DYNAMIC

Question 1

Measuring mixed venous oxygen?

Answer 1

MvO2 (mixed venous oxygen) reflects the amount of oxygen in the venous blood after returing from upper body and arms via SVC, lower body and gut via IVC and coronary sinus.

It is measured best via a pulmonary artery cathetar (also called PA saturation)

Normal values for PA sat/MvO2 : 65-80%

Note: Central IJ lines can be used as a surrogate but these only consist of venous blood returing via SVC from arms and head. The normal value is usualy 5-10% higher.

Question 2

Determinants of oxygen delivery to tissues?

Answer 2

1. FiO2 or PaO2: As air enters the alveoli the higher the partial pressure of O2 the more it can then bind Hb.
2. Increasing the Hb content
3. Increasing the cardiac output

Oxygen Delivery (DO2) = Cardiac Output (HR X Stroke Volume) X Oxygen Content (Hb X SaO2)

As hemoglobin molecules pass out of the right side of the heart and through the lungs/alveoli, four molecules of oxygen become attached to each individual hemoglobin molecule. This oxygenated blood then passes through the left side of the heart and out to the tissue. Upon reaching the capillary beds, an average patient extracts one molecule of oxygen from each hemoglobin molecule, leaving the red blood cells 75% saturated with oxygen as they return back to the right side of the heart

Question 3

Compensatory mechanisms when O2 delivery decreases?

Answer 3

Tissues require oxygen in order to make ATP (energy). If the amount of oxygen being received by the tissues falls below the amount of oxygen required (because of an increased need, or decreased supply), the body attempts to compensate as follows:

1. The cardiac output is increased in an effort to increase the amount of oxygen being delivered to the tissues
2. Tissues begin to remove or extract a higher percentage of oxygen from the arterial blood. This results in a reduced amount of oxygen remaining in the blood as it returns to the right side of the heart (decreased SvO2).
3. If the tissues fail to receive an adequate supply of oxygen, anaerobic metabolism becomes the only mechanism to produce tissue ATP. Anaerobic metabolism is inefficient, producing a large amount of metabolic waste (e.g. lactic acid) that is difficult for the body to eliminate quickly.

Question 4

MvO2 and Cardiac output monitoring?

Answer 4

If SvO2 decreases, it indicates that the tissues are extracting a higher percentage of oxygen from the blood than normal. In otherwords, a decreased SvO2 indicates that the cardiac output is not high enough to meet tissue oxygen needs.

Question 5

4 fundamental causes of drop in MvO2:

Answer 5

1. The cardiac output is not high enough to meet tissue oxygen needs > Tissues start extracting more
2. The Hb is too low
3. The SaO2 is too low
4. Oxygen consumption has increased without an increase in oxgyen delivery

Question 6

Acute on chronic systolic heart failure with following:

• Low output state (very low EF, low CI)
• Warm (perfused, SBP high)
• Wet (evidence of volume overload)

Answer 6

In these patients with a low output state we increase cardiac outpur by using an ionotrope and vasoldilators to decrease SVR > Start milrinone/dobutamine + hydralazine/Ace or ARB/Entresto

We also diurese with lasix/bumex for net -1.5 to 2L /day

Note: If patient was cold or hypotensive we won’t consider afterload reducing agents

Question 7

Initial rate control for atrial flutter with RVR?

Answer 7

Can consider giving IV diltiazem 17.5 mg or IV lopressor push

Question 8

Rate control for atrial flutter if IV push unsuccesful?

Answer 8

Can start diltiazem ggt and once stable can transition to PO metoprolol or Cardizem immediate release 30 q6

Question 9

Anticoagulation for atrial flutter?

Answer 9

Every patient with atrial flutter should be on anticoagulation (CHAD-VASC) just like atrial fibrillation

Question 10

Atrial fibrillation with RVR but hemodynamically stable, rate control with?

Answer 10

Can give IV lopressor pushes or IV Cardizem pushes.

If still not controlled can start Cardizem ggt

Note: Don’t use CCBs if reduced EF

Question 11

Hemodynamically unstable patient with Atrial fibrillation?

Answer 11

Consider cardioversion if patient has severe hypotension with RVR >110. Or they have chest pain, AMS or acute heart failure.

• Discuss with patient get consent
• Place pads : anterior-posterior preferred over anterior-lateral

Sedation: Etomidate start with 0.1mg/kg IV; repeat with 0.05 mg/kg just prior to shock. Ketamine: Start with 0.5mg/kg IV. Both of these won’t drop blood pressure. Ketamine will cause longer sedation. Can also use IV midazalom if blood pressure tolerates.

• Start anticoaglation with heparin
• Prepare for cardioversion: Synchronised (make sure on R or S wave and not T wave as that can induce Vtach)
• Deliver initial 200J, if no response an additional 200 or 360J
• Place pressure (weights) on pads in obese patients to decrease transthoracic impedence to current flow
• Improve blood pressure using phenylephrine a selective A1 agonist that won’t increase HR and also bring BP high before starting AV nodal agents. Dose (push): 50-200 mcg q1-2 mins PRN (goal diastolic >60). Dose (drip): 40-180 mcg/min, titrated to goal
• Control rate with agents that won’t bring blood pressure down too quickly. In the crashing patient, Amiodarone is a better choice because it doesn’t negatively affect the blood pressure as much as the previously mentioned medications. Dose: Give a 150 mg bolus (slow push or over 10 mins) followed by 1 mg/min IV infusion..Can re-dose 150 mg 2 additional times if the rate does not respond after 30-40 minutes.Esmolol, a cardioselective beta-blocker, is another good option because of its quick “on/off properties”. It quickly takes effect, can be titrated to effect, and has a short half-life, which means we can turn it off and quickly have it out of their system if their blood pressure drops. Dose: Bolus loading dose of 500 mcg/kg over 1 minute followed by 50 mcg/kg/min infusion for 4 minutes. If the desired effect is not reached, may increase in 50 mcg/kg per minute increments until the max dose of 200 mcg/kg per minute. If you do choose to use Diltiazem, don’t give a big push dose like we do for stable patients; instead, use a slow drip, or small frequent doses. Once you achieve the rate you want, you’ll need to either start a drip, or give an oral dose of Diltiazem to maintain lasting rate control.2,6 It is currently recommend to avoid the use of the non-dihydropyridine calcium channel blockers in patients with heart failure with reduced ejection fraction due to the negative inotropic effects (this is true for both the crashing and stable patient!). Dose (initial): 2.5 mg/min over 10-15 minutes 2 OR 5 mg doses every 1 minute. Dose (once desired rate achieved): Drip at 5-15 mg/hr OR 30-60 mg PO
• Check electrolytes (give Mg if <2)
• Correct underlying causes

Question 12

Amiodarone dose for rate control in atrial fibrillation?

Answer 12

150 mg over at least 10 minutes, followed by 0.5 to 1 mg/minute; may administer repeat boluses of 150 mg IV over at least 10 minutes as needed.

Note: Alternatively can give IV 300 mg over 1 hour, then 10 to 50 mg/hour over 24 hours followed by an oral maintenance dose

Question 13

Esmolol for rate control in atrial fibrillation?

Answer 13

IV: Loading dose (optional): 500 mcg/kg over 1 minute; follow with a 50 mcg/kg/minute infusion for 4 minutes; response to this initial infusion rate may be a rough indication of the responsiveness of the ventricular rate.

Infusion may be continued at 50 mcg/kg/minute or, if the response is inadequate, titrated upward in 50 mcg/kg/minute increments (increased no more frequently than every 4 minutes) to a maximum of 200 mcg/kg/minute.

To achieve more rapid response, following the initial loading dose and 50 mcg/kg/minute infusion, rebolus with a second 500 mcg/kg loading dose over 1 minute, and increase the maintenance infusion to 100 mcg/kg/minute for 4 minutes. If necessary, a third (and final) 500 mcg/kg loading dose may be administered, prior to increasing to an infusion rate of 150 mcg/kg/minute. After 4 minutes of the 150 mcg/kg/minute infusion, the infusion rate may be increased to a maximum rate of 200 mcg/kg/minute (without a bolus dose). The ACC/AHA/HRS supraventricular tachycardia guidelines recommend a maximum dose of 300 mcg/kg/minute (ACC/AHA/HRS.

Note: If a loading dose is not administered, a continuous infusion at a fixed dose reaches steady-state in ~30 minutes. In general, the usual effective dose is 50 to 200 mcg/kg/minute; doses as low as 25 mcg/kg/minute may be adequate. Maintenance infusions may be continued for up to 48 hours.

Question 14

Atrial flutter with RVR in a stable patient chronic HFrEF?

Answer 14

Try not to use CCBs

Beta-blockers preferred. IV esmolol ggt

A bolus of 0.5 mg/kg is infused over one minute, followed by 50 µg/kg per min

If, after four minutes, the response is inadequate, another bolus is given followed by an infusion of 100 µg/kg per min

If, after four minutes, the response is still inadequate, a third and final bolus can be given followed by an infusion of 150 µg/kg per min.

If necessary, the infusion can be increased to a maximum of 200 µg/kg per min after another four minutes

Alternatively, an infusion can be started at 50 µg/kg per min without a bolus, and the rate of administration can be increased by 50 µg/kg per min every 30 minutes.

Note: IV digoxin can be used in comination with a beta-blocker

Question 15

Atrial flutter with RVR in a patient with decompensated chronic systolic heart failure (hypotensive)?

Answer 15

These patients cannot tolerate a BB.

In these patients we should use Amiodarone after starting anticoagulation. Give a bolus of 150 IV once followed by 1/mg/min for 6 hours and then 0.5 mg/min for 18 hours..

Note: This is ideal in patients who were on long term anticoagulation as if they cardiovert the risk of thromboemolism is low. Caution should be used in starting amiodarone in patients not on anticoagulation as this can cause embolism. Explore other options like whether beta-blockers can be tolerated.

Question 16

Patient with shortness of breath, JVD, peripheral edema but echocardiogram showing normal LVEF?

Answer 16

In such a case we have to see if the volume overload and pulmonary hypertension is secondary to left heart disease (Valvulvar vs diastolic) or due to pulmonary disease.

The best way to establish this is to do a right heart cath which will help us determine if it’s Group II or another Group. Even though the patient has presevred EF it can be still be Group II from diastolic dysfunction/valvular disease.

Question 17

Chronic right heart failure treatment?

Answer 17

In such patient treatment options include:

(1) . Diuretics: This is important because these patients will usually have signs of volume overload with shortness of breath, peripheral edema, JVD and congestive hepatopathy. IVC usually dilated and non collapsible. However, there should be cautious use of diuretics in these patients due to preload dependence and also because there is less forward flow to the LV. Furthermore, a dilated RV causes the septum to buldge towards the LV making the septal LV not relax properly and causing diastolic dysfunction.
(2) . For contractility we can start patient on digoxin
(3) . For RV afterload reduction we can consider sildenafil

Question 18

Acute RV failure & shock?

Answer 18

• Determine etiology (inferior MI with RV involvement, take to cath lab)
• Consider RV support (RV impella, protec duo are mechanical RV choices)
• Chemical RV support (We can consider dobutamine for RV support but it can cause hypotension so it is important to bring their blood pressure up with first vasopressors such as levophed)
• These patients are usually preload dependent, don’t diurese aggressively and CVP goal should be a bit higher 14-16 and don’t give nitro!)

Question 19

Variants of Takotsobu?

Answer 19

Common Takotsobu cardiomyopthy has a hypocntractile apex (ballooning) with a hyperkinetic base. There are many other variants and these include reverse Takotsobu where the base is hypokinetic and apex is hyper dynamic. There is also mid-ventricular/cavity Takotsobu where the base and apex are hypercontractile but the mid cavity isnt moving well.

Question 20

Treatment for orthostatic hypotension?

Answer 20

1. Make sure patient has received adequate amount of fluids. It could be that patient is dehydrated because of which ANS is unable to mount a response on standing up.
2. Stop medications that cause volume loss such as thiazides or inhibit the SANS response such as Beta and Ca channel blockers
3. If above measure fail, compression stocking up to the thigh and standing up slowly
4. Other treatments include midodrine and then fludocortisone

Question 21

If patient has dilated RV, peripheral edema and signs of right heart failure and normal LV on echo but RHC shows normal PVR and high PCWP then diagnosis?

Answer 21

This could be secondary to LV disease, valvular disease. Diastolic dysfunction when the EF is preserved.

Question 22

Mechanical MV and anticoagulation?

Answer 22

Any patient with a mechanical MVR who has a subtherapeutic INR or needs Warfarin to be stopped must be initiated on heparin.

Question 23

VT storm

(Patient with ICD comes in with multiple shocks)

Answer 23

Important to think about 1) Electrolytes 2) Ischemia

For treatment in a patient with ICD we can:

(1) ATP
(2) Amiodarone (we can give 150 mg IV bolus as a push x 2 followed by 1mg/min amiodarone ggt)
(3) . Lidocaine (we can give a 1 mg/kg bolus followed by 1-2 mg/min drip)
(4) . Can try giving pushes of Versed 2-4 mg IV

If patient is still refractory we should then intubate the patient and start propofol

Question 24

Treatment of sustained V-tach in a stable patient?

Answer 24

Amiodarone (Bolus then ggt)

Lidocaine (bolus then ggt)

Cardioversion (Class I indication)

Question 25

Posterior fasicular block?