Contents

 

A & P Back to Basics

Page 2

Principles of Haemodynamic Monitoring

 

Page 7

Shock

Page 11

Pulmonary Artery Flotation Catheters - Swans

 

Page17

Principles of Inotropes

Page 24

PiCCO

Page 37

 

Introduction

 

I Hope you find this booklet valuable and are able to use it for your own reference or when teaching others.

More information is accessible through my website at:

 

http://www.rocket.pwp.blueyonder.co.uk/

 

Please feel free to contact me through the “E Mail” link on the website or directly on the ITU on Ext 2400 if you have any problems or queries.

 

Lorraine

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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.

 

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

w 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 ¯ 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 

 

 

 

Principles of haemodynamic monitoring

 

 

Haemodynamic monitoring refers to the monitoring of blood flow and pressure within the cardiovascular system. Indirect monitoring usually suggests a non invasive method of assessment i.e. a manual BP recording with a sphygmomanometer. Direct or invasive monitoring involves cannulating the patient and allows the continuous and ongoing assessment of critical pressures associated with cardiovascular function. In short Direct monitoring provides the most accurate physiological data in the I.C.U.

 

For monitoring purposes in the ICU three components are needed:-

 

1. A catheter or cannula of some kind

 

2. A transducer- to provide the conversion of the pressure into an observable waveform

 

3. A monitor- to display and store the data

 

All pressure monitoring systems need to be connected to an IV solution to it to stop the line and catheter from becoming occluded. The fluid in the line is pressurised to 300mmhg by the use of a pressure bag; this is to prevent back flow of blood up the line and into the solution itself.

 

 

 

Nursing management of pressure lines

 

 

Each ICU has it’s own protocol for the care of IV pressure lines though nurses must be able to recognise fundamental issues related to their management. These are mainly issues of infection control bleeding and embolic complications.

 

 

Safety and emergency procedures - pressure lines

 

 

1. Don’t become complacent ....arterial lines and Swan-Ganz catheters are common place in most ICU’s and nurses are very familiar with their uses etc. However ...these lines carry potential fatal consequences for the patient if they are not managed correctly

 

2. Always ensure that you can see the line- a patient in the ICU who is critically ill may have 10 or more infusions going at once!...they can easily become knotted and twisted and confusingly spaghetti-like! If the line is an arterial one inserted into a radial artery or dorsalis pedis (foot) You must be able to see the line at all times. Should the line be hidden under the sheets the patient could have become inadvertently disconnected and be slowly (or if their BP is good)....quickly ...exhanguinating!!

 

3. Observe all sites for signs of infection

 

4. Assess the patients overall general condition ...not just the data on the chart

 

5. NEVER EVER ALLOW INJECTIONS TO BE GIVEN INTO ARTERIAL LINES. In the ICU we like to think we give safe and effective INTRAVENOUS injections not INTRAARTERIAL ones....( Which can cause immediate arterial sclerosis and ischaemia leading to the patient requiring amputation )

Make doubly sure that your injection ports on an arterial line are blanked off with a small blank cap....not an injection bung!!

 

6. Secure all lines firmly to the patient and inform the patient of it’s purpose and function.

Wherever practical mark the lines “ARTERIAL” 

 

7. No air please!!!.....not even a tiny bit!

 

 

 

The haemodynamic profile.

 

 

A haemodynamic profile can be extremely useful in building up a picture of the patients overall cardiovascular function. The reason for the degree of dysfunction are many, though it is reasonable to say that a patient requiring continuous haemodynamic monitoring will have one or more of the following conditions:

 

 

Cardiac failure

 

Pulmonary oedema

 

Respiratory failure

 

Major trauma

 

Sepsis

 

Profoundly shocked

 

Why do we need haemodynamic monitoring?

 

To determine the effectiveness of cardiovascular function

 

As an evaluation of treatment (particularly inotropes)

 

As an assessment of their volaemic state (i.e. burns and trauma)

 

A typical haemodynamic profile.

 

Systemic arterial pressure i.e. systolic and diastolic

Mean arterial pressure usually  80 - 90 mmHg

 

Central venous pressure (or right atrial pressure)

4 - 10 mmHg (12 – 15 mmHg IPPV)

 

Pulmonary artery pressure

15 - 25 mmHg systolic

8 - 10 mmHg diastolic

 

Pulmonary artery wedge pressure

6 - 12 mmHg (10 – 17 mmHG IPPV)

 

Cardiac output

4 - 8 litres/minute

 

Cardiac index

2.5 -4.2 l/min/m2

 

 

 

Systemic vascular resistance (or SVR)

900 - 1600 dynes/sec/cm5

 

Pulmonary vascular resistance

20 - 120 dynes/sec/cm5

 

Stroke volume

60 - 100 ml

 

 

Calculation of haemodynamic parameters.

 

Mean arterial pressure

 

Diastolic X 2 + Systolic

3

 

 

Systemic vascular resistance

 

 

(Mean arterial pressure - CVP) X80

Cardiac output

 

 

Pulmonary vascular resistance

 

(Mean PA pressure - Wedge X80

Cardiac Output

 

 

 

 

 

 

 

 

 

 

 

 

 

Shock !!!

 

DEFINITION: -  Inadequate delivery of oxygen to the tissues.

 

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

 

There are five types of shock:-

 

w        ANAPHALACTIC

w        HYPOVOLAEMIC

w        NEUROGENIC

w        CARDIOGENIC

w        SEPTIC (Distributive)

 

Hypovolaemic Shock.

 

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

 

Causes: -

 

w        HAEMORRHAGE

w        DEHYDRATION

w        BURNS

w        ASCITES, PERITONITIS

w        EXCESSIVE DIURESIS

 

Clinical Features