Swan Ganz Catheters - A Learning Guide.

I am a Sister working at the Royal Liverpool University Hospital Intensive Care Unit. which is a large ITU that admits around 485 patients per year. There is a very wide spectrum of pathology provided by the medical and surgical patients admitted from both within and outside the hospital.

In recent years the development of arterial pulse contour cardiac output and trans pulmonary thermodilution (PiCCO)
has meant there has been a decline in the use of pulmonary artery catheters,  however it is still important to understand the principles of Swan Ganz Catheters
.  


The information on this site has been provided by:

Sr. Lorraine Burgess - Nurse Audit Lead, Joint Nurse Lead for the Cheshire and Merseyside Critical Care Network

Sr. Andrea Fazakerley - Critical Care Outreach Educator

Dr. Richard Wenstone - Consultant Intensivist

Contact Author  (Please let me know your comments, is the page useful? What do you do in your hospital?)     

 Down load this website Click Here

Introduction

Back to Basics

History                                                                                          

What is a "Wedge"?

How ? Care of the patient

Why ? Shock – signs and symptoms

Cardiac Output Measurement using Thermodilution

When ? Titration of vaos active drugs, diagnostic.

Cardiac Output Studies - An Expanded Role

PiCCO Information


 

Introduction

Looking after a patient with a pulmonary artery catheter (PA) is probably "the" most daunting experience for a nurse new to ITU. Yet those more experienced staff can do the job of caring for these patients easily and with little apparent stress, it becomes second nature a bit like driving a car. However there is never room for complacency complications are rare but they happen and they can be fatal so it is important to reinforce to both new and experienced staff the rationale for their actions so that hopefully at the end of this learning guide all staff will feel happier and more confident in caring for these patients.

We will be revisiting some old favorites like A&P, nursing care and do’s and don’ts.  

 

Back To Basics

Cardiac output is the rate which the heart pumps blood, often defined as: The volume of blood pumped out of the left ventricle into the aorta in one minute." This is calculated by multiplying the Stroke volume (the volume of blood pumped out with each contraction) by the heart rate.

Therefore Cardiac output (CO) = Stroke volume (SV) x heart rate (HR)

For example an adult at rest has a heart rate of about 72 beats/min and a stroke volume of 70mls therefore CO = 72 x 70 = 5 litres per minute.

At rest normal cardiac output is about 5 litres per minute.

This can increase to 25 litres/min during exercise or 35 litres for an athlete. When an increased cardiac output is needed to supply other organs e.g. the gut during digestion or muscles during exercise it is achieved by increasing the heart rate or the stroke volume.

The mechanisms by which the HR & SV can be altered.

A. Control of the Heart.

In the absence of nervous or hormonal control the sinoatrial node discharges spontaneously and rhythmically @ 100 beats per minute

Factors altering the heart rate: -

1. Nervous:

Most important is the influence of the autonomic nervous system. The heart is supplied by both the sympathetic and parasympathetic nerves.

Sympathetic nerves to the heart originate in the cardiovascular centre (group of neurones within the medulla) these affect the SA node, AV node and portions of the myocardium. Stimulation causes an increase in heart rate.

Parasympathetic nerves to the heart (vagus nerve) also originates in the medulla. This affects SA node And AV node. Stimulation causes decrease in the heart rate.

At rest HR is usually 60 to 80 / minute. This is rather less than the inherent rate of the discharge of the cardiac pacemaker (SA node) Therefore at rest the parasympathetic influence is dominant.

Primarily the heart rate is regulated by the slowing effects of the parasympathetic and the accelerating effects of the sympathetic.

2. Hormonal

Adrenaline (released from the adrenal medulla) causes increase in heart rate by stimulating the b receptors in the cardiac muscle conduction system.

3. Stretch

The stretching of the left atrium wall by increased venous return causes increase in heart rate by 10 to 15 % because stretch receptors in the atrial wall/superior vena cava and the inferior venacava send impulses that stimulate sympathetic output this is called the Bainbridge Reflex.

4. Temperature.

Rise in temperature causes increase in HR because it increases the rate of discharge from the SA node. Converse also applies.

5. Drugs.

To increase the HR - Isoprenaline / Adrenaline.

To reduce to HR - Beta-blockers e.g. propanolol.

The HR is also sensitive to plasma electrolyte concentrations and hormones other than adrenaline.

The heart rate is usually faster in females and declines with age.

B Control of Stroke Volume.

In the normal heart the most important factor that controls the amount of blood pumped from a ventricle with each heart beat (Stroke Volume) is the amount of blood in the ventricle immediately before contraction. This is called the ventricular end diastolic volume. V.E.D.V.

The more blood in the ventricles the greater the amount pumped -Starlings Law: The force of the muscle contraction is proportional to the initial muscle fibre length (i.e. Stretch).

 

1 Venous Return.

The force of contraction adjusts according to the volume of blood in the ventricles this is called auto regulation.

Blood volume: - reduced circulating volume e.g. Due to bleeding leads to reduced venous return.

The position of the person e.g. Trendelenburg, will increase venous return.

Intrathoracic pressures caused by I.P.P.V. Will reduce venous return.

2. Nervous.

Sympathetic nervous stimulation increases ventricular and atrial contractility.

Normally when the ventricles contract they do not empty completely. When contractility improves, the ventricles empty more completely therefore increasing SV.

Sympathetic stimulation not only causes a more forceful contraction but also a more rapid contraction. This is important when an increase in HR reduces the time available for diastolic filling of the ventricles; because if contraction can be made more rapid there will be a larger fraction of the cardiac cycle available for filling, and coronary blood flow during diastole.

 

 

Drugs affecting contractility.

Inotropic drugs.

Those increasing contractility are called positive e.g. dobutamine and adrenaline

Those decreasing contractility are called negative inotropes e.g. b blockers.

3 Hormonal Regulation: - Circulating catecholamines, adrenaline & noradrenaline produce changes in myocardial contraction (and hence in S.V.)

4 Arterial Blood Pressure: - An increase in the resistance to the ejection of blood from the ventricles can reduce the S.V. This is caused by the ability of the large arteries to expand and contract. This is called Afterload. Arterial blood pressure gives an indication of the degree of afterload.

If the B.P. is high and the force of contraction is constant then the ventricles will not empty as much and S.V. will be reduced.

In a normal heart changes in blood pressure do not affect the overall cardiac output as the heart can self adjust.

Drugs that can reduce afterload are nitrates like Isoket.

Summary: - A normal functioning heart will pump out all of the blood that is returned to it from the veins. Therefore venous return is the prime factor in determining cardiac output, and vice versa.

 

Basic principles of fluids, pressure, flow & resistance.

 

All fluids when in a confined space exert a pressure.

Hydrostatic pressure refers to the force that a fluids exerts against the walls of it’s container.

The pressure that blood exerts in the vascular system is called: -

Blood Pressure

BP Is the result of blood flow and vascular resistance.

Blood Flow: - The circulation is a closed system therefore total flow leaving the heart must equal the total flow returning to the heart - This blood flow equals cardiac output.

Blood pressure = cardiac output X total peripheral resistance

B.P. Can be maintained or altered by manipulation of cardiac output and or total peripheral resistance.

Systolic pressure: - is determined by the amount of blood being forced into the aorta or arteries with each ventricular contraction i.e. The S.V. and the force of the contraction. Increase in either will raise systolic pressure and vice versa. Also increase in afterload caused by vascular disease will also raise systolic pressure. In old age the vascular tree is more rigid so systolic hypertension is common.

Diastolic pressure: - This reflects peripheral resistance.

If there is vasoconstriction the diastolic will rise.

If there is vasodilation the diastolic will fall.

Drugs to vasodilate e.g. hydralazine will lower diastolic pressure.

If the heart rate falls then the diastolic will fall as there is an increased time for the blood to flow out of the arteries (& vice versa)

The difference between the systolic and diastolic is called the Pulse Pressure.

Mean Arterial Pressure:- This represents the pressure driving blood through the systemic circulation. This is estimated by adding 1/3 of the pulse pressure to the diastolic pressure.

If BP = 120/70mmHg Then Pulse pressure = 50 mmHg

1/3 of 50 = 17

Add 17 to the diastolic of 70 = 87

Therefore M.A.P. = 87mmHg.

Glossary

Afterload = The resistance of the ejection of blood offered by the systemic circulation

Cardiac Output = The amount of blood ejected by the left ventricle in one minute

Contractility = The ability of myocardial cells to contract (shorten) in response to an electrical impulse.

Oxygen consumption = The amount of oxygen used by the tissues in one minute.

Oxygen delivery = The amount of oxygen delivered to the tissues in one minute.

Preload = Ventricular end diastolic pressure

Pulmonary capillary wedge pressure = Reflects left ventricular end diastolic pressure

Stroke volume = Volume of blood ejected per ventricular contraction.

Systemic vascular resistance = MAP - CVP X 80 CO

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A Bit of History

 

The pulmonary artery flotation catheter.

During the late 60’s and early 70’s Drs H.J.C. Swan and William Ganz developed a balloon tipped flotation catheter. The function of the catheter was to be able to continuously measure at the bedside certain intracardiac pressures. Before this the patient would have to have been transferred to a cardiac catheterization lab; and then only intermittent measurements would be obtained.

By floating a flexible catheter into the pulmonary artery and using a balloon to occlude it then indirect measurements can made of the pressure in the left ventricle.

Since the initial design there have been many modifications so that now we are able to continuously measure cardiac output and venous oxygen saturation, as well as infuse drugs and measure right sided heart pressure.

Incidentally the first Swan Ganz catheter to be inserted in this country was done in a Liverpool Hospital !!

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What is a Wedge?

 

Pulmonary Artery Wedge Pressure:- When the tip of the Swan is properly positioned in the PA, a wedge pressure can be obtained. By inflating the balloon the tip will "float" into a smaller branch of the PA and occlude forward flow. When this occurs there is an unrestricted vascular chamber from the pulmonary artery through the pulmonary vascular system, the pulmonary vein, the left atrium, the open mitral valve and the left ventricle. therefore the theory is, the pressure in front of the occluded catheter tip is the same as the pressure in the left ventricle during diastole (because this is the time when all of the valves are open and the heart is filling with blood)

 

Nursing responsibilities during insertion of a Swan Ganz Catheter.

1. Ensure the comfort of the patient

2. Make sure the transducer is flushed and re zeroed and ready to read P.A.

3. Observe the monitor for signs of dysrhythmias

4. Observe the waveforms as the catheter passes through the different chambers of the heart

Nursing Care :-

Nursing care of the patient with a "Swan" is complex, the nurse must be able to interpret the data obtained as well as being able to alert medical staff of potential or actual complications.

1. Prevention of infection is paramount

2. The position of the tip may change forward migration will be indicated by a wedge trace with a deflated balloon spontaneous wedging, this may cause pulmonary infarction. Notify a doctor to reposition the catheter.

3. Over inflation of the balloon may cause the PA to rupture, prolonged inflation may result in pulmonary infarction and insertion of air into a ruptured balloon could cause an air embolus.

4. Inflation of the balloon should be done slowly while observing the pressure tracing on the monitor. When the pressure changes from PA to Wedge no more air should be inserted. There should be a slight resistance felt, if there is no resistance and a wedge trace can not be obtained then a balloon rupture should be suspected. The syringe should be therefore labeled as ruptured and medical staff informed.

5. After wedging the catheter always make sure the monitor returns to a PA trace.

The clinical information obtained from invasive pressure monitoring is truly beneficial in the care of the critically ill patient. The role of the nurse in the prevention and detection of complications is pivotal.

Nursing management of these patients does not begin and end with writing numbers on a chart the psychological care of the patient and their families is very important, they will ask questions want to know what you are doing and what all of the numbers mean .So you need to confident in your ability to explain to them what, why and when !!!! In a way they will understand.

 

 

CHARACTERISTIC INTRACARDIAC PRESSURE WAVEFORMS DURING THE INSERTION OF A SWAN GANZ CATHETER.

 

 

 

 

Site

Pressure (mmHg)

Right atrium Mean

0-7

Right Ventricle

Systolic

End diastolic

15-25

0-8

Pulmonary artery

Systolic

Diastolic

Mean

15-25

8-15

10-20

Pulmonary Artery Wedge

Mean

6-12

 

 

These are "Normal" Intra cardiac pressures for a spontaneously breathing patient (a bit rare in I.T.U.!!!)

Remember to add 5 mmHg plus PEEP for ventilated patients.

 

 

Troubleshooting guide !!!

 

Problem

Possible cause

Nursing actions

Rationale

Damped pressure trace:

Shows as low amplitude tracing (low systolic/high diastolic pressure)

Clot occluding catheter

 

 

 

 

 

 

 

 

 

Catheter kinked touching the vessel wall, or malpositioned

 

 

Air in the system

Blood on the transducer

 

Equipment fault/error

Check patency by aspirating: continue until blood flows back easily then flush. If no blood can be aspirated do NOT flush.

 

 

 

 

 

 

Ask the patient to cough deflate the balloon and gently flush may need medical staff to reposition. Check X ray

 

Check flush bag and obturators for bubbles

Flush the system check the pressure bag

Check taps are open correctly and that settings on the monitor are correct

Risk of pulmonary emboli. All clots should be cleared. Risk is minimized by use of a constant flushing system and use of a heparinised solution. An occluded catheter should be removed.

Coughing and flushing may help displace the catheter

 

 

Air will distort readings

Blood on the transducer will distort readings

Methodical checking can be very revealing!

Wedge pressure unobtainable

Monitoring problem

Balloon over/under inflated

 



Balloon rupture

 

Catheter displaced

 

 

Monitor may be still set on Zero

Contact technician

Deflate balloon and reinflate

 

 

 

No resistance to inflation. Do NOT inject

Inform medical staff to reposition


Check settings


Over inflation may cause vessel damage or balloon rupture. Risk of air embolus

Risk of air embolus

Catheter may require repositioning or replacing

Sudden changes in pressures or configuration

Patient in pain or agitated.

 

 

Transducer not at correct level.

Catheter displaced spontaneous wedging

 

Ensure adequate sedation or analgesia reassure patient to ally anxiety

 

Re Zero

 

Inform medical staff to reposition

Pressures may rise in response to pain

 

Should be done regularly

Risk of pulmonary infarction

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Why!?

Most I.T.U. patients will probably have a P.A. catheter inserted at some point during their stay. The main reason being cardiovascular instability due to shock of one kind or another.

So what is Shock?

DEFINITION :- Inadequate delivery of oxygen to the tissues.

" A syndrome characterized by a reduction in blood flow and inadequate perfusion, leading to tissue hypoxia and failure of cell function"

There are five types of shock:-

ANAPHYLACTIC

HYPOVOLAEMIC

NEUROGENIC

CARDIOGENIC

SEPTIC

Hypovolaemic Shock.

Caused by a reduction in circulating volume. The body can cope with a loss of 10 to 15 %.

Causes:-

HAEMORRHAGE

DEHYDRATION

BURNS

ASCITES, PERITONITIS

EXCESSIVE DIURESIS

Clinical Features

HYPOTENSION

TACHYCARDIA

SWEATING COLD AND CLAMMY

OLIGURIA

REDUCED L.O.C.

TACHYPNOEA

CYANOSIS

HYPOTHERMIA

DYSRHYTHMIAS

THIRST

N & V

Hypotension :- Reduced venous return - reduced SV - reduced CO - Hypotension.

Tachycardia :- Reduced BP reduced stimulation of the carotid baroreceptors - increased sympathetic activity of the cardiovascular centre in the brain - increase in HR.

Sweating Cold and Clammy:-  sympathetic stimulation leads to peripheral vaso constriction (stimulation of alpha receptors) also causes stimulation of sweat glands.

Oliguria:-Vasoconstriction  reduced renal blood flow therefore reduced filtration and reduced urine output. Rennin is released ( Quick reminder of the renin angiotensin pathway-)

Renin - enzyme that splits angiotensinogen into angiotensin I Angiotensin I is converted into Angiotensin II under the influence of A.C.E. Angiotensin II causes the secretion of aldosterone from the adrenal gland allowing Na and water to be retained to increase circulating volume, further reducing urine output.

In response to stimulation of osmo and volume receptors A.D.H. is released this allows more water to be retained by increasing the permeability of the distal tubules.

Reduced L.O.C:- Confusion caused by cerebral hypoxia.

Tachypnoea :- Reduced oxygen to the cells - anaerobic metabolism- increase in lactic acid production - lactic acidosis. Central chemoreceptors sense the increase in hydrogen ions therefore stimulates the respiratory centre in the brain to increase the respiratory rate in order to "blow off" excess hydrogen H+ HCO3 ~ H2CO3 ~ H2O + CO2

Reduced oxygen level in the blood also stimulates the resp. Centre to increase rate.

Cyanosis:- Reduced peripheral oxygen. Increased amounts of reduced haemoglobin of more than 5g/dl = blue.

Hypothermia:- Anaerobic metabolism does not create much heat therefore leading to reduction of core body temperature.

Dysrhythmia Kidneys retain potassium to excrete hydrogen. Hyperkalaemia causes Dysrhythmia .Reduced coronary artery blood flow leads to ischaemia. Lactic acid is also cardiotoxic.

Thirst:-It is thought that osmoreceptors and A.D.H. production stimulates the "thirst " centre in the brain.

N&V:- Due to reduced blood flow to the G.I.T. Causing  G.I.T.ischaemia,  this could also lead to stress ulceration. Acidosis also makes one feel nauseous.

This list is not exhaustible and some of the reasons may be debatable.

In our ITU we tend to see three of the main causes of shock that require invasive haemodynamic monitoring, so we will look at these in a little more detail.

Management of Hypovolaemic shock:-

Oxygenation - Main problem is that of hypoxaemia therefore 100% oxygen is needed and early I.P.P.V. Should be considered. Although I.P.P.V. May worsen hypotension due to the increase in intrathoracic pressure causing a reduced venous return.

Fluids - ­ circulating volume, replace lost fluids, good I.V. access is needed use of H.A.S. and

Blood. Stop further loss of fluid e.g. Go to theatre if A.A.A.

 

Monitoring - Arterial line, C.V.P. E.C.G. Urine output, pulse oxymeter blood gases, monitor L.O.C.

Once fluid level is optimum may need inotropes.

Treat underlying cause.

Complications:-

i. Renal failure:- acute tubular necrosis (A.T.N.)

ii. A.R.D.S.

iii. Heart failure / dysrhythmias due to ¯ cardiac output

iv. G.I.T. Ischaemia - stress ulceration

v. Liver failure ¯ detoxification and ¯ clotting

vi. D.I.C.

Cardiogenic Shock:- End stage of heart failure, Shock due to dysfunction of the heart and pump failure.

Causes:-

v M.I.

v Tamponade

v Myopathy

v Arrhythmia

v Following cardiac surgery e.g. Heart transplant

v Chest trauma

v Mitral and Aortic regurgitation

v Infection

Treatment:- prognosis is very poor. Mortality of 80 - 90%. Try to treat the underlying cause to prevent shock from occurring.

Swan Ganz Catheter:- To monitor the effect of inotropes and fluid therapy. Use of nitrates to ¯ afterload and hopefully increase cardiac output. Less resistance in the aorta allows for a bigger to S.V. To occur.

Intra Aortic Balloon Pump (I.A.B.P.):- Inflates at the start of diastole and forces blood into the coronary artery system. During systole it deflates and the sudden drop in pressure reduces afterload and allows for a larger stroke volume.

Surgery:- to remove the underlying cause e.g. Emergency C.A.B.G. Aneurysm repair etc.

 

 

SEPTIC SHOCK.

In a previously fit and well person "septic" shock has a mortality rate of 50% which is even higher if there is a significant existing morbidity

Clinical features:- Septic shock occurs in two distinct but overlapping phases.

Warm Shock (hyperdynamic):- This is the first stage of septic shock and is characterised by a high cardiac output and a low vascular resistance. Vasodilation causes a relatively reduced circulating volume together with an increased capillary permeability, results in a rapid hypotension despite a high cardiac output. Fever and chills may develop as an immune system response and urine output may fall. However if compensating mechanisms are present then it may be difficult to first see the potential danger as the patient looks well perfused . An increase in circulating catecholamines causing blood pressure to be normalised.

Cold Shock (hypodynamic):- This is a late presentation and often irreversible phase of septic shock. It is characterised by vasoconstriction, hypotension, hypoperfusion decreased venous return and decreased cardiac output. The symptoms may include:-

A rapid thready pulse

Cold clammy skin

Subnormal or elevated temperature

Depressed level of consciousness

Eventually patients with cold shock develop multiple system failure e.g. A.R.D.S., D.I.C., liver and kidney failure.

A comprehensive description of the pathophysiology of septic shock is beyond the scope of this guide - as there is still debate, discussion and research being done in this complex field.

What we can say is that the events that lead from sepsis to full blown septic shock are probably initiated by the presence of a large number of bacteria , which have not been controlled by the immune response.

The problems are caused by endotoxins that are released when the bacteria are destroyed and the cell membranes are broken down

Endotoxins stimulate the release of various vaso active substances:- including histamine and prostaglandin. These potent vasodilators cause a decrease in peripheral vascular resistance and an increase in capillary permeability, allowing fluid to enter the interstitial spaces from the intravascular spaces resulting in volume depletion and relative hypovolaemia.

 

 

Management:-

1. Identify and treat the underlying cause. The patient may need U.S.S., C.T., B.A.L. Blood cultures, surgery or a line change. In an ideal world antibiotics should not be started until a sensitivity is obtained. Practically cultures are sent than blind antibiotics are commenced

2. Oxygen therapy usually I.P.P.V. A.R.D.S. is a common complication of this condition patients have a high oxygen requirement and there are bilateral lung field infiltrates on the chest X Ray that look like pulmonary oedema however a normal P.A.O.P. indicates a non cardiogenic cause

3. Invasive monitoring using a Swan Ganz catheter.

4. Replace circulating volume using colloids other clotting factors and blood may be needed.

5. Inotropes to increase vascular resistance and blood pressure. These can be titrated according to cardiac output measurements.

6. Support of failed renal system with H.D./H.F.

7. Psychological care of the patient and family. The patient may be very anxious if he is not already sedated and families need a lot of reassurance and explanation of current treatment and progress or deterioration.

8. Good life insurance!!!!!!

We have established our "basics" now we will look at how the P.A. Catheter can help make accurate diagnosis’ and enable the titration of vaso active drugs.

 

Cardiac Output Measurement Using The Thermodilution Method.

In the early 1950’s , Fegler first described measuring cardiac output using the thermodilution method. It was not until the early 1970’s that Drs Swan and Ganz demonstrated reliability of this technique with a special temperature sensing pulmonary artery catheter. Since that time the thermodilution method has become the standard for clinical practice.

The thermodilution method uses a known amount of solution (10 mls of 5% dextrose) at a known temperature (room air) which is then rapidly injected into the C.V.P. Lumen of the Swan. This cooler solution mixes with and cools the blood, and the temperature is measured downstream by a thermistor bead embedded in the tip of the catheter. The resultant change in temperature is then plotted on a time-temperature curve.

A normal curve will characteristically show a sharp upstroke from the rapid injection followed by a smooth downslope back to the baseline. The area under the curve is inversely proportional to the cardiac output. The computer in the monitor uses an equation to make the exact calculation. Usually several measurements are made and an average result taken.

There are conditions where the thermodilution method may produce unreliable results for example those that have a back flow of blood on the right side; tricuspid or pulmonary valve regurgitation and ventricular or atrial septal defects.

Direct Measurements:-

v Heart Rate

v Blood Pressure

v Pulmonary Artery Pressure

v Central Venous Pressure

v Cardiac Output

 

Derived Parameters:-

v Mean Arterial Pressure

v Cardiac Index

v Stroke Volume

v Systemic Vascular Resistance

v Pulmonary Vascular Resistance

v Stroke Work Index

Cardiac Index

Cardiac Output

205 – 4.2 L/min/m2

4 – 8 L/min

Heart Rate

70 – 120 beats/min

Mean Arterial Pressure

70 – 90 mmHg

Mean pulmonary artery pressure

< 30 mmHg

Right Atrial pressure (CVP)

12 – 20 mmHg

Pulmonary artery wedge pressure

12 – 20 mmHg

Systemic vascular resistance (SVR)

900 – 1600 dyne/sec/cm5

Pulmonary vascular resistance (PVR)

20 – 120 dyne/sec/cm5

SvO2

70 – 75%

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Inotropes.

 

General Principles:-

i. Defence of blood pressure in critically ill patients forms the basis of haemodynamic resuscitation and organ perfusion.

ii. Hypovolaemia is the most common cause of hypotension and low cardiac output in critically ill patients and must be assiduously monitored and corrected.

iii. The main indication for inotropes is to increase myocardial contractility for a given preload or afterload. Unresponsive to fluid replacement therapy.

iv. MAP and CO should be interpreted within the context of the pre morbid state.

v. The use of inotropes in anything other than tiny doses require invasive monitoring with an arterial line and a PA catheter.

vi. Inotropes primarily increase cardiac output and MAP however all of these agents have variable effects on heart rate and vascular resistance which are neither predictable nor constant.

vii. No single drug or combination have been proved to be superior to another.

 

 

Mechanism of different Inotropes.

Digitalis Glycosides:- Inhibits Na+ and K= pump and causes impaired transport of Na+ and K+ out of the cardiac cell.

This leads to a rise in intracellular Na+

Na+ is exchanged for Ca++

Increases intracellular Ca++ leads to

Increased contractility.

Catecholamines:-( dopamine, noradrenaline, and adrenaline) Stimulate sympathetic receptors

(different doses of these drugs affect receptors in different ways however in low doses β effects dominate) Stimulation of β1 receptors results in Increased contractility.

Phosphodiesterase inhibitors:-( e.g. Enoximone) Phosphodiesterase is an enzyme that converts active cAMP into inactive cAMP. By inhibiting this reaction there is an Increase in intracellular active cAMP which allows for a greater influx of Ca++ . As we know increased intracellular Ca++ causes Increased contractility.

 

 

β1 effects:-

Increase contractility (inotropy)

Increase heart rate (chronotropy)

β2 effects:-

Increase inotropy

Vasodilation

Bronchodilation

α1 effects:-

Increase inotropy

α2 effects

Increase inotropy

Vasoconstriction

 

 

Agent

Infusion dose

Uses

Adrenaline

β effects @ low doses

α effects @ high doses

6 mg in 100mls of 5% dextrose

ml/hr = mcg/min

Resuscitation

Severe sepsis

Cardiogenic shock

Acute asthma

Anaphylaxis

Maintenance of cerebral perfusion pressure

Medical pacing

Noradrenaline

α effects at high doses

6mg in 100ml of 5% dextrose

ml/hr = mcg/min

Vasodilated states e.g. septic shock

Dopamine

α & β effects

400mg in 100 mls of 0.9% Na+Cl or 5% dextrose

ml/hr = mcg/kg/min

No advantage over Adrenaline or noradrenaline "Renal dose" is no longer advocated

Dobutamine

β effects mild α 2 effects

1 gram in 250 mls 0.9% Na+Cl or 5% dextrose

Primarily a vaso dilator with weak Inotropic action. Traditionally used in cardiogenic shock in low output high afterload states

 

Enoximone

100 mg diluted up to 50 mls with saline = 2 mg/ml

Cardiogenic shock due to Pump failure and high afterload


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