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34 **CVS**

CVS Examination

Vascular Guidelines Superchart

BHF Factfiles

Cardiology Rural Health West

Heart Foundation au

Cardiology Explained NCBI Bookshelf

Long term CVS Conditions BJGP Nov 2011

 Coronary Heart Disease  vs Cardio Vascular Disease
CHD Coronary artery disease CAD
angina/ACS/CABG etc
CVD Coronary artery disease CAD
+ cerebrovascular disease+ peripheral vascular disease PVD/PAD
CVD risk  =  CHD risk  x 1.3
1° Prevention CHD/CVD risk > 20%but no history of disease/events
2° Prevention patients with CHD CVD  (+/- diabetes)
Audit Targets (QOF etc) TC < 5.0 LDL <3
Aspirational Targets  TC < 4.0 LDL < 2


Cardiology lectures





Cardiac anatomy and physiology







Chest Pain

NICE CG95 Mar 10 Chest Pain

rural health west com.au july 2011 chest pain


Atypical chest pain

Tietze costochondritis

Chest Wall Syndrome Verdon et al 2007






Angina pathophysiology




Canadian angina grading

Canadian CVS Angina Grading
G1 angina on strenuous activity
G2 angina on ordinary activity eg uphill or >1 flight of stairs
G3 marked limitation of normal activityeg 1 fight of stairs
G4 angina on any activity & at rest


Angina guidelines

NICE Aug 2011 Offer optimal drug treatment initially in Stable Angina

Management of stable angina CG126QRG

BMJ Summary of NICE Angina Management

MeReC Rapid Review

North West Medicines Information Service Nice Bites Aug 11 Stable Angina

SIGN Angina guidelines 96, 2007

(GP Update)

Angina drug Rxto relieve symptoms and improve prognosisOptimise dose of each agent before adding another
GTN for all treating acute attacksprophylactically before activity known to trigger angina1 puff of GTN every 5 minutes and if still in pain >5 mins ring 999).
B-Blockers first line treatment to prevent attacks+ secondary prevention benefitse.g. atenololtitrate up to max tolerated dose.
Rate Limiting Ca Blockers if BB contraindicated/not toleratedverapamil, diltiazemsypmptomatic relief onlycontraindicated in heart failure, bradycardia and AV block
Non rate limiting Ca Blocker amlodipine, nifedipine felodipinecan given in combination with beta-blockers
Long-acting nitrates symptomatic reliefpatient should have at least 12 nitrate-free hours each day to prevent toleranceISMN can be given in conjunction with beta-blockers or calcium-channel blockers to achieve better symptom control.
Nicorandil potassium-channel activator2nd line in addition to BBlocker ie NRL20 mg bdsymptomatic relief and decreases the risk of hospital admission and recurrent vascular events
Refer Cardiology Refer for diagnosis via exercise tolerance test+ if symptom control fails with GTN prn, BB + one other agent.Myocardial perfusion scintigraphy if unable to do ETT/pre-existing abnormal ECGCABG for triple vessel or left main stem diseasePercutaneous approach if single/double vessel disease
Aspirin (75mg)statin
ACE inhibitorfor all (whether have LVD or not)
To prevent new vascular events
Definite evidence for ACE in LVSD, probable benefit without LVSD
Screen for depression


Investigations in angina
Bloods  FBC, TSH (if abnormal then do T3 and T4), Cr and LFTs (most will need a statin), fasting blood sugar, fasting lipids (cholesterol & LDL)
CXR not routinely indicated
Echo All patients post MI to assess ventricular function re ? adding in Eplerenone (all should be on a betablocker and ACE post MI).All patients with suspected CCF/LVF/heart murmur
Stress test Confirmation of suspected angina.Evaluation of residual ischaemia post MI.Abnormal in 85% of patients with angina.
Perfusion scan Patient unable to exercise.Equivocal exercise stress test
Angiography Strongly positive stress test.Acute coronary syndrome.Angina poorly controlled with medical treatment.Assessment for further Rx – angioplasty & stent or CABG.Angina after further Rx.Prior to valvular surgery


Secondary Prevention Post MI (NICE May 2007)
Lifestyle advice Smoking Cessationincreased dietary oily fish to > 3x per week.Annual flu vaccination irrespective of agepneumovac.
Aspirin 75mg
Clopidogrel Additional  75mg a day for 12/12 post NSTEMI or post eluting stent insertionthereafter continue with aspirin 75mg alone but in STEMI Clopidogrel for 2/52 post non-eluting stentuse Clopidogrel for 4/52Long term use of Clopidogrel alone is only used in patients allergic to Aspirin
Betablockers for all <12/12 post MI Indefinite treatmentif the patient presents >12/12 post MI and is not on a betablocker arrange an echo, as betablockers are not indicated in asymptomatic patients with preserved LV function, unless high risk or other compelling reasons
Statins for all  ‘treat to target’ e.g. Simvastatin 40mg, then Simvastatin 80mg and then Rosuvustatin 20mg. The mimimum audit target = Cholesterol < 5.0 and LDL <2.5 but an aspirational target of Cholesterol < 4.0 and LDL < 2.0
Adosterone antagonists e.g. spironolactone if symptoms/signs of CCF & LVSDstart within 3-14 days of MI, preferably after the ACE.Monitor U&E’s as per CCF protocol.Halve dose or stop them if hyperkalaemia is a problem.
Refer Cardiology CABG for triple vessel or left main stem diseasePercutaneous approach if single/double vessel diseaseif symptom control fails with GTN prn, betablocker + one other agent.

Beware PPIs negate the benefit of Clopidogrel! So if you have to treat clopidogrel related dyspepsia consider a H2 Blocker (evidence of value still being debated).


Aortic dissection
CTD – Marfans, Ehrs Danlos SLE
Congenital Heat disease eg coarctation
Trauma inc atrogenic
Crack cocaine
youtu.be.com/dZLX2MD_w78Aortic Dissection Easily Missed BMJ Jul 2011Acute aortic syndromes EHJ Jul 2011

Degeneration of medial smoth muscle leads to tear in aortic intima  causing a flase lumen between inner and outer tunica media with obliteration and vascular insufficiency of aortic tributaries – carotids,  coronaries, subclavian, anterior spinal coeliac and renal.

Sudden excruciating central tearing chest pain assoc with differential pulse and BP.


Acute coronary syndrome
angina chest pain due to cardiac ischaemia when myocardial oxygen demand exceeds supply – brought on by exhertion – relieved by restusually due to chronic (stable) athersclerosis
MI sudden complete occlusion of coronary artery due to ruptur of an atheromatous plaque wuith secondary thrombus formation
unstable angina acute coronary syndrome without ST-segment changes or evidence of myocardial injury.
NSTEMI no ST segment elevation but evidence of myocardial injury as assessed by elevated enzymes
STEMI ST-elevation myocardial infarctionischaemic chest pain plus ST-segment elevation on the ECGneed urgent reperfusion



NICE Unstable Angina & STEMI CG 94 Mar 2010 Quickref

SIGN 93 ACS Feb 2007

SIGN Heart Disease QRF

Hyperglycaemia in ACS NICE CG BMJ Nov 2011








ACS management

Arrange immediate admission

High flow oxygen.

iv Tramadol 50mg over 3 mins and iv Maxalon 10mg.

Oral aspirin 300mg – decreases mortality by 25% (ISIS II study).

Oral clopidogrel 300mg stat.

Thrombolysis within 6 to 12hrs of the onset of symptoms – decreases mortality by 25% (ISIS II study).

Beta blockade within 24hrs (ISIS 1 study & NICE 2007).

Early angioplasty (if available) is replacing thrombolysis. Please note the new rules with respect to the duration of clopidogrel use in combination with aspirin vary depending upon the type of MI and the type of stent used.

Drug treatment of ST-elevation myocardial infarction

All patients should have ECG monitoring in an environment where defibrillation and pacing can be performed.

Aspirin 300 mg chewewd should be given to all patients unless there are clear contraindications.

Intramuscular injections should be avoided because of the increased muscle enzyme activity and high risk of bleeding if thrombolytics are administered.

Diamorphine administered intravenously is generally considered to be the drug of first choice unless severe hypotension and/or respiratory depression are present. Metoclopramide is probably the safest anti-emetic for reducing opiate-induced nausea and vomiting.

Oxygen – Ventilation/perfusion abnormalities occur secondary to pulmonary oedema and associated hypoxaemia, and require treatment with oxygen.

Nitrates – Sublingual or intravenous organic nitrates can be used to reduce chest pain provided that the patient is not hypotensive. Particular caution is required to right ventricular infarcts, as venodilatation can precipitate severe hypotension. Nitrates have no effect on mortality.

Beta-adrenoceptor antagonists Early administration of a beta-blocker reduces infarct size and life-threatening arrhythmias. Patients with elevated blood pressure, tachycardia, atrial fibrillation and recurrent chest pain are most likely to benefit, while those with bradycardia, hypotension and conduction problems are most likely to experience adverse effects.

ACE inhibitors ACE inhibitors or the angiotensin-II-receptor antagonist valsartan should also be administered within 24 hours after an ST-elevation infarction or for those with left bundle branch block. Most benefit is due to improvement in left ventricular function.

Acute coronary syndrome without ST elevation

BMJ 2007;334:1265-9

Drug therapy should include:

Aspirin for life– reduces relative risk of further vascular event by 50% (ATC trial, BMJ 2002;324:71-86).

Clopidogrel for up to 12 months post event (reduces risk of vascular event by an additional 20% compared to aspirin alone, (NEJM 2001;345:494-502), but 1% absolute risk increase in bleeding.

BBlockers – to decrease myocardial O2 demand by reducing heart rate and blood pressure and reducing risk of arrhythmias.

Vasodilators (nitrates, calcium channel blockers) for coronary artery vasodilatation and to lower blood pressure. Although neither BBlockers or vasodilators have been shown to reduce the risk of MI or death!

The role of gycoprotein2b/3a receptor inhibitors (eg abciximab) is unclear: theoretically they should be beneficial as they inhibit platelets. However benefit appears only in those who have Percutaneous coronary interventions, not those managed conservatively.

Modify all cardiovascular risk factors (statins, ACE inhibitor for cardio-protection, smoking cessation, screen for diabetes, obesity reduction, increase physical activity).



For patients with ST-segment elevation, thrombolysis results in reperfusion in 50-70% of those treated.

This is translated into improved left ventricular function, and reduced arrhythmias, cardiogenic shock and mortality. The best results occur if percutaneous coronary intervention is performed soon after drug administration. The greatest benefit is achieved with early thrombolysis, especially if given within 4 hours of the onset of chest pain.

Adverse effects and contraindications Bleeding, symptomatic hypotension and allergic reactions are the most common and serious reactions associated with streptokinase therapy. However, hypertension can be associated with reperfusion, due to successful thrombolysis and recanalisation. Allergic reactions which include fever, rashes, serum sickness, polyneuropathy and (rarely) anaphylaxis occur in about 12% of patients treated. These reactions are rarely seen with other thrombolytic agents, e.g. alteplase, and severe reactions usually occur on re-exposure.

Any condition which increases the risk of bleeding represents a relative or absolute contraindication to the use of streptokinase and other thrombolytic agents. A previous history of an allergic reaction to streptokinase is an absolute contraindication. Great care is also required when giving thrombolytic drugs to patients who are already receiving anticoagulants and antiplatelet drugs.

Streptokinase Inexpensive AntigenicOccasional allergic reactionHypotensionNeed heparin
Anistreplase Rapid effect with prolonged actionAntigenic Occasional allergic reactionModerately expensive
Alteplase Short half-lifeNon-antigenicHighly clot selectiveVery expensive




All patients following an acute coronary syndrome or who have undergone percutaneous coronary intervention should receive clopidogrel. A loading dose of 300 mg followed by a maintenance dose of 75 mg was the regimen used in the outcome trials. This should be combined with 75 mg of aspirin. To date there is no evidence of clinical benefit beyond 1 year for the combination.


NSTEMI  and unstable angina

differs from that of STEMI in a number of key areas:

Thrombolytic therapy is of no proven value.

Rate-limiting calcium-channel blockers such as verapamil or diltiazem are useful adjuvants to analgesics, nitrates and beta-blockers.

HMG CoA reductase inhibitors have been shown to reduce mortality and recurrent myocardial infarction when administered in the acute setting.

Glycoprotein-llb/llla antagonists have been shown to protect patients with NSTEMI and unstable angina from death and non-fatal myocardial infarction during the acute phase of their presentation and for 24 hour following intervention.

Unfractionated and low-molecular-weight heparin reduces the risk of further myocardial infarction, often combined with antiplatelet drugs.


NICE Ticagrelor Guidance via NELM Oct 2011


Drug therapy in CVD and post MI
ACE inhibitor ACE inhibitors should continue for life even in the absence of LVF/LVSD.ARBs if allergy/intolerance of ACE
Aspirin 300mg in suspected ACS then 75mg od indefinately.A PPI should be given to those with a history of dyspepsia. Those with a history of aspirin induced gastrointestinal haemorrhage should be considered for aspirin therapy with full dose PPI protection. Only those truly intolerant to aspirin may be considered for monotherapy with clopidogrel.For those on warfarin for some other reason (eg. recurrent DVT) and who are at low risk of bleeding consider aspirin and warfarin with a PPI.
Clopidogrel Patients given aspirin and clopidogrel within the first 24 hrs post MI should continue to take both for 1 month,then aspirin alone.Those with non-ST elevation acute coronary syndrome should be given aspirin with clopidogrel for 12m.
B-Blocker BBlockers reduce mortality after MI & in heart failure & are 1st line drug in angina.BBlockers are no longer the drug of choice for most people with hypertension.
Statins give to all post-MI regardless of their cholesterol level


Cardiac rehabilitation


British Heart Foundation Cardiac Rehabilitation Factfile

Aims is to restore patient to the best possible function after ACS and to minimise risk of recurrence.

Cardiac rehabilitation improves risk, morbidity, mortality and psychosocial outcome.

May reduce mortality by 20-25%.



Intimal fibrosis, reduplication of elastic lamina, smooth muscle hypertrophy, hyaline arteriosclerosis.

NWMIC Nice Bites 34 Sep 2011





Measuring Blood Pressure

Patient sat comfortably, rested, no recent nicotine or caffeine. arm fully exposed and resting in slight flexion supported on desk with brachial artery at heart level.

Choose appropriate size cuff for size of arm. Wrap neatly and tightly round arm with lower end approx 2-3 cm above antecubital fossa.

Ensure dial visible and set to zero. Tighten air valve palpate radial artery and inflate quickly till pressure obliterates radial/brachial pulse. Let down pressure and note approx systolic pressure when pulse returns.

Place stethoscope over radial artery. Reinflate cuff to 30mm above this value. Release pressure steadily approx 2-3 mm per second.

Note the appearance  of audible sounds 1st Korotoff = systolic pressure.

Note complete disappearance  (not muffling) of audible sounds  2nd Korotoff sound = diastolic pressure



NICE CG127 Hypertension Aug 2011 QRG

NPC Rapid Review Oct 2011


NPC Rapid Review Oct 2011

Management of hypertension: summary of NICE guidance BMJ Aug 2011

Choice of diuretic in hypertension: saving the baby from the bathwater Heart Jul 2011

30 min BP measurement compares favourably to standard office-based BP measurement NPC Rapid Review Sep 11

New evidence supports more rigorous measurement of blood pressure for the diagnosis of hypertension NPC Rapid Review Oct 2011

Pulse learning hypertension module

whatever happened to the thiazides? DTB Dec 11


Hypertension grades 
Systolic Diastolic Action
Normal <130 <85 recheck 5 years
G1mild 140-159 90-99 clinic readings ≥140/90 and average ABPM/HBPM ≥135/85 recheck monthly if low CHD risk (<20%) no TOD and no DM – recheck CHD risk annually If >20% or TGO or DM confirm over 12w then treat
G2moderate 160-179 100-109 clinic readings ≥160/100 and ABPM/HBPM ≥150/95 recheck 1w if low risk – treat if remains high over 4-6 weeks If risk high or TOD or DM observe over 3-4 weeks then treat
G3severe >180 > 110 confirm over 1-2 weeks then treatconsider immediate Rx/referrral
G4v severe >210 >120  malignant = 200/130?
IsolatedSystolicgrade 1 140-159 <90
IsolatedSystolic grade 2 >160 <90


Hypertension drugs
A ACE/ARB first line < 55less effective blackscaution RAS/atherosclerosis undiagnosed murmur unstable anginalisinopril 5-40 mg odramipril 2.5 5 mg bdARB if truly intolerant
C Ca channel blocker black/over 55/concomitant anginablack= african/caribbean not mixed race asian or chineseBeta-blockers and ACE ineffective in this groupamlodipine 510mg odcoracten XL 3060 mg odDiltiazem XL (rate limiting)
D thiazide diuretic consider first line black or elderlyavoid in gout ask about impotencebendrofluazide 2.5mg odor thiazide like diuretic chlorthalidone or indapamide


Hypertension Initial Rx
ACE(ARB) in white under 55(BB if younger, intolerant, fertile, high sympathetic drive)CCB if black or over 55


Hypertension step 2
A+CA+D if CCB not tolerated or heart failureIf initially on BB add A cf D (DM risk)If going to A+C in blacks then ARB not ACE


Hypertension step 3


Hypertension step 4
A+C+D + 4th agentfurther diuretic (higher-dose thiazide-like diuretic or spironolactone, depending on K)or alpha blocker or beta blockerspecialist advice


NeLM BMJ Editorial: Personalised medicine for hypertension July 2011

UKMi How should ankle oedema caused by calcium channel blockers be treated?




Regional Drug And Therapeutics Centre (Newcastle)

Which angiotensin receptor blocker?


ACEs in CV disease
Ramipril Hypertensioninitially 1.25 mg od Usual 2.5 mg – 5mg od max 10mg odHeart Failureinitially 1.25 mg od under supervision Target 10mg daily in 1 or two divided dosesPost MIInitially 2.5mg bd Increase 48hrs to 5mg bdMaintainance 2.5-5mg bd2 prevention 2.5mg 0d then 5mg od then 10mg od
Lisinopril HypertensionInitially 2.5 -10mg od Maintainance 10-20mg od max 80mgodHeart Failureinitially 2.5mg under supervision Target 30-35mg odPost MI 5mg within 24 hrs then 5mg next day then 10mg od halve dose if SBP <120
Perindopril Hypertension 4mg od half in elderly/CKDmax 8mg odHeart Failure 2mg am then 4mg od before food 4mg od increase to 8mg od in 2w halve in elderly >70 yrs


ARBs in CVS disease
Candesarten  Hypertension 8mg od (usual maintainance) 2mg hepatic impairement 4mg renal impairementIncrease 4 weekly max 32 mg odHeart Failure 4mg odincrease 2 weekly to max 32 mg od
Losarten Hypertension 50mg od (25mg od elderly/CKD) Max 100 mg od
Valsartan  HF post MI 20mg bd increase over several weeks to 160mg bd
Irbesartan  CKD DM BP


Measuring Electrolytes in patients on ACEs

Check baseline U&Es plus a single U&E check while dose is being titrated up + an annual check (if all normal)

ACE inhibitors should be withdrawn if the creatinine rises by >50% of its baseline value, or exceeds 200 mmol/l whichever is less.

Dual Blockade BMJ Feb 2012


Resistant hypertension

Antihypertensive use in patients with resistant hypertension Hypertension Nov 2011


Accelerated hypertension

BP 200>130 mmHg.

Headache nausea vomitting blurred vision scotoma  seizures heart failure.




  • Coarctation of the aorta
  • Renal
  • Endocrine – DM hyperthyroidism, COnns Cushing hyperparathyroidism CAH acromegaly
  • Eclampsia
  • Pill / Phaeocromocytoma


Hypertension in elderly

ACCF/AHA 2011 Expert Consensus Document on Hypertension in the Elderly Apr 2011

Immediate and late benefits of treating very elderly people with hypertension BMJ Jan 2011


Heart failure

Failure of cardiac output to match metabolic needs of the tissues.

Heart failure
left-sided failure mainly left ventriclepulmonary oedema
right-sided failure mainly right ventricleoedema ascites hepatomegaly
Biventricular failure both ventricles
Systolic failure forward failureLV fails to eject blood (reduced LVEF)CO may fall and reduce tissue perfusionsymptoms of LVF – Breathless patientAND echo findings of left ventricular hypertrophy and left atrial enlargementAND evidence of raised left atrial pressure (diagnosed by elevated Btype natriuretic peptide (BNP) or on new echo indices).BMJ ‘Practice’ article looks at the use of beta blockers for heart failure with reduced ejection fraction NELM Sep 2011
Diastolic failureHFNEF signs and symptoms of LVF but ejection fraction is preservedstiff LV cannot relax in diastole so cannot fill properly

High out put failure (CO cannot match increased demand – anaemia, pregnancy, Pagets Beri Beri AVM)

NYHA heart failure classification
Class 1662F no limitation of activitySymptoms occur only on severe exertion; almost normal lifestyle possible Treat BP lipids and diabetes Smoking Cessation Exercise lifestyle adviceACE and betablocker (unless contraindicated)
Class 2662G some limitationSymptoms occur on moderate exertion; patients have to avoid certain siluations (e.g. carrying shopping up stairs  x
Class 3662H severe limitation of normal activitySymptoms on mild exertionactivity markedly restricted above plus Low Na dietavoid or withdraw antiarrhythmics, most calcium blockersfurther drug Rx – diuretics digoxin aldosterone antagonists ARBs hydrallazine nitrates
Class 4662I symptomatic at rest Endstage requiring specialist treatmentAs above plus mechanical assist devices, inotrope infusion palliative care


BNP – B type natriuretic peptide
<100pg/ml heart failure unlikely
>100pg/ml + clinical picture of failuremakes the diagnosis more likelyecho indicated.

Hormone secreted by the left ventricle in response to strain.

Raised in LV dysfunction, hypertrophy, ischaemia and failure.

Reduced renal excretion in renal failure (Cr>200) may artificially increase BNP.

BHF FF116 BNP in heart failure

HF treatments
reduce preload loop diuretics to reduce plasma volume and venous pressuresalt restriction also to reduce fluid overload
reduce afterload  vasodilators to increase venous capacitance
improve contractile function  inotropes
improve prognosis  ACE BB (additive)
devices  cardiac resynchronisation devices and defibrillators

Target all areas of RAS and SNS to slow or prevent further myocardial dysfunction & remodelling – aim for mid therapeutic dose ranges before adding in another drug



ACEI enalapril perindopril ramipril inhibit intracardiac RAS myocardial hypertrophy and remodelling -slowing progression and improving survival.

Betablockers bisoprolol carvedilol reduce chronic sympathetic overactivity slowing progression and improving survival.

Loop  diuretics

Aldosterone antagonists spironolactone eplerenone additional Rx improving survival in mod severe heart failure.  Helpful also in hypokalaemia.

ARB if ACE intolerant or …dual blockade if persistant symptoms despite optimum RX ?? Beware hyperkalaemia.

Hydralazine + Nitrates persistant symptoms esp AfroCaribean




Heart failure annual review

Check NYHA classification, BMI, smoking status/cessation advice, alcohol intake, BP, Cr&Es, fasting lipids (cholesterol & LDL), fasting blood sugar etc within the last 12 months.

patient pathway –

Patients, as a result of remembering their annual review date or having a reminder on their prescription will ring to book their annual review. The reception team will book a fasting bloods & BP appointment with one of the HCAs.

The HCAs will review the patients comorbidities using the SystmOne chronic disease icons page (checking for COPD, Asthma, HT, IHD/TIA/CVA) to decide the tests they have to perform. They will also arrange a 20 minute review with a Practice Nurse but a 30 minute appointment if they have asthma, COPD or a history of MI, angina, TIA or stroke.

The Practice nurses on completing the annual review, where no action is deemed to be necessary, will also document and inform the patient of their next planned review date and task the appropriate GP to code the medication review and reauthorise the prescriptions. Patients requiring further assessment or a change in medication will be referred to the GP.


Atrial fibrillation

Rapid chaotic ineffective atrial electrical activity producing pulse irregularly irregular in rate and volume with difference between apical and radial rates.

May be permanent persistant or paroxysmal.

ECG shows uneven baseline with absent o waves and irregular  QRS.


Hyperthyroidism, acute and chronic alcohol excess

IHD, RHD, hypertension, cardiomyopathy, pericarditis SSS atrial myxoma,

Pneumonia PE bronchial Ca

Atrial fibrillation

Rhythm Control DC cardioversion (after anticoagulation)Drugs – amodarone flecainide sotalol
(Ventricular)RateControl  digoxinverapamilbetablockers
Anticoagulation  see CHADS2

AFA – Clinicians Area

NICE CG36 Atrial fibrillation Jun 2006

NeLM New treatment options for AF Oct 07


CHADS2 warfarin or aspirin in AF
H Hypertension (systolic >160) 1
A Age over 75 years 1
D Diabetes 1
S Previous stroke or TIA 2


CHADS2 Score
0 aspirin
1 aspirin or warfarin
2 or more warfarin


Dabigtran (pradaxa)


Non-valvular AF plus or more risk factors 150mg bd

European Medicines Agency update on safety of Pradaxa Nov 2011

MHRA:Renal function testing of patients receiving dabigatran


Stroke TIA

Stroke = sudden loss of neurological function (due to a vascular cause) lasting for more than 24 hours.

Transient ischaemic attack (TIA) lasts less than 24 hours


SIGN 104 Stroke TIA management QRG Dec 08

SIGN 119 Dysphagia in Stroke Jun 2010 QRG

SIGN 118 Stroke Rehab Jun 2010

NICE CG68 Stroke Jul 2008

iTunes U CVA Rock Valley College


SIGN 108, 2008


999  Rapid transport to hospital and early brain imaging.
Thrombolysis within 3-4.5 hrs
within 24-48 hrs 300mg reducing to 75mg
BP Hypertension in the immediate 48hrs post-stroke period should NOT be treated (unless hypertensive encephalopathy etc) as this may cause extension.Pre-stroke antihypertensives should be stopped for 1-2 weeks and blood pressure monitored during this period, following which they may be re-introducedHypertension persisting more than 2-4 weeks after a stroke should be treatedStroke risk can be reduced by up to 40% if the diastolic BP is reduced by 6mmHg or the systolic BP is reduced by 10-12mmHg (irrespective of whether the BP is elevated or not)Lower BP to 140/85 mmHg (or to 130/80 mmHg in diabetic patients)
AF Check for atrial fibrillation and, if present, consider warfarinisation.
Statins  Statins are indicated as part of a secondary prevention treatment plan for patients following a stroke or TIA.NICE recommends 40mg of simvastatin for all first line.SIGN recommends 80mg of atorvastatin first lineAll CVA and TIA patients with a cholesterol of >3.5 mmol/l should be offered a statin unless contraindicated.This is in order to reduce the risk of a further CVA, but also to reduce the risk of MI; most patients who have had a CVA have a ~30% 10-year risk of CHD.
Thiazides and/or ACE inhibitors SIGN recommendeds even if the patient is normotensive and, in this case, BP should be reduced to the lowest level that the patient can tolerate.
Carotid endarterectomy Benefit of surgery relates to the degree of stenosis.Carotid endarterectomy for asymptomatic carotid stenosis reduces the risk of stroke by 30% over three years (Cochrane Review 2005).Early carotid scanning (SIGN) and consider endarterectomy in those with a carotid artery teritory stroke (unless severely disabled) or TIA, if stenosis is 50-99% in men, 70-99% in women.Recommended to be done within 2 weeks of admission. endarterectomy most beneficial if done within 12 weeks of TIA


ABCD2 TIA stroke risk score
A Age >60 1
B Blood pressure >140/90 mmHg 1
C Clinical features of the TIA unilateral weakness 2
speech disturbance without weakness 1
D1 Duration of symptoms >60 min 2
10-59 min 1
<10 min 0
D2 Diabetes DM 1


ABCD2 score
Risk of subsequent stroke at 2 days


Modifiable risk factors for stroke



fruit and veg


NICE TA210 Dec 2010 Clopidogrel and modified release dipyridamole in the prevention of occlusive vascular events


Antiplatelet drugs in CVA
Ischaemic CVA TIA PAD/MV
Clopidogrel aloneDipyridamole MR + aspirin if clopidogrel intoleratant Dipyridamole MR + aspirinDipyridamole MR alone if aspirin intolerant Clopidogrel alone


Clopidogrel 75mg (prasugrel 10mg od) stop 5d b4 surgery/dental extraction (discuss cardiologist)

dipyrimidole – increase up to 200mg bd over 2 weeks to minimise headache side effect

See also Aspirin and clopifogrel in MI NICE CG48 and CG94


Dyspepsia on aspirin
In patients experiencing dyspepsia, try a switch to enteric coated aspirin
If not, then add Omeprazole 20mg if the symptoms are not settling.
Those patients still experiencing dyspepsia on aspirin plus PPI, should be considered for Clopidogrel, and the PPI should be discontinued, except in high risk GI patients, where long term PPI cover should be considered. Persisting dyspepsia on Clopidogrel should require investigation.Even in patients with history of peptic disease can be treated with PPI plus aspirin.

EEP Infopoems Antithrombotic therapy after stent in patients already using anticoagulant



aspirin plus warfarin

MeReC Extra No. 28, 2007

A systematic review looked at whether aspirin added to warfarin in those at high risk of arterial thromboembolism (defined as MI, unstable angina requiring hospitalisation, CVA, TIA, systemic embolism) (Arch Int Med 2007;167:117-24).

Subgroup analysis showed the most significant advantage was in those with mechanical heart valves, who had a significant reduction in thrombotic events with a risk of GI bleed no greater than the other subgroups (ie. higher than with warfarin alone, but not higher than the overall risk for those on warfarin and aspirin).

American Heart Association recommends that aspirin (75mg) should be added to those on warfarin with mechanical heart valves.


QOF CHD Targets



Primary prevention CVS


fixed factors modifiable factors
agesexpremature FH (1st deg male <60 risk x1.5)ethnicity (south asia x1.4)premature menopause smoking statusweight/BMI/abdo circumferencealcohol consumptionBPDM/IGTlipid profile (LDLC/HDLC/TG)


NICE PH15 Identifying and supporting people most at risk of dying prematurely Sep 2008 QRG

Effectiveness and cost effectiveness of cardiovascular disease prevention in whole populations: modelling study BMJ May 2011

Total-C 10 yr risk Measures Reassess – Actions
<5 <15% Lifestyle 5 years
>15% LifestyleLipid breakdownCorrect secondary causes Annually
>5 <15% Correct secondary causes Annually
>5 >15% Correct secondary causesTrial of lipid lowering dietRecheck at 1 and 3 months Dietician Annually when stable
>7.5 Consider Familial Hypercholesterolaemia Refer (Coales)


CVD risk asssessment

CVD Scoring Tools





Joint British Societies coronary risk prediction chart




SIGN 97 2007 CVD risk estimation

For adults 30-75 years (NB Vasc Screening 40-75) with the following:

Hypertension, Smoking, FH premature CHD, clinical signs dyslipidaemia, Diabetes (in fact treat as 2ndry or use UKPDS)

For hypertensive patients on treatment, pretreatment levels should be used where possible when assessing risk.

Clinical judgement needs to be used for patients who have been well controlled for years and for whom a pre-treatment level is not available; however, if using treatment BP levels, bear in mind that the patient’s CVD risk is probably higher than expected.

Do not asses CVD risk already have established CVD, or Diabetes and over 40, FHC – treat as high risk anyway.

Lifestyle advice for all regardless of risk


in house patient pathway CVD prevention
Primary prevention Secondary prevention
No history of IHD, TIA, CVA, PVD includes patients on registers for IHD, CVA,TIA, PVD, diabetes
Well person check or referral by GP for CVD risk assessmentAppointment booked with  HCA for fasting bloods and BPHCA checks bloods according to the guideline; also to record BP.Patient asked to see PN in one week for resultsGP will action the pathology results in their in-box “to see nurse”Practice Nurse calculates CVD risk using QRisk2 using BMI, smoking status and FH of CVD Ensure lipid levels treated to target (TC <5.0 and LDL<2.5)if not refer to GPReturn to have BP if not at target(QOF standard <150/<90 for CVD, TIA or CVA)Refer to GP if BP on second occasion not at target


CVD risk
 <10%  reassure, lifestyle advice, no further action needed
10-19%  risk; lifestyle advice and offer 5 yearly checks.
> 20% to see the PN for lifestyle advice and arrange repeat fasting lipids and CVD risk assessment in 3 months.If then >20% then ask the patient to make an appointment with a GP having discussed statins using the PDA.Also refer the patient to a GP if the repeated total cholesterol is >7.5 or LDL>4.9 to assess the possibility of familial hyperlipidaemiaAnybody who has a primary CVD risk of >20% should be considered for statin – 40mg simvastatin F&Ftreat more intensively  TTT if established CVD


Vascular screening       NHS Healthcheck
1 face–to-face assessmentall patients 40 – 74 not already on a disease register for CHD, DM or HypertensionExceptions: Patients for whom it is not appropriate to review the chronic disease parameters due to particular circumstances e.g. terminal illness, extreme frailty,Informed dissentersClinical assessment will includeAge Ethnicity Sex BP BMI Waist circumferenceTotal cholesterol (near patient testing)Blood glucose monitoring (near patient testing)Medical history Family historyLifestyle Assessment Diet Exercise Smoking Alcohol
3 Communication of risk to all patients who undergo vascular assessment
4 Lifestyle advice to be given to all patients who undergo vascular assessment regard lessof risk score
5 Management of high risk patients including appropriate medication and referrals
6 Appropriate recall date recorded on patient’s computerised clinical record
7 System to follow-up DNAs


CVD Secondary Prevention   NICE CG48 2007 pdf
Patients with cinically evident confirmed or established CAD, CVD, PVD (+/- DM)
Statins eg simvastatin 40 mg TTT
ACE inhibitor
aspirin and clopidogrel for 12 months in the case of non-ST segment elevation acute coronary syndrome
Smoking cessation
Diet and lifestyle
Cardiac rehabilitation Offer to all patients who are stable.Sex can be resumed (after uncomplicated MI) after about 4w post MI.Phosphodiesterase inhibitors can be used from 6m post MI unless on nitrates/nicorandil


Lifestyle targets for all JBS 2005
Diet Total dietary fat <30% of total energy intakeSaturated fats <10% of total fat intake.Dietary cholesterol  < 300 mg/day.Replace saturated fats with an increased  MUFAat least five portions per day fresh fruit and vegetablesRegular (> 2 servings/week) intake of fish and other sources of omega-3 fatty acids
Salt  < 100 mmol/l day  –  <6 g NaCl or < 2.4 g Na
Smoking  Stop
Exercise regular aerobic physical activity for at least 30 minutes per day most days of the weeke.g. fast walking, swimmingrecent advice on this
Weight BMI 20-25 kg/m2 and avoid central obesityWC Caucasians < 102 cm men  < 88 cm  womenfor  Asians < 90 cm men < 80 cm women
Alcohol < 21 u/week men or < 14 u/week  women


Cholesterol and Triglycerides
Total Cholesterol <5.5 mmmol/l
LDL 2.0-3.4 mmmol/l
HDL 0.9-2.2 mmol/l
Triglycerides <2.0 mmol/l


<2.3 no Rx
>2.3 correct secondary causesstart trial of lipid lowering diet – 6mthen commence nicotinic acid or fibratemonitor 3m
>4.5 risk of pancreatitis – refer lipid clinic


Lipid guidelines for primary prevention
Target Population aged 40-74 no history of cardiovascular disease no diabetes Over 75s may be at high CV risk, especially if they smoke or have high BP, but most data on CV risk, including the Framingham data, include very few people >74y, and most risk calculators stop at 74y.NICE recommends balancing comorbidities, benefits and risks and treating according to clinical judgement,
Perform ‘prior risk assessment’ guestimate of  CVD risk when some of the data required for a formal risk assessment is absentallows those at highest risk to be identified and targeted for a full formal risk assessment with up to date data Perform formal CVD risk assessment if ‘prior risk assessment’ >20%/10yUse Framingham 1991 risk equation (including average of at least 2 systolic BPs, and data on LVH).
Adjust for ethnicity South Asian origin multiply CVD risk by 1.4
Adjust for FH Family history of coronary heart diseaseMale first degree relative under 55 with CHDOR Female first degree relative under 65 with CHD Multiply risk by 1.5 if one relative affected (ie. act if 10y CVD risk =13.3%)Multiply risk by 2 if 2 or more relatives affected (ie. act if 10y CVD risk = 10%).
Consider false negatives with CVD risk score below 20% but in whom the risk estimation may be falsely low:Low socioeconomic statusOn antihypertensives or lipid lowering drugsBMI >40Recently stopped smokingChronic condition that increases CVD risk (CKD, SLE, HIV, on antipsychotics). Use clinical judgement to determine whether to treat these individuals as high risk.
Offer statins to all at high risk



Lipid Guidelines  Secondary Prevention (RCN Clinical Craft Card)
Secondary prevention patients Angina ACS MI TIA CVA PAD
Other Risk factor modifications Smoking Cessation Diet Weight BP Antiplatelets bblocker/ACE in CHD
Established CVS disease Initiate rx with simva 40mglower dose or alternative if contraindications
Targets not achieved on initial doseTotal C 4mmol/l or LDL-C < 2 mmol/l Switch to HIS
Statins not tolerated consider fibrates, resins, nicotinic acid or ezetimibe
ACS Offer HIS immediatelyMeasure fasting lipids at 3m
Annual Review for all Repeat LFTs at 3 and 12m only unless otherwise indicatedReview lipids and risk factors annuallyNo routine CK


TC/ HDL ratio

should be less than 6

or if total cholesterol /hdl ratio is less than 6 then a  higher TC level is OK (?)

confusingly sometimes reported as HDL/TC ratio  (RC 44PF)


 V for Villains

VLDL carries endogenous TGs from liver to cells for storage and metabolism

H for Heroes

HDL carries cholesterol away from peripheral cells to liver for excretion

Serum cholesterol levels can vary by up to 20% through the course of the day – current guideles are for morning sample

NICE. Statins for prevention of cardiovascular events QRG 2006

Statins for primary prevention in people at low cardiovascular risk: a meta-analysis NelM )ct 2011


Primary preventionrisk > 20% but no history of CVDno target – fire and forget
Secondary preventionhistory of CVDcholesterol <4, LDL <2(audit standard chol <5 LDL<3)or a reduction of 30% in either


Starting and monitering statins

Simvastatin 40mg is advocated for first line use because of cost and efficacy.

Effective for lowering LDL cholesterol, but can increase HDL cholesterol (especially rosuvastatin) and lower triglycerides.

Other agents will be needed in some patients when a statin alone is insufficient for reducing LDL cholesterol, when they are intolerant of a statin, or when the triglyceride levels are very high.

Most authorities state the benefits of statin therapy in large populations greatly outweigh the adverse effects.

The main adverse effects liver damage,  rhabdomyolysis and peripheral neuropathy develops.

These adverse effects are more common when statins are combined with fibrates (especially gemfibrozil).

No need to monitor patients on 10 mg simvastatin.

All other patients should have baseline liver function tests which should be repeated 1-3 months after treatment is initiated. Thereafter, LFTs should be checked at intervals of 6 months for the first year of treatment, and then annually.

Only check CK   if patient develops  muscle pain/tenderness/weakness.

Start with e.g. Simvastatin 40mg and warn the patient about common side or serious side effects e.g. myalgia.

Check fasting lipids and ALT at 4 weeks. Uptitrate the dose if not at target  and repeat in another 4 weeks.

If that fails to achieve target try titrating to target using Atorvastatin 20mg then  40mg, then  80mg)

Stop statin if ALT x3 upper limit of normal or if has suspected myopathy with CK> 5 x normal.

If they have myalgia with a normal CK then try switching to Simvastatin 20mg or Pravastatin 40mg as an alternative.

If that fails consider Ezetimibe, Ciprofibrate or an anion exchange resin.

remember less than half of patients on treatment will reach their target  – don’t pursue blindly


Clinical scenario Use
Post ACS HIS Atorvostatin 80mg Rosuvostatin 20/40mg
Secondary Prevention S 40mg titrating up to S80 or equivalentAtorvostatin 10 -20mgif CI try lower dose of alternative eg pravastatin or atorvostatin 10mg and titrate up
Type 2 DM Over 40yrs +high risk S40
CKD Caution Simva CKD 4-5 Atorvorstatin Ok Pravastatin in transplants
CHF no indication for statins in HF

NICE CG67 Lipid modification May 2008



Fish oils omega 3 fatty acids


Omacor (fish oil) within 3m and up to 4y post MI

nelm.nhs.uk Fish oil and omega 3 fatty acids in CVD



Reduces cholesterol absorption from the intestine, is well tolerated and can be added to a statin to achieve the cholesterol target (increased rhabdomyolysis risk), or used alone in patients who are intolerant or uncontrolled on a standard or HIS.



Ezetimibe for the treatment of primary (heterozygous-familial and non-familial) hypercholesteroloemia


Nicotinic acid

(in secondary prevention only).

Abbott Laboratories has announced the discontinuation of nicotinic acid (Niaspan) due to commercial reasons. The only nicotinic acid-containing product now available is Tredaptive, a combination of laropripant and nicotinic acid. AUG 2011


Plant sterols and stanols

Naturally occuring compounds incorporated into consumer food products

Benecol and Flora Pro-active. Compete with cholesterol for intestinal absorption, lowering serum cholesterol concentration – 1 teaspoon a day is the maximum needed for cholesterol-lowering effects.



Fibrates are mainly used for mixed hyperlipidaemia, and can be added to a statin under specialist advice


Anion exchange resins


Familial hypercholesterolaemia Simon Broome criteria
Definite FH Possible FH
Children <16 yrscholesterol >6.7 mmol/l LDL >4.0 mmol/lAdultscholesterol >7.5 mmol/l LDL >4.9 mmol/l
PLUS tendon xanthomata in patient or 1st/2nd degree relative Plus either FH Mi in 2nd degree relative < 50 yearsor <60 years in 1st degree relative
OR DNA confirmation:LDL receptor mutation/familial defective apo B100/PCSK9 mutation OR FH of cholesterol > 7.5mmol/l in 1st or 2nd degree relativeor greater than 6.7 mmol/l in child, brother or sister aged younger than 16 years

NICE CG71 Familial hypercholesterolaemia Aug 2008

BHF Factfiles FH Nov 2009




Cholesterol controversies

Kendric etc





Low cost combined low dose combination of thiazide  atenolol  ramipril  simvastatin  and aspirin (or similar). Give to anyone at high risk plus all over 55s. Reduce simultaneously the four cardiovascular risk factors (low density lipoprotein cholesterol, blood pressure, serum homocysteine, and platelet function) regardless of pretreatment levels.

One-third of people taking this pill from age 55 would benefit, gaining on average about 11 years of life free from an IHD event or stroke.

source GPUpdate

The Indian Polycap Study (TIPS) Lancet 2009

First polypill data show promise Heart.org Mar 2009

Wald NJ, Law MR (BMJ 2003)





Other CVS risk factors

Resting HR

Xanthelasmata, arcus, and ischaemic vascular disease  BMJ Jul 2011





NICE CG109 Transient loss of consciousness in adults and young people Aug 2010

BMJ 2010:340:c880


Arrythmias SIGN

Arrythmias in CHD SIGN 94 Feb 2007


Long QT



Long QT syndrome BMJ 2010


Supraventricular tachycardia SVT







Amiodarone-lite – less effects on thyroid and lung function.



Acute, subacute or chronic inflammation of pericardium.  x
Idiopathic  x
Infective  x
CTD  x
Post MI (immediate)  x
Post MI (delayed) Dresslers Syndrome  x
Malignancy  x
Metabolic  x
Radio RX  x
thoracic surgery  x


Presents with sharp pleuritic chest pain relieved by leaning forward.



Pericardial effusion

Pericardial sac contains a thin film of fluid (<50mls) produced by the visceral pericardium



Pericardial effusion PUK

Pericardial effusion Medscape


Constrictive pericarditis

Thickened fibrotic pericardium adherent to myocardium restricting diastolic filling causing RHF.

  • Causes
  • acute viral or bacterial pericarditis
  • cardiac surgery
  • radiotherapy
  • TB

Rheumatic fever

Inflamatory multisystem reaction to following on 2-5 weeks after  group A beta haemolytic streptococcal infection in children. Rare in developed countries.










Rheumatic fever medscape

Rheumatic fever PUK

Rheumatic fever NHS Direct encyclopaedia Wales


Endocarditis Dukes Criteria
Major Definitive  blood cultures or

echocardiographic evidence

Minor Predisposing structural abnormality



suggestive cultures

suggestive echocardiography

2 major or 1 major + 3 minor or 5 minor

See also Duckett Jones Criteria



Endocarditis Prophylaxis and Dental Rx – Nobody requires endocarditis prophylaxis

NICE CG64 Prophylaxis against infective endocarditis Mar 2008



Acute myocardial  inflammation and necrosis.

  • Infections – Coxsackie B, EBV, CMV, influenza, Lymes, diptheria , fungal, Chagas
  • CTD – SLE sarcoid polymyositis
  • Drugs and toxins – Chemotherapy  Radiotherapy cocaine heavy metals
  • Idiopathic






EHJ Oct 2011


Sudden cardiac death in young people


Cardiac disease in the young (CRY) youtube channel



Dilated  post viral alcohol drugs familial post partum haematochromatosis thyerotoxicosis
Hypertrophic HOCM  familial
Restrictive  amyloid sarcoid haematochrmatosis





HOCM Medscape

BHF Cardiomyopathy

Cardiac Risk in the Young

US HOCM guidelines NeLM Nov 2009


Heart sounds and murmurs


Heart sound sites









Littmann education heart lung-sounds






Valvular heart disease


Valvular heart disease John Hopkins Medicine

Valvular heart disease AAFP 2001

Valvular heart disease heartpoint.com


Mitral valve disease

Mitral valve disease PUK





Mitral Stenosis



Mitral Stenosis
Tapping apex beat, parasternal heave (RVH)diastolic thrill at apex.
Rough rumbling mid-diastolic apical murmerbest heared in left lateral recumbant positionmore prominent after exercise (eg 10 sit ups).May be presystolic accentuation if patient in SR (cf AF)
Loud S1 + opening snap (short sharp high-pitched sound localised at or just inside the apex) after S2 ( the sooner the more severe the stenosis)
Mitral valve narrowing causing resistance to blood flow  from LA to LV.Increased left atrial pressure causes left atrial dilatation with pulmonary hypertension (with malar flush)May be AF.

Presents with SOB, fatigue, peripheral emboli.Occ small volume puse in advanced stenosis.

Signs of CCF – and pulmonary hypertension (a wave in JVP)

Signs of infective endocarditis – clubbing splinter haemhorrhages splenomegaly


Mitral Incompetence
strong localised apex beat displaced left  and downwards(LVH)apical systolic thrill
pansystolic atrial murmer radiating to  left axilla
Quiet S1 +/- S3 (regurgitated left atrial blood)
May be signs of pulmonary hypertensioneg Loud P2 + parasternal heave + malar flush
Retrograde flow of blood from LV to LA during systole.Causesacute papillary muscle rupture

rheumatic fever


mitral valve prolapse

left venricular dilatation



Tricuspid incompetence

Backflow of blood from RA to RV during systole.

Relatively uncommon amongst valve lesions.

  • Congenital (ebstein anomaly, ostium primum defect)een in carcinoid.
  • Functional in RV dilatatin eg pulmonary hypertension.
  • Rheumatic HD and Endocarditis ( esp IV drug users)
  • Metabolic (cirrhosis, carcinoid)




Tricuspid valve disease PUK


Aortic valve disease





Aortic stenosis
Slow rising small amplitude pulse +/- anacrotic notch.Heaving displaced apex (LVH) + systolic thrill.
midsystolic ejection murmer – may radiate to right of neck.Heard all over chest but loudest at base
Quiet or absent S2
Presents with angina, syncope or LVF.
Commonest valve disease in UK.Causes pressure overload in LV with LVH and low output failure. May be angina/MI and syncope/dizzyness/sudden death on exercise.causespost Rheumatic

due to calcification of congenital bicuspid valves

or calcification/degeneration of normal valves in elderly – sclerosis cf true stenosis)





Aortic regurgitation
Collapsing/water-hammer pulse(Bisferins in combined AS/AI)Corrigans pulse at carotid arteries.May be signs LVH.
Early diastolic murmer at LSE (RSE in Marfans and syphilitic aortitis)patient sat up and holding breath in max inspiration.
Femoral pulses are dimished and delayed compared to radial and BP lower in legs
CausesValve leaflet damage  – Endocarditis Rheumatic heart diseaseDilatation of aortic root – hypertension CTD Ankylosing spondilitis, Syphilis and MarfansReflux of blood from aorta into LV during diastole causing diminished pulse volume and volume overload in LV – (initially increasing stroke volume then leading to dilatation and LVF) 







Aortic valve disease PUK


Pulmonary stenosis


Rare – occurs as part of congenital heart conditions.



Pulmonary regurgitation

Pulmonary regurgitation medscape

Pulmonary regurgitation mykentuckyheart.com

Pulmonary valve disease PUK


Pulmonary Hypertension

Persistant raised pulmonary arterial pressure

  • Idiopathic
  • Left Heart Disease
  • Chronic Lung disease
  • Recurrent PE
  • CTD
  • drugs (amiodarone)


Congenital heart disease









Congenital Heart Disease NHS Choices


Cyanotic congenital heart disease

Conditions involving right to left shunting of venous blood into the systemic circulation.



Transposition of great arteries

Reversal of pulmonary artery and aorta, usually with asosciated PDA (physiological correction).

Presents at birth (if not detected antenataly) with cyanosis requiring immediate surgery.




Failure of closure shortly after birth allows persistant right to left shunt.

May lead to Eisenmengers if uncorrected.




Tetralogy of Fallot
1 overriding aorta
3 pulmonary stenosis
Commonest cyanotic heart disease presenting in infancy



Uncorrected left to right shunting causes pulmonary hypertension and increased right sided pressures with reversal of the shunt and venous blood entering the general circulation.



Acyanotic congenital heart disease




Coartction of the aorta
Systolic murmer over precordium +/- LVHMay be visible pulsations on the back
Femoral pulses are dimished and delayed compared to radial and BP lower in legs


Hypoplastic left heart syndrome



Left parasternal heave due right ventricular enlargement.
Mid-systolic nurmer 3rd left intercostal space
Wide relativel fixed split S2
Direct communication between the atria with left to right shunt.May be asymptomatic or present with SOB CCF or CVA.Large untreated defects can lead to Eisenmengers.http://youtu.be/e46jtin-H50http://youtu.be/Gros-u7YCTk



Commonest congenital heart defect.

Smaller lesions may cause asymptomatic  left to right shunt but uncorrected larger defects lead to heart failure, pulmonary hypertension and Eisenmengers.






Pulmonary atresia

Pulmonary atresia



SIGN 2006, 89 BMJ IC

NICE TA 223 May 2011

Drug therapy: cilostazol (a peripheral vasodilator)

Recommended in claudication after walking short distances, stopping after 3 months if no improvement in symptoms.

Antiplatelets Don’t use aspirin and warfarin together in PAD to reduce cardiovascular complications.

Antiplatelet agents for intermittent claudication Cochrane 17/11/11

Differential diagnosis (BMJ 2007;334:746).

SIGN 89 2006



ABPI measurement
<0.9  significant
<0.8  risk of ulceration
<0.5  critical ischaemia / P

see also


With the patient lying down put the sphyg. cuff around the lower leg, above the ankle.

Find the dorsalis pedis pulse (or posterior tibialis) and using a doppler to listen to this, inflate the cuff slowly until the pulse disappears.

Then deflate slowly noting the pressure at which the pulse becomes returns.

Repeat on this leg then do it twice on the other leg.

Take the highest of the four readings.

Then measure the brachial systolic pressure in the usual way.


Cardiac investigations
Echocardiography http://youtu.be/QdkJ6qzMfNEhttp://youtu.be/SaORcN29CtMhttp://youtu.be/QdkJ6qzMfNEEchocardiography PUK
Trans-oesophageal Echocardiography (TEE) http://youtu.be/9Us9mXXILSkhttp://youtu.be/zLB_mY57B8M
Treadmill (stress) test  http://youtu.be/KsHXCebWMec
Tilt Table Test http://youtu.be/F0RQPI7ndnohttp://youtu.be/LBTjIxFisnQ
Radionucleotide Scanning http://youtu.be/2tHSAliJgQo
Cardiac Catherization http://youtu.be/xwh3tlFaVm0


Coronary Angioplasty
PTCA http://youtu.be/smVhcKYkYSkhttp://youtu.be/gvRtP3wl_AY
Stenting (PTCS) http://youtu.be/SKmCJ-nEDhg
drug eluting stents http://youtu.be/SKmCJ-nEDhg


electrophysiological studies
Electrophysiological Studies  http://youtu.be/iwdZb1_FexM
Radio-frequency Ablation  http://youtu.be/J1jAwbbTfAg
Brachytherapy radiation
Permanent Pacemaker Implantation http://youtu.be/UdaTqPSO3Rshttp://youtu.be/9nccIc3Qflo
Bi-Ventricular Pacing for Heart Failure http://youtu.be/A-MLRYuCRIM
Automatic Implantable Cardiovertor-Defibrillator http://youtu.be/UdaTqPSO3Rshttp://youtu.be/9nccIc3Qflo
Automated External Defibrillators http://youtu.be/UdaTqPSO3Rshttp://youtu.be/9nccIc3Qflo


Cardiac imaging




British Society of Cardiac Imaging

British Heart Foundation BHF Factfile Cardiac Imaging

MD-CT angiogram & MR angiogram

Coronay calcium scoring



Cardiac catheterisation values
Mean arterial pressure SBP+2xDBP/3 70-105 mm Hg
CVPRAP 2-6 cm H20 2-8 mm Hg
Right Ventricle Pressure 20-30 mm Hg systolic0-8 mm Hg diastolic
Pulmonary Artery Pressure 20-30 mm Hg systolic PAS8-15 mm Hg diastolic PAD10-20 mm Hg mean PAM
Pulmonary Artery Wedge Pressure 4-12 mm Hg
Cardiac output Heart rate X stroke Volume 4-8 l/ min
Cardiac Index CO/Body Surface Area BSA 2.5 – 4 l/min/m2
Stroke Volume CO/HR 60-100 ml/beat
Stroke Volume Index SV/BSA 30-60 ml/beat/m2
Systemic Vascular Resistance MAP-RAPx80 / CO 900-1200 dynes/sec/cm5
Systemic Vascular resistance index MAP-RAPx80 / CI 1360-2200 dynes/sec/cm5/m2



Pacemaker Codes
1st letter Chamber thats paced Atria Ventricle Dual Other/Not applicable
2nd letter Chamber thats sensed Atria Ventricle Dual Other/Not applicable
3rd letter Pulse Generators response Inhibited Triggered Dual (both) Other/not applicable
4th letter Pacemakers programmability Programmable – basic functions Multiple parameters Communication eg telemetry Rate Responsiveness None
5th letter Pacemakers response to tachycardia Paciong Shock Dual Shock and Pace Other ie none (ERFIQ Lippincott 2007)


Cardiac surgery

Coronary Artery Bypass Graft (CABG) and MIDCAB




Transmyocardial Revascularization (TMR,DMR,PMR)


Myocardial Reduction Surgery


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