Cardiology COPY Flashcards
How would you treat bradycardia (e.g. someone presents with syncope, SOB, chest pain)?
Atropine is used in the first instance when someone has bradycardia and adverse clinical features (shock, syncope, ischemia i.e chest pain, HF). Dose: 500mcg IV Frequency: can repeat 3-5mins up to max of 3mg (administer up to 6 times). If bradycardia persists: 2nd line: Transcutaneous pacing (external pacing). 3rd line: isoprenaline/adrenaline infusion titrated to response
What extra drug can you use for bradycardia caused by CCB or B-blockers?
IV glucagon
What are important things to assess when someone presents with bradycardia?
1-Identifying the presence of signs indicating haemodynamic compromise - ‘adverse signs’: -shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness -syncope -myocardial ischaemia -heart failure 2-The following are risk factors for asystole. Even if there is a satisfactory response to atropine specialist help is indicated to consider the need for transvenous pacing: -complete heart block with broad complex QRS -recent asystole -Mobitz type II AV block -ventricular pause > 3 seconds
What do you know about Amiodarone?
1-class III antiarrhythmic agent used in the treatment of atrial, nodal and ventricular tachycardias. 2-MOA: blocks potassium channels= inhibits repolarization= prolongs the action potential. Can also block sodium channels. 3-Limitations: -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. 4-Monitoring: TFT, LFT, U&E, CXR prior to treatment TFT, LFT every 6 months 5-Adverse E.: thyroid dysfunction: both hypothyroidism and hyper-thyroidism corneal deposits pulmonary fibrosis/pneumonitis liver fibrosis/hepatitis peripheral neuropathy, myopathy photosensitivity ‘slate-grey’ appearance thrombophlebitis and injection site reactions bradycardia lengths QT interval
IE in IVDU affects which valve?
Tricuspid valve
What is MOA of Alteplase?
Activates plasminogen to form plasmin. This degrades fibrin = breaks the thrombi.
Examples of thrombolysis agents? Indications, CI & side effects?
Examples: alteplase tenecteplase streptokinase Indicatations: STEMI, acute ischemic stroke, PE in haemodynamically unstable patient. CI: active internal bleeding recent haemorrhage, trauma or surgery (including dental extraction) coagulation and bleeding disorders intracranial neoplasm stroke < 3 months aortic dissection recent head injury severe hypertension Side-effects: haemorrhage hypotension - more common with streptokinase allergic reactions may occur with streptokinase
How would a posterior MI present on ECG?
Tall R waves in V1-V2 Coronary artery: Left circumflex & right coronary
How would you Ix a suspected PE? What next Ix to consider if negative?
Well’s score >4 = CTPA If CTPA is negative and a DVT is suspected= proximal leg vein ultrasound. *D-dimer is used to exclude PE in patients with Well’s score <4. Its ideally performed within 4hrs of presentation. *V/Q scans are offered as an alternative first-line investigation for patients with a Wells score greater than 4 who cannot tolerate CTPA due to contrast media allergy, severe renal impairment or high risk from irradiation.
What are the components of Well’s score?
Clinical feature Points 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
If PE is suspected or likely, but there’s a delay in CTPA, what to do?
Interim therapeutic anticoagulation.
What ECG findings in hypokalaemia?
In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT
U waves small or absent T waves (occasionally inversion) prolong PR interval ST depression long QT
Patient, 70 yr old male at GP has BP 190/110 twice at separate times. He denies any headache, blurred vision, chest pain or palpitations but has dyspnoea at rest & O/E has bibasal crepitations to mid-zones. Fundocopy is normal.
Respiratory rate 12
SpO295% on room air
Temperature36ºC
Blood pressure190/110mmHg
Heart Rate50bpm
What is the next step in Mx?
If new BP >= 180/120 mmHg + new-onset confusion, chest pain, signs of heart failure, or acute kidney injury then admit for specialist assessment.
Other same-day specialists referrals in the setting of severe HTN: retinal haemorrhages, papilloedema (signs of accelerated hypertension) or suspected phaeochromocytoma.
When would you use contrast-enhanced CT coronary angiography (CTCA)?
Typical angina
Atypical angina
Non-cardiac chest pain but a positive resting ECG e.g. Q wave abnormalities, ST-T wave changes
Management of NSTEMI & Unstable Angina?
Aspirin 300mg
Fondaparinux 2.5mg s/c for 48-72hrs (if PCI isnt planned immedietly)
Calculate GRACE score (6-month mortality)
- Low risk (<= 3%): Conservative with Tricagrelor
- Intermediate/high risk (>3%): 1- PCI (immediate if clinically unstable- within 72hrs if stable)
2-Give Tricagrelor or Prasugrel
3-Give Unfractioned heparin
What is the management of STEMI once its been confirmed?
2 Types of coronary reperfusion therapies to consider:
1- Primary coronary intervention (PCI) via drug-eluting stents= if presentation within 12 hours AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given
OR if >12hrs but evidence of ongoing ischemia
2-Fibrinolysis/Thrombolysis= within 12 hrs onset but PCI cannot be delivered within 120 mins. Alteplase (fibrinolytic therapy) which needs antithrombin e.g Heparin.
*if patient ECG taken 90 minutes after fibrinolysis failed to show resolution of ST Elevation then PCI
What drug therapy is given for STEMI patients during PCI?
PCI via radial access: unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI)
PCI via femoral access: Bivalirudin with bailout GPI
A-What drug should be given during fibrinolysis at the same time?
B-What drug should be given following fibrinolysis procedure?
A- Antithrombin drug
B-Ticagrelor
Post-MI compliations: Acute pulmonary oedema/ CHF Mx?
IV furosemide (IV has more bioavailability in acutely ill patients)
ACE-Inhibitors + B-blockers improve long-term prognosis of patients with CHF
Symptoms of Acute PO: productive cough, SOB, anxiety & sweatiness, raised JVP, widespread end-inspiratory crackles. Low Sats, tachycardia & tachypnoea.
A-How to diagnose ACS in a patient with chest pain PC?
B- Specify ECG changes
A-Its acute in nature, and you get ECG changes+/- biochemical markers of myocardial necrosis
B-ECG: T wave inversion, ST depression, ST elevation, New LBBB, Q waves. Troponin T + (NSTEMI/STEMI) - (Unstable angina)
ACS:
A- IR to Chest pain- what is the nature of cardiac chest pain?
B-What other associated factors with chest pain?
A-Central/retrosternal position, heaviness/pressure/band-like constriction, non-pleuritic, radiates to jaw,neck,arm,shoulder.
B- 1->15 mins 2-Occurs at rest (UA), 3-Inc. in frequency (crescendo angina) 4-Severe 5- Nausea/Vomiting/Sweating 6-Not resolving with nitrates 7-SOB
What are the independent risk factors of ACS? what about non-modifiable?
1-hyperlipidemia, smoking, HTN, DM, CKD
2-Age, Male sex, FH (m <55, F <65), South asian ethnicity, previous MI
Silent MI- who would present with it & what other symptoms they might present with?
People with autonomic dysfunction (DM or elderly). Might present with delirium, hypotension or epigastric pain.
Initial Ix for ACS:
1- 12 lead ECG (15-30 mins apart)
2-CXR (to exclude non-cardiac causes of chest pain e.g. pneumothorax/pneumonia & to assess for HF & aortic dissection.
3-Bloods: a) biomarkers: Troponin T or I (6hrs apart/serial) b) FBC (anaemia) c)Urea & creatinine: impaired renal function can cause false + troponin/ need baseline for ACE inhibitors d)LFT’s: baseline for STatins, hepatic impairment is CI to ticagrelor e)Electrolytes: HypoK &HyperK cause arrhythmias f)Lipid profile g)Glucose: control DM
What to keep in mind about Troponin?
It has high sensitivity (can be detected easily even at very low levels) but low specificty to MI (other conditions e.g. acute HF, Myocarditis, pericarditis, PE, renal failure & sepsis)
What does the presence of Q wave mean?
Full thickness (transmural) infarction. No Q wave= subendocardial infarction
STEMI: ECG Changes?
ST-Elevation of >/ 1mm in limb leads or >/2mm in 2 adjacent chest leads OR new LBBB in the context of cardiac sounding chest pain (ST segments cannot be meaningfully assessed if LBBB. (not all new LBBB=acute coronary occlusion)
NSTEMI: ECG Changes?
ST depression, T wave inversion, Flat T waves, pseudonormalisation of T waves, no ECG changes!
Initial Mx for ALL ACS patients:
MONAC: IV Morphine 2.5mg bolus + IV metoclopramide,
O2 if deSat <94% or <88-92% in COPD,
Nitrates sublingually,
Aspirin (300mg STAT) + Dual antiplatelet loading dose (clopidogrel 300mg STAT or ticagrelor 180mg STAT)
Continious cardiac monitoring & Coronary Artery unit.
Steps after PCI for STEMI: ABCDE 2xG!
A-ACE Inhibitor: Ramipril 1.25mg OD (CI= Renal failure of BP S <90mmHg.)
B- B-Blocker: Bisoprolol 2.5mg OD
C- Cholestrole lowering: Atorvastatin 80mg.
D-Dual antiplatelet therapy: Aspirin for life 75mg +Clopidogrel 75mg OD/Ticagrelor 90mg BD for at least 1 year.
E-Echo: to assess Left ventricle & HF signs.
G-Gastroprotection: Lansoprazole 30mg OD
G-Glucose= keep b/w 4-11mmol/L (Start IV insulin if >11)
Lifestyle Cautions for ACS:
Driving: 1-week after angioplasty. 4-weeks if no angioplasty.
Sexual intercourse- 1 week (inc. physical exercise). Air travel- 2 months.
Complications of ACS: Sudden death on PRAED Street
Sudden Death (VT or VF), P- Pump failure or Pericarditis R-Rupture (LV free wall, septum or papillary m.-MR) A-Aneurysm or Arrhythmia E-Embolism (ischemic leg or stroke) D-Dressler Syndrome
What useful test to assess a recurrent MI or re-occlusion?
CK-MB biomarker: useful in detecting reinfarction upto 36hours because when level drop after MI then Increase again it could mean a second infarction while Troponin takes 14 days to normalise.
Stable Angina (NOT ACS):
A- What are the causes?
B-Key features to differentiate between ACS & Stable Angina?
A-Causes: 1- Atheroscleorosis 2- Aortic Stenosis =LVH (to compensate O2 demand) Worsens-Anaemia, HCM, Tachyarrhythmias.
So basically: mismatch b/w O2 supply and demand→ Myocardial Ischemia.
B-
- constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms <15mins
- precipitated by physical exertion
- relieved by rest or GTN in about 5 minutes
patients with all 3 features have typical angina
patients with 2 of the above features have atypical angina
patients with 1 or none of the above features have non-anginal chest pain
Ix of Stable Angina:
Diagnosis is often clinical.
For patients in whom stable angina cannot be excluded by clinical assessment alone NICE recommend the following (e.g. symptoms consistent with typical/atypical angina OR ECG changes):
1st line: CT coronary angiography
2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia)
3rd line: invasive coronary angiography
Non-invasive Ix examples:
myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT) or
stress echocardiography or
first-pass contrast-enhanced magnetic resonance (MR) perfusion or
MR imaging for stress-induced wall motion abnormalities
Mx of Stable Angina?
Management: Lifestyle changes, Medication, Percutaneous Coronary Intervention & Surgery.
① Medication→
1-All patients receive Aspirin, Statin (esp. if total cholesterol >4mmol/l) and Sublingual GTN or Spray (Glyceryl Trinitrate) for pain symptom.
2-First line: Either Beta-Blocker or Calcium Channel Blocker (monotherapy rate limiting ones) e.g. Verapamil or Diltiazem *NEVER PRESCRIBE VERAPAMIL + B-BLOCKER= Complete Heart Block
If poor response to first-line then titrate medication to max-tolerated e.g. Atenolol 100mg od
Second-line: if titration doesn’t work then: Combination therapy of B-Blocker and CCB L-Type= long-acting modified release dihydropyridine e.g. Nifedipine) .
Third-Line: If still Symptomatic then add a 3rd drug whilst waiting for PCI or CABG. e.g. (Nicorandil, Ivabradine, Ranolazine).
*Nitrate→ Prophylaxis: Isosorbide Mononitrate (have 8hr free period to prevent tolerance).
②Modifying lifestyle: DM and HTN control, stop smoking, exercise and weight loss.
③ Percutaneous Transluminal Coronary Angioplasty (PCTA): → A balloon that dilates stenotic vessel (Stent).
NOTES: *angina + asthma =verapamil, CCB is CI in LV dysfunction. B-blockers short acting can be trialed as not every asthma is triggered by it.
Statins:
A- Q Risk >10% Mx?
B-What if the patient has a pre-existing CVD?
If QRisk3 is >10% then offer atorvastatin 20mg for primary prevention.
If patient has pre-existing CVD = 80mg for secondary prevention.
LFTs should be measured within 3months of starting treatment & at 12 months. (Statins are safe to start as long as liver transaminase results are less than 3x upper limit of normal).
CI to nitrates?
*It’s important to remember that Nitrates should be give if Systolic BP >90mmHg/60mmHg (otherwise vasodilation will cause hypotension). It’s given for pain as well.
What ECG changes = Coronary Artery?
Anterior: V1-V4 = Left anterior descending
Lateral: I, aVL +/- V5-6 = Left circumflex
Inferior: II, III, aVF = Right coronary
Posterior: Tall R waves V1-2 = Left circumflex + right coronary
Acute presentation symptoms of HF?
Acutely unwell (pale,clammy, cyanosis, frothy blood in sputum, cardiac wheeze & use of accessory muscle)
Left ventricular failure signs: Sinus tachycardia or AF, Systolic hypotension, Signs of cardiomegaly on CXR, 3rd/4th heart sounds, right sided or bilateral pleural effusions/oedema.
Right ventricular signs: elevated JVP, Hepatomegaly, Ascites, peripheral oedema.
Other Clinical Features: Dyspnoea, Orthopnoea & paroxysmal nocturnal dyspnoea
HF Ix?
Investigations:
1-Bloods: FBC, U&E’s, LFT’s TFT’s, Lipid levels & glucose
2-Assess BNP (released upon myocardial stretch): if >=100pg/ml Ix & refer within 6 weeks. If >=400pg/ml, refer to ECHO & specialist within 2w.
3-CXR: ABCDE (alveolar oedema (bat-wing), Kerley B-lines, cardiomegaly, Upper lobe diversion, Pleural effusion)
4-ECHO: to assess ventricular function (EF), valvular function & structural abnormalities.
5-ECG: to check for potential causes (remember that HF must be caused by soemthing)
Others if needed: Angiography, CT, cardiac MRI
Mx of acute HF?
Oxygen 15L/min via non-rebreathe mask or consider CPAP in ITU if not improving or developing acute respiratory acidosis.
IV opiates= only if chest pain or distress
Loop Diuretic = IV furosemide 40mg
Vasodilators = If systolic BP >90mm give IV GTN or IV isosorbide infusion
Inotropic agents = if systolic <90mm Dobutamine
Others:
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.
Chronic HF: how would you classify the severity?
NYHA classification:
I= no limitation or symptoms during ordinary activity
II=Normal at rest, ordinary activity produces mild symptoms
III= Normal at rest, less than ordinary activity produces symptoms (e.g. walking short distances of 20-50m)
IV=Symptoms at rest, patient is bed-bound
Chronic HF: Mx?
Management:
Aim is to manage symptoms & reduce episodes of acute on chronic decompensation.
Lifestyle Modification: Smoking cessation – adequate fluid & salt restriction (<3g salt/day). Can weight body to assess fluid. – alcohol restriction & optimise diet & exercise.
Medication:
First-line (combined therapy): ACE-Inhibitor + B-blocker (bisoprolol, carvedolol, nebivolol)
Second-line (becomes triple therapy): Aldosterone antagonist (spironolactone, eplerenone)
** both ACE-I & Spironolactone cause hyperkalaemia so K+ must be monitored.
Third-line (when triple therapy fails):
Initiated by specialist, one of these:
Ivabradine: Sinus rhythm >75/min & LVEF <35%
Sacubitril-valsartan: LVEF <35% & symptomatic on ACE-I or ARBs (should allow wash out period of ACE-I & ARBs)
Digoxin: improves symptoms due to inotropic properties. Indicated esp. with co-existing AF
Hydralazine in combo with Nitrate: in afro-Caribbean patients
Cardiac resynchronisation therapy: if widened QRS (e.g. LBBB)
Other: If fluid overload = Loop diuretics, Annual influenza vaccine, One-off pneumococcal vaccine (although booster every 5 years in CKD, Asplenia or splenic dysfunction)
What drugs improve mortality in patients with HF?
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.
ACE-inhibitors and beta-blockers have no effect on mortality in heart failure with preserved ejection fraction
Whats the difference between acute pericarditis vs. constrictive pericarditis?
Acute Pericarditis: inflammation of pericardium (the membrane that encloses heart)
Constrictive Pericarditis:
Chronic pericarditis → fibrosis → constrictive pericarditis
Clinical features of acute pericarditis?
TRIAD: chest pain = Sharp retrosternal that’s worst on leaning back & better forward (e.g. patient sat up in tripod position) Can have associated
Friction rub = via stethoscope
ECG changes = diffuse ST Elevation (Saddle-shaped) or PR depression
How would you diagnose Infective Endocarditis?
A-Whats the pathological criteria?
B-List the Major criteria:
C-List the Minor criteria:
Via Modified Duke’s Criteria:
- Pathological Criteria Positive, or
- 2 major criteria, or
- 1 major & 3 minor, or
- 5 minor
*As Tom Jones would say, ‘Me and Mrs Jones, we got a thing going on’. If that is indeed the case, then they very well might need a room (RHEUM) for the night. Jones criteria = Rheumatic fever
*En’duke’arditis = Duke’s criteria for IE :)
A-Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)
B:
1-Positive blood cultures:
●2 positive blood cultures showing typical IE organisms (e.g. strep viridans & HACEK group)
HACEK group: gram -ve bacteria H-haemophilus species A-Actinobacillus species C-Cardiobacterium hominis E-Eikinella corrodens K-Kingella kingii
●2 positive blood cultures taken >12hrs apart (persistent bacteraemia) OR 3 or more positive cultures where the pathogen is less specific/atypical to IE e.g. staph aureus & staph epidermidis
●Positive serology for Coxiella Burnetti, Bartonella species or chlamydia psittaci or an antiphase IgG antibody titre of >= 1/800
2-Echo:
●Oscillating mass, abscess or dehiscence of prosthetic valve
● New valvular regurgitation
C:
1-Microbiological evidence does not meeting major criteria.
2-Vascular phenomena (splinter haemorrhage, janeway lesion, major emboli, splenomegaly, clubbing, petechiae or purpura)
3-Predisposing heart disease or IVDU
4-Fever >38C
5-Immunological phenomena (e.g. glomerulonephritis, Osler’s nodes, Roth spots)
Causes of pericarditis?
Causes: Idiopathic, viral (EBV,echovirus, coxsackie, SLE/sarcoidosis, dressler syndrome post-MI, drugs (Hydralazine, Isoniazid, Procainamide, penicillin) , Uraemia.
How would you Ix acute pericarditis?
Ix:
Bloods: Troponin, BNP, CRP, WCC. If troponin is high this signify myocardial involvement & ischemia!
ECG: wide-spread ST elevation (no reciprocal changes).
CXR: Pulmonary infiltrate + rule out other causes
Echo: to check if the myocardium is involved (myocarditis) not just pericardium which will present itself by LV dysfunction (IRL RHF might follow & see both clinical signs). Also: Pericardial effusion
Mx of acute pericarditis?
Management:
1-NSAID or Aspirin until CRP is normal
2-Colchicine: to prevent further recurrance
3-Corticosteroids: if underlying cause is connective tissue disease, immune-mediated or uraemic.
4-If LVF from myocarditis= treat like HF acutely as needed e.g. IV furosemide if fluid over-load. Long-term longevity Rx as well: e.g. ACE-Inhibitors, B-blockers & Spironolactone
A-Symptoms of constrictive pericarditis?
B-Mx?
Symptoms: Kussmaul’s sign (breath in = raised JVP) + Symptoms similar to RHF
Treatment:
- Lower the pre-load (diuretics & salt restriction)
- Pericardiectomy
Typical presentation of Aortic Dissection?
Signs?
Sudden onset tearing central chest pain radiating to the back with a PMH of HTN. Pain is maximal at onset.
Other: Neurological symptoms due to occlusion of carotid, vertebral or spinal arteries, vasa nervorum of peripheral nerves, hypotensive cerebral perfusion deficit. So symptoms can include hypotension, frontal headache, neck pain.
Findings: sinus tachycardia, BP is super high (OR hypotensive), radio-radial delay of pulses.
How would you manage Aortic Dissection: Type A + Type B?
Whats the BP aim for type A?
If type A- Ascending aorta: control BP (IV labetalol) + Surgical
If type B- Descending aorta (distal to the left subclavian origin): Control BP (IV labetalol) only (+/-supportive treatment)
Type A BP: Systolic 100-120mmHg whilst awaiting surgery
Aortic Dissection: Ix findings?
CXR: widened mediastinum
CT angiography of chest, abdo & pelvis (for stable patients + surgery): A false lumen
TOE (for unstable patients)
What’s IE?
Most common organisms?
IE: infection of the endocardium and all its structures (valves, chordae tendinae) Acute-Subacute-Chronic presentations.
Most common organisms involved in infective endocarditis (in order of incidence) are:
Staph. aureus = Intravenous drug use - predisposition to Staph. aureus infection and right-sided valve disease e.g. tricuspid endocarditis
Strep. viridans
Enterococci
Coagulase negative staphylococci e.g. Staph. epidermidis
Strep. bovis - often in patients with colonic lesions, e.g. IBD or carcinoma
Fungi
HACEK organisms - Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella
Whats the Mx of HTN?
Note: Black African or African Caribbean patients with DM who are diagnosed with HTN= first line is ARB e.g. Losartan regardless of age.
Cardiac Tamponade: Features, Causes, Ix & Mx?
Features: Patients complain of SOB & Chest Pain (without evidence of MI on ECG or bloods)
Beck’s Triad: (DDD)
Distention of Jagular Vein (high JVP)
Distant heart sound
Decreased blood pressure: Pulsus Paradoxus (low BP when we inspire)
Causes: Trauma, Uremia, malignancy, proximal aortic dissection with rupture.
Ix: ECG (electrical alternans)
Mx:Urgent Pericardiocentesis.
ALS: Reversible causes of cardiac arrest?
The ‘Hs’:
Hypoxia
Hypovolaemia
Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
Hypothermia
The ‘Ts’:
Thrombosis (coronary or pulmonary)
Tension pneumothorax
Tamponade – cardiac
Toxins
How does acute pulmonary oedema present? & how would you manage acute pulmonary oedema?
Patients present with acute SOB & a PMHx of IHD & HF. O/E: Bilateral bibasal crackles (can go upwards like to mid-zone).
Mx First-line urgently: IV furosemide
Next: sublingual glyceryl trinitrate (veno-dilation and reduce preload) for quicker onset of action, intravenous morphine (treats the dyspnoea), oxygen and being positioned upright. This is to reduce the amount of fluid in the lung and improve symptoms.
Atrial Fibrillation: Definition, Epidemiology, Causes?
- Def: Uncoordinated atrial activity leading to an irregularly irregular heart rate
- Epidemiology: Extremely common – most common tachyarrhythmia
-
Cause: CHAMP
- Cardiac (HTN, Valvular disease, IHD/CAD, CCF)
- Hyperthyroidism
- Alcohol
- Metabolic (↓Mg, ↓K)
- Pulmonary causes, pneumonia/any infection
Atrial Fibrillation: Features & Investigations?
-
Features: Spectrum – symptoms get worse as ventricular rate gets faster/higher
- Asymptomatic (20%)
- Palpitations
- Heart failure
- Syncope
Ix: ECG= No p-wave, irreg irreg
Atrial Fibrillation: Acute AF Management algorithm?
Onset <48 hours: 1-Heparin 2- below:
1-Haemodynamically unstable (chest pain, syncope, signs of HF) = emergency electrical cardioversion (restores sinus rhythm)
2-Haemodynamically stable = rate or rhythm control (if rhythm control is the preferred choice, its usually via pharmacological cardioversion)
Onset >48 hours:
1-Haemodynamically stable = rate control
2-Rhythm control is not usually the preferred choice but if seniors decide that it is the preferred choice you must anti-coagulate for atleast 3 weeks prior elective pharmacological cardioversion
*(An alternative strategy is to perform a transoesophageal echo (TOE) to exclude a left atrial appendage (LAA) thrombus. If excluded patients may be heparinised and cardioverted immediately).
Acute AF: A- Rate control drugs?
B-Rhythm control drugs (pharmacological cardioversion)?
A-
Rate control drugs:
1- Beta blockers (metoprolol is short-half life so can adjust easily, bisoprolol or carvedalol). If patient has CI to B-blockers (e.g. Asthma) then 2- rate-limiting CCB (e.g. Diltiazem hydrochloride or Verapamil hydrochloride)
*These should be given as monotherapy & NEVER together = complete heart block)
3-Digoxin can be used for sedentary patients & HF only(cause of its positive inotropic affect)
B-_Pharmacological cardioversion (rhythm restoration)- using antiarrhythmic drugs:_
1- IV Flecanide: if no structural heart disease
2-Amiodarone (can achieve both rhythm & rate control BUT IV is avoided due to long-term SE, thats why its only used in special circumstances when patients have severe LVF)
*after electrical cardioversion, if sinus rhythm is needed to be maintained by a drug, sotalol (b-blocker) is usually used.
Atrial Fibrillation: Long-term/chronic Mx with thromboprphylaxis?
You can decide if the patient is suitable for thromboprophylaxis using the CHADVASc & HASBLED scores:
If the score is 0= offer TTE to exclude valvular heart disease, which in combination with AF is an absolute indication for anticoagulation. If its excluded & still 0 (anti-coagulation is contraindicated) then give Aspirin AND clopedigrol combo.
If indicated: Anticoagulant= DOAC/ NOAC (e.g. dabigatran, edoxaban, rivaroxaban, or apixaban) OR Warfarin
Pulmonary Embolus:
