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Haemodynamics

by Patrick Neligan 1998

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All tutorials located on this site are the property of Patrick Neligan and are for personal study purposes only. They are not peer reviewed and no responsibility is taken for inaccuracies. These tutorials must not be reproduced without permission or used in any other publication.

Contents

1. Clinical Scenarios
2. A primer of Applied Cardiovascular Physiology.
3. Shock: the manifestation of cardiovascular failure.
4. High Output versus low output states.
5. Cardiovascular measurement.
6. How to treat cardiovascular failure.
7. How do you know your treatment is working
8. Solution to clinical scenarios
9. Key points.

A 72 year old female is admitted complaining of weakness, sweating and dysuria. Her temperature is 39⁰C, pulse 130, BP 76/44, warm peripherally, lung fields: reduced air entry bilaterally, oliguria, Hb 16 g/dl, WCC 27, PO2 8.2, MSU gram -ve bacilli, >10⁵ organisms.

What is your diagnosis?

How would you classify this patients haemodynamic status?

How would you manage this patient?

A 56 year old male presents to A&E. He is cold, clammy, dysphoric and complaining of central chest pain. His pulse is 130, blood pressure is 84/50, lung fields: bilateral crackles, a third heart sound is audible. ECG reveals ST segment elevation leads V2 to V4.

What is the diagnosis?

How would you classify this patients haemodynamic status?

How would you manage this patient?

A 79 year old female presents with central abdominal pain radiating through to the back. Background history of hypertension, treated with nifedipne 20 mg bd and enalapril 10 mg mane. She is cold and clammy. ECG normal. Pulse 100. Blood Pressure 100/60. Femoral pulses impalpable. Catheterised: only 10 ml of urine in the bladder. Haemoglobin 6.0.

How would you classify this patients haemodynamic status?

How would you manage this patient?

The same patient undergoes surgery. On day 3 you are called to review her in the ICU. Her urinary output has been less than 30 ml/hr for the last 6 hours. Her creatinine today is 270 (yesterday it was 190, and the previous day it was 80). Her blood pressure is 90/40. You prescribe 500 ml of haemaccel. Two hours later you are called because this has had no response. The nurse suggests renal dose dopamine.

How would you manage this patient?

A 27 year old male is involved in an RTA. He sustains a burst fracture of T2 with complete neurological deficit below this level. Fours hours following admission his SpO2 is 85%, his blood pressure is 80/40 and his heart rate is 45.

How would you classify this patients' haemodynamic status?

How would you manage this patient?

The function of the cardiovascular system is to deliver oxygen to the tissues and to remove waste products, transferring them to the kidneys, liver and lungs.

The cardiovascular system consists of four components:

1. A pump, the heart.
2. An oxygenating system, the alveolar capillary interface.
3. A transport system, the peripheral circulation.
4. A transport solution, the blood.

The cardiovascular system fails if any of these four components fails.

One formula explains the whole of cardiovascular and respiratory intensive care:

The Delivery of oxygen to the tissues is determined by:

The amount of oxygen in the blood: the oxygen binding capacity of haemoglobin x the concentration of haemoglobin x the amount of dissolved oxygen

Multiplied by the Cardiac Output.

Cardiac Output = Heart rate x Stroke Volume

Heart rate is controlled by the autonomic nervous system.

Stroke volume is determined by Preload, Afterload and Contractility;

Preload = end diastolic volume (or wall tension), which is in effect the circulating volume.

Afterload = determined by:

1. The total peripheral resistance (which is determined by the sympathetic tone, baroreceptor activity, the renin-angiotensin-aldosterone axis, and the tissue oncotic pressure), and
2. The systolic wall tension (which follows the:
    law of laplace = TMP x r / 2 h [transmural pressure x radius / 2 x wall thickness]).

Contractility = the ability of the heart to contract independently of preload and afterload. The ejection fraction is SV/EDV, and Starling's law matches these variables and demonstrates contractility.

The starling Concept equates preload with stroke volume.

Stroke volume = EDV-ESV

Ejection fraction = EDV – ESV x 100% / EDV

Contractility is increased by inotropic agents:

Adrenaline / Nor adrenaline
Dobutamine / Dopamine
Calcium

Contractility is decreased by:

Acidosis
Hypoxia
Hypocalcaemia

"Acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in generalized cellular hypoxia."

• Pump
• Fluid
• Tubing

• Acute myocardial infarction
• Acute aortic incompetence
• Ischaemic mitral regurgitation
• LV aneurysm
• Myocardial contusion
• ~ 40% of myocardium damaged leading to  Shock

• Outflow obstruction ->pulmonary embolus
• Inflow obstruction -> Cardiac tamponade

• Exogenous loss  from  haemorrhage
• Endogenous loss -> third space loss & capillary leak syndrome

• A state of relative hypovolaemia (eg. loss blood oncotic pressure).
• Impaired distribution and oxygen utilisation.

Classic examples: septic shock, spinal shock, anaphylactic shock, AV shunting.

The management of shock involves reversal of the physiological abnormalities:

For cardiogenic shock: an inotropic agent with vasodilatory properties, or some other form of afterload reducing agent.

For hypovolaemic shock: volume, preferably replacing what has been lost – crystalloid for free water loss, colloid / rcc for plasma / blood loss.

For spinal shock: for a high spinal injury: an chronotropic agent with vasoconstrictive properties. For a lower injury a vasoconstrictor.

For septic shock: an inotrope and mild vasoconstrictor

All circulatory failure thus does not involve low cardiac output or, indeed myocardial dysfunction. A good rule of thumb follows:

1. Coronary care type patients have primary myocardial dysfunction: they shut down in response to an insult and become cold and clammy. Low cardiac output high SVR (systemic vascular resistance). There is usually signs of cardiac dysfunction eg. ECG findings.
2. Intensive care patients usually have peripheral circulatory failure, with varying degrees of myocardial dysfunction. They are usually hot and sweaty. High cardiac output, low SVR. There is usually additional signs of sepsis – high temperature, high WCC, CXR infiltrates, coagulopathy etc.

It is essential to identify whether the patient’s hypotension is due to a high or a low output state. There is often, but not always, obvious on physical examination and deductive reasoning.

However, in, for example, a patient post cardiac surgery with low blood pressure and poor urinary output, the answer may nor be so obvious.

Certain monitoring procedures may be useful:

• Invasive BP monitoring
• Pulse Oximetery
• Central venous pressure
• Pulmonary Artery Catheterisation
• Transoesophageal echocardiography

1. The presence of a low CVP and low systemic blood pressure is strongly suggestive of relative or absolute hypovolaemia. The treatment is fluid loading.
2. The presence of a normal CVP in the presence of hypotension is suggestive of peripheral circulatory failure. The treatment is inotropes / inoconstrictors.
3. The presence of a high CVP in the presence of a low blood pressure is suggestive of congestive heart failure, right ventricular infarction, constrictive pericarditis or cardiac tamponade.

However, the CVP only tells you what the right heart filling pressures are like in the right side of the heart. It only suggests preload. It tells you nothing about myocardial function: ie. High CVP caused by constrictive pericarditis, the myocardium may be normal. Using the CVP alone gives you only a "best guess" idea of the function of the left side of the heart. All bets are off if the patient has significant coronary heart disease or a previous MI. CVP monitoring gives you no idea of cardiac output or systemic vascular resistance.

If you want to measure cardiac output and left sided pressures you need to canulate the left side of the heart. Direct canulation is not feasible. However if a balloon tipped catheter is "floated" into the pulmonary artery. This measures PA pressure. If the balloon is advanced, inflated, into to the artery until it jams into the distal blood vessel, occluding it, the pulmonary artery occlusion (Wedge) pressure is measured. The theory is that a direct column of blood is formed between the left atrium and this point, and therefore you’re measuring the left atrial pressure. From this you can infer the LVEDV and preload. This assumes that the patient does not have mitral stenosis, mitral regurgitation, tricuspid regurgitation or an atrial myxoma.

The cardiac output can also be measured using a PA (Swan Ganz) catheter. This can be performed intermittantly using a thermodilution technique (cold saline is injected into the right side of the heart and the temperature is measured on the left side, the decrease in blood temp allows calculation of the CO / Ci). More modern continuous cardiac output monitors are available now, which include a heated filament on the PA catheter; the calculation are made in a similar way. Systemic vascular resistance is calculated using the formula: MAP – CVP x 90 / CO

The problem with PA catheters is that the have a hefty number of associated complications: rupture of the heart or pulmonary artery, arrhythmias, infection etc. Moreover, nobody has ever proved that PA catheters make any difference to patients’ outcome.

 In fact Conors, in a landmark study in JAMA December 1996, demonstrated a higher mortality rate in septic patients who were "swanned" than in those who weren’t. Consequently there has been a movement away from using PA catheters in septic patients. The device retains common usage in cardiac anaesthesia.

Transoesophageal Echocardiography (anything you can do!)

Transoesophageal echo is capable of estimating Cardiac output, ejection fractions, regional wall motion abnormalities (acute ischaemia), filling pressures, diagnosing pulmonary emboli, dissecting aneurysms, demonstrating regurgitant valves e.t.c. It can do anything a PA catheter can do except measure mixed venous oxygen saturations.

Only problem: it takes years to learn how to use TOE.

• Fluids
• Inotropes
• Vasoconstrictors
• Vasodilators

Crystalloids: Hartmanns solution, Normal saline

Colloids: Haemaccel, Gelofusin, Hetastarch, Dextran 40 & 70, Albumin 5% & 20%, frozen plasma and Red cell concentrate.

"Horses for Courses" - what drug to use when:

There are very few clinical endpoints of value:

1. Improved blood pressure.

2. Improved thermoregulation (cardiogenic warms up, septic cools down).

3. Improved urinary flow.

4. Improved PaO2.

5. Reduced base deficit and lactate.

6. Shift of mixed venous O² concentration towards normal.

7. Improved gastric mucosal pH (ie. Less acidic).

8. The core-peripheral temperature gradient narrows.

9. Cardiac index / output returns to normal.

10. The patient "looks better".

• Vaso vagal attacks
• Pulmonary infarction
• Cardiac tamponade
• "Flash pulmonary oedema".
• Anaphylaxis.
• Other drug effects (sedatives decrease blood pressure), vancomycin.
• Liver failure.

A 72 year old female is admitted complaining of weakness, sweating and dysuria. Her temperature is 39⁰C, pulse 130, BP 76/44, warm peripherally, lung fields: reduced air entry bilaterally, oliguria, Hb 16 g/dl, WCC 27, PO2 8.2, MSU gram -ve bacilli, >10⁵ organisms.

A 56 year old male presents to A&E. He is cold, clammy, dysphoric and complaining of central chest pain. His pulse is 130, blood pressure is 84/50, lung fields: bilateral crackles, a third heart sound is audible. ECG reveals ST segment elevation leads V2 to V4.

1. Oxygen therapy, minimal 40%

2. Intavenous morphine.

3. Aspirin 300mg to chew.

4. Dobutamine infusion.

5. Thrombolysis if appropriate.

A 79 year old female presents with central abdominal pain radiating through to the back. Background history of hypertension, treated with nifedipne 20 mg bd and enalapril 10 mg mane. She is cold and clammy. ECG normal. Pulse 100. Blood Pressure 100/60. Femoral pulses impalpable. Catheterised: only 10 ml of urine in the bladder. Haemoglobin 6.0.

The same patient undergoes surgery. On day 3 you are called to review her in the ICU. Her urinary output has been less than 30 ml/hr for the last 6 hours. Her creatinine today is 270 (yesterday it was 190, and the previous day it was 80). Her blood pressure is 90/40. You prescribe 500 ml of haemaccel. Two hours later you are called because this has had no response. The nurse suggests renal dose dopamine.

A 27 year old male is involved in an RTA. He sustains a burst fracture of T2 with complete neurological deficit below this level. Fours hours following admission his SpO2 is 85%, his blood pressure is 80/40 and his heart rate is 45.

1. Delivering oxygen to the tissues is the prime objective of cardiovascular ICM:

2. Cardiac output depends on preload, afterload and contractility.

3. Cardiovascular interventions manipulate these factors.

4. There are 4 types of shock: cardiogenic, obstructive, hypovolaemic and distributive.

5. Each of these has a different haemodynamic profile and consequently a different management strategy.

6. The prime objective of any of these strategies is to return blood pressure to baseline, and maintain tissue perfusion and oxygenation.

7. Dobutamine is the drug of first choice in most coronary care scenarios, adrenaline is the drug of choice in ICU scenarios.

8. The degree of illness determines the amount of invasive monitors placed. CVP monitoring can be misleading. PA catheters may not influence outcome.

9. By and large simple clinical observations are the most effective ways of assessing response to treatment. Invasive monitoring such as lactate, mvO2, and pHi are neither sensitive nor specific.

10. Regardless of the cause of shock, follow your ABCs, and that means Airway and ventilation come first.

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