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Cardiovascular System. HLT 43407 ClareShalders/2009. Heart failure Underlying heart failure impairment of the pumping ability of the heart Nature of impairment depends on the side of the heart involved.

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Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

Cardiovascular System

HLT 43407

ClareShalders/2009


Cardiovascular system

Heart failure

Underlying heart failure impairment of the pumping ability of the heart

Nature of impairment depends on the side of the heart involved

CLARE SHALDERS/GOTAFE/2008


Cardiovascular system

Right side of heart fails, blood accumulates in the venous circulation, causing organ congestion and peripheral tissue oedema

Left side fails blood accumulates in the pulmonary circulation, resulting in pulmonary congestion, and fluid in the lungs.

CLARE SHALDERS/GOTAFE/2008


Cardiovascular system

The impairment of ventricular ability results in significant volume of blood remaining in the chamber after contraction.

This stress is called preload

CLARE SHALDERS/GOTAFE/2008


Cardiovascular system

Left side of the heart is called CCF

Eventually impairment of one side of the heart leads to involvement of both sides


Cardiovascular system

To compensate for decreased cardiac output, compensatory mechanisms take place.

Long term these mechanisms amplify the problem rather than overcome it.

The increase in workload called afterload, means that the myocardium requires more oxygen

CLARE SHALDERS/GOTAFE/2008


Terms

CLARE SHALDERS/GOTAFE/2008

Terms

Inotropes: affect the force of the heart muscle contraction

Positive inotropes increase force of myocardial contraction eg. Adrenaline, digoxin, dobutamine

Negative inotropes decrease the force of myocardial contraction e.g Beta blockers eg. propanolol


Terms1

CLARE SHALDERS/GOTAFE/2008

Terms

Chronotropic drugs affect heart rate

Positive chronotropic speed up by increasing impulse formation in SA node, eg. Adrenaline

Negative chronotropic has opposite effect, slows rate down, e.g. digoxin

Dromotropic drugs affect conducting system velocity (speed)

Positive action e.g. adrenaline Negative: digoxin, calcium channel blockers eg. verapamil


Adrenergic receptors

CLARE SHALDERS/GOTAFE/2008

Adrenergic Receptors

Sympathomimetic drugs (adrenergic agonists) directly stimulate alpha and beta adrenoceptors

Alpha receptors 1&2

Vasoconstrict arterioles of the skin

Pupil dilation

Relaxation of the gut


Adrenoceptor antagonists

CLARE SHALDERS/GOTAFE/2008

Adrenoceptor antagonists

Beta adrenoceptor antagonists drugs

Beta blockers

Beta 1 selective blockers cardioselective

Beta 1 & 2 non selective adrenoceptor antagonists

Cardiac muscle contains mainly beta 1

Smooth muscle contains mainly beta 2


Beta adrenoceptor blocking agents

CLARE SHALDERS/GOTAFE/2008

Beta Adrenoceptor Blocking Agents

Beta Blockers – inhibit the effect, of catecholmines at beta adrenergic receptor sites.

Some agents have equal affinity for beta 1 and beta 2 receptors. ( non cardioselective propanolol/ cardioselective atenolol, metoprolol) may reduce the incidence of bronchospam


Beta blockers

CLARE SHALDERS/GOTAFE/2008

Beta Blockers

Depress myocardial contractility and reduce the heart rate.

In addition reduces oxygen demand, B Blockers may also increase the perfusion of the ischaemic area, because the decrease in heart rate increases the duration of diastole and hence the time available for coronary blood flow

Two types alpha and beta

Beta blockers block the beta receptor

Some also block the alpha receptor


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

Action

Block the adrenoceptors, thereby reducing some of the responses of the body to adrenaline, noradrenaline and isoprenaline.

Some are more specific for receptors dominant in the heart (beta 1) others block receptors in the lungs (beta 2) as well as the beta 1 receptors


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

Beta Blockers Action

Reduces cardiac rate and force of contraction

Reduced cardiac output and cardiac demand

Reduced BP

Reduced response to stress

Inhibition of renin release from kidney


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

Beta Blockers Use

Hypertension

Angina pectoris (temporary interference with blood flow that reduces oxygen and nutrient supply to heart muscle)

Cardiac arrythmias

Myocardial infarction

Tacycardia


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

Adverse effects:

Bronchospasm (uncommon but serious)

Bradycardia, postural hypotension

Nausea, vomiting, diarrhoea, constipation, indigestion and dry mouth

Cold extremities

Fatigue, dizziness, headache, malaise

Depression ,mood changes

Effect on lipid and glucose metabolism

Sleep disturbances


Beta blockers1

CLARE SHALDERS/GOTAFE/2008

Beta Blockers

Beta blockers should not be stopped suddenly

Most effective when used with an ACE

Client should have sitting systolic BP above 85mmHg, and heart rate above 55bpm before commencing beta blockers


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

Cardioselective

Inhibit 1 receptors in cardiac smooth muscle

Examples include

Metoprolol(Betaloc, Lopresor)

Atenolol(Tenormin, Noten)

Safe for use in people with respiratory conditions or prone to bronchospasm


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

Non – Cardioselective

> Inhibit B1 receptors in cardiac smooth muscle and B2 receptors in bronchial and vascular muscle

> Examples include

Pindolol (Visken)

Labetalol (Trandate)


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

Implications for nursing

Monitor blood pressure for effect of medication

Monitor patient for any breathing difficulties or bradycardia

Side effects are weakness and drowsiness

Can cause wheezing and should be used with caution in patients with asthma, bronchitis or emphysema


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

Angiotensin converting enzyme (ACE) inhibitors

Act as antagonist of the renin-angiotensin system

Interfere with the conversion of angiotensin 1 to angiotensin 2 by inhibiting the angiotensin converting enzyme


Cardiovascular system

This results in the dilation of peripheral blood vessels and a reduction in blood pressure excretion of sodium and water is enhanced and potassium is retained.

Inhibition of aldosterone release, reducing sodium and water reabsorption

Eg. captopril (Capoten) and enalapril ) (Renitec)


Cardiovascular system

Cardiac after load is reduced and aldosterone mediated sodium and fluid retention is diminished.

Major advantage of this group is they produce there effects without compromising cardiac function by reducing cardiac output or altering heart rate.

Eg. captopril (Capoten) and enalapril ) (Renitec)

CLARE SHALDERS/GOTAFE/2008


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

Are indicated for:

Hypertension, heart failure, diabetic nephropathy, left ventricular dysfunction and after myocardial infarction

Preserving kidney function in diabetes

Most of these drugs maintain antihypertensive effect for up to 24 hours allowing once daily dosing


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

Adverse reactions

Persistent dry cough

Headache

Diarrhoea

Loss of taste

Weakness

Nausea

Dizziness

Hypotension

Rash

Fever

Joint pain


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

The suffix pril useful guide to identifying individual generics

One of major advantages are they produce their affects without compromising cardiac function

Caution in patients with renal impairement

Caution with use of NSAIDS during ACE therapy as can reduce the effectiveness of the ACE.


Cardiovascular system

First dose of ACE may cause severe hypotension, commenced with low dose and titrated.

Can be given in combination with diuretics.

Potassium sparing diuretics not recommended due to risk of hyperkalaemia.

CLARE SHALDERS/GOTAFE/2008


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

Angiotensin Receptor Antagonists

Agents such as candersartan, irbesartan, losartan block the receptors for angiotensin 11

Inhibit vasoconstriction and the increase in aldosterone release( similar to ACE)


Cardiovascular system

Losartan

Duration of action 24 hours

Metabolised in liver and excretion in bile (60%) and urine(35%)

Adverse reactions – headache tiredness dizziness, hypotension and GIT disturbances

Cause less cough then ACE,


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

Action

They prevent angiotensin from binding to it’s receptor in the walls of the blood vessels.

Resulting in lower blood pressure

Do not cause a cough as a side effect

Can help kidney function

Anti inflammatory effect on the walls of the blood vessels

Eg. Atacand


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

Angina Medications

Control the symptoms of angina caused by blocked or narrowed coronary arteries.

They can not fix the blockage


Cardiovascular system

Angina Medications

Only bypass or angioplasty can resolve the blockages

Angina patients commonly treated with asprin, helps prevent narrowing in artery from progressing to a full blown heart attack


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

Angina Medications

Medications to prevent angina from occurring include

Long acting nitrates

Beta Blockers

Calcium Channel Blockers

Lowering the serum cholesterol levels helps the arteries of the heart dilate


Coronary vasodilators

CLARE SHALDERS/GOTAFE/2008

Coronary Vasodilators

Drugs that dilate the coronary blood vessels are primarily used on the treatment of angina pectoris

A condition characterised by either an imbalance in the supply and demand of oxygen by cardiac tissue or by obstruction or narrowing of the coronary arteries caused by atherosclerosis

Nitrates are very useful in the treatment of angina


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

NITRATES

Their action results in the relief of ischaemia in coronary blood vessels

They improve the delivery of oxygen to ischaemic tissue by increasing coronary blood flow

They reduce oxygen consumption of the heart by dilating peripheral blood vessels.

GTN (Glyceryl trinitrate) is shown to be effective in 90% of people with angina within 5 minutes


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

If the body exposed to nitrates continuously the body becomes tolerant to them

Essential to have a nitrate-free interval every day

Most commonly done at night, when at rest

Sublingual tablets are used for acute attacks. Should be placed under the tongue and dissolve. Repeated at five minute intervals total of three. If chest pain not relieved in 15 minutes should call ambulance.

Transient headache and flushing may occur post dose.


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

NITRATES

GTN comes in many forms

Tablets for sublingual administration

Patch for transdermal application

Ointment for transdermal application

Liquid for intravenous infusion

Isosorbide Trinitrate has a longer duration of action and is administered as an oral tablet

Used in the prevention of angina


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

NITRATES - GTN

Volatile substance

Quickly rendered inactive by light, heat, air and moisture

Sublingual tablet is the most predictable form

Tolerance can develop so use of the smallest effective dose is recommended


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

GTN – Nursing implications

Common side effects include

Headache

Hypotension

Syncope

Nausea

Ensure regular haemodynamic monitoring

Start with the smallest dose

Use oxygen therapy

Educate patient about how to take medication


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

GTN – Nursing implications

With sublingual GTN

Ask patient to take a sip of H2O prior to tablet

Do not chew or swallow

Encourage patient to rest/do not move until episode of angina has resolved

Educate patient about how to store GTN products properly

Look up Glyceryl Trinitrate


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

CARDIAC GLYCOSIDES

Digitalis demonstrates a herbal recipe, used by common people for dropsy

Term digitalis glycoside refers to cardiac glycosides derived from digitalis species and includes digoxin


Cardiovascular system

A very effective treatment for congestive heart failure which is often the result of the sustained presence of one or more underlying cardiovascular diseases

Symptoms of heart failure include weight gain, oedema, shortness of breath, pulmonary congestion


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

Works by exerting a positive inotropic action on the heart

> Increases the force of contraction and thereby improve the mechanical efficiency of the heart as a pumping organ

>Results in a reduction in heart size

>They also slow heart rate and slow conduction

>Increases blood flow to the kidneys


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

Example – Most widely used Digoxin (Lanoxin)

Increases the amount of calcium inside the cells of the heart and caused the heart muscle to beat stronger

Loading doses are used to start therapy

Regular blood tests to ensure therapeutic dose

Low therapeutic index ie. Therapeutic dose is close to toxic dose

Symptoms of toxicity

GIT upset – N&V, diarrhoea

Neurological – Drowsiness, confusion, lethargy

Cardiac arrythmias

Hypokalaemia (low K)

Renal impairment


Cardiovascular system

CLARE SHALDERS/GOTAFE/2008

Nursing Implications

Close monitoring to look for signs of toxicity

Narrow therapeutic range

Regular serum digoxin levels

Caution is required when patient is taking Quinidine and Digoxin as quinidine enhances digoxin

Look up digoxin


Heart failure medications

CLARE SHALDERS/GOTAFE/2008

Heart Failure Medications

Usually treated with

Diuretics

ACE Inhibitors

Beta blockers

Digoxin


Heart failure

CLARE SHALDERS/GOTAFE/2008

Heart Failure

Diuretics

Used to remove excess fluid

Minimise shortness of breath and swelling

ACE Inhibitors

Dilate blood vessels making it easier for the heart to pump blood

Improve symptoms and can prolong survival

If ace inhibitors not tolerated combination of nitrates and hydralazine can be substituted


Heart failure1

CLARE SHALDERS/GOTAFE/2008

Heart Failure

Heart failure patients often have high levels of adrenaline in their blood stream

Beta blockers block this adrenaline effect

Metoprolol was the first beta blocker for this indication

Carvedilol beta blocker with other properties that was specifically developed for patients with heart failure

Digoxin strengthens the heart muscle to improve the symptoms of heart failure

Spironolactone a diuretic inhibits hormone called aldosterone that is deleterious to the failing heart in addition to its fluid removing effects.


Antihypertensive agents

CLARE SHALDERS/GOTAFE/2008

Antihypertensive agents

Hypertension is defined as an abnormal increase in arterial blood pressure

Blood pressure is dependant on two factors

> Cardiac output and peripheral resistance

Virtually all forms of antihypertensives affect one or both of these systems

There are several types

Beta bockers

Alpha blocker

Diuretics

Angiotensin converting enzyme (ACE inhibitors)

Calcium channel blocker


Antihypertensives

CLARE SHALDERS/GOTAFE/2008

Antihypertensives

Antihypertensive agents act indirectly such as vasodilators or directly such as angiotensin converting enzyme (ACE)

They treat by improving blood volume, cardiac output.


Antihypertensive agents1

CLARE SHALDERS/GOTAFE/2008

Antihypertensive agents

Used in the treatment of heart disease, stroke, vascular disease, renal impairment where elevated blood pressure is significant

When instituting drug therapy the lowest dose of the chosen drug is used and adding a second drug from a different drug class if necessary


Antihypertensive agents2

CLARE SHALDERS/GOTAFE/2008

Antihypertensive agents

Management of Hypertension we may need to use:

Diuretics plus beta blocker

Ace inhibitor plus calcium channel blocker

Beta blocking agents

Vasoldilators


Antihypertensives1

CLARE SHALDERS/GOTAFE/2008

Antihypertensives

Peripherally acting adrenergic agents

Work by blocking the post synaptic adrenoreceptors resulting in dilation of both arterioles and veins and a lowering of blood pressure

Eg. Minipress (Prazocin)

Nursing implications – can cause syncope in the early phase. Best given at bedtime to reduce likelihood of syncope


Antihypertensive agents3

CLARE SHALDERS/GOTAFE/2008

Antihypertensive agents

Clonidine

Centrally acting A2 agonist.

Reduces systolic and diastolic blood pressure by stimulating central receptors

Blood pressure lowered as result of decreased cardiac output, heart rate and peripheral vascular resistance.

Used for hypertension, migraine, opiod withdrawel, ADD and phaeocromocytoma.


Antihypertensive agents4

CLARE SHALDERS/GOTAFE/2008

Antihypertensive agents

Methyldopa

Exact hypotensive effect unknown

Peak effect occurs in 4-6 hours

Duration of action 12-24 hours

Adverse reactions

Drowsiness, dry mouth, headaches, oedema of the legs and feet, fever postural hypotension


Antihypertensives2

CLARE SHALDERS/GOTAFE/2008

Antihypertensives

Adverse effects:

Depend on drug chosen:

Dizziness, weakness, sweating, flushing, tacycardia or bradycardia, nausea and vomiting, diarrhoea, dry mouth, blurred vision hypotension, headache, dry non productive cough etc


Antihypertensive agents5

CLARE SHALDERS/GOTAFE/2008

Antihypertensive agents

Look up

Methyldopa

Clonidine

Captopril

Enalapril

Ramipril


Calcium channel blockers

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Calcium Channel Blockers

Block the inward movement of calcium through the slow channels of the cell membranes of cardiac and smooth muscle cells

This relaxes the muscle in the walls of the arteries, resulting in dilatation of the arteries. Therefore lowers blood pressure and improves blood supply to the heart.

All of these effects allow the heart to make do with a reduced blood supply and help treat symptoms of angina


Calcium channel blockers1

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Calcium Channel Blockers

Used for:

Lowering blood pressure

Controlling angina

Preventing migraines

Eg.Phenylalkylamine type (verapamil)

Benzothiazepine type (diltiazem)

Dihydropyridine type (amlodipine, felodipine nifedipine,nimodipine, lercandipine


Calcium channel blockers2

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Calcium Channel Blockers

Diliazem and verapamil slow the heart rate, which further helps to control angina

Also helpful in controlling abnormally fast heart rhythms

Side effects include

Constipation (verapamil)

Most common S/E

Dizziness, flushing, hypotension, headaches, and


Potassium channel activators

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Potassium Channel Activators

May be used as an alternative to long acting nitrates to reduce the frequency of angina attacks

They relax smooth muscle by acting on ATP sensitive potassium channels

Nocorandil

Diazoxide

Minoxidil


Potassium channel activator

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Potassium Channel Activator

Nicorandil

Acitvation of potassium channels, lead to arterial vasodilation, relaxes venous vascular system

Absorbed rapidly (30-60 mins) rapid elimination phase

Adverse effects: nausea, flushing, headache, dizziness palpitations

Dosage: 10-20 mg BD


Arrythmias

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Arrythmias

Arrythmias occur because of abnormality

in spontaneous initiation of an impulse or abnormality in impulse conduction are subdivided

Antiarrythmic drugs are subdivided into various classes depending on their effect on the hearts electrical conduction


Antiarrhythmic drugs

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Antiarrhythmic Drugs

Adverse effects:

Dizziness, headache, confusion, nervousness, seizures, dyspnoea, nausea and vomiting, hypotension, bradycardia

Precautions: contr in pregnancy. Used cautiously in clients with liver or renal disease


Antiarrhythmic drug

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Antiarrhythmic Drug

Nursing Implications:

If IV can cause severe hypotension

Photosensitivity can occur

Monitor blood pressure, heart rate and ECG therapy

Clients need to know how to monitor pulse rate if using long term therapy


Antidysrhymic drugs

Antidysrhymic drugs

A dysrhythmia is an abnormality in the rythym of the heart due to an impairment of the conduction system

The dysrhythmias that respond best to drug therapy are rapid rythyms.

Anti dyarryhthmic agents act by impeding the movement of ions across the membrane of myocardial cells

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Antidysrhymic drugs1

Antidysrhymic drugs

Best in treatment of ectopic beats and increase in heart rate because they act to suppress and stabilise the excitable myocardial tissue

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Antidysrhymic drugs2

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Antidysrhymic drugs

Adenosine

Activates specific adenosine receptors on the myocardium

Used for SVT (supraventricular taccycardia)

Common adverse effects facial flushing, dyspnoea, and chest tightening

Half life less than 30 seconds


Cholesterol

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Cholesterol

High cholesterol level is significant contributor to heart disease

Lowering cholesterol slows or prevents the growth of atherosclerotic plaques in the arteries.

Statin medication appears to prevent inflammation of the atherosclerotic plaque, this inflammation may cause plaque to rupture and cause a heart attack


Hypolipidaemic agents

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HYPOLIPIDAEMIC AGENTS

ATHEROSCLEROSIS

A disease characterised by the accumulation of fatty substances on the inner wall of large and medium sized arteries such as the aorta and the coronary, cerebral and renal arteries.

Will eventually lead to coronary heart disease, cerebro-vascular disease as well as renal disease or failure


Hypolipidaemic agents1

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HYPOLIPIDAEMIC AGENTS

Our bodies contain good cholesterol (HDL)

HDL protein takes cholesterol out of the lining of our blood vessels and protects against heart disease

Bad cholesterol (LDL)

Cholesterol attached to the LDL protein is what damages our blood vessels

Many people have high chol part due to genetic abnormality that causes the liver to manufacture to much chol

Diet will help by about 11%-40%


Lipoproteins

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LIPOPROTEINS

VLDL – contain a high proportion of lipid and are secreted in the liver, derived from a fatty meal, high in triglycerides

LDL – contain the greatest proportion of cholesterol of all of the lipoproteins, which raises blood cholesterol

HDL – the smallest lipoproteins and contain the greatest proportion of protein. Thought to actually be useful in preventing coronary artery disease. We want to have a high HDL


Hypolipidaemic agents2

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HYPOLIPIDAEMIC AGENTS

Many drugs have been shown to reduce the plasma concentrations of various lipoproteins, particularly cholesterol, but there is little evidence to show that these can reverse any existing atherosclerosis

It is also still unclear whether the use of these drugs actually affects morbidity or mortality


Cholesterol lowering medications

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Cholesterol Lowering Medications

Resins

These bind bile that was secreted into the intestine and prevent it from being reabsorbed

These medications lower LDL level not triglyceride level

Side effects

GIT upset especially constipation


Cholesterol lowering medication

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Cholesterol Lowering Medication

Taste of powders can be a problem

Mix with noncarbonated beverage

Take with meals to help side effects

Increase fibre intake

They can prevent absorption of other medications


Cholesterol lowering medication1

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Cholesterol lowering medication

Fibrates

Medications lower LDL chol and triglycerides as well as raise HDL levels

They inhibit production of proteins containing fat and chol by the liver and release triglycerides from fat stores in the body

Fibrates also have anti inflammatory effect on the walls of the blood vessels


Cholesterol lowering medication2

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Cholesterol Lowering Medication

First line anytihyperlipidaemic agents are the statins

Eg Simvastatin, pravastatin, atorvastatin

They have very few side effects even in long term therapy


Statins

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Statins

Statins

Inhibit an enzyme in the liver that is responsible for manufacturing cholesterol

Primarily lower LDL raise HDL and sometimes lower triglycerides also

Also mild blood thinning and anitiinflammatory effect on the walls of the blood vessels

Side effects

Be alert for muscle aches and pains

Liver makes cholesterol mostly at night, these medications should be taken in the evening


Hypolipidaemic agents3

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HYPOLIPIDAEMIC AGENTS

STATIN drugs

Eg. Simvastatin (Zocor)

Pravastatin (Pravachol)

Atorvastatin (Lipitor)

Used as adjunctive therapy to diet in the treatment of high cholesterol, and in people with multiple heart disease risks


Cholesterol absorption inhibitors

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Cholesterol Absorption Inhibitors

Prevent intestines from absorbing cholesterol in the food we eat

They lower the level of bad LDL

Side effects rare and minor


Hypolipidaemic agents4

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HYPOLIPIDAEMIC AGENTS

Eg. GEMFIBROZIL

Used for severe hypertriglyceridaemia, diabetic dyslipidaemia and heart disease risk reduction

Reduces the synthesis of triglycerides in the liver, reducing LDL and VLDL concentrations

Useful for people who do not respond adequately with diet therapy alone

Contraindicated in people with severe hepatic or renal dysfunction, gall bladder disease, pregnancy and lactation

Trade names include:- Lopid, Ausgem, Genhexal, Jezil


Hypolipidaemic agents5

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HYPOLIPIDAEMIC AGENTS

Niacin

Nicotinic acid lowers LDL chol and triglycerides and raises HDL chol

It accomplishes this by inhibiting the production of fat and cholesterol containing protiens by the liver

The large doses result in GIT irritation and pruritis. May also cause flushing itching and hypotension because of its vasodilating action


Cardiovascular system

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Take with food or cold beverage, avoid hot

One asprin a day helps decrease side effects

Start at low dose

Has an antinflammatory effect


Implications for nursing

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IMPLICATIONS FOR NURSING

Patient should have cholesterol studies before drug therapy and at regular intervals

Ensure related conditions are also treated at the same time

Ensure that patient understands that treatment is long term

Encourage dietary and exercise management


Activity

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Activity

Group 1 – Investigate Ca Channel Blockers

Group 2 – Investigate Nitrates

Group 3 – Investigate Beta Blockers

Group 4 – Investigate ACE inhibitors


Cardiovascular system

CSHALDERS/GOTAFE/2008

THE CLOTTING PROCESS

Injury to the wall of a blood vessel triggers a complex series of events which involves the activation of many different clotting factors. This injury, and its subsequent events, results in the formation of a fibrin clot. Any defect in the sequence of events can prevent the formation of a clot and, if not properly controlled, may result in a serious haemorrhagic risk.


Cardiovascular system

CSHALDERS/GOTAFE/2008

Any number of drugs are now available in Australia affect the clotting of blood. These include the anticoagulants, the thrombolytic agents, tissue plasminogen activator, and the haemostatic agents


Cardiovascular system

CSHALDERS/GOTAFE/2008

Used either to prevent the formation of a thrombus or to inhibit the extension of existing ones by inhibiting the formation or action of one or more clotting factors


Cardiovascular system

Individuals can suffer from intravascular clots (thrombi) formed in intact blood vessels

Thrombi form in cerebral or coronary vasculature

Common cause of thrombi – stasis of blood

CSHALDERS/GOTAFE/2008


Cardiovascular system

Thrombus


Cardiovascular system

Emboli


Cardiovascular system

In persons prone to thrombus we can prevent clot formation.

But must be very careful not to over stimulate this and lead to a bleeding disorder.

CSHALDERS/GOTAFE/2008


Cardiovascular system

Thrombus in right atrium


Cardiovascular system

Coronary bypass graft completely occluded by acute thrombosis.


Cardiovascular system

Heparin

Is a mucopolysaccharide that occurs naturally in the body principally within mast cells

Heparin is obtained from animal tissues, pig intestines and lungs of cattle

Not available orally as strongly ionic

CSHALDERS/GOTAFE/2008


Cardiovascular system

Heparin augments the function of antithrombin 111, factor Xa and thrombin

This binds directly to a clotting factor molecule to inactivate it.

Measured in international units

CSHALDERS/GOTAFE/2008


Cardiovascular system

Adverse effects

Mainly bleeding

If this occurs the antidote is protamine sulphate (prepared from salmon sperm)

CSHALDERS/GOTAFE/2008


Cardiovascular system

Clinical considerations

In IM form can cause painful haematoma therefore s/c or IV

Need APPT to obtain therapeutic levels

Advise to report nose bleeds, black stools, or bleeding gums

CSHALDERS/GOTAFE/2008


Cardiovascular system

Heparin is high molecular weight molecule, therefore variable subcutaneous absorption

Use of low molecular weight heparins such as enoxaparin (clexane)

CSHALDERS/GOTAFE/2008


Cardiovascular system

These type of heparins bind to antithrombin 111 but complex with only factor Xa and not thrombin

They have relatively long half lives, require less monitoring greater subcutaneous bioavailability

CSHALDERS/GOTAFE/2008


Cardiovascular system

The LMWH are more expensive than heparin

More effective in reducing thromboembolic episodes

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Cardiovascular system

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Since prothrombin (factor II) is depressed by these drugs, then measuring serum ‘Prothrombin Time’ is an accurate means of monitoring patient therapy.

Have a greater potential for clinically significant drug interactions than any other class of drugs


Cardiovascular system

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Oral anticoagulants

Inhibit clotting by interfering with the synthesis of Vitamin K-dependent clotting factors (II, VII, IX, X)


Cardiovascular system

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Synthesis of these factors in the body is dependent upon a sufficient supply of this vitamin.

Unlike heparin, the action of oral anti-coagulants is not evident for at least 12-24 hours after the first dose has been administered. This delay is due to the time required for normal removal of circulating clotting factors to take place.


Cardiovascular system

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Metabolised by the liver

Overdosage of anticoagulants may be seen as bleeding, increased bruising

Effect of oral anti-coagulants is reversed by parenteral Vitamin K


Cardiovascular system

Drugs which can interact with oral anti-coagulants causing an increased rate of metabolisation include:-alcohol

Tegretol

Dilantin

Grisovin

Rifampicin


Cardiovascular system

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WARFARIN is generally considered the agent of choice for this class because it has a more predictable action and a lower incidence of side effects.


Cardiovascular system

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Warfarin

Inhibits epoxide reductase and thus depletes active vitamin K from the liver

Takes several days to take effect

As Vitamin K is not interfered with directly by warfarin, need to watch excess of vitamin k in the diet.


Cardiovascular system

-Therapy with warfarin requires extreme care and close monitoring

-Dosage must be individually determined for each patient and controlled by periodic blood tests

-Dosage is usually adjusted to maintain a prothrombin time from 1.5 to 2.5 times the control value.


Cardiovascular system

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Individual responses varied important to determine effect on each individual

Clotting mechanisms assessed until stabilisation occurs

INR(International Normalised Ratio)

2.0-4.0


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Adverse Effects

Heamorrhage

Necrosis of skin

Alopecia rarely


Cardiovascular system

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Clinical considerations

Can be effected by other drugs and certain foods

Avoid foods high in Vitamin K

Critical consistency achieved

Herbal medicines can also interact, chamomile, garlic Ginkgo biloba


Cardiovascular system

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Vitamin K acts as an antidote in case` of hemorrhage

Must take tablets at same time each day

Regular blood tests for INR

Notify doctor immediately if bleeding or bruising occurs


Cardiovascular system

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ANTI-PLATELET AGENTS

Antiplatelet agents work by preventing the platelets in the blood from clumping by preventing thromboxane A2 synthesis. Used at low doses to treat myocardial infarction and to prevent thrombus formation in other high risk patients.

.


Cardiovascular system

Examples of antiplatelets include aspirin, clopidogrel, ticlopidine, and dipyridamole.


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Asprin

NSAID, analgesic, antipyretic, anti inflammatory

Also anti platelet properties

It renders the enzyme COX inactive leaving platelets unable to form TXA for their lifespan

The anti inflammatory activity of asprin also thought to contribute to a reduction in atherosclerotic plaque rupture and its consequences


Cardiovascular system

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Adverse Effects

Minimal in low dose antiplatelet therapy

GIT upset, and allergy, chronic ingestion papillary necrosis- irreversible renal failure

Stop 7 days before surgery


Cardiovascular system

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Clopidogrel

Inhibits the aggregation of platelets by irreversibly inhibiting the binding of ADP to its receptor on platelets

May be useful for those who experience asthma

Can be combined with asprin particularly after coronary stent surgery


Cardiovascular system

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Antiplatelet agents, including aspirin, can have serious and potentially fatal side effects if not taken properly and should be taken under adequate supervision and after suitable education


Cardiovascular system

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THROMBOLYTIC AGENTS

Thrombolytic enzymes act to convert the substance known as plasminogen to the enzyme fibrinolysin. This enzyme dissolves fibrin clots as well as other plasma proteins. These substances are present in thrombi and emboli. So thrombolytic enzymes work by dissolving potentially life-threatening vascular obstructions.

Available as intravenous preparations that can be used to avert a myocardial infarction or pulmonaryemboli.


Cardiovascular system

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Adverse effects

Heamaturia

Tarry stools

Excessive vaginal bleeding

Abdominal flank or joint pain

Headaches

Changes in neurological status

Heamatemesis

Nose or gum bleeds


Cardiovascular system

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NURSING IMPLICATIONS – Patient education

Oriented towards patient comfort and safety

Advise patient to avoid trauma

Advise patient to have regular contact with health professional

Avoid laxatives and drastic dietary changes

Patients should carry medical information detailing drug therapy

Avoid pregnancy


Cardiovascular system

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Antithrombotic agents are used in the prophylaxis and management of inappropriate clot formation in an intact circulation

Antiplatelet drugs are used in long term treatment of thrombotic disorders

Fibrinolytic drugs are used in emergency treatment of thrombotic disorders. They act to enhance conversion of plasminogen into plasmin, which dissolves the fibrin lattice of the clot


Cardiovascular system

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Fibrinolytic agents are administered within 6-12 hours of the onset of chest pain in an AMI

Most common adverse effect is hemorrhage


Cardiovascular system

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Bullock, S. Manias, E. Galbraith, A. Fundamentals of Pharmacology. 5th Edition

Ref Bryant, Knights, Salerno, 2ND Edition. Toronto 2005

Marieb, E. 2006, Essentials of Human Anatomy & Physiology, 8th Edition, Pearson, Benjamin, Cummings. USA


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