: He is an insulin dependent diabetic, has chronic hypertension, and smokes cigarettes. He sleeps sitting up and takes prevacid due to his severe acid reflux.

Meds: Prevacid, Dobutamine, Lasix, NPH insulin

Allergies: NKDA

PE:

VS: P = 106, BP = 95/52, SpO2 = 89%, Temp = 36.6 C
Airway: Mallampati II, full cervical ROM
Pulmonary: bilateral crackles
CV: Regular rate; systolic ejection murmur

CXR: Left heart prominence; Kerley B lines and peribronchial cuffing are noted

EKG: ST-segment depression in the anterolateral leads; Q-waves in the inferior leads

Heart Cath: 4+ mitral regurgitation

ABG: pH = 7.43; paCO2 = 43; PaO2 = 71; SpO2 = 89% on 10L O2 by simple mask

Lab: Hgb = 11.3 gm/dL, GLucose = 174 mg/dL, Na+ = 140 mEq/L, K+ = 3.8 mEq/L)

Vigorous inflation of the lungs following cardiopulmonary bypass serves two function.

  • First, it aids in the recruitment of collapsed alveoli.
  • Second, the positive pressure results in increased blood flow through the pulmonary vasculature, displacing air into the left heart where it can be more easily removed with a vent.

De-airing of the heart is important to prevent the end-organ damage that can occur with embolization of air into cerebral or coronary arteries.

TEE can be helpful in ensuring adequate de-airing of the left ventricle prior to the start of left ventricular ejection.

7

Intra-operative Management:

The patient is normothermic and an attempt is being made to wean him from cardiopulmonary bypass.

During this process, the pulmonary artery pressure increases and the systemic pressure decreases. What do you think?

(A 67-year-old, 128 kg, 5'8", male presents for quadruple CABG and mitral valve replacement. He complains of worsening chest pain.

PMHx: He is an insulin dependent diabetic, has chronic hypertension, and smokes cigarettes. He sleeps sitting up and takes prevacid due to his severe acid reflux.

Meds: Prevacid, Dobutamine, Lasix, NPH insulin

Allergies: NKDA

PE:

VS: P = 106, BP = 95/52, SpO2 = 89%, Temp = 36.6 C
Airway: Mallampati II, full cervical ROM
Pulmonary: bilateral crackles
CV: Regular rate; systolic ejection murmur

CXR: Left heart prominence; Kerley B lines and peribronchial cuffing are noted

EKG: ST-segment depression in the anterolateral leads; Q-waves in the inferior leads

Heart Cath: 4+ mitral regurgitation

ABG: pH = 7.43; paCO2 = 43; PaO2 = 71; SpO2 = 89% on 10L O2 by simple mask

Lab: Hgb = 11.3 gm/dL, GLucose = 174 mg/dL, Na+ = 140 mEq/L, K+ = 3.8 mEq/L)

Increasing pulmonary artery pressures combined with decreasing systemic pressures is suggestive of -- left ventricular failure.

There are multiple complications that could lead to left heart failure in this patient:

  1. increased afterload secondary to mitral valve replacement (the low resistance flow back into the atrium is no longer available);
  2. graft failure (kinking, air, clot);
  3. inadequate myocardial preservation during cardiopulmonary bypass;
  4. inadequate coronary blood flow (hypotension, coronary emboli, coronary spasm, tachycardia with decreased diastolic perfusion time);
  5. myocardial infarction;
  6. valve failure;
  7. hypoxemia;
  8. inadequate preload (hypovolemia, loss of atrial kick);
  9. reperfusion injury;
  10. acidemia; and
  11. electrolyte abnormalities.

8

Intra-operative Management:

How might recent mitral valve replacement contribute to the risk of left ventricular failure coming off bypass?

(A 67-year-old, 128 kg, 5'8", male presents for quadruple CABG and mitral valve replacement. He complains of worsening chest pain.

PMHx: He is an insulin dependent diabetic, has chronic hypertension, and smokes cigarettes. He sleeps sitting up and takes prevacid due to his severe acid reflux.

Meds: Prevacid, Dobutamine, Lasix, NPH insulin

Allergies: NKDA

PE:

VS: P = 106, BP = 95/52, SpO2 = 89%, Temp = 36.6 C
Airway: Mallampati II, full cervical ROM
Pulmonary: bilateral crackles
CV: Regular rate; systolic ejection murmur

CXR: Left heart prominence; Kerley B lines and peribronchial cuffing are noted

EKG: ST-segment depression in the anterolateral leads; Q-waves in the inferior leads

Heart Cath: 4+ mitral regurgitation

ABG: pH = 7.43; paCO2 = 43; PaO2 = 71; SpO2 = 89% on 10L O2 by simple mask

Lab: Hgb = 11.3 gm/dL, GLucose = 174 mg/dL, Na+ = 140 mEq/L, K+ = 3.8 mEq/L)

Replacement of the mitral valve results in the loss of the low resistance outflow tract into the left atrium, which then results in increased left ventricular afterload.

This increase in afterload may unmask left ventricular dysfunction, making it necessary to administer inotropes, vasodilators (to reduce afterload), and/or fluids (to increase preload).

Other factors that increase the likelihood of needing post cardiopulmonary bypass inotropes include --

  • the severity of regurgitation,
  • the presence of pulmonary hypertension,
  • low pre-operative left ventricular ejection fraction, and
  • prolonged aortic cross-clamp time.

9

Intra-operative Management:

Would an intra-aortic balloon pump (IABP) facilitate weaning this patient from cardiopulmonary bypass (CPB)?

(A 67-year-old, 128 kg, 5'8", male presents for quadruple CABG and mitral valve replacement. He complains of worsening chest pain.

PMHx: He is an insulin dependent diabetic, has chronic hypertension, and smokes cigarettes. He sleeps sitting up and takes prevacid due to his severe acid reflux.

Meds: Prevacid, Dobutamine, Lasix, NPH insulin

Allergies: NKDA

PE:

VS: P = 106, BP = 95/52, SpO2 = 89%, Temp = 36.6 C
Airway: Mallampati II, full cervical ROM
Pulmonary: bilateral crackles
CV: Regular rate; systolic ejection murmur

CXR: Left heart prominence; Kerley B lines and peribronchial cuffing are noted

EKG: ST-segment depression in the anterolateral leads; Q-waves in the inferior leads

Heart Cath: 4+ mitral regurgitation

ABG: pH = 7.43; paCO2 = 43; PaO2 = 71; SpO2 = 89% on 10L O2 by simple mask

Lab: Hgb = 11.3 gm/dL, GLucose = 174 mg/dL, Na+ = 140 mEq/L, K+ = 3.8 mEq/L)

If left ventricular failure is preventing weaning from CPB despite significant inotropic support, an IABP may prove beneficial by improving coronary perfusion during diastole and reducing afterload during systole.

This is the only intervention that serves to reduce myocardial oxygen demand, while at the same time, increasing myocardial oxygen supply.

The IABP should be positioned so that the tip is at the junction of the aortic arch and descending aorta (below the left subclavian artery to prevent cerebral emboli).

It should then be synchronized with the cardiac cycle using either the arterial pressure wave form or the electrocardiographic QRS complex, timed so that balloon inflation occurs with aortic valve closure (dicrotic notch of the arterial wave form & the middle of the T-wave on the ECG), and set at a ratio of 1:2 to allow for comparison of the natural ventricular beats to augmented beats, which aids in the optimization of timing and efficacy.

This 1:2 ratio can then be adjusted to further optimize cardiac function and/or wean from CPB.

10

Intra-operative Management:

Describe the appropriate timing for inflation and deflation of an intra-aortic balloon pump (IABP)? Why is it important?

(A 67-year-old, 128 kg, 5'8", male presents for quadruple CABG and mitral valve replacement. He complains of worsening chest pain.

PMHx: He is an insulin dependent diabetic, has chronic hypertension, and smokes cigarettes. He sleeps sitting up and takes prevacid due to his severe acid reflux.

Meds: Prevacid, Dobutamine, Lasix, NPH insulin

Allergies: NKDA

PE:

VS: P = 106, BP = 95/52, SpO2 = 89%, Temp = 36.6 C
Airway: Mallampati II, full cervical ROM
Pulmonary: bilateral crackles
CV: Regular rate; systolic ejection murmur

CXR: Left heart prominence; Kerley B lines and peribronchial cuffing are noted

EKG: ST-segment depression in the anterolateral leads; Q-waves in the inferior leads

Heart Cath: 4+ mitral regurgitation

ABG: pH = 7.43; paCO2 = 43; PaO2 = 71; SpO2 = 89% on 10L O2 by simple mask

Lab: Hgb = 11.3 gm/dL, GLucose = 174 mg/dL, Na+ = 140 mEq/L, K+ = 3.8 mEq/L)

It is important to set the timing of the IABP so that inflation of the balloon occurs with aortic valve closure (the start of diastole), and thus increasing aortic diastolic pressures and augmenting coronary perfusion pressure.

Rapid balloon deflation timed to occur just prior to ventricular contraction promotes forward flow by reducing ventricular afterload.

Inappropriate timing of balloon inflation or deflation can lead to increased left ventricular afterload and/or reduced augmentation of coronary perfusion.

Therefore, in order to optimize the benefits of the IABP, it is critical to establish appropriate timing, control heart rate, and aggressively treat any developing cardiac dysrhythmias.

11

Intra-operative Management:

If this patient had a pacemaker, could you use an IABP?

(A 67-year-old, 128 kg, 5'8", male presents for quadruple CABG and mitral valve replacement. He complains of worsening chest pain.

PMHx: He is an insulin dependent diabetic, has chronic hypertension, and smokes cigarettes. He sleeps sitting up and takes prevacid due to his severe acid reflux.

Meds: Prevacid, Dobutamine, Lasix, NPH insulin

Allergies: NKDA

PE:

VS: P = 106, BP = 95/52, SpO2 = 89%, Temp = 36.6 C
Airway: Mallampati II, full cervical ROM
Pulmonary: bilateral crackles
CV: Regular rate; systolic ejection murmur

CXR: Left heart prominence; Kerley B lines and peribronchial cuffing are noted

EKG: ST-segment depression in the anterolateral leads; Q-waves in the inferior leads

Heart Cath: 4+ mitral regurgitation

ABG: pH = 7.43; paCO2 = 43; PaO2 = 71; SpO2 = 89% on 10L O2 by simple mask

Lab: Hgb = 11.3 gm/dL, GLucose = 174 mg/dL, Na+ = 140 mEq/L, K+ = 3.8 mEq/L)

Yes.

While a pacemaker could interfere with synchronization when using older systems,

most current IABP consoles are able to distinguish a QRS complex from a pacer spike.

Another option would be to use the arterial waveform as a trigger instead of the QRS complex.

12

Post-operative Management:

As you are transporting the patient to the ICU, the medical student asks you to explain the difference between radial artery pressure and central aortic pressure immediately following CPB.

(A 67-year-old, 128 kg, 5'8", male presents for quadruple CABG and mitral valve replacement. He complains of worsening chest pain.

PMHx: He is an insulin dependent diabetic, has chronic hypertension, and smokes cigarettes. He sleeps sitting up and takes prevacid due to his severe acid reflux.

Meds: Prevacid, Dobutamine, Lasix, NPH insulin

Allergies: NKDA

PE:

VS: P = 106, BP = 95/52, SpO2 = 89%, Temp = 36.6 C
Airway: Mallampati II, full cervical ROM
Pulmonary: bilateral crackles
CV: Regular rate; systolic ejection murmur

CXR: Left heart prominence; Kerley B lines and peribronchial cuffing are noted

EKG: ST-segment depression in the anterolateral leads; Q-waves in the inferior leads

Heart Cath: 4+ mitral regurgitation

ABG: pH = 7.43; paCO2 = 43; PaO2 = 71; SpO2 = 89% on 10L O2 by simple mask

Lab: Hgb = 11.3 gm/dL, GLucose = 174 mg/dL, Na+ = 140 mEq/L, K+ = 3.8 mEq/L)

Due to the peripheral vasodilation that occurs with rewarming,

radial arterial pressures may be as much as 30 mmHg lower than central aortic pressures following CPB (femoral artery catheters correlate well with central aortic pressures).

This pressure gradient usually resolves within 45 minutes of separation from cardiopulmonary bypass.

Prior to the resolution of the pressure gradient, the surgeon can estimate aortic pressure by direct palpation or, if a more accurate central aortic pressure is required, by connecting a transducer to an aortic vent or a needle inserted into the aorta.

13

Post-operative Management:

Which ventilator setting would you order upon arrival in the ICU?

(A 67-year-old, 128 kg, 5'8", male presents for quadruple CABG and mitral valve replacement. He complains of worsening chest pain.

PMHx: He is an insulin dependent diabetic, has chronic hypertension, and smokes cigarettes. He sleeps sitting up and takes prevacid due to his severe acid reflux.

Meds: Prevacid, Dobutamine, Lasix, NPH insulin

Allergies: NKDA

PE:

VS: P = 106, BP = 95/52, SpO2 = 89%, Temp = 36.6 C
Airway: Mallampati II, full cervical ROM
Pulmonary: bilateral crackles
CV: Regular rate; systolic ejection murmur

CXR: Left heart prominence; Kerley B lines and peribronchial cuffing are noted

EKG: ST-segment depression in the anterolateral leads; Q-waves in the inferior leads

Heart Cath: 4+ mitral regurgitation

ABG: pH = 7.43; paCO2 = 43; PaO2 = 71; SpO2 = 89% on 10L O2 by simple mask

Lab: Hgb = 11.3 gm/dL, GLucose = 174 mg/dL, Na+ = 140 mEq/L, K+ = 3.8 mEq/L)

If the patient did not demonstrate any respiratory effort,

I would order a mode of ventilation that would provide full support, such as assist-control or synchronized intermittent mandatory ventilation (SIMV).

Along with this setting, I would add a small amount of PEEP to prevent atelectasis.

---

If, however, the patient did demonstrate respiratory effort, I would order a weaning mode of ventilation, such as SIMV.

Along with this setting, I would add pressure support ventilation (PSV) and continuous positive airway pressure (CPAP).

SIMV allows me to set a basal respiratory rate that is synchronized to avoid initiating a mechanical breath during a patient initiated spontaneous breath.

The addition of PSV reduces the work of breathing during spontaneous breaths;

the addition of CPAP helps to reduce/prevent atelectasis that can lead to increased right-to-left shunting of blood in the pulmonary circuit (physiologic shunt).

14

Post-operative Management:

A few hours later you are called to see the patient. His blood pressure has dropped to 76/43 mmHg. What is your differential?

(A 67-year-old, 128 kg, 5'8", male presents for quadruple CABG and mitral valve replacement. He complains of worsening chest pain.

PMHx: He is an insulin dependent diabetic, has chronic hypertension, and smokes cigarettes. He sleeps sitting up and takes prevacid due to his severe acid reflux.

Meds: Prevacid, Dobutamine, Lasix, NPH insulin

Allergies: NKDA

PE:

VS: P = 106, BP = 95/52, SpO2 = 89%, Temp = 36.6 C
Airway: Mallampati II, full cervical ROM
Pulmonary: bilateral crackles
CV: Regular rate; systolic ejection murmur

CXR: Left heart prominence; Kerley B lines and peribronchial cuffing are noted

EKG: ST-segment depression in the anterolateral leads; Q-waves in the inferior leads

Heart Cath: 4+ mitral regurgitation

ABG: pH = 7.43; paCO2 = 43; PaO2 = 71; SpO2 = 89% on 10L O2 by simple mask

Lab: Hgb = 11.3 gm/dL, Glucose = 174 mg/dL, Na+ = 140 mEq/L, K+ = 3.8 mEq/L)

My differential for this decrease in blood pressure would include --

  • myocardial ischemia/infarction,
  • left or right ventricular failure,
  • continued myocardial stunning,
  • IABP malfunction/complication (if still in place),
  • tension pneumothorax,
  • hypo/hypervolemia,
  • dysrhythmia,
  • cardiac tamponade,
  • metabolic disturbances (electrolyte abnormalities, acid-base disorder, hyper/hypoglycemia), and
  • cardiovascular depression secondary to pain medication and/or sedative drugs.

Establishing a diagnosis would be aided by observing the ECG, evaluating data provided by the CVP and/or PAC (if present), and, possibly, utilizing TEE.

15

Post-operative Management:

What are the clinical manifestations of cardiac tamponade?

(A 67-year-old, 128 kg, 5'8", male presents for quadruple CABG and mitral valve replacement. He complains of worsening chest pain.

PMHx: He is an insulin dependent diabetic, has chronic hypertension, and smokes cigarettes. He sleeps sitting up and takes prevacid due to his severe acid reflux.

Meds: Prevacid, Dobutamine, Lasix, NPH insulin

Allergies: NKDA

PE:

VS: P = 106, BP = 95/52, SpO2 = 89%, Temp = 36.6 C
Airway: Mallampati II, full cervical ROM
Pulmonary: bilateral crackles
CV: Regular rate; systolic ejection murmur

CXR: Left heart prominence; Kerley B lines and peribronchial cuffing are noted

EKG: ST-segment depression in the anterolateral leads; Q-waves in the inferior leads

Heart Cath: 4+ mitral regurgitation

ABG: pH = 7.43; paCO2 = 43; PaO2 = 71; SpO2 = 89% on 10L O2 by simple mask

Lab: Hgb = 11.3 gm/dL, Glucose = 174 mg/dL, Na+ = 140 mEq/L, K+ = 3.8 mEq/L)

In the awake patient who has not recently undergone cardiac surgery,

increasing pericardial pressures result in -- dyspnea, tachycardia, hypotension, orthopnea, jugular venous distension, muffled heart sounds, and pulsus paradoxus.

Unfortunately, the clinical presentation is often atypical and difficult to diagnose in the mechanically ventilated patient following cardiac surgery.

The atypical presentation is partly due to the fact that the pericardium is left open following cardiac surgery, resulting in -- regional versus homogenous compression of the cardiac chambers from blood and/or clot.

A loculated or localized hematoma/clot can cause regional compression that produces a clinical picture inconsistent with classical tamponade physiology, where an equalization of diastolic pressures occurs throughout the heart.

Rather, the clinical picture may mimic left and/or right heart failure.

Therefore, a high degree of clinical suspicion and the use of transesophageal echocardiography may help to produce a timely diagnosis.

Diastolic collapse of the right atrium, right ventricle, and/or left ventricle, as determined by TEE, is the most sensitive and specific sign of cardiac tamponade.

16

Post-operative Management:

Can cardiac tamponade occur when the pericardium is no longer intact?

(A 67-year-old, 128 kg, 5'8", male presents for quadruple CABG and mitral valve replacement. He complains of worsening chest pain.

PMHx: He is an insulin dependent diabetic, has chronic hypertension, and smokes cigarettes. He sleeps sitting up and takes prevacid due to his severe acid reflux.

Meds: Prevacid, Dobutamine, Lasix, NPH insulin

Allergies: NKDA

PE:

VS: P = 106, BP = 95/52, SpO2 = 89%, Temp = 36.6 C
Airway: Mallampati II, full cervical ROM
Pulmonary: bilateral crackles
CV: Regular rate; systolic ejection murmur

CXR: Left heart prominence; Kerley B lines and peribronchial cuffing are noted

EKG: ST-segment depression in the anterolateral leads; Q-waves in the inferior leads

Heart Cath: 4+ mitral regurgitation

ABG: pH = 7.43; paCO2 = 43; PaO2 = 71; SpO2 = 89% on 10L O2 by simple mask

Lab: Hgb = 11.3 gm/dL, Glucose = 174 mg/dL, Na+ = 140 mEq/L, K+ = 3.8 mEq/L)

As I mentioned, a loculated or localized hematoma can result in regional compression of the heart even when the pericardium is no longer intact.

The presentation, however, is often inconsistent with classical tamponade physiology due to the uneven distribution of blood and/or clots around the heart, which results in regional versus homogenous compression of the cardiac chambers.

17

Post-operative Management:

What is pulsus paradoxus?

(A 67-year-old, 128 kg, 5'8", male presents for quadruple CABG and mitral valve replacement. He complains of worsening chest pain.

PMHx: He is an insulin dependent diabetic, has chronic hypertension, and smokes cigarettes. He sleeps sitting up and takes prevacid due to his severe acid reflux.

Meds: Prevacid, Dobutamine, Lasix, NPH insulin

Allergies: NKDA

PE:

VS: P = 106, BP = 95/52, SpO2 = 89%, Temp = 36.6 C
Airway: Mallampati II, full cervical ROM
Pulmonary: bilateral crackles
CV: Regular rate; systolic ejection murmur

CXR: Left heart prominence; Kerley B lines and peribronchial cuffing are noted

EKG: ST-segment depression in the anterolateral leads; Q-waves in the inferior leads

Heart Cath: 4+ mitral regurgitation

ABG: pH = 7.43; paCO2 = 43; PaO2 = 71; SpO2 = 89% on 10L O2 by simple mask

Lab: Hgb = 11.3 gm/dL, Glucose = 174 mg/dL, Na+ = 140 mEq/L, K+ = 3.8 mEq/L)

Pulsus paradoxus is = an exaggeration of the normal variation in systolic pressure and pulse that occurs during the inspiratory phase of respiration.

Normally, with inspiration, intrathoracic pressure becomes more negative resulting in increased venous return to the heart, which in turn results in increased right ventricular volume and bulging of the intraventricular septum toward the left ventricle.

This bulging reduces the left ventricular capacity and filling volume, which in turn reduces stroke volume and systolic pressure.

The reduction in systolic pressure (normally = 10 mmHg) then leads to an increase in heart rate secondary to the baroreceptor reflex.

This normal variation in blood pressure may be exaggerated (>/= 10 mmHg) with certain medical conditions such as --

cardiac tamponade, airway obstruction, COPD, and pulmonary embolism.

18

Post-operative Management:

Echocardiography confirms that the patient has cardiac tamponade. What would you do?

(A 67-year-old, 128 kg, 5'8", male presents for quadruple CABG and mitral valve replacement. He complains of worsening chest pain.

PMHx: He is an insulin dependent diabetic, has chronic hypertension, and smokes cigarettes. He sleeps sitting up and takes prevacid due to his severe acid reflux.

Meds: Prevacid, Dobutamine, Lasix, NPH insulin

Allergies: NKDA

PE:

VS: P = 106, BP = 95/52, SpO2 = 89%, Temp = 36.6 C
Airway: Mallampati II, full cervical ROM
Pulmonary: bilateral crackles
CV: Regular rate; systolic ejection murmur

CXR: Left heart prominence; Kerley B lines and peribronchial cuffing are noted

EKG: ST-segment depression in the anterolateral leads; Q-waves in the inferior leads

Heart Cath: 4+ mitral regurgitation

ABG: pH = 7.43; paCO2 = 43; PaO2 = 71; SpO2 = 89% on 10L O2 by simple mask

Lab: Hgb = 11.3 gm/dL, Glucose = 174 mg/dL, Na+ = 140 mEq/L, K+ = 3.8 mEq/L)

If the patient remained relatively hemodynamically stable,

I would alert the surgical team (if not already done),

deliver 100% oxygen,

administer fluids for volume expansion,

consider the administration of catecholamines,

treat any bradycardia (i.e. atropine),

correct any metabolic acidosis (which can contribute to cardiac depression), and

transport the patient to the operating room with full monitoring and emergency cardiovascular drugs immediately available during transport.

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If I felt there was not enough time to get him to the operating room, I would consider reopening his chest in the intensive care unit.

In the latter situation, I would likely avoid any anesthesia in order to avoid the attenuation of compensatory mechanisms that are sustaining vital cardiac output and organ perfusion.

However, I would administer anesthetic drugs as soon as pericardial pressure was relieved and cardiovascular function improved.