In this podcast we talk about shock, cyanosis and heart failure in neonates.

Dr Joe Nemeth provides a 3 minute summary.

Dr Adam Michael takes us over some important pearls.

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Hypotension

Positive pressure ventilation secondary to intubation, increases intrathoracic pressure which increases right atrial pressure resulting in decreased pressure differential and less blood coming back into the heart.

What may help

• Volume resuscitation may increase cardiac output
• If patients are not fluid responsive, vasopressors may be used: Noradrenaline is the drug of choice.
• Adrenaline 10-50mcg boluses can be used as needed for BP
•  Metaraminol can be used: Increases peripheral vascular resistance, Increases force of myocardial contraction
•  Beware induction agents: Benzodiazepines and Propofol- Sympatholytic effect- myocardial depression and decreased vascular tone. Ketamine is the preferred agent gives sympathetic surge
• Identify patients susceptible to hypotension post intubation have pre-intubation hypotension and a Shock Index > 0.8
•  Aim for higher BP ie SBP of 140 mm Hg
•  

Hypoxaemia

What may help

• Maximise oxygenation: Nasal canula at 15L/min + NRB or BVM (with PEEP)
• HFNC
• CPAP with PEEP  

Severe Metabolic Acidosis

What may help

• Avoid intubating these patients
•  No evidence that Bicarb helps but HCO3-> H20 + CO2
•  Can use NIPPV
•  If have to intubate the patient, avoid paralysis if possible, or use very short acting neuromuscular blocker such as suxamethonium.
•  Allow the patient to maintain their spontaneous respirations. Beware of Fatigue and air trapping
• Consider Pressure assisted VAPOX.

Right Ventricular Failure

What may help

• Beware fluid challenge as the volume overloaded right ventricle can can affect LV filling decreasing stroke volume. Bedside ECHO can tell us about the RV
•  Pre-oxygenate
•  Use haemodynamically neutral induction agents eg., ketamine
•  Noradrenaline can increase mean arterial pressure > pulmonary arterial pressure.

Please also read the review of Cardiac Arrest Complicating Emergency Airway Management

References

1. Zuercher M et al . Cardiac arrest during anesthesia. Curr Opin Crit Care 2008;14:269–74.
2. Heffner AC et al. Incidence and factors associated with cardiac arrest complicating emergency airway management. Resuscitation 84(2013) 1500-1504.

• Consider every case a difficult Intubation due to effects on anatomy and physiology
• Normal airway techniques may not be effective.
• Positioning of the patient is critical- aim for head up.
• Pre-oxygenation techniques are crucial
• Appropriate medication dosing is important
• Video laryngoscopy may provide an edge
• Mechanical Ventilation needs to be tailored

Anatomy and Physiology in the obese patient can make every case difficult

• A BMI greater than 30 kg/m2 is considered obese. BMI’s greater than 40 kg/m2 considered severely CLASS III obese.
• For example a 168cm person weighing 85kg is considered obese. We need to keep some perspective on these. It’s not just the absolute weight. I know a lot of rugby players that fall into that range.
• Obese patients have a decreased overall, lung capacity and an increase in metabolic activity. This results on increased oxygen consumption and an increased work of breathing.
• The adipose tissue produces increased metabolic activity as well as increasing airway resistance and potentially causes increased risk of pharyngeal wall collapse with paralysis.
• The ability to adequately pre-oxygenate give safe apnoea times is affected as the functional residual capacity is also decreased. Safe apnoea times are decreased to one to two minutes.
• The displacement of the diaphragm makes ventilation in the supine position more difficult and can lead to desaturation more readily, in this position.
• Obese patients are more difficult to ventilate and they desaturate far more rapidly.

Normal Airway techniques may not be effective.

• The airway in the obese patient must always be assumed to be a difficult airway. The risk of rapid desaturation is high and the increase in airway resistance makes BVM ventilation more difficult (1,2); a 2 hand technique (2 operator) being required.
• Use a PEEP valve at 10cm H20.
• The use of airway adjuncts, such as nasopharyngeal and oropharyngeal (unless contraindicated) may help with ventilation (3)
• Laryngoscopy can prove difficult due extra adipose tissue resulting in an alteration of the anatomy.
• A predictor of difficult intubation is a large neck circumference and a high Mallampati Score (4).
• Laryngeal masks can be used in the obese patient (5)
• Performing a surgical airway on these patients is extremely difficult due to the inability to identify important anatomical landmarks (6). Bedside ultrasound may assist in identifying the anatomy (7,8)

Patient positioning is critical

• Patients should be placed in the upright position, to allow the diaphragm to fall and allow greater ventilation of the lungs.
• If it’s not possible to sit the patient upright eg., in trauma, with cervical precautions, a reverse Trendelenburg position is recommended.
• In preparation for intubation, the ramped, head-up position where the auditory canal is aligned with the sternal notch, provides a better position for visualisation of the glottis. (9,10), with improvements of over 50% when head elevation is used, as compared to supine positioning (11).

Pre-oxygenation is crucial

• Given that obese patients desaturate very rapidly, adequate pre-oxygenation is imperative, if time allows.
• Non-Invasive ventilation such as CPAP can improve oxygenation (12,13). A minimum of 5-10 minutes may be needed.
• Apnoeic Oxygenation via high flow nasal prongs should also be used during the procedure.

Appropriate medication dosing

The pharmacokinetics of some medications is altered by obesity. Obese patients have a higher glomerular filtration rate, causing renally excreted drugs to have shorter half-lives.

We need to which medications should be given according to ideal body weight versus total body weight doses. Induction and paralysis medications are shown below:

• Propofol: Ideal Body Weight. There is a significant risk of hypotension if larger doses are used.
• Ketamine: Ideal body weight
• Suxamethonium: Total body weight.
• Rocuronium: Ideal body weight. It appears that the duration of action is prolonged if total body weight is used, however the time to relaxation may not be different (14)

Video laryngoscopy for Intubation

• Awake intubation may be an option to consider for the obese patient, assuming they can maintain saturations.
• Normal laryngoscopy may need some modifications including a short handle laryngoscope and larger blade sizes.
• Video laryngoscopes have resulted in better views of the glottis and produced views of the glottis (15,16,17)

Mechanical Ventilation

• Use ideal body weight for tidal volumes of 6-8mL/kg.
• Higher respiratory rates will be needed as obese patients have spontaneous respiratory rates of 15-20 breaths per minute.
• Positioning in the reverse Trendelenburg position may improve oxygenation and ventilation
• PEEP of 10-15cmH20 may be needed.

Summary

• Consider every case a difficult Intubation due to effects on anatomy and physiology
• Increased airway resistance
• Increased tissue results in higher metabolic rates and rapid desaturation
• Increased tissue may cause pharyngeal wall to collapse
• Normal airway techniques may not be effective.
• Two handed BVM should be used
• Airway adjuncts such as oropharyngeal and nasopharyngeal airway may help
• Positioning of the patient is critical- aim for head up.
• Sitting position or head up is better for pre-oxygenation
• Reverse Trendelenburg may assist
• Ramp up and ear to sternal notch positioning for intubation
• Pre-oxygenation techniques are crucial
• Rapid desaturation
• Pre-oxygenate in upright position
• Use CPAP
• Use high flow apnoeic oxygenation
• Appropriate medication dosing is important
• Use total body weight for suxamethonium dosing
• Use ideal body weight for Propofol, Ketamine and Rocuronium dosing
• Video laryngoscopy may provide an edge
• Video Laryngoscopy gives a better view than Direct Laryngoscopy
• Mechanical Ventilation needs to be tailored
• Use ideal body weight for Tidal Volume
• Increase respiration rates are needed.
• Use PEEP 15-20cm H20

REFERENCES

1. Levi D, et al. Critical care of the obese and bariatric surgical patient. Crit Care Clin 2003; 19:11.
2. Varon J, Marik P. Management of the obese critically ill patient. Crit Care Clin 2001; 17:187.
3. Gerstein NS, et al. Efficacy of facemask ventilation techniques in novice providers. J Clin Anesth 2013; 25:193.
4. Brodsky JB, et al. Morbid obesity and tracheal intubation. Anesth Analg 2002; 94:732.
5. Zoremba M, et al. Comparison between intubation and the laryngeal mask airway in moderately obese adults. Acta Anaesthesiol Scand 2009; 53:436.
6. Aslani A, et al. Accuracy of identification of the cricothyroid membrane in female subjects using palpation: an observational study. Anesth Analg 2012; 114:987.
7. Dinsmore J, et al. The use of ultrasound to guide time-critical cannula tracheotomy when anterior neck airway anatomy is unidentifiable. Eur J Anaesthesiol 2011; 28:506.
8. Siddiqui N, et al. Ultrasound Improves Cricothyrotomy Success in Cadavers with Poorly Defined Neck Anatomy: A Randomized Control Trial. Anesthesiology 2015; 123:1033.
9. Rao SL, et al. Laryngoscopy and tracheal intubation in the head-elevated position in obese patients: a randomized, controlled, equivalence trial. Anesth Analg 2008; 107:1912.
10. Collins JS, et al. Laryngoscopy and morbid obesity: a comparison of the "sniff" and "ramped" positions. Obes Surg 2004; 14:1171.
11. Lee BJ, et al. Laryngeal exposure during laryngoscopy is better in the 25 degrees back-up position than in the supine position. Br J Anaesth 2007; 99:581.
12. Delay JM, et al. The effectiveness of noninvasive positive pressure ventilation to enhance preoxygenation in morbidly obese patients: a randomized controlled study. Anesth Analg 2008; 107:1707.
13. El-Khatib MF, et al. Noninvasive bilevel positive airway pressure for preoxygenation of the critically ill morbidly obese patient. Can J Anaesth 2007; 54:744.
14. Leykin Y, et al. The pharmacodynamic effects of rocuronium when dosed according to real body weight or ideal body weight in morbidly obese patients. Anesth Analg 2004; 99:1086
15. Marrel J, et al. Videolaryngoscopy improves intubation condition in morbidly obese patients. Eur J Anaesthesiol 2007; 24:1045.
16. Andersen LH, et al. GlideScope videolaryngoscope vs. Macintosh direct laryngoscope for intubation of morbidly obese patients: a randomized trial. Acta Anaesthesiol Scand 2011; 55:1090.
17. Ruetzler K, et al. McGrath Video Laryngoscope Versus Macintosh Direct Laryngoscopy for Intubation of Morbidly Obese Patients: A Randomized Trial. Anesth Analg 2020; 131:586.

Earlier that morning the patient developed central chest pain and felt dizzy. When the ambulance arrived the patient had the following vitals:

• Afebrile
• HR 72bpm
• BP 65/42
• Sats 97% on Room air.

ECG showed a normal sinus rhythm with no ST elevation or depression.

Following an unsuccessful fluid challenge, the ambulance commenced Adrenaline and gave Aspirin.

On arrival to the ED the patient is still complaining of chest pain and has the following vitals:

• HR 128bpm
• BP 132/68

There are still no signs of ischaemia on the ECG, it is normal sinus rhythm.

What percentage of patients with early AMI have ECG changes?

What percentage of patients with proven MI( history and Troponin) do not develop ST elevation or Depression?

What would you do now?

I stop the adrenaline and put up Noradrenaline. The ambulance state the patient has an advanced directive.

We talk about advanced directives and what they mean.

We also talk about Troponins and mortality.

Kaura et al. Association of troponin level and age with mortality in 250000 patients; cohort study across five UK acute care centres. BMJ 2019;367:16055

Below is a great graph from the above study. It shows that the hazard ratio for a high troponin is highest in the younger patients and decreases in the elderly. Why would that be?

Much of the literature quotes one study from 1999:

Hochman J et al. Early revascularisation in acute myocardial infarction complicated by cariogenic shock. August 26, 1999, 341(9): 625-634.

We also look at another study:

Ratcovich HL et al. Outcome in elderly patients with cardiogenic Shock Complicating Acute myocardial Infarction.Shock March 2022 57(3);327-335.

This was a retrospective, registry study. It quite interestingly showed amongst other things that for elderly patients who survived almost 70% were still alive at one year.

We look at the CardShock study:

Harjola V-P et al. Clinical picture and risk prediction of short term mortality in cardiogenic shock. Europe J Heart Fail. 2015. 17: 501-509

Finally we look at the American Heart Association statement:

Cardiogenic Shock in Older Adults: A Focus on Age-Associated Risks and Approach to Management: A Scientific Statement From the American Heart Association. Circulation 2024;149:e1051-e1065

Suggestions for clinical practice:

1. "Inconsistent definitions of older adults and CS, along with limited recommendations within clinical practice guidelines, especially for individuals ≥75 years of age, create a knowledge gap for evidence- based recommendations in older adults.
2. Clinical decision-making frequently places significant emphasis on chronological age, resulting in a disregard for the critical link between in-hospital outcomes and individual patient characteristics, including the presence of geriatric conditions such as multimorbidity, polypharmacy, cognitive decline, delirium, and frailty.
3. HF-CS has emerged as the primary cause of CS. Older adults are more likely to develop AMI-CS com- pared with younger individuals. With the increasing prevalence of HF among the older adult population, a rise in HF-CS cases may be anticipated.
4. Regardless of shock cause, CS mortality remains high and increases incrementally with advancing age.
5. Age is recognized as a contributing factor to increased mortality risk in older adults with CS; however, it should not be regarded as the sole determinant. Individualized assessments consider- ing a range of contributing factors are necessary.
6. A comprehensive assessment by an interdisciplin- ary team is crucial in the evaluation of the multi- factorial heightened mortality risk in older adults, taking into account baseline patient factors, clinical trajectory, ...... read them all in the Papercut review of this study here. 

How do we choose the right pressor in shock? Below is a brief discussion of pressors and their properties as well as 4 cases, where we choose the pressor to use, with reasoning.

If I were to use one general guide, it is, that unless we need to increase the heart rate, then NorAdrenaline, can be used in nearly all cases. 

Below are 4 cases to think about. Try them and then scroll down and read on the properties of all these medications.

CASE 1

A 68 yo male is brought to your emergency department in what appears to be septic shock. He has had a recent urine infection. Over the last 24 hours he has become quite febrile and lethargic according to his wife. This morning he felt unwell and felt like he was going to collapse each time he tried to get out of bed.

On arrival he is alert and oriented. He feels unwell. His vitals are as follows:

• Temperature 38.9
• Heart Rate 115 bpm
• Blood Pressure 65/42
• Sats 96% on room air.

The ambulance have given him one litre of Normal Saline and he is on his second Litre.

You make the diagnosis of Septic Shock most likely due to urinary cause and immediately give antibiotics. The second litre of fluids is now in, with no change in blood pressure.. 

Our Approach:

Given that there is no issue with heart rate at the moment, isoprenaline can be removed. We can also assume no cardiac dysfunction, so we can remove inodilators. This leaves us with:

• Adrenaline
• Noradrenaline
• Vassopressin

The drug of choice to start with is NorAdrenaline. Vasopressin may also be used.

CASE 2

In this case we have exactly the same patient as in case 1 with urosepsis, however, the patient has an added history of atrial fibrillation for which he is on Sotalol. At presentation the patient has a heart rate of 28 beats per minute, and it is a junctional rhythm. He also has acute renal failure and potassium of 7.8mmol/l.

How would you treat this patient’s blood pressure and heart rate now?

This was the case of Septic Shock resulting in acute renal failure, which decreased clearance of Sotalol and resulted in the bradycardia.

Our Approach: A first approach may be to start with isoprenaline and see if there is a rapid change in heart rate and thus blood pressure. If improvement in the heart rate occurs, then Noradrenaline may be added if further blood pressure support is needed. An alternative is to simply commence Adrenaline, which will improve both the heart rate and the blood pressure. Beware in the ischaemic patient.

CASE 3

A 65 yo male is brought in by ambulance. He has had chest pain for the previous 3 hours.He is diaphoretic and looks unwell. His BP is 71/50 and he is speaking in single words, with saturations of 90% on a non-rebreather. His chest examination has widespread crepitations.

He has no relevant past medical history.

Hi ECG is shown below:

A probable LAD occlusion is diagnosed and that the patient is in cardiogenic shock. Your hospital doesn’t have a Cath lab and so you decide to thrombolyse. However, you also need to sort out the cardiac failure and the blood pressure.

How would you treat this patients’s cardiogenic shock?

Our Approach: GTN is not an option for managing the ischaemia, due to the cariogenic shock. The patient is placed on CPAP to assist with breathing. The optimal blood pressure management for this patient would have been to start NorAdrenaline and then we could add Dobutamine if needed. Milrinone may be a substitute in patients with known poor ejection fraction ie., known significant heart failure.

CASE 4

A 68 yo patient has been sent to the ED from oncology outpatients, where he was receiving chemotherapy. He has a sinus tachycardia of 132, pleuritic chest pain and a tender right calf and his saturations are 92% on room air. On arrival back into the ED following a CTPA, which confirmed a larger central pulmonary embolism, his heart rate stays at 130bpm, his saturations drop to 88% on 6 L of oxygen and his blood pressure is now 68/36.

How would you treat this patient’s blood pressure now?

Our Approach: This is a patient with hypotension secondary to pulmonary embolism and there would be an expected increase in pulmonary vascular resistance. The performance of the right ventricle may be affected. The definitive treatment is thrombolysis, however if the blood pressure is controlled, anticoagulation is also possible (Read more on Pulmonary Embolism)

We started with intravenous fluids in this patient however, to much fluid can be harmful here, especially if there is a suspected right ventricular dysfunction. Volumes should be limited to 250-500 mL. Remember that fluid does very little when ‘the pipes are blocked’ by a clot.

Noradrenaline is the preferred agent in most cases, primarily as it is effective in increasing the BP, and doesn’t result in tachycardias, as might occur with Adrenaline. It is also less arrhythmogenic. It can result in a small increase in pulmonary vascular resistance, however not as much as Adrenaline. Once Noradrenaline is commenced, if the patient still has hypotension, Dobutamine can be added. Beware to start with noradrenaline, as although Dobutamine increases myocardial contractility, it also has an initial vasodilatory effect and can make hypotension worst if given on its own.

An alternative medication is Vasopressin as it has no effect on pulmonary vascular resistance.

Vasopressor vs Inotrope?

A Vasopressor increases systemic vascular resistance and an Inotrope increases cardiac contractility A third property to consider is that some medications result in Vasodilation. Some of these medications also have potentially significant side effects. Perhaps the most important is a risk of arrhythmias. A second but also very important effect to consider, is the effect on the right ventricle via pulmonary vascular resistance.

I will not be discussing Dopamine as part of these as it is both highly arrhymogenic and increases pulmonary vascular resistance. The medications we will be looking at include:

• Adrenaline
• Noradrenaline
• Dobutamine
• Milrinone
• Isoprenaline
• Vasopressin

α1 = vascular(arterial) smooth muscle

β1 = Heart: Increases rate and force of contraction

β2 = Bronchial Smooth muscle dilatation

INOPRESSORS: Adrenaline and NorAdrenaline

Adrenaline (αβββ)

It is a non-selective adrenergic agonist, that is both a chronotrope and inotrope. It acts on α and β receptors. At low doses, it acts on β2 receptors causing vasodilation. At higher doses its effect are on α1 and β1, resulting in positive inotropy and vasoconstriction (of peripheral vasculature and pulmonary arterial and venous circulation). It’s use is mostly in anaphylaxis and cardiac arrest as other drug combinations have been found to be better for both septic and cariogenic shock.

NorAdrenaline (αααβ)

It acts on vascular α1 adrenergic receptors, causing vasoconstriction and thus increasing systolic and diastolic blood pressures. It has chronotropic effect at high doses. It can cause tachycardia and increase myocardial oxygen demand. It is the first line management of septic shock and may be used with other medications.

INODILATORS: Dobutamine and Milrinone

Dobutamine (αββ)

Dobutamine, a synthetic catecholamine, acts on β1 receptors increasing cardiac contractility. It also has α1 and β1 effects on peripheral vasculature resulting in vasodilatation at lower doses, thus increasing cardiac output. At doses above 5mcg/kg/min it can result in vasoconstriction. It is usually used with an inopressor in cardiogenic shock. Higher doses of dobutamine is not preferred in patients with recent myocardial ischemia, as it can increase myocardial oxygen demand and induce tachycardia.

Milrinone

It is a Phosphodiesterase Type 3 inhibitor(PDE3) used as an inotropic agent in patients with cardiogenic shock. It inhibits PDE3, which results in more calcium ions entering the myocardial cell, increasing cardiac contractility. It also acts on peripheral and pulmonary vasculature leading to vasodilatation as well as inotropic effect. It does not act on the beta adrenergic pathway. Another feature of the mechanism of action of milrinone is that the same intracellular processes is activated in smooth muscle cells of the peripheral and pulmonary vasculature, leading to a net vasodilatory effect in addition to its positive inotropic effect.

In a sub-group analysis of the OPTIME-CHF trial, it was found to increase mortality in patients with heart failure of ischaemic origin.

Isoprenaline (ββββ)

It acts on β1 and β2 receptors and increases heart rate and contractility. It’s main use is in significant heart blocks and bradyarrhythmias.

VASOPRESSOR: Vasopressin

Vasopressin (V1 V2)

Vasopressin acts on V1 and V2 receptors leading to vasoconstriction and increasing systemic vascular resistance. It also acts to increase renal water absorption. It...]]>Cases in Shock: Choosing Inotropes and Vasopressors

How do we choose the right pressor in shock? Below is a brief discussion of pressors and their properties as well as 4 cases, where we choose the pressor to use, with reasoning.

If I were to use one general guide, it is, that unless we need to increase the heart rate, then NorAdrenaline, can be used in nearly all cases. 

Below are 4 cases to think about. Try them and then scroll down and read on the properties of all these medications.

CASE 1

A 68 yo male is brought to your emergency department in what appears to be septic shock. He has had a recent urine infection. Over the last 24 hours he has become quite febrile and lethargic according to his wife. This morning he felt unwell and felt like he was going to collapse each time he tried to get out of bed.

On arrival he is alert and oriented. He feels unwell. His vitals are as follows:

• Temperature 38.9
• Heart Rate 115 bpm
• Blood Pressure 65/42
• Sats 96% on room air.

The ambulance have given him one litre of Normal Saline and he is on his second Litre.

You make the diagnosis of Septic Shock most likely due to urinary cause and immediately give antibiotics. The second litre of fluids is now in, with no change in blood pressure.. 

Our Approach:

Given that there is no issue with heart rate at the moment, isoprenaline can be removed. We can also assume no cardiac dysfunction, so we can remove inodilators. This leaves us with:

• Adrenaline
• Noradrenaline
• Vassopressin

The drug of choice to start with is NorAdrenaline. Vasopressin may also be used.

CASE 2

In this case we have exactly the same patient as in case 1 with urosepsis, however, the patient has an added history of atrial fibrillation for which he is on Sotalol. At presentation the patient has a heart rate of 28 beats per minute, and it is a junctional rhythm. He also has acute renal failure and potassium of 7.8mmol/l.

How would you treat this patient’s blood pressure and heart rate now?

This was the case of Septic Shock resulting in acute renal failure, which decreased clearance of Sotalol and resulted in the bradycardia.

Our Approach: A first approach may be to start with isoprenaline and see if there is a rapid change in heart rate and thus blood pressure. If improvement in the heart rate occurs, then Noradrenaline may be added if further blood pressure support is needed. An alternative is to simply commence Adrenaline, which will improve both the heart rate and the blood pressure. Beware in the ischaemic patient.

CASE 3

A 65 yo male is brought in by ambulance. He has had chest pain for the previous 3 hours.He is diaphoretic and looks unwell. His BP is 71/50 and he is speaking in single words, with saturations of 90% on a non-rebreather. His chest examination has widespread crepitations.

He has no relevant past medical history.

Hi ECG is shown below:

A probable LAD occlusion is diagnosed and that the patient is in cardiogenic shock. Your hospital doesn’t have a Cath lab and so you decide to thrombolyse. However, you also need to sort out the cardiac failure and the blood pressure.

How would you treat this patients’s cardiogenic shock?

Our Approach: GTN is not an option for managing the ischaemia, due to the cariogenic shock. The patient is placed on CPAP to assist with breathing. The optimal blood pressure management for this patient would have been to start NorAdrenaline and then we could add Dobutamine if needed. Milrinone may be a substitute in patients with known poor ejection fraction ie., known significant heart failure.

CASE 4

A 68 yo patient has been sent to the ED from oncology outpatients, where he was receiving chemotherapy. He has a sinus tachycardia of 132, pleuritic chest pain and a tender right calf and his saturations are 92% on room air. On arrival back into the ED following a CTPA, which confirmed a larger central pulmonary embolism, his heart rate stays at 130bpm, his saturations drop to 88% on 6 L of oxygen and his blood pressure is now 68/36.

How would you treat this patient’s blood pressure now?

Our Approach: This is a patient with hypotension secondary to pulmonary embolism and there would be an expected increase in pulmonary vascular resistance. The performance of the right ventricle may be affected. The definitive treatment is thrombolysis, however if the blood pressure is controlled, anticoagulation is also possible (Read more on Pulmonary Embolism)

We started with intravenous fluids in this patient however, to much fluid can be harmful here, especially if there is a suspected right ventricular dysfunction. Volumes should be limited to 250-500 mL. Remember that fluid does very little when ‘the pipes are blocked’ by a clot.

Noradrenaline is the preferred agent in most cases, primarily as it is effective in increasing the BP, and doesn’t result in tachycardias, as might occur with Adrenaline. It is also less arrhythmogenic. It can result in a small increase in pulmonary vascular resistance, however not as much as Adrenaline. Once Noradrenaline is commenced, if the patient still has hypotension, Dobutamine can be added. Beware to start with noradrenaline, as although Dobutamine increases myocardial contractility, it also has an initial vasodilatory effect and can make hypotension worst if given on its own.

An alternative medication is Vasopressin as it has no effect on pulmonary vascular resistance.

Vasopressor vs Inotrope?

A Vasopressor increases systemic vascular resistance and an Inotrope increases cardiac contractility A third property to consider is that some medications result in Vasodilation. Some of these medications also have potentially significant side effects. Perhaps the most important is a risk of arrhythmias. A second but also very important effect to consider, is the effect on the right ventricle via pulmonary vascular resistance.

I will not be discussing Dopamine as part of these as it is both highly arrhymogenic and increases pulmonary vascular resistance. The medications we will be looking at include:

• Adrenaline
• Noradrenaline
• Dobutamine
• Milrinone
• Isoprenaline
• Vasopressin

α1 = vascular(arterial) smooth muscle

β1 = Heart: Increases rate and force of contraction

β2 = Bronchial Smooth muscle dilatation

INOPRESSORS: Adrenaline and NorAdrenaline

Adrenaline (αβββ)

It is a non-selective adrenergic agonist, that is both a chronotrope and inotrope. It acts on α and β receptors. At low doses, it acts on β2 receptors causing vasodilation. At higher doses its effect are on α1 and β1, resulting in positive inotropy and vasoconstriction (of peripheral vasculature and pulmonary arterial and venous circulation). It’s use is mostly in anaphylaxis and cardiac arrest as other drug combinations have been found to be better for both septic and cariogenic shock.

NorAdrenaline (αααβ)

It acts on vascular α1 adrenergic receptors, causing vasoconstriction and thus increasing systolic and diastolic blood pressures. It has chronotropic effect at high doses. It can cause tachycardia and increase myocardial oxygen demand. It is the first line management of septic shock and may be used with other medications.

INODILATORS: Dobutamine and Milrinone

Dobutamine (αββ)

Dobutamine, a synthetic catecholamine, acts on β1 receptors increasing cardiac contractility. It also has α1 and β1 effects on peripheral vasculature resulting in vasodilatation at lower doses, thus increasing cardiac output. At doses above 5mcg/kg/min it can result in vasoconstriction. It is usually used with an inopressor in cardiogenic shock. Higher doses of dobutamine is not preferred in patients with recent myocardial ischemia, as it can increase myocardial oxygen demand and induce tachycardia.

Milrinone

It is a Phosphodiesterase Type 3 inhibitor(PDE3) used as an inotropic agent in patients with cardiogenic shock. It inhibits PDE3, which results in more calcium ions entering the myocardial cell, increasing cardiac contractility. It also acts on peripheral and pulmonary vasculature leading to vasodilatation as well as inotropic effect. It does not act on the beta adrenergic pathway. Another feature of the mechanism of action of milrinone is that the same intracellular processes is activated in smooth muscle cells of the peripheral and pulmonary vasculature, leading to a net vasodilatory effect in addition to its positive inotropic effect.

In a sub-group analysis of the OPTIME-CHF trial, it was found to increase mortality in patients with heart failure of ischaemic origin.

Isoprenaline (ββββ)

It acts on β1 and β2 receptors and increases heart rate and contractility. It’s main use is in significant heart blocks and bradyarrhythmias.

VASOPRESSOR: Vasopressin

Vasopressin (V1 V2)

Vasopressin acts on V1 and V2 receptors leading to vasoconstriction and increasing systemic vascular resistance. It also acts to increase renal water absorption. It may also have an effect on pulmonary vascular dilatation. It is a pure vasopressor and has no inotropic or chronotropic effect.

It has been used in cardiac arrest, but is primarily used in cases where there is shock secondary to vasodilatation, such as in septic shock.

DRUGS + ReceptorsWHEN TO USESIDE EFFECTSADRENALINE

α+++++

β1+++++

β2+++

Cardiac Arrest 

Anaphylaxis

Shock (cardiac/vasodilatory)

Bronchospasm

BradycardiaArrhythmogenic ++

Pulmonary Vascular resistance -/+

NORADRENALINE

α+++++

β1+++

β2++

Shock (cardiac/vasodilatory)Arrhythmogenic +

Pulmonary Vascular resistance +

DOBUTAMINE

α+ 

β1+++++

β2+++

Low cardiac output:

-heart failure

-cardiogenic shock

-sepsis leading to myocardial dysfunctionArrhythmogenic ++

Pulmonary Vascular resistance –

MILRINONE

cAMP

Low cardiac output states in heart failureArrhythmogenic +

Pulmonary Vascular resistance –

ISOPRENALINE

β1+++++

β2++++++

BradycardiasArrhythmogenic +

Pulmonary Vascular resistance nil

VASOPRESSIN

V1 V2

Shock (cardiac and vasodilatory)

V1 V2

References

1. De Baker D et al. Comparison of Dopamine and Norepinephrine in the treatment of shock. N Engl J Med 2010; 362:779-789
2. Levy B, et al. Comparison of norepinephrine-dobutamine to epinephrine for hemodynamics, lactate metabolism, and organ function variables in cardiogenic shock. A prospective, randomized pilot study. Crit Care Med. 2011;39:450–5.
3. Tarvasmaki T, et al. Current real-life use of vasopressors and inotropes in cardiogenic shock – adrenaline use is associated with excess organ injury and mortality. Crit Care. 2016;20:208
4. Felker GM et al. Heart failure etiology and response to milrinone in decompensated heart failure: results from the OPTIME-CHF study. J Am Coll Cardiol. 2003;41:997–1003. 
5. Bistola V et al. Inotropes in Acute Heart Failure: From Guidelines to Practical Use: Therapeutic Options and Clinical Practice. Card Fail Rev. 2019 Nov; 5(3): 133–139
6. Maggioni AP et al. EURObservational Research Programme: the Heart Failure Pilot Survey (ESC-HF Pilot) Eur J Heart Fail. 2010;12:1076–84

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