cardiology - 1 file download

Maysah Al-Mulla OHCM, Passmedicine

Cardiology

OBJECTIVES

- Chest pain

ACS

MI

Angina

- Heart murmurs

- HTN

- Arrhythmia

- DVLA

- Cardiovascular diseases in pregnancy

- Heart failure

- Pericardial disease

- Valvular disease

- Rheumatic heart diseases

Causes of Chest pain

Condition Characteristic exam feature Myocardial infarction Cardiac-sounding pain

heavy, central chest pain they may radiate to the neck and left arm

nausea, sweating elderly patients and diabetics may experience no pain

Risk factors for cardiovascular disease

Pneumothorax History of asthma, Marfan's etc Sudden dyspnea and pleuritic chest pain

Pulmonary embolism Sudden dyspnea and pleuritic chest pain Calf pain/swelling Current combined pill user, malignancy

Pericarditis Sharp pain relieved by sitting forwards May be pleuritic in nature

Dissecting aortic aneurysm

'Tearing' chest pain radiating through to the back Unequal upper limb blood pressure

Gastro-oesophageal Burning retrosternal pain


reflux disease Other possible symptoms include regurgitation and dysphagia

Musculoskeletal chest pain

One of the most common diagnoses made in the Emergency Department. The pain is often worse on movement or palpation.

May be precipitated by trauma or coughing

Shingles

Pain often precedes the rash

NICE guidelines on assessing a patient you suspect having a cardiac chest pain

Patients presenting with acute chest pain

Immediate management

GTN ASA 300mg. NICE do not recommend giving other antiplatelet

agents (i.e. Clopidogrel) outside of hospital Do not routinely give oxygen, only give if sats < 94%*

- People with oxygen saturation (SpO2) of less than 94% who

are not at risk of hypercapnic respiratory failure, aiming for SpO2 of 94-98%.

- People with chronic obstructive pulmonary disease who are at risk of hypercapnic respiratory failure, to achieve a target SpO2 of 88-92% until blood gas analysis is available

Perform an ECG as soon as possible but do not delay transfer to hospital. A normal ECG does not exclude ACS

Referral Current chest pain or chest pain in the last 12 hours with an abnormal ECG:

- Emergency admission Chest pain 12-72 hours ago:

- Refer to hospital the same-day for assessment Chest pain > 72 hours ago

- Perform full assessment with ECG and troponin measurement before deciding upon further action

Patients presenting with stable chest pain

Anginal Pain Constricting discomfort in the front of the chest, neck,

shoulders, jaw or arms Precipitated by physical exertion

Relieved by rest or GTN in about 5 minutes

Patients with all 3 typical angina Patients with 2/3atypical angina

Patients with 0/3Non angina chest pain


Cardiovascular risk factors

Smoking hx DM

HTN Dyslipidemia

Family hx of premature CKD

Other cardiovascular diseases Estimation of risks Typical angina + risk of CAD>90%

Men older than 70 Women older than 70 with high risk and typical symptoms

No diagnostic tests Treat as known CAD

Risk of CAD 61-90% Women older than 70

Coronary angiography

Risk of CAD 30-60% Functional imaging

SPECT Stress echo MR perfusion MR for stress induced wall

motion abnormalities

Risk of CAD 10-29% CT calcium scoring

Angina pectoris

Types Causes Management (NICE 2011)

Stable with activity relieved by rest

Can be induced by cold, heavy meals or emotions

Atheroma AS, HOCM, anemia

Modify risk factors ASA+statins GTN for attacks BB or CCB CCB if alone should

be rate limiting (verapamil or diltiazin)

CCB+BB (use long

acting dihydroperidine CCB)

SEQUENCE: Increase doses of monotherapy

Add combination If can’t tolerate a combination therapy:

- Long acting nitrate

Unstable with no activity or with Decubitus

when lying flat

Variant coronary artery spasm


- Ivabradine - Nicorandil - Ranolazine

If on combination, add third only if before CABG or

PCI NO BB+CCB heart

block if nitrate

tolerancetake second dose after 8 hrs

Ivabradine Act on *funny* channelsreduce HR Referral Diagnostic uncertainty

New angina of sudden onset

Recurrent angina if past MI or CABG Angina uncontrolled by drugs Unstable angina

Heart Sounds

S1 S2 S3 S4 Closure of mitral and

tricuspid valve

Closure of aortic and

pulmonary valves

Diastolic filling of the

left ventricle

Atrial contraction

against stiff ventricle

Normal is <30 yrs Causes of a loud

S1 - mitral stenosis

- left to right shunts

- short PR interval, atrial premature

beats - hyperdynamic

states

Causes of a quiet

S1 - mitral

regurgitation


Unmodifiable risk factors Modifiable risk factors

Increasing age Male gender Family history

Smoking Diabetes mellitus Hypertension

Hypercholesterolaemia Obesity

ACS

STEMI NSTEM I Unstable angina


ACUTE CORONARY SYNDROME

Diagnosis Elevated cardiac exams (then they decrease) And either:

- Symptoms of ischemia - ECG changes

Symptoms Acute central chest pain >20 mins Dyspnea, nausea, sweating Silentno chest pain DM and Old Sometimes you may have stroke, syncope, MI, pulmonary edema

Signs Anxiety, pallor

Tachy or bradycardia Hypo or hypertension S4 Signs of heart failure Pansystolic murmur

Low grade fever Investigations ECG (* see booklet)

CXR: - Cardiomegaly - Pulmonary edema - Widened mediastinum Cardiac enzymes: - Trop I and T rise in 3-12 hours peak in 24-48 hrs decrease in

5-14 days - CKMB rise in 3-12 hours peak in 24 hours decrease in 48-72

hours

Types Unstable angina STEMI

NSTEMI Complications Cardiac arrest (most common cause of death, caused by VF) ACLS

Cardiogenic shock use inotropes Chronic heart failure Loops diuretics, ACEI, BB Tachyarrhythmias (VF, VT) Bradyarrhythmias (AV block after inferior MI) Pericarditis (48 hrs) - Dressler syndrome 2-6 weeks) fever, pleuritic pain, pericardiac effusion, high ESR NSAIDs

Left ventricular aneurysm persistent ST elevation Left ventricular free wall rupture (1-2 weeks) patients present with

HF and cardiac tamponade pericardiocentesis/thoracotomy

VSD (1 week) HF with pansystolic murmur ECHO to rule out MR do surgical correction

Acute MR (with infero-posterior MI) early to mid diastolic


murmur vasodilator therapy and surgical correction RV infarction ST elevation in V3/4 give fluids and avoid diuretics

and nitrates

Management Pre-Hospital Arrange ambulance

ASA 300mg, GTN, morphine, metoclopramide

Hospital STEMI PCI if symptoms within 12 hours from presentation, and you can facilitate PCI within 90 mins

Thrombolysis if PCI cannot be done (target is <30min from admission but contraindicated if >24hrs from

symptoms) but if ECG within 90mins still has <50% improvement the transfer to PCI

BB ACEI within 24 hrs of MI even if normotensives (especially

if LV dysfunction or HF)

Dual antiplatelet for 12 months NSTEMI BB and nitrates

Antithrombotic fondaparinux if low bleeding risk and no angiography planned in the next 24 hrs

If angiography is planned within 24 hrs or Cr is >265 the unfractionated heparin is the choice

Assess the GRACE risk Coronary angiography within 96 hours if 6 months

mortality is more than 3% or the patient is unstable High risk patients: GPIIb/IIIa antagonists and angiography within 96 hrs, clopidogrel and ASA for up to 12 months Low risk patients: Clopidogrel for 12 months Discharge troponin if negative

Subsequent management

Address modifiable risk factors - Diet: Mediterranean style diet, NO oily fish or omega 3

- Exercise: 20-30 mins

- PDE5 inhibitors can be used 6 months after MI but not with nitrates Prophylaxis against thromboembolism

ASA Long term B blockage

ACEI Statins

Aldosterone antagonists within 3-14 days after MI (preferably after ACEI) for HF or LV dysfunction

Dose adjusted insulin infusion to keep the glucose less than 11 Discharge after 5-7 days


Return to work after 2 months Avoid intercourse for 1 month Avoid travels for 2 months Don’t return to work if airtravel pilot, air traffic control, divers If heavy manual labor advise light work 5 weeks FU for symptoms

3 months FU for lipid profile Thrombolysis ECG criteria:

- ST elevation >1mm in 2 or more limb leads or >2mm in 2 or more chest leads

- LBBB - Posterior changes (deep ST depression and tall R waves in leads V1-

V3) Examples:

- Alteplase (should be followed by unfractionated heparin), Tenecteplase (preferred in out of hospital setting) (both less death but more stroke)

- Streptokinase Contraindications: - GI bleed <1 month - Non compressible punctures <24 hrs - Recent hemorrhage, trauma or surgery (including dental extraction)

<3 weeks

- coagulation and bleeding disorders - intracranial neoplasm - stroke < 3 months - aortic dissection - recent head injury - pregnancy or <1 week postpartum - severe hypertension >180/110

PCI Poor response or intolerance to medical rx Refractory angina in patients not suitable for CABG

Previous CABG Post thrombolysis in patients with severe stenosis, symptoms or

+stress test Complications:

- Restenosis - Emergency CABG

- MI - Death

CABG Indications: - Left main disease - Triple disease involving the proximal part of the LAD


Arrhythmias (look at the 2015 UK resuscitation guidelines)

Causes Cardiac: MI

CAD LV aneurysm

Mitral valve disease

Cardiomyopathy Myocarditis, pericarditis

Non cardiac: Caffeine

Smoking/alcohol Drugs (B2 agonist, L dopa, digoxin)

Metabolic imbalance Pheochromocytoma

Presentation Palpitations, chest pain

Syncope/presyncope Hypotension Pulmonary edema

Investigations CBC, FBS

Electrolytes TFTs

ECG, 24 hrs ECHO MS, HCM

Bradycardia HR >40 with no symptoms drugs, sick sinus, hypoth - No treatment, avoid the drugs HR<40 with symptoms - 0.6-1.2mg atropine IV (up to 3) - Temporary pacing wire - Isoprenaline infusion - External cardiac pacing

Narrow complex

tachycardia (no

adenosine in asthma, give

Verapamil)

Sinus tachycardia rate control if necessary Atrial tachyarrhythmia

- AF no P waves

- Atrial flutter atrial rate 260-340, ventricular rate 150 (2;1 block) - Atrial tachycardia give digoxin specific antibody, keep K 4-5

- Multifactorial atrial tachycardia in COPD, correct the hypoxia and hypercapnia, consider verapamil or BB if HR >110

- Junctional P wave is either buried in the QRS complex or right after the QRS vagal maneuvers, adenosine, and ablation. If recurrence

give BB or amiodarone - WPW:

ablation, flecanide, satolol (DON’T GIVE IN AFIB), amiodarone


Wide complex tachycardia

VT/VF Torsade de pointe (VT)

Holiday heart

syndrome

Binge drinking conduction disturbances

Ventricular tachycardia

Types Monomorphic - Caused by MI Polymorphic - Torsade de pointe (long QT) MgSO4 over 10 min 2g (can lead to VF

and death)

Long QT Causes Congenital

Jervel-Lange-Neilsen (deafness with abnormal K channel)

Romano-Ward (no deafness) Drugs

TCA Chloroquine

Amiodarone, satolol, class 1a anti arrhythmic Erythromycin, anti-histamines

Others: Electrolytes hypo Ca, hypo K, hypo Mg

MI, myocarditis Hypothermia SAH

Types Long QT 1

Exertional syncope (swimming) Long QT 1

Syncope after emotional stress, exercise or auditory stimuli Long QT3

Events occur at night or rest

Management Avoid precipitating factors

BB (NOT SATOLOL) Implantable defibrillator

Management See 2015 UK resuscitation guidelines Drugs - Amiodarone (thru central line)

- Lidocaine (careful if LV dysfunction )

- Procainamide If fails use EPS or ICD

NO VERAPAMIL IN VT


Atrial fibrillation

Rate Atrial rate is 300-600 Causes Cardiac

MI HF Cardiomyopathy

Mitral valve disease Extra-Cardiac

Thyroid disease Pneumonia Caffeine Alcohol Post-op K/Mg imbalance

Symptoms Chest pain Palpitations SOB Fainting

Investigations ECG Blood tests (CBC, electro, TFTs) Echo

Classifications First detected episode Recurrent episodes if 2 or more - If the episode terminates spontaneously less than 7 days

Paroxysmal - Non limiting more than 7 days Persistent

- Permanent cant cardiovert do rate control and anticoagulation Rate control and maintenance of sinus rhythm

Rate control (Risk of bradycardia if BB+CCB (like verapamil and diltiazem)

- BB - CCB (diltiazem)

- Digoxin (not first line, only in HF) Rhythm control (<65 yrs, new onset, correctable, symptomatic, CHF)

- Satolol - Amiodarone - Flecainide

Cardioversion Acute (<48 hrs)

- Ill, unstable electrical cardioversion - Stablepharmacological or elective electrical cardioversion

- Start LMWH >48 hrs - At least 3 weeks of anticoagulation before cardioversion


- TEE to exclude left atrial thrombus if excluded then heparinize and cardiovert immediately (electrical)

- If high risk of cardioversion failure, give at least 4 weeks of amiodarone or satolol prior to cardioversion

- Post cardioversion anticoagulation for at least 4 weeks

Anticoagulation CHA2DS2-VASc score (see below)

Apixaban - Prior stroke or TIA

- 75 yrs or more - HTN

- DM - Symptomatic HF

Dabigatran - Previous stroke, TIA or embolus

- LV EF <40% - NYHA class 2 or more - Age 75 or more - Age 65 or more if DM, HTN or CAD Rivaroxaban - Prior stroke or TIA - CHF - DM, HTN - 75 yr or more

Warfarin (INR 2-3)

Post-stroke Following a stroke, Warfarin is the choice of anticoagulation In acute stroke and absence of hemorrhage commence

anticoagulation after 2 weeks (unless large cerebral infarction) Atrial flutter

Manage same as Afib (it is more sensitive to cardioversion, also ablation of tricuspid isthmus is curative)

CHA2DS2-VASc SCORE for need of anticoagulation

Risk factor Points C Congestive heart failure 1

H Hypertension (or treated hypertension) 1 A2 Age >= 75 years 2

Age 65-74 years 1

D Diabetes 1

S2 Prior Stroke or TIA 2

V Vascular disease (including ischemic heart disease and peripheral arterial disease)

1

S Sex (female) 1


Scoring

0 No treatment 1 Males: consider anticoagulation

Females: No treatment 2 or more

Offer anticoagulation

HASBLED SCORE (for risk of bleeding with anticoagulation)

Risk factors Score

H Hypertension, uncontrolled, systolic BP > 160 mmHg 1

A Abnormal renal function (dialysis or creatinine > 200) Or

Abnormal liver function (cirrhosis, bilirubin > 2 times normal, ALT/AST/ALP > 3 times normal

1 for any renal abnormalities

1 for any liver

abnormalities

S Stroke, history of 1 B Bleeding, history of bleeding or tendency to bleed 1

L Labile INRs (unstable/high INRs, time in therapeutic range < 60%) 1 E Elderly (> 65 years) 1

D Drugs Predisposing to Bleeding (Antiplatelet agents, NSAIDs) Or Alcohol Use (>8 drinks/week)

1 for drugs 1 for alcohol

3 or more means high risk of bleeding

General cardiac investigations and management

Pacing Indications for temporary pacing Symptomatic bradycardia Anterior MI with AV block Inferior MI if AV block Drug resistant SVT and VT

Indications for permanent pacing Complete AV block

Mobitz II Persistent AV block after anterior MI

HF Drug resistant tachyarrhythmias

CRT HF with EF <35% and QRS >120ms

ECG Look at the booklet

Exercise ECG Indication IHD

Exercise induced arrhythmias


Contraindications Recent Q waves MI <5 days or unstable angina

Severe AS Uncontrolled HTN, arrhythmia orHF

Myocarditis / pericarditis

PE/aortic dissection Stop if

Chest pain, dyspnea, cyanosis Feeling faint or exhausted ST >1mm Arrhythmia Fall in BP more than 10mmhg from baseline 90% of max HR achieved (220-age)

Heart Failure

Classification Systolic dysfunction - EF <40

- Causes IHD, MI, cardiomyopathy Diastolic dysfunction

- EF>50% - Causes Pericarditis, restrictive cardiomyopathy, HTN

Left ventricular failure - PND, orthopnea, SOB, nocturnal cough with pink sputum, wheeze,

weight loss, cold peripheries Right ventricular failure - Causes Pulmonary stenosis, lung diseases - Symptoms LL edema, ascites, TR Low output HF

- Pump failure and negative inotropes drugs - Excessive preload like MR or volume overload (NSAID cause fluid

retention)

- Chronic excessive afterload like AS and HTN High output HF

- Pregnancy, anemia, hyperthyroidism NYHA classification

Class I - No limitation, no symptoms Class II - Mild symptoms

- Slight limitation with ordinary physical activities

Class III - Moderate symptoms - Marked limitation with less than ordinary activities


Class IV - Severe symptoms - Unable to carry out any activities without symptoms, even at rest

Diagnosis With previous MI - ECHO in 2 weeks

With no previous MI - Measure BNP If high echo in 2 weeks if raised echo in 6 weeks

BNP levels - High >400pg/ml - Raised 100-400 - Normal <100

High BNP - LVH - Ischemia - Tachycardia - HYpoexemia - GFR<60, liver cirrhosis - COPD - Diabetes - Sepsis

Low BNP - Obesity

- Diuretics - ACEI, BB, ARBs, aldosterone antagonists

Management Acute management Sit up O2 Diamorphine 1.25-5mg IV slowly (careful in liver disease or

COPD) Furosemide 40-80mg IV slowly (more in renal failure) GTN (NOT if SBP<90) If SBP ≥100 start nitrate infusion 2-10mg/hr

If still no improvement

Further dose of furosemide 40-80mg CPAP Increase nitrate infusion If SBP< 90 treat as cardiogenic shock

Chronic management Mortality improvement (no improvements with furosemide or digoxin)

- ACEI - Spironolactone 25mg/day (risk of hyperkalemia)

- BB - Hydralazine with nitrates


NICE guidelines

First line ACEI+BB Second line aldosterone antagonists OR angiotensin II receptor

blocker OR hydralazine+nitrite If no symptomatic relief CRT or Digoxin

Influenza and pneumococcal vaccine Diuretics (you can give bumetanide 1-2mg/day or metolazone 5-

20mg/day) be careful of low K caused by any conditions in combination with digoxin as

toxicity increases

Murmurs

Innocent murmurs

Soft blowing in pulmonary area or buzzing in aortic area No radiation

Vary with posture No thrills or added sounds No diastolic component Asymptomatic

Type of Murmur Conditions

Ejection systolic Aortic stenosis

Pulmonary stenosis, HOCM ASD, Fallot's

Pan-systolic Mitral regurgitation (blowing) Tricuspid regurgitation (blowing)

VSD

Late systolic Mitral valve prolapse Coarctation of aorta

Early diastolic Aortic regurgitation (blowing) Graham-Steel murmur (pulmonary regurgitation)

Mid-late diastolic Mitral stenosis (rumbling)

Austin-Flint murmur (severe aortic regurgitation) Rumbling

Continuous PDA (machinery)


Hypertension

BP ranges NICE definitions Clinical BP readings persistently ≥140/90

24 BP monitoring ≥135/85 Causes Essential HTN 90%

Secondary HTN

- Renal disease GN Pyelonephritis APKD Renal artery stenosis

- Endocrine Primary hyperaldosteronism Pheochromocytoma Cushing, acromegaly

Primary adrenal hyperplasia (11 betahydroxylase def) - Others

Coarctation of the aorta Glucocorticoids, NSAIDs, OCPs

Pregnancy Classifications Stage I

- Clinic BP ≥140/90, AMBP or HBPM ≥135/85 Stage II

- Clinic BP ≥160/100, AMBP or HBPM ≥ 150/95 Severe - Systolic ≥180 or diastolic BP ≥110

Symptoms Headaches, visual disturbances, seizures Investigations U&E, urinary proteins renal disease

HbA1C coexisting DM Lipids hyperlipidemia

ECG LVH Funduscopy hypertensive retinopathy

Diagnosis Clinic measurement in both arms, repeat of >20mmhg difference, if still

repeat measurement in arm with higher BP Take 2nd reading at clinic (if >140/90), with the lowest to determine

further plan

AMBP or HBPM if BP ≥140/90

AMBP - 2 readings per hour, average of 14 readings

HBPM - For each BP recording, two consecutive measurements need to be


taken, at least 1 minute apart and with the person seated - BP should be recorded twice daily, ideally in the morning and evening - BP should be recorded for at least 4 days, ideally for 7 days - Discard the measurements taken on the first day and use the average

value of all the remaining measurements

Management Lifestyle modification

Drugs (see below)

When to treat AMBP/HBPM ≥ 135/85

- <80 years, with one of the following: Target organ damage

Cardiovascular diseases Renal disease

DM 10 cardio risk is ≥20%

AMPB/HBPM ≥ 150/95 - Drug treatment regardless of age BP ≥180/110 - Immediate treatment should be considered - If there are signs of papilledema or retinal hemorrhages same day

assessment by a specialist - Referral if a pheochromocytoma is suspected

Trials in HTN

STOP-2 The 1999 Swedish Trial in Old Patients with Hypertension-2 study looked at whether older drugs (beta-blockers or thiazides) or newer drugs (ACE inhibitors or calcium channel blockers) were better at preventing fatal cardiovascular disease. Main results

old and new antihypertensive drugs were similar in prevention of cardiovascular mortality or major events

decrease in blood pressure was the most important factor in the prevention of cardiovascular events in this age group

ALLHAT The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial was

a large randomized controlled trial that was started in 1994 and reported in 2002. ALLHAT compared amlodipine, chlorthalidone (a thiazide), lisinopril and doxazosin.

Over 40,000 patients aged 55 years or older who had hypertension with one other risk factor (for example diabetes) were included in the trial.


Main results

chlorthalidone outperformed lisinopril in preventing cardiovascular disease, a surprising finding which has been debated since (particularly in relation to the large number of black patients in the trial (ACE inhibitors are known to be less effective in this group)

the doxazosin arm was stopped prematurely due to a higher incidence of

heart failure 60% of patients reached the target blood pressure of 140/90 mmHg (it was

generally thought prior to the trial that blood pressure targets were more difficult to achieve)

ASCOT The 2003 Anglo-Scandinavian Cardiac Outcomes Trial - Blood Pressure Lowering Arm was a double-blinded, randomized controlled trial of around 20,000 patients with hypertension and other risk factors. Patients were randomized to either atenolol (with the addition of bendroflumethiazide if needed) or amlodipine (with the addition perindopril if needed). The primary outcome was non-fatal myocardial infarction (MI)

and fatal ischemic heart disease (IHD).

Main results

the study was stopped prematurely because of a higher death rate in the atenolol assigned group

the group receiving amlodipine-based regimes had a non-significant 10% reduction in primary outcomes (non-fatal MI plus fatal IHD) and significant

reductions in nearly all secondary cardiovascular endpoints and new-onset

diabetes


Drug Mechanism of action Common side-effects

Notes

ACEI Inhibit the conversion angiotensin I to angiotensin II

Cough Angioedema Hyperkalaemia

First-line treatment in younger patients (< 55 years old)

Less effective in Afro-Caribbean patients

Must be avoided in pregnant women

Renal function must be check 2-3 weeks after starting due to the risk

of worsening renal function in patients with renovascular disease

Drug names end in '-pril' CCB Block voltage-gated

calcium channels relaxing vascular

smooth muscle and force of myocardial

Flushing

Ankle swelling Headache

First line in older patients (>= 55

years old)


contraction

Thiazides Inhibit sodium absorption at the

beginning of the distal convoluted tubule

Hyponatraemia Hypokalaemia

Dehydration

Have a very weak diuretic action

ARBS Block effects of angiotensin II at the AT1 receptor

Hyperkalaemia In patients who cant tolerate ACEI (cough)

Drug names end in '-sartan'

Rheumatic fever

History (Group A beta hemolytic) Strep pyogen infection 2-6 weeks prior to presentation

ASOR >200iu/ml History of scarlet fever

+throat swab High Dnase B titre

Criteria 2 major OR 1 major+2 minor (Jones criteria)

Major criteria - Erythema marginatum

- Sydenham's chorea - Polyarthritis

- Carditis (endo-, myo- or peri-) - Subcutaneous nodules

Minor criteria - Raised ESR or CRP - Pyrexia - Arthralgia (not if arthritis a major criteria) - Prolonged PR interval

Management Bed rest until CRP is negative for 2 weeks Benzylpenicillin 0.6-1.2g IV stat then penicillin V 250-500mg Q6 for 10

days if allergic, give erythro or azithro NSAIDs or ASA for pain

Immobilization for arthritis Haloperidol or diazepam for chorea

Secondary prophylaxis

Penicillin V 250mg BD If carditis+valve disease continue until age of 40 If carditis but NO valve disease continue for 10 yrs

If no carditis 5 years prophylaxis (until age 21)


Valvular disease

Mitral stenosis Causes Rheumatic fever

Mucopolycassaridosis Fibroelastosis

Carcinoid

Presentation When valve area is <2cm sq Dyspnea

Fatigue Palpitations

Chest pain Hemoptysis and a picture of bronchitis

Signs Features - mid-late diastolic murmur (best heard in expiration)

- loud S1, opening snap - low volume pulse - malar flush - atrial fibrillation

Features of severe MS - length of murmur increases - opening snap becomes closer to S2

Investigations ECG - P mitrale

- RVH - RAD

Chest x-ray

- left atrial enlargement may be seen

Echocardiography - The normal cross sectional area of the mitral valve is 4-6 sq cm. A 'tight'

mitral stenosis implies a cross sectional area of < 1 sq cm

Management If in AF rate control and anticoagulation Diuretics Balloon vulvoplasty, open valvotomy, valve replacement

Mitral regurgitation

Causes Functional (LV dilatation) Annular calcification (elderly)

Rheumatic fever Infection endocarditis Mitral valve prolapse, ruptured chordea, papillary muscle dysfunction Connective tissue, cardiomyopathy


Signs Displaced hyperdynamic apex AF Soft S1, split S2, loud P2 Pansystolic murmur radiating to axilla

Investigations ECG

- P mitrale

- LVH - Left atrial enlargement

Chest x-ray

- LA/LV enlargement

Echocardiography (to assess LV function but do TEE for assessing severity and ability to repair)

Management If in AF rate control and anticoagulation

Diuretics Surgery

Mitral valve prolapse (most common) leads to sudden death Symptoms Asymptomatic

Atypical chest pain or palpitations Autonomic dysfunction

Signs Mid systolic click or late systolic murmur

Diagnosis ECHO

Management BB for palpitations Surgery for severe regurg

Aortic stenosis

Causes Degenerative calcification (>65 years ) Bicuspid valve (<65 years)

William’s (supravalvular aortic stenosis) Rheumatic fever

HOCM (subvalvular)

Symptoms Chest pain Exertional dyspnea

Syncope Triad angina, syncope, HF

Features Narrow pulse pressure (parvus et tardus) Slow rising pulse

Heaving non displaced apex Delayed ejection systolic murmur Soft/absent S2/A2 S4 Ejection click LVH or failure


Investigations ECG - P mitrale - LVH - LAD - Poor R wave progression, LBBB, complete AV block

CXR - LVH

- Calcific aortic valve

ECHO (Diagnostic) - Severe stenosis if gradient ≥50 mmhg and valve area <1cm sq - Aortic jet velocity >4 or increasing by >0.3/yr more complications

Management Asymptomatic

Observe Asymptomatic with valve gradiet >50 + features of left systolic

dysfunction Surgery

Symptomatic Valve replacement

Prognosis Symptomatic with no surgery Angina and syncope 2-3 yrs Cardiac failure 1-2 yrs Moderate to severe with medical intervention 50% mortality

at 2 yrs Aortic regurgitation

Causes Valve disease - Rheumatic fever - IE - CTD - Bicuspid aortic valve Aortic root disease - Aortic dissection

- Spondylarthropathies - HTN

- Syphilis - Marfan’s, Ehler Danlos

Symptoms Exertional dyspnea Orthopnea

PND Palpitations, angina, syncope

Features Early diastolic murmur

Collapsing pulse


Displaced hyperdynamic apex Wide pulse pressure Mid diastolic Austin Flint murmur (in severe AR) Corrigon sign

Carotid pulsation De Musset sign

Head nodding with each heart beat Quincke’s sign

Capillary pulsation in nail beds Duroziez’s sign

In the groin, if you press on the femoral pulse, put your stethoscope 2 cm proximal you’ll get a systolic murmur, distal you’ll get diastolic murmur

Traube’s sign Pistol shot sound over the femoral arteries

Diagnosis ECHO

Management ACEI (reduce the HTN) ECHO every 6-12 months to monitor Surgery

Increasing symptoms Enlarging heart T wave inversion on lateral leads Failure of medical treatment

Prognosis Poor post-operative survival EF <50% NYHA class III, IV Duration of CCF >12months

Tricuspid Regurgitation

Causes Functional (RV dilatation) Rheumatic fever

IE (IV drug abusers) Carcinoid

Symptoms Fatigue Hepatic pain Ascites Edema Dyspnea and orthopnea (if LV dysfunction)

Signs Giant V wave and Y descent in JVP Pulsatile hepatomegaly Pansystolic murmur head best at lower sternal boarder on inspiration

Management Digoxin, ACEI, diuretics Surgery


Tricuspid stenosis

Causes Rheumatic fever IE

Congenital Signs Giant a wave and slow y descent in JVP

Opening snap Early diastolic murmur heard at left sternal edge on inspiration

Diagnosis ECHO

Management Diuretics Surgery

Pulmonary stenosis

Causes Congenital (Turner’s, william’s, Noonan’s) Acquired (rheumatic fever, carcinoid)

Dyspnea Fatigue Edema Ascites

Dysmorphic facies Prominent a wave on JVP Ejection systolic murmur radiating to the shoulder Widely split S2 In severe stenosis longer murmur, obscured A2, soft P2

ECG - P pulmonale - RVH - RBBB

Diagnosis Cardiac catheterization Management Vuloplasty/ vulvotomy

Pulmonary regurgitation

Graham steel murmur if associated with MS and Pulmonary HTN Valve replacement

Biological valves Mechanical valves Origin Bovine or porcine Bileaflet valve

Disadvantages Structural deterioration or calcification over time

High risk of thrombosis

Anticoagulation No long term anticoagulation

Warfarin for the first 3 months

ASA long term

Long term anticoagulation

ASA is added

INR target Aortic 2-3

Mitral 2.5-3.5


Infective endocarditis

Affected patients Previously normal valve (50%) Rheumatic valve disease

Prosthetic valve Congenital heart defects

IV drug users

Causes Streptococcus viridans (most common cause - 40-50%). Streptococcus mitis and Streptococcus sanguinis

Staphylococcus epidermidis prosthetic valves

Staphylococcus aureus acute presentation IVDUs

Streptococcus bovis colorectal cancer

Non-infective Systemic lupus erythematosus (Libman-Sacks) Malignancy: marantic endocarditis

Culture negative causes

prior antibiotic therapy Coxiella burnetii Bartonella Brucella

HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

Diagnosis Dukes criteria (one of these) - Pathological criteria +

- 2 major - 1 major + 3 minor

- 5 minor

Pathological criteria Positive histology or microbiology of pathological material

obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)

Major criterial - Positive blood cultures

2 positive blood cultures showing typical organisms

consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group

persistent bacteremia from two blood cultures taken > 12 hours apart or three or more positive blood cultures where


the pathogen is less specific such as Staph aureus and Staph epidermidis

positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci

positive molecular assays for specific gene targets - Evidence of endocardial involvement

positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of

prosthetic valves), or new valvular regurgitation

Minor criteria - predisposing heart condition or intravenous drug use - microbiological evidence does not meet major criteria - fever > 38ºC

- vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura

- immunological phenomena: glomerulonephritis, Osler's nodes, Roth spots

Management Antibiotics - Bling therapy for native valve

Amoxicillin 2g Q4 IV ± gentamicin 1mg/kg Q12 IV Penicillin allergy Vanco 1g Q12 IV + gentamicin 1mg/kg

Q12 IV If negative organism meropenem 2g Q8 IV+ vanco

(trough 15-20) - Blind therapy for prosthetic valve

Vanco + genta + rifampicin 300-600 BD - Staph with native valve

Flucloxacillin >4 weeks (vanco + rifamp if allergic) - Staph with prosthetic valve

Fluclo + genta + rifamp >6 weeks - Strep

1.2g Q4 IV for 4-6 weeks - Entercoccus & HACEK

Amoxi 4 weeks + genta 2 weeks Surgery

HF Valvular obstruction Repeated emboli

Fungal endocarditis Persistent bacteremia

Myocardial abscess


Prevention NICE recommends the following procedures do not require prophylaxis: Dental procedures Upper and lower gastrointestinal tract procedures GU tract; this includes urological, gynecological and obstetric

procedures and childbirth Upper and lower respiratory tract; this includes ear, nose and

throat procedures and bronchoscopy

if a person at risk of infective endocarditis is receiving antimicrobial therapy because they are undergoing a gastrointestinal or genitourinary

procedure at a site where there is a suspected infection they should be given an antibiotic that covers organisms that cause infective endocarditis

Diseases of the heart muscle Myocarditis

Causes Viral Coxsackie, HIV, Mumps, Rubella, Polio

Bacteria Diphtheria, clostridia, TB

Spirochaetes Lyme disease, syphilis

Protozoa Chagas' disease, Toxoplasmosis

Autoimmune Drugs

Doxorubicin, cyclophosphomide, penicillin, spironolactone Carbamazepine, methyl dopa

Presentation Acute SOB, chest pain, fatigue

Investigation In absence of MI, they have +trop Negative antimyosin scintigraphy excludes it

Cardiomyopathies (New WHO Classification) Primary Cardiomyopathy

Genetic (AD) HOCM

- Basics Leading cause of adult sudden death Mutation in B myosin heavy chain protein C

- Features

Often asymptomatic Dyspnea, angina, syncope


Sudden death (most commonly due to ventricular arrhythmias), arrhythmias, heart failure

Jerky pulse, large 'a' waves, double apex beat Ejection systolic murmur: increases with Valsalva maneuver

and decreases on squatting

- Associations Friedreich's ataxia

Wolff-Parkinson White

- Echo - mnemonic - MR SAM ASH Mitral regurgitation (MR) Systolic anterior motion (SAM) of the anterior mitral valve

leaflet Asymmetric hypertrophy (ASH)

- ECG

Left ventricular hypertrophy Progressive T wave inversion

Deep Q waves Atrial fibrillation may occasionally be seen

Arrhythmogenic right ventricular dysplasia

- Basics 2nd most leading cause of sudden death Mutations in desmosomes genes

- Presentation

Syncope, palpitations, sudden death

- Investigations Epsillon notch/terminal notch in QRS Echo hypokinetic RV

MRI fibrofatty tissue

- Management Drugs satolol

Ablation ICD

Naxos disease is AR variant (ARVC+ palmoplantar keratosis + woolly hair)


Mixed Dilated cardiomyopathy

- Features Dilated heart leading to systolic (+/- diastolic) dysfunction All 4 chambers affected but LV more so than RV Features include arrhythmias, emboli, mitral regurgitation

Absence of congenital, valvular or ischemic heart disease

- Causes Alcohol: may improve with thiamine

Postpartum HTN Inherited Infections e.g. Coxsackie B, HIV, diphtheria, parasitic Endocrine e.g. Hyperthyroidism

Infiltrative* e.g. Haemochromatosis, sarcoidosis Neuromuscular e.g. Duchenne muscular dystrophy

Nutritional e.g. Kwashiorkor, pellagra, thiamine/selenium deficiency Drugs e.g. Doxorubicin

- Investigations

Low NA indicates poor prognosis ECHO global hypokinetic heart and low EF

- Treatment Digoxin, diuretics, ACEI, anticoagulation, biventricular pacing, ICD

Restrictive cardiomyopathy

- Causes Idiopathic Amyloidosis

Hemochromatosis Sarcoidosis

Scleroderma

- Diagnosis Cardiac cath

Acquired Peripartum

- Between last month of pregnancy and 5 months post partum

Takotsubo - Stress induced, transient


Secondary cardiomyopathies

Infective Coxacki

Chagas Infiltrative

Amyolidosis

Storage Hemochromatosis

Toxicity Doxorubicin

Alcohol Inflammatory

Sarcoidosis Endocrine

DM Thyrotoxicosis Acromegaly

Neuromuscular Friedreich’s ataxia Duchenne muscular dystrophy

Nutritional Beriberi (thiamine)

Autoimmune

SLE

Pericardial diseases Acute pericarditis

Features Chest pain: may be pleuritic. Is often relieved by sitting forwards Other symptoms include non-productive cough, dyspnea and flu-

like symptoms Pericardial rub

Tachypnea Tachycardia

Causes viral infections (Coxsackie)

tuberculosis uremia (causes 'fibrinous' pericarditis) trauma post-myocardial infarction, Dressler's syndrome connective tissue disease

hypothyroidism

Investigations ECG - widespread 'saddle-shaped' ST elevation - PR depression: most specific ECG marker for pericarditis


Treatment Analgesics Colchicine if relapse Steroids if relapse

Constrictive pericarditis Causes Any cause of pericarditis (particularly TB)

Features Dyspnea

right heart failure: elevated JVP, ascites, oedema, hepatomegaly JVP shows prominent x and y descent

pericardial knock - loud S3 Kussmaul's sign is positive

Investigations CXR Pericardial calcification

Both Y and X present in JVP (compared to tamponade where you have absent Y)

Pericardia effusion

Causes infectious pericarditis: viral, tuberculosis, pyogenic spread from septicemia and pneumonia

uremia idiopathic

post myocardial infarction (including Dressler's syndrome) malignancy

heart failure nephrotic syndrome hypothyroidism trauma

Features Dyspnea Raised JVP Bronchial breathing at left base

Diagnosis CXR Enlarged and globular heart

ECG Low voltage QRS

ECHO

Echo free area surrounding the heart Management Pericardiocentesis

Cardiac Tamponade Causes Any pericarditis

Aortic dissection Hemodialysis

Features Dyspnea

Raised JVP, with an absent Y descent - this is due to the limited right ventricular filling

Tachycardia


Hypotension Muffled heart sounds Pulsus paradoxus Kussmaul's sign (much debate about this)

Investigations Beck’s triad

- Falling BP

- Rising JVP - Muffled heart sounds

CXR

- Big globular heart

ECG - Electrical alternans, low voltage QRS

Diagnosis ECHO

- Echo free area surrounding the heart Management Pericardiocentesis

DVLA: Cardiovascular diseases

Hypertension - can drive unless treatment causes unacceptable side effects, no

need to notify DVLA. If Group 2 Entitlement the disqualifies from driving if resting

BP consistently 180 mmHg systolic or more and/or 100 mm Hg diastolic or more

Angioplasty (elective) - 1 week off driving

CABG - 4 weeks off driving

Acute coronary syndrome- 4 weeks off driving, 1 week if successfully treated by

angioplasty

Angina - driving must cease if symptoms occur at rest/at the wheel

Pacemaker insertion - 1 week off driving

Implantable cardioverter-defibrillator (ICD): if implanted for sustained

ventricular arrhythmia: cease driving for 6 months. If implanted prophylactically

then cease driving for 1 month. Having an ICD results in a permanent bar for

Group 2 drivers

Successful catheter ablation for an arrhythmia- 2 days off driving

Aortic aneurysm of 6cm or more - notify DVLA. Licensing will be permitted

subject to annual review. An aortic diameter of 6.5 cm or more disqualifies

patients from driving

Heart transplant: DVLA do not need to be notified


Surgical Chest pain

Dissection of thoracic aorta

Tearing interscapular pain Discrepancy in arterial blood pressures taken in both arms

May show mediastinal widening on chest x-ray

Diffuse oesophageal spasm

Spectrum of oesophageal motility disorders Caused by uncoordinated contractions of oesphageal muscles May show "nutcracker oesophagus" on barium swallow Symptoms include dysphagia, retrosternal discomfort and dyspepsia

Gastro-oesphageal reflux

Common cause of retrosternal discomfort Usually associated with symptoms of regurgitation, odynophagia and

dyspepsia Symptoms usually well controlled with PPI therapy Risk factors include obesity, smoking and excess alcohol

consumption

Boerhaaves syndrome

Spontaneous rupture of the oesophagus Caused by episodes of repeated vomiting often in association with

alcohol excess Typically there is an episode of repetitive vomiting followed by

severe chest and epigastric pain Diagnosis is by CT and contrast studies

Treatment is surgical; during first 12 hours primary repair, beyond this usually creation of controlled fistula with a T Tube, delay beyond 24 hours is associated with fulminent mediastinitis and is usually fatal.

Achalasia Difficulty swallowing, dysphagia to both liquids and solids and sometimes chest pain

Usually caused by failure of distal oesphageal inhibitory neurones Diagnosis is by pH and manometry studies together with contrast

swallow and endoscopy

Treatment is with either botulinum toxin, pneumatic dilatation or cardiomyotomy


Cardiovascular diseases in pregnancy

Chest pain in pregnancy Aortic dissection • Predisposing factors in pregnancy are

hypertension, congenital heart disease and Marfan's syndrome

• Mainly Stanford type A dissections • Sudden tearing chest pain, transient

syncope • Patient may be cold and clammy,

hypertensive and have an aortic regurgitation murmur

• Involvement of the right coronary artery may cause inferior myocardial infarction

Surgical correction

- <24 weeks

Aortic repair with fetus kept in utero

- 28-32 weeks

Dependent on fetal condition

- >32 weeks Primary cesarean section

followed by primary aortic repair at the same operation

Mitral stenosis • Leading cause of mortality in pregnancy • Half dose scintigraphy; CT chest if

underlying lung disease should aid diagnosis

• Treatment with low molecular weight heparin throughout pregnancy and 4-6

weeks after childbirth • Warfarin is contra indicated in

pregnancy Hypertension in Pregnancy

High risk of hypertensive diseases take ASA 75mg OD from 12 weeks until the birth of the baby Hypertensive disease during previous pregnancies

Chronic kidney disease Autoimmune disorders such as SLE or antiphospholipid syndrome

Type 1 or 2 diabetes mellitus


Hypertension in pregnancy in usually defined as:

systolic > 140 mmHg or diastolic > 90 mmHg or an increase above booking readings of > 30 mmHg systolic or > 15 mmHg

diastolic

Pre-existing hypertension Pregnancy-induced hypertension

(PIH, also known as gestational hypertension)

Pre-eclampsia

A history of hypertension before pregnancy or an elevated blood pressure > 140/90

mmHg before 20 weeks gestation

No proteinuria, no edema

Occurs in 3-5% of pregnancies and is more common in older women

Hypertension (as defined above) occurring in the second half of pregnancy (i.e. after

20 weeks) No proteinuria, no

oedema Occurs in around 5-

7% of pregnancies Resolves following

birth (typically after one month). Women with PIH are at

increased risk of future pre-eclampsia

or hypertension later in life

Pregnancy-induced hypertension in association with proteinuria (> 0.3g / 24 hours)

Edema may occur but is now less commonly used as a criteria

Occurs in around 5% of pregnancies

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