Cardiology Flashcards
Pulmonary oedema presentation
Investigations and what they show
- Acute worsening SOB, dyspnoea
- Orthopnoea
- PND – wake up gasping for breath
- Productive cough – pink frothy sputum
- Chest pain
- Collapse, cardiac arrest or shock
On examination • Distressed, pale sweaty • Tachycardic • Tachypnoeic • Tend to be hypertensive • Crackles on auscultation • Raised JVP
Investigations
• CXR – to confirm diagnosis. Look for
- Interstitial shadowing; Enlarged hila; Prominent upper lobe vessels; Pleural effusions; Kerley B lines (thin linear pulmonary opacities caused by fluid or cellular infiltration into the interstitial of the lungs); May or may not be cardiomegaly
- Exclude pneumothorax, PE and consolidation
• ECG – check rhythm
- ?any cardiac arrhythmia
- ?Evidence of acute ST changes
- ?Evidence of underlying heart disease (LVH, p mitrale)
• ABG
- low PaO2. PaCO2 may be low (hyperventilation) or high depending on severity
- Pulse oximetry may be inaccurate if peripherally shut down
• Bloods
- FBC: ?Anaemia or leucocytosis indiciating precipitant
- inc. BNP (serial for treatment). BNP <100 rules out acute HF
- U&Es (baseline of renal function)
- +/- trop
- Echo (not immediately but for HF diagnosis)
Pulmonary oedema management
Acute
Follow up
- Sit upright
- High flow O2 – give 100% oxygen if no pre-existing lung disease
- Gain IV access + take bloods
- Monitor ECG – cardiac monitoring
- Treat any arrhythmias if contributing e.g AF
- Do other investigations as above whilst continuing treatment
3.
- Give 40-80mg Furosemide IV – Should act quickly. Monitor BP when giving.
- Give 1.25-5mg Diamorphine IV to aid respiratory distress (careful in liver failure + COPD)
- Give 2 puffs GTN spray – vasodilates to get fluid off (Don’t give if sBP <90)
4.
- If sBP >100 start a GTN infusion – to reduce preload
- If pt worsening, give further dose of furosemide/infusion
- Give NIV e.g. CPAP – to keep airways open that would collapse because of fluid and push fluid off their chest
- If sBP <100, treat as cardiogenic shock and refer to ICU
Once stable and improving:
• Check obs at least QDS
• Daily weights, aim reduction of 0.5kg/day
• Change to oral furosemide or bumetanide
• Consider adding thiazide if on a large dose of loop diuretic bendroflumethiazide or metolazone 2.5–5mg daily
• ACEi if LVEF <40%.
• Consider beta blocker and spironolactone if LVEF <35%
• Is pt suitable for biventricular pacing or cardiac transplantation
• Consider digoxin warfarin, especially if AF
Hypertension end-organ damage
Proteinuria Hypertensive retinopathy 1) Arteriolar narrowing 2) AV nipping 3) Flame haemorrhages + cotton wool spots 4) Papilloedema LVH
Tests
- Urine dip
- Fundoscopy
- ECG + Echo
- Bloods - electrolytes, glucose, lipids, renal function
Raised troponin causes
MI Myocarditis Takotsubo cardiomyopathy Massive PE Critical illness e.g. shock, sepsi
Contraindications to thrombolysis
Previous intracranial haemorrhage or stroke of unknown cause
Recent ischaemic strokeischaemic stroke
HCM
Main symptoms
ECG
Most important test
Syncope
Angina
Dyspnoea
Palpitations
Signs on examination
- Systolic murmur
- Systolic thrill (L lower sternal edge)
- Jerky peripheral pulse
- Double apical beat
- ?bisferens pulse
ECG
- T wave and ST segment abnormalits
- LVH
- Q waves (hypertrophied septum mimics old MI)
Most important test = exercise test
- Lack of normal change in BP = risk factor for sudden death
Management of HCM
High risk individuals need ICD
BB or Verapamil: for symptomatic patients
Amiodarone for arrhythmias
Anti-coagulate for paroxysmal AF or Systemic emboli
Avoid vasodilators
What is cor pulmonale
Causes
Signs
Hypertrophy of the right ventricle and right heart failure that are caused by pulmonary arterial hypertension
Causes
- COPD
Signs Are of R sided HF - Hepatomegaly - Peripheral oedema - Raised JVP
Left sided heart failure features
Orthopnoea, PND, SOB on exertion
Hypothermia results on investigations
ECG
Bloods
ECG: J waves, long qt, bradycardia, 1st degree HB
Bloods: Hb and haematocrit can be elevatved
- Platelets and WBC may be low (sequestration in spleen)
- Hypokalaemia (shift into intracellular space)
Causes of arrhythmia
Cardiac IHD structural changes Cardiomyopathy Pericarditis Myocarditis
Non-cardiac Caffeine Smoking Pneumonia/PE Metabolic in balance: Potassium potassium, calcium, magnesium, hypercapnia, metabolic acidosis, thyroid disease Pheochromocytoma
Investigation of arrhythmia
Bloods FBC You and EV Glucose Magnesium TFT
ECG - signs of IHD - signs of AF - short PR - long QT - U waves Echo
Mitral regurgitation
Causes
Symptoms
Signs
Management
Causes
1) Primary
- Degenerative mitral valve disease (prolapse, calcification, ruptured chordae tendinea)
- Rheumatic fever
- Infective carditis
- Connective tissue disorders
2) Secondary
- CAD, prior MI causing papillary muscle involvement
- DCM and left HF
Symptoms
- Signs of LV failure
- Dyspnoea
- Fatigue
- Palpitations
Signs
- AF - common in chronic MR with a dilated LA
- Raised JVP If pulmonary HTN and R HF or fluid retention
- Dilated Apex beat
- RV heave
- Sodt S1, Split S2
- Pansystolic murmur radiating to axilla
ECG - AF and p mitral
CxR - large LA and LV
Echo - main assessment
MI must be ruled out in patient preenting with severe MR
Management
- control rate if fast AF
- Diuretics improve symptoms
- Surgery if symptoms worsen - repair preferred. Abx for prophylaxis
Mitral valve prolapse
What is it
Symptoms
Signs
Complications
Tests
Management
Most common valvular abnormality 1/20. Occurs alone or with cardiomyopathy, Turner, WPW, PDA
Symptoms
- usually asymptomatic
- may get chest pain, palpitations
Signs
- mid diastolic click and late systolic murmur
Complications
- MR
- Cerebral emboli
- Arrhytmias, sudden death
Echo diagnostic
Treatment
- bb may help palpitations and chest pain
- surgery if severe MR
Mitral stenosis
Causes
Symptoms
Signs
Tests
Management
Causes
- Rheumatic fever - most most common
- IE
- Congenital
- SLE
Symptoms
- Dyspnoea, fatigue, palpitations, chest pain
- systemic emboli, haemoptysis, chronic bronchitis
Signs
- Malta flush (low CO)
- AF due to LA strain
- Tapping NON displaced apex beat
- Loud S1, rumbling mid diastolic murmur
Tests
- ECG - AF, RVH/RAD, p mitrale
- Echo diagnostic
Management
- Rate control and anticoagulation in AF
- Diuretics
- Balloon mitral valvuloplasty to open valve
- Valve replacement
Complications
- AF
- Pulmonary HTN
- Emboli
- Large LA puts prqessude on structures e.g. Laryngeal nerve
Aortic regurgitation
Causes
Symptoms
Signs
Management
Reflux of blood from aorta into LV during diastole
Causes
- Acute: Rheumatic fever, IE, aortic dissection, chest trauma
- Congenital - aortic valve anbnormalitis, connective tissue disorders, Rheumatic fever, RA, SLE, ank spond
Symptoms
- often asymptomatic with only exertional Dyspnoea
- orthopnoea and paroxysmal nocturnal Dyspnoea
- palipiataions, angina, syncope
Signs
- collapsing pulse
- wise pulse pressure
- displaced apex beat
- early diastolic murmur ( sat forward and expiration)
- corrigans sign - carotid pulsitations in neck
- De musset - he’s nodding with each HB
- Quincke signs - capillary pulsation in nail bed
- Austin flint murmur - heard at apex - early diastolic rumbling murmur caused by blood flowing back through the aortic valve and over mitral valve leaflets
Management
- Aim to reduce systolic HTM
- Aim to replace valve before significant dysfunction
- Abx prophylaxis against IE
- Vasodilators: ACEi or Nifedipine
Complications
- LV failure
- pulmonary oedema
Infective endocarditis
Causes
Risk factors
Signs and symptoms
Causes
- bacteraemia - s. Aureus, strep vridans (subacute), staph epidermis, staph bovis (associated with colorectal ca)
- fungal infection - usually in IV drug users, immunocompromised, prosthetic valves
- rarely HaCEk
- SLE
- Maliganncy
Risk factors
1) on normal valves
- Dermatitis
- IV injection
- Renal failure
- immunosuppressed/ organ transplant
- DM
- Post op wound
2) on abnormal valves
- Aortic or mitral valve disease
- Triscupid valves in IVDU
- Coarctation
- PDA
- Prosthetic valves
Signs and Simpson’s
- Sepsis - fevers, rights, night sweats, weight loss, splenomegaly, clubbing
- cardiac - murmur (new or changed),
- immune complex deposition - vascularising, microscopic haematuria, glomeruolonephritis/AKI, Roth spots, splinter haemorrhages, Oslerd nodes
- Emobolic - abscesses in relevant organ e.g. brain, heart, kidney, spleen, gut or skin (Janeway lesions)
Infective endocarditis critieria
Management
Modified dukes criteria. Need 2 major or 1 major + 3 minor or 5 minor
Major - BE
- Blood culture +ve 2 x 12 h apart
- Endocardial involvement from Echo
Minor - FEEVER
- Fever >38
- Echo findings (not major)
- Vascular findings - splenomegaly, clubbing, splinter haemorrhages, janeway lesions, petechiae, major haemorrhage
- EEvidence from micro/immnunology (2 evidences)
- Risk factors e.g. drug abuse, valve disease
Management
- speak to micro and cardio
- give antibiotics
- consider surgery if severe valve incompetency etc.
Tricuspid regurgitation
Causes
Symptoms
Signs
Management
Causes
- RV dilation due to pulmonary HTN induced by LV failure or PE
- Rheumatic fever
- Infective endocarditis
- carcinoid syndrome
- Congenital
- Drugs
Symptoms
- fatigue, SOB, palpitations, hepatic pain on exertion, ascites, oedema and symptoms of cause
Signs
- giant V waves in raised JVP
- Parastermal RV heave
- Pansustolic murmur ( in inspiration)
- Pulsatile hepatomegaly, jaundice, ascites
Management
- Treat cause
- Give diuretics, digoxin and ACEi
- Valve repair if needed
Causes of raised JVP
Cause of absent A waves
Cause of large A waves
Cause of large V waves
Increased RA pressure
1) HF
2) Fluid overload
3) Constrictive pericarditis
4) Cardiac tamponade
Cause of absent A waves
- AF
Cause of large A waves
- RVH due to Pulmonary HTN or PS
- Tricuspid stenosis
Cause of large V waves
- Tricuspid regurgitation
Stages of JVP
A wave = atrial contraction
- blood passed through tricuspid to RA
- Also up so blood in IJV increases
X descent = atrial relaXation
- blood flows into relaxed atria from IJV
- also blood from atria to ventricles
c wave = start of systolic Contraction
- RV contracts squeezing blood to pulmonary artery
- pressure pushes into closed tricuspid - bulges into RA
X descent = end of RV contraction
- RV squeezed small -= space in pericardium = space for atria to fill out and suck in blood
V wave = atrial relaXation
- RA starts to fill with blood (tricuspid closed)
- As fills more, filling occurs higher up
Y descent = tricuspid opens
- Emptying of RA
What is the Leriche’s syndrome
Peripheral artery disease at level of aortic bifurcation or bilateral occlusion of iliac arteries = classic triad
1) Bilateral buttock, hip or thigh claudicatipn
2) Erectile dysfunction
3) Absent/ diminished femoral pulses
What is bifasicular block and trifasicular block
Bifasicular block = RBBB with LAD
Trifasicular block = RBBB with LAD and 1st degree heart block
Who gets statins
Dose for actor OST’s tin
- all with establish CVD ( IHD, Stroke, TIA, PAD)
- all with 10 year Cv risk 10% or more
- AsSess T2 diabetics with QRISK2
- T1DM If dx more than 10 y ago, older than 40 or established nephropThy
Atorvostatin dose
- 20mg for primary prevention
==> increase the dose if non-HDL has not reduced for >= 40%
- 80mg for secondary prevention
Causes of long QT
1) Genetic
2) electrolytes
- hypomagnesaemia
- hypocalcaemia
- hypokalaemia
3) Drugs
- Anti arrhythmic e.g, amiodarone, SOTALOL
- antibiotics e.g. erythromycin, clarithromycin, ciprofloxacin
- psychotropic drugs e.g. SSRI, TCA, Neuroleptic
Causes of sinus bradycardia
Young athletic
Sleep
Chronic degeneration of sinus or AV nodesu or atria
Drugs e.g. Bb, morphing, amiodarone, CCB, lithium, propafenone
Increased Vagal tone - vasovagal attack, N&V, carotid sinus hypersentivify
Hypothyroid
Hypothermia
MI or ischaemia of the sinus node
Raised ICP
Wells score for PE
Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) 3
An alternative diagnosis is less likely than PE 3
Heart rate > 100 beats per minute 1.5
Immobilisation for more than 3 days or surgery in the previous 4 weeks 1.5
Previous DVT/PE 1.5
Haemoptysis 1
Malignancy (on treatment, treated in the last 6 months, or palliative) 1
> 4 – CTPA
4 or less – D dimer
AF need for anti-coagulation
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 ischaemic heart disease and peripheral arterial disease) 1 S Sex (female) 1
Strategy based on score 0 No treatment 1 Males: Consider anticoagulation Females: No treatment (this is because their score of 1 is only reached due to their gender) 2 or more Offer anticoagulation
Warfarin INR targets
Venous thromboembolism
AF
Mechanical valves
Venous thromboembolism: 2.5, if recurrent 3.5
AF: 2.5
Mechanical heart valves, target INR depends on the valve type and location. Mitral valves generally require a higher INR than aortic valves.
beta blocker CIs
Side effects
Uncontrolled HF
Concurrent verapamil: May precipitate severe bradycardia
Asthma
Sick sinus syndrome
Side effects
- Bronchospasm
- Trouble sleeping
- ED
- Fatigue
- Cold peripheries
ACE-i CIs
Side effects
Pregnancy + breast feeding
Bilateral RAS
Aortic stenosis
Side effects
- Cough
- Angiodema
- Hyperkalaemia
HF cxr findings
Alveolar oedema kelley B lines (expansion of interstitial space by fluid) Cardiomegaly Dilated upper lobe vessels Effusions (pleural)
P450 Inhibitors
Examples
Effect
Examples Antibiotics: ciprofloxacin, erythromycin Isoniazid Cimetidine,omeprazole Amiodarone Allopurinol Imidazoles: ketoconazole, fluconazole SSRIs: fluoxetine, sertraline ritonavir Sodium valproate Acute alcohol intake quinupristin
Cause an increase in INR - often rapid
P45O Inducers
Examples
Effect
Antiepileptics: phenytoin, carbamazepine barbiturates: phenobarbitone rifampicin St John's Wort chronic alcohol intake griseofulvin smoking (affects CYP1A2, reason why smokers require more aminophylline)
Causes decrease in INR - often takes a while
Standard heparin (unfractionated) MOA
Adverse effects
Administration
Duration of action
Monitoring
Advantage over LMWH
Activates antithrombin III. Forms a complex that inhibits thrombin, factors Xa, IXa, Xia and XIIa
Adverse effects
- Bleeding
- Thrombocytopenia - HIT
- Osteoporosis and an increased risk of fractures
- Hyperkalaemia - this is thought to be caused by inhibition of aldosterone secretion
Administration
IV
Duration of action
Short
Monitoring
APTT
Advantage over LMWH?
Useful in situations where there is a high risk of bleeding as anticoagulation can be terminated rapidly. Also useful in renal failure
LMWH MOA
Adverse effects
Administration
Duration of action
Monitoring
Advantage over LMWH
Activates antithrombin III.
- Forms a complex that inhibits factor Xa
Adverse effects
- Bleeding
- Lower risk of HIT and osteoporosis with LMWH
Administration
Subcut
Duration of action
Long
Monitoring
Anti-Factor Xa (although routine monitoring is not required)
Advantage over LMWH
Now standard in the management of venous thromboembolism treatment and prophylaxis and acute coronary syndromes
Causes of AF
What to look for o/e
Investigations
Management
Complications
Cardiac: IHD (MI, CAD), Mitral valve disease, Pericarditis, Cardiomyopathy, Rheumatic heart disease
Pulmonary: PE/Bronchial carcinoma
Systemic: Sepsis/Infection, Thyrotoxicosis, HTN, Alcohol, Caffeine
O/E
- Irregularly irregular pulse, difference in apical beat and radial pulse
- Valvular disease/thyroid disease?
- Tachy/palpitations/stroke
Investigations
ECG
Bloods
Echo
Management
1) Haemodynamically unstable: DC cardioversion
2) Rate control if long standing/mitral stenosis: BISOPROLOL or CCB (Verapamil/Diltiazam) if asthma. 2nd line: Add digoxin
3) Rhythym control
If paroxysmal or new onset - Pt choice unless unstable - DC cardiversion vs amiodarone/flecanice
4) Stroke risk prevention
- Use CHA2DS2VASc - 1 (M) or 2 (F) needs anticoagulation with NOAC unless prosthetic valve AF
Complications
- Thromboembolism
- HF/ Worsening of HF
Narrow complex tachycardia
Differentials
SVT = Narrow complex (<0.12s), + HR >100
Differentials
1) Sinus tachycardia
2) Atrial: AF, Atrial Futter, Atrial tachycardia
3) AVNRT
3) AVRT
Broad complex tachycardia differentials
VT causes
VT
Torsades de Pointes
SVT with BBB
VT causes
IM QVICK
1) Infarction (esp. ̄c ventricular aneurysm)
2) Myocarditis
3) QT interval↑
4) Valve abnormality: mitral prolapse, AS
5) Iatrogenic: digoxin, antiarrhythmics, catheter
6) Cardiomyopathy (esp. dilated)
7) K↓, Mg↓, O2↓, acidosis
Stable angina management
Complications of stable angina
Lifestyle: Stop smoking; Diet; Activity;
Aspirin 75mg OD
Statin
Sublingual GTN for episodes
BB for symptoms
CCB if bb not working
Can try ivabradine + long acting nitrates, Nicorandil, Ranolazine
If angina persists –> consider CABG or PCI
Complications
- Unstable angina
- MI
- Stroke
- QOL
Localising MI
RCA - Inferior - leads II, III, avF
- RA, RV, Inferior aspect of LV, Posterior Septal area
Circumflex - Lateral - leads I, avL, v5-6
- LA, Posterior aspect of LV
LAD - Anterior - leads v1-v4
- Anterior aspect of LV, Anterior aspect of septum
LCA - Anteroleateral - leads I, avL, v3-v6
STEMI management acute
MONA - as for all ACS
- Morphine 1-10mg IV, Metoclopramide 10mg IV
- Oxygen (if needed)
- GTN spray
- Aspirin 300mg + Ticagrelor 180mg
Reperfusion if within 12 h onset
- PCI if within 120mins
- Fibrinolysis if PCI not available in 120 mins (Activates plasminogen to form plasmin, which breaks down fibrin)
NSTEMI management acute
MONA as for all ACS
- Morphine 1-10mg IV, Metoclopramide 10mg IV
- Oxygen (if needed)
- GTN spray
- Aspirin 300mg + Ticagrelor 180mg
BANE
1) BB e.g. metoprolol (unless CI - use CCB if so)
2) Anti-coagulate: Fondaparinux 2.5mg OD SC or LMWH e.g. Enoxaparin 1mg/kg BD (This should be UF heparin if going for angiography)
3) IV nitrates if pain continues e.g. GTN 50mg in 50ml 0.9% saline
4) ECG (whilst in pain) - determine risk
Invasive (high-risk pt)
- Rise in trop
- Dynamic ST/T wave changes
- Secondary criteria: DM, CKD, LVEF <40%, Early angina post MI, recopt PCI, prior CABG, Intermediate to high grace score
==> Infusion of GpIIb/IIIa antagonist (e.g. tirodiban) and refer for angioplasty as inpatient (within 72h)
1) Urgent (<120mins) if ongoing angina despite Rx + evolving ST changes, signs of cardiogenic shock or life threatening arrhythmia
2) Early (<24h) if grace score >140 and high risk pt
3) Within 72h if lower risk pt
Conservative strategy (low risk pt) - No recurrence of chest pain - No signs of HF - Normal ECG - Negative baseline + 6-9h Trop - No inducible ischaemia ==>May be discharged if a repeat trop is -ve. Treat medication and arrange further ivg e.g. stress test, angiogram Risk score - GRACE
Secondary prevention for MI
Aspirin 75mg OD + Another anti-platelet for 12months
Atorvostatin 80mg OD
ACEi e.g. ramipril 10mg
Atenolol (or other beta blocker)
Aldosterone antagonist for those with clinical HF
NB dual antiplatelet therapy varies following PCI depending on stent use
MI complications
Poor prognostic factors ACS
Death Rupture of septum of papillary muscle Eodema - HF Aneurysm + Arrhythmia Dressler's syndrome
ACS poor prognosis Age Development (or history) of heart failure - crackles Peripheral vascular disease Reduced systolic blood pressure Killip class* Initial serum creatinine concentration Elevated initial cardiac markers Cardiac arrest on admission ST segment deviation
Chronic HF management
1st line for all = ACE-inhibitor and a beta-blocker*. (start one drug at a time
2nd line: Aldosterone antagonist, angiotensin II receptor blocker or a hydralazine in combination with a nitrate
If symptoms persist:
- CRT or DIGOXIN to be considered
- An alternative supported by NICE in 2012 is ivabradine.
The criteria for ivabradine include that the patient is already on suitable therapy (ACE-inhibitor, beta-blocker + aldosterone antagonist), has a heart rate > 75/min and a left ventricular fraction < 35%
Diuretics should be given for fluid overload
Offer annual influenza vaccine
Offer one-off*** pneumococcal vaccine
Other drugs
sacubitril-valsartan is considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs
sacubitril-valsartan should be initiated following ACEi or ARB wash-out period
A number of drugs have been shown to improve mortality in patients with chronic heart failure: ACE inhibitors (SAVE, SOLVD, CONSENSUS) spironolactone (RALES) beta-blockers (CIBIS) hydralazine with nitrates (VHEFT-1)
No long-term reduction in mortality has been demonstrated for loop diuretics such as furosemide.
Contraindications to thrombolysis
Contraindications: AGAINST Aortic dissection GI bleeding Allergic reaction previously Iatrogenic: recent surgery Neuro: cerebral neoplasm or CVA Hx Severe HTN (200/120) Trauma, inc. CPR
What is acute pericarditis
Inflammation of the pericardium lasting <6 weeks
Causes
- VIRUS e.g. coxsackie B, echovirus, HIV
- Other: Uraemia, Trauma, Infection + Malignancy
Presentation
- Sharp retrosternal chest pain
- relieved by leaning forwards
- May be worse on inspiration and radiate to the neck
May be pericardial friction rub (may be transient)
Dx: ECG: Saddle shaped ST segment elevation
CXR - may show enlargement of cardiac shadow
Echo: useful if suspision of pericardial effusion (normal kn uncomplicated pericarditis)
Ddx: DISSECTION
Management
- Treat underlying cause and NSAIDs (unless in few days after MI as risk of myocardial rupture)
- If resistant - steroids
Complications
- Chronic pericarditis
- Chronic pericarditis
HTN management
ABPM/HBPM >= 135/85 mmHg (i.e. stage 1 hypertension)
treat if < 80 years of age AND any of the following apply; target organ damage, established cardiovascular disease, renal disease, diabetes or a 10-year cardiovascular risk equivalent to 10% or greater
- if >80 just lifestyle advice
ABPM/HBPM >= 150/95 mmHg (i.e. stage 2 hypertension)
offer drug treatment regardless of age
Statins MOA
Asdverse effects
Statins inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis.
Adverse effects
1) Myopathy: includes myalgia, myositis, rhabdomyolysis and asymptomatic raised creatine kinase. Risks factors for myopathy include advanced age, female sex, low body mass index and presence of multisystem disease such as diabetes mellitus. Myopathy is more common in lipophilic statins (simvastatin, atorvastatin) than relatively hydrophilic statins (rosuvastatin, pravastatin, fluvastatin)
2) Liver impairment: the 2014 NICE guidelines recommend checking LFTs at baseline, 3 months and 12 months. Treatment should be discontinued if serum transaminase concentrations rise to and persist at 3 TIMES BASELINE
There is some evidence that statins may increase the risk of intracerebral haemorrhage in patients who’ve previously had a stroke. This effect is not seen in primary prevention. For this reason the Royal College of Physicians recommend avoiding statins in patients with a history of intracerebral haemorrhage
Cardiac tamponade
features
Signs
Cardiac tamponade is characterized by the accumulation of pericardial fluid under pressure.
Classical features - Beck’s triad:
hypotension
raised JVP
muffled heart sounds
Other features: dyspnoea tachycardia an absent Y descent on the JVP - this is due to the limited right ventricular filling pulsus paradoxus - an abnormally large drop in BP during inspiration Kussmaul's sign - much debate about this ECG: ELECTRICAL ALTERNANS Management = Urgent pericardiocentesis
Adenosine Use
MOA
CI:
Adverse effects
denosine is most commonly used to terminate supraventricular tachycardias. The effects of adenosine are enhanced by dipyridamole (antiplatelet agent) and blocked by theophyllines. It should be avoided in asthmatics due to possible bronchospasm.
Mechanism of action
causes transient heart block in the AV node
agonist of the A1 receptor in the atrioventricular node, which inhibits adenylyl cyclase thus reducing cAMP and causing hyperpolarization by increasing outward potassium flux
adenosine has a very short half-life of about 8-10 seconds
Adenosine should ideally be infused via a large-calibre cannula due to it’s short half-life,
Adverse effects chest pain bronchospasm transient flushing can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)
Acute HF Drugs
Management options in acute heart failure include:
oxygen
loop diuretics
opiates - reduce anxiety and reduce dyspnoea
vasodilators
inotropic agents
CPAP
ultrafiltration
mechanical circulatory assistance: e.g. intra-aortic balloon counterpulsation or ventricular assist devices
Consideration should be given to discontinuing beta-blockers in the short-term.
Pulmonary artery occlusion pressure monitoring
Results
Interpretation of PAOP PAOP mmHg Scenario Normal 8-12 Low <5 Hypovolaemia Low with pulmonary oedema <5 ARDS High >18 Overload
Informing DVLA after MI
If PCI and car driver - no need, can drive in 4 weeks
If lorry driver - notify DVLA, stay off for 6 weeks then DVLA will assess
ejection systolic murmur, fixed splitting of S2
ASD
Risk
- Stroke as embolism may pass from venous system to left side of heart causing a stroke
Acute MI ECG changes
1) hyperacute T waves are often the first sign of MI but often only persists for a few minutes
2) ST elevation may then develop
3) T waves typically become inverted within the first 24 hours. The inversion of the T waves can last for days to months
4) pathological Q waves develop after several hours to days. This change usually persists indefinitely
INR dropped below 2 on warfarin - management
Start LMWH, Increase warfarin dose
Ejection systolic murmurs
Aortic stenosis
Pulmonary stenosis, hypertrophic obstructive cardiomyopathy
Atrial septal defect, tetralogy of Fallot
Continuous machine-like murmur
PDA
Management of orthostatic hypotension
Dx
Causes
Education and lifestyle measures such as adequate Hydration and salt intake
Discontinuation of vasoactive drugs e.g. nitrates, antihypertensives, neuroleptic agents or dopaminergic drugs
If symptoms persist, consider compression garments, fludrocortisone, midodrine, counter-pressure manoeuvres, and head-up tilt sleeping
Dx of orthostatic hypotension
A symptomatic fall in systolic BP > 20 mmHg or diastolic BP > 10 mmHg or decrease in systolic BP < 90 mmHg is considered diagnostic
Causes
Hypovolaemia
Autonomic dysfunction: diabetes, Parkinson’s
Drugs: diuretics, antihypertensives, L-dopa, phenothiazines, antidepressants, sedatives
alcohol
An inferior myocardial infarction and AR murmur s
Think proximal aortic dissection
Other features may include pericardial effusion, carotid dissection and absent subclavian pulse.
DVLA rules post CABG
4 weeks off driving
Features of hypercalcaemia
Features 'bones, stones, groans and psychic moans' corneal calcification shortened QT interval on ECG hypertension
Causes of a collapsing pulse
aortic regurgitation
patent ductus arteriosus
hyperkinetic states (anaemia, thyrotoxic, fever, exercise/pregnancy)
MOA of
Aspirin
Clopidogrel
Enoxaparin
Fondaparinux
Bivalridun
Abciximab, eptifibatide, tirofiban
Aspirin
Antiplatelet - inhibits the production of thromboxane A2
Clopidogrel
Antiplatelet - inhibits ADP binding to its platelet receptor
Enoxaparin
Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa
Fondaparinux
Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa
Bivalirudin
Reversible direct thrombin inhibitor
Abciximab, eptifibatide, tirofiban
Glycoprotein IIb/IIIa receptor antagonists
CTPA vs V/Q scan
V/Q if renal impairment
What is Takayasu’s
Features
Associations
Management
Takayasu’s arteritis is a large vessel vasculitis. It typically causes occlusion of the aorta and questions commonly refer to an absent limb pulse. It is more common in females and Asian people
Features
systemic features of a vasculitis e.g. malaise, headache
unequal blood pressure in the upper limbs
carotid bruit
intermittent claudication
aortic regurgitation (around 20%)
Associations
renal artery stenosis
Management
steroids
Reason for and causes of
S3
S
S3
Caused by diastolic filling of the ventricle
Considered normal if < 30 years old (may persist in women up to 50 years old)
Heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mitral regurgitation
S4
Caused by atrial contraction against a stiff ventricle
therefore coincides with the P wave on ECG
May be heard in aortic stenosis, HOCM, hypertension
in HOCM a double apical impulse may be felt as a result of a palpable S4
Causes of radio-femoral delay
Causes of radio-femoral delay
A significant delay between the radial and femoral pulse suggests aortic coarctation distal to the left subclavian artery.
- Aortic co-arctation
Causes of radio-radial delay If present, a delay between bilateral radial pulses suggests narrowing of the aorta proximal to the left subclavian artery - classically in the context of coarctation of the aorta. - Aortic coarctation - Subclavian stenosis - Takayasu arteritis
Rx of pts on warfarin needing emergency surgery
If surgery can wait for 6-8 hours - give 5 mg vitamin K IV
If surgery can’t wait - 25-50 units/kg four-factor prothrombin complex
Constrictive pericarditis
Causes
Features
Signs
Investigation findings
Causes
any cause of pericarditis
particularly TB
Features dyspnoea right heart failure: elevated JVP, ascites, oedema, hepatomegaly JVP shows prominent x and y descent pericardial knock - loud S3 Kussmaul's sign is positive
CXR
pericardial calcification
Signs
- KUSSMAUL SIGN (differentiates from cardiac tamponade)
Vit K heavy foods to avoid on warfarin
Broccoli, spinach, kale and sprouts are all high in vitamin K so should be avoided in excess by patients taking warfarin.
Amiodarone
Monitoring
Factors that limit use
class III antiarrhythmic agent used in the treatment of atrial, nodal and ventricular tachycardias. The main mechanism of action is by blocking potassium channels which inhibits repolarisation and hence prolongs the action potential. Amiodarone also has other actions such as blocking sodium channels (a class I effect)
Monitoring of patients taking amiodarone
TFT, LFT, U&E, CXR prior to treatment
TFT, LFT every 6 months
Factors that limit use
very long half-life (20-100 days). For this reason, loading doses are frequently used
should ideally be given into central veins (causes thrombophlebitis)
has proarrhythmic effects due to lengthening of the QT interval
interacts with drugs commonly used concurrently (p450 inhibitor) e.g. Decreases metabolism of warfarin
numerous long-term adverse effects (see below)
Axillary/brachial artery embolus
Which is more common
Symptoms
Cause
50% of upper limb emboli will lodge in the brachial artery
30% of upper limb emboli will lodge in the axillary artery
Symptoms
Sudden onset of symptoms; pain, pallor, paresis, pulselessness, paraesthesia
Cause
Sources are left atrium with cardiac arrhythmia (mainly AF), mural thrombus
Cardiac arrhythmias may cause result in impaired consciousness in addition to the embolus
Cervical rib
Cause
Symptoms
Management
0.2-0.4% incidence
Consist of an anomalous fibrous band that often originates from C7 and may arc towards, but rarely reaches the sternum
Congenital cases may present around the third decade, some cases are reported to occur following trauma
Bilateral in up to 70%
Symptoms
Compression of the subclavian artery may produce absent radial pulse on clinical examination and in particular may result in a positive Adsons test (lateral flexion of the neck away from symptomatic side and traction of the symptomatic arm- leads to obliteration of radial pulse)
Treatment is most commonly undertaken when there is evidence of neurovascular compromise. A transaxillary approach is the traditional operative method for excision
Brain death testing
1) Fixed pupils which do not respond to sharp changes in the intensity of incident light
2) No corneal reflex
3) Absent oculo-vestibular reflexes - no eye movements following the slow injection of at least 50ml of ice-cold water into each ear in turn (the caloric test)
4) No response to supraorbital pressure
5) No cough reflex to bronchial stimulation or gagging response to pharyngeal stimulation
6) No observed respiratory effort in response to disconnection of the ventilator for long enough (typically 5 minutes) to ensure elevation of the arterial partial pressure of carbon dioxide to at least 6.0 kPa (6.5 kPa in patients with chronic carbon dioxide retention). Adequate oxygenation is ensured by pre-oxygenation and diffusion oxygenation during the disconnection (so the brain stem respiratory centre is not challenged by the ultimate, anoxic, drive stimulus)
The test should be undertaken by two appropriately experienced doctors on two separate occasions. Both should be experienced in performing brain stem death testing and have at least 5 years post graduate experience. One of them must be a consultant. Neither can be a member of the transplant team (if organ donation contemplated).
