cardio/ resp Flashcards
What signs are associated with mitral stenosis?
malar flush on cheeks.
regular, low-volume pulse
mid-diastolic murmur loudest with the patient leaning to left, at apex, opening snap
Can cause AF due to atrial enlargement
Thinks ARMS - atrial regurg early murmur, followed by MS with mid murmur
What signs are associated with aortic regurgitation?
early diastolic murmur over aortic area: intensity of the murmur is increased by the handgrip manoeuvre
collapsing/ waterhammer/ corrigans pulse
wide pulse pressure
Quincke’s sign (nailbed pulsation)
De Musset’s sign (head bobbing)
What are all MI patients discharged on?
beta blocker
aspirin
ticagrelor / second line anti-platelet (DAPT - this is stopped at 12 months post MI
ACE inhibitor
statin
1st, 2nd line and 3rd line mx of HF?
1st - BB (carvedilol or bisoprolol) + ACE-i (or ARB)
2nd - spironolactone (also think of SGLT-2 inhib if diabetic) then consider SGLT-2 inhib - in hfref
3rd- initiated by a specialist. Options include ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin and cardiac resynchronisation therapy
It cardiac arrest is witnessed on a monitor how should ALS be done
Witnessed cardiac arrest while on a monitor - up to three successive shocks before CPR
When do patients get fibrinolysis for a STEMI?
should be offered within 12 hours of the onset of symptoms if primary PCI cannot be delivered within 120 minutesof the time when fibrinolysis could have been given. Should be given wtih an antithrombin drug eg fondaparinux. drug used in fibrinolysis is alteplase
dresslers syndrome - what is it?
dresslers syndrome is pericarditis secondary to MI, occurs 3-6 weeks after MI
What is Beck’s triad?
What can cause it? what do you see on ecg?
Muffled heart sounds + JVP raised + hypotension indicate Beck’s Triad -> cardiac tamponade
LV free wall rupturet MI
on ecg get tachy + electrical alternans
Treatment for angina (initial)? 2nd line add in if uncontrolled? 3rd line?
Initial: bisoprolol, GTN, aspirin and statin OR if BB CI then start rate limiting CCB eg verapamil
2nd: longer-acting dihydropyridine calcium channel blocker should be added eg Nifedipine, amlodipine
3rd: a long-acting nitrate (Isosorbide mononitrate)/ ivabradine/ nicorandil/ ranolazine/ hydrolazine + refer to cardiology for PCI assessment
What can be found on CXRs for bronchiectasis?
Parallel line shadows (often called tram-lines) are common in bronchiectasis and indicate dilated bronchi due to peribronchial inflammation and fibrosis.
What is the 4th line management for BP?
if potassium < 4.5 mmol/l add low-dose spironolactone
if potassium > 4.5 mmol/l add an alpha- or beta-blocker
When are prophylactic abx used in COPD? Which abx are used?
250mg azithromycin three times per week if:
Non-smoking
On maximum medical mx
Had pulmonary rehab
4 acute exacerbations in the last year (producing sputum), requiring hospital admission at least once.
Howdo you interpret lung function tests?(restrictive vs obstructive) When should it be done?
Done Post bronchodilator in COPD for diagnosis, pre and post in asthma
FVC - reduced, FEV1 - reduced FEV1/FVC - normal.
Restrictive lung disease - scarring of lung means reduced compliance and capacity.
Reduced forced vital capacity (FVC) as decreased compliance. FEV1 decreases at same rate so means when devided is normal.
FEV1 - reduced, FEV1/FVC - reduced
obstructive diseases eg COPD, asthma, or bronchiectasis
Obstruction to airflow which means it is hard to exhale. FEV1 is reduced. FVC is normal/ slightly low. So ratio is low.
Mx of spontaneous pnuemothorax? High risk features?
High risk features:
haemodynamically unstable
hypoxia
bilateral
underlying lung disease
>50 with sig smoking history
haemopneumothorax
If patient asx/ pneumothorax not big enough to drain - conservative mx
If patient sx + high risk + >2cm on CXR —> chest drain
If patient sx + low risk + >2cm on CXR —> needle aspiration/ ambulatory device
What are electrolyte causes of prolonged QT and potential VT?
hypocalcaemia, hypokalaemia, hypomagnesaemia
osler nodes vs janeway lesions?
Janeway lesions - erythematous macular or nodular lesions caused by septic emboli
osler nodes - painful erythematous lesions caused by immune complex deposition
what venturi mask should you use on CO2 retainers if NOT critically ill
28% Venturi mask at 4 litres/min is used prior to the results of blood gases in patients with risk factors for hypercapnia aiming for oxygen saturation of 88-92%.
If critically ill just whack on 15L
What are the rate limiting CCB? What are the dihydropyrodine CCB?
rate-limiting one such as verapamil or diltiazem
onger-acting dihydropyridine calcium channel blocker e.g. amlodipine, modified-release nifedipine
What is the mx of COPD?
1st line: SABA/ SAMA
2nd line:
If asthma features (diagnosis prev of asthma/ atopy/ raised eosinophils/ diurnal variation in peak flows) - add ICS + LABA
If no asthma features add LAMA + LABA
3rd line: all three - ICS +LABA +LAMA
What do the different leads on the ecg correspond to in terms of coronary arteries and what complications post MI can they lead to?
RCA - inferior leads - supplies AV node - so get AV block
LAD - anterior leads - left ventricle thrombus / ventricle free wall rupture/ VSD
Circumflex - lateral leads
ECG changes in pericarditis?
the changes in pericarditis are often global/widespread, as opposed to the ‘territories’ seen in ischaemic events
‘saddle-shaped’ ST elevation
PR depression: most specific ECG marker for pericarditis
How does miliary TB look on CXR?
scattered, fine nodules throughout lungs
What is moderate vs severe vs very severe copd?
The severity of COPD is based upon FEV1 readings. mildis >80% Moderate is FEV1 50-79%, severe is 30-49%, and very severe is <30%.
What ECG findings would you see in cardiac tamponade?
electrical alternans - alternation of QRS complex
Mx of asthma in <12? vs >12?
<12
SABA —> add ICS —> add LTRA —> refer
> 12
Low dose ICS/ fometerol –> low dose MART –> moderate dose MART —> check FeNO and eosinophil count, if raised refer if not —> trial LTRA/ LAMA for 8-12 w –> refer
What medications are given for pharmacological cardioversion?
flecainide or amiodarone if there is no evidence of structural or ischaemic heart disease or
amiodarone if there is evidence of structural heart disease.
What coronary artery is affected in new LBBB?
anterior/ anteroseptal
What lung cancer type has the highest incidence after asbestosis exposure?
Bronchogenic carcinoma
What are two causes of treatment resistant HTN?
coarctation of the aorta (aorta narrowed distal to ductus arteropsusto upper limb BP higher than lower branches)
renal artery stenosis
After DC cardioversion for AF how long should anti-coagulation be continued?
forever even once sinus rhythm maintained
HOCM ECG findings?
left ventricular hypertrophy
non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen
deep Q waves
Which HF medications reduce their mortality?
ACE-inhibitors/ ARBs
Beta-blockers
Aldosterone antagonists
Hydralazine and nitrates
What is seen on CXR for an aspergilloma?
The air crescent sign on chest x-ray is a characteristic finding of aspergilloma where a crescent of air that surrounds a radiopaque mass present in a lung cavity is visible.
Ball shaped opacity in apices
Presentation of digoxin toxicity?
generally unwell, lethargy, nausea & vomiting, anorexia, confusion, yellow-green vision
arrhythmias (e.g. AV block, bradycardia)
gynaecomastia
When can you restart sildenafil post MI/ stroke?
6 months
When do you recieve a bioprosthetic valve vs mechanical?
Bioprosthetic are used in >65s as no need for life-long anti-coagulation and have lower risk of VTE, however do not last as long as mechanical
Mx of pleural paques?
Pleural plaques are the most common form of asbestos-related lung disease and are benign. They are not associated with an increased risk of lung cancer or mesothelioma. This patient should be reassured and advised that no follow-up of these specific plaques is necessary, although an ongoing review of his lung disease is encouraged.
What medication is CI in HOCM?
ACE-i
nitrates
inotropes
rs can reduce afterload which may worsen the LVOT gradient.
What are some SE/ big CI to adenosine?
adenosine can cause a brief sensation of flushing and intense chest pain, but the side-effects should resolve fastly. This medication should not be administered to asthmatics as it can cause bronchospasm.
Which cardiac med can patient develop tolerance to?
Patients may develop tolerance to this medication necessitating a change in dosing regimeIsosorbide mononitrat
When would you record a posterior ECG?
Posterior MI is suggested by the following changes in V1-3:
Horizontal ST depression
Tall, broad R waves (> 30ms)
Upright T waves
What is pancoasts syndrome?
apical lung ca
leads to horner’s syndrome + brachial plexus invasion
Needs MRI chest
How should you treat MI secondary to cocaine use?
IV benzodiazepines
ECG features in hypokalaemia?
U waves
small or absent T waves (occasionally inversion)
prolong PR interval
ST depression
long QT
How is asthma diagnosed in adults?
Adults with suspected asthma should have both a FeNO test and spirometry with reversibility
What is lights criteria?
Light’s criteria are used for establishing an exudative effusion using protein or lactate dehydrogenase (LDH):
Pleural fluid protein / serum protein greater than 0.5
Pleural fluid LDH / serum LDH greater than 0.6
Pleural fluid LDH greater than 2/3 of the normal upper limit of the serum LDH
pH not part of criteria
Exudative vs transudative pleural effusions?
Exudative – a high protein content (more than 30g/L) eg cancer, RA, infection
Transudative – a lower protein content (less than 30g/L) eg HF, Hypothyroidism, meigs syndrome, hypoalbuminaemia, liver + renal failure
When do you use adrenaline in ALS and dose?
adrenaline 1 mg as soon as possible for non-shockable rhythms
during a VF/VT cardiac arrest, adrenaline 1 mg is given once chest compressions have restarted after the third shock
repeat adrenaline 1mg every 3-5 minutes whilst ALS continues
When do you use amiodarone in ALS and doses?
amiodarone 300 mg should be given to patients who are in VF/pulseless VT after 3 shocks have been administered.
a further dose of amiodarone 150 mg should be given to patients who are in VF/pulseless VT after 5 shocks have been administered
mx of following if tachycardia with no life-threatening features:
polymorphic VT eg torsades de pointes
VT
SVT
If tachycardia with life threatening features?
No life threatening features and
polymorphic VT eg torsades de pointes: magnesium 2g
VT: amiodarone 300mg IV —> synchornised DC shock up to x3
SVT: vagal manouveres –> adenosine 6mg –> adenosine 12mg –> adenosine 18mg –> verapamil/ BB
If tachycardia with life threatening features:
synchornised DC shock up to x 3 –> amiodarone 300mg IV —> repeat shock
When do you give atropine for bradycardia? Dose? next steps if doesn’t work?
If at risk of haemodynamic compromise: clinical shock, syncope, MI, HF or complete heart block with broad complex QRS, recent asystole, Mobitz type II AV block, ventricular pause > 3 seconds need to treat
Atropine (500mcg IV) 1st line tp to maximum of 3mg –> transcutaneous pacing or isoprenaline/adrenaline infusion titrated to response
Most common cause of arrest post MI?
VF
What are the different complications of a MI?
Immediate: Cardiogenic shock (low ejection fraction and poor output);
tachyarrthymias;
bradyarrthymias (most common is AV block in inferior MI)
Short-term: pericarditis (48 hrs, has pericardial rub and typical sx);
LV aneurysm (weakness in myocardium causes peristent ST elevation and LV filure -need anti-coag due to thrombus risk)
intermediate term: dresslers syndrome (2-6 weeks, fever, effusion, raised ESR, pleuritic pain, mx with NSAIDs);
LV free wall rupture (1-2 weeks post MI, acute HF due to tamponade so need urgent pericardiocentesis);
VSD (in first week, rupture of septum, causes HF and pansystolic murmur, need echo and sugrery, anteior MI);
Acute mitral regurgitation (?pansystolic murmur, most commonly infero-posterior MI, can be due to rupture papillary muscle, hypotension, early-to-mid systolic rupture, give vasodilator therapy, often need surgery)
Long term: Chronic heart failure
Bacterial causes of IE and their associations?
Staphylococcus aureus - most common cause overall, associated with IVDU
step viridans - associated with dental procedures
Staphylococcus epidermidis - associated with prosphetic valves and lines
Streptococcus bovi-
associated with colorectal cancer
What pulls trachea away vs towards white out on CXR?
towards:
Pneumonectomy
Complete lung collapse e.g. endobronchial intubation
Pulmonary hypoplasia
away:
Pleural effusion
Diaphragmatic hernia
Large thoracic mass
pneumothorax also pushes away
CI to thrombolysis in STEMI (ie alteplase)?
Contraindications to thrombolysis
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
presentation and mx of lung abscess
Lung abscess, often occur due to aspiration pneumonia, cause fever, foul smelling productive cough, gen unwell, air fluid level on CXR
treat with clindamycin 4-6w
if doesn’t work percutaneous drainge
how long does someone need anti-coag for in considering carioversion for AF (in those who are stable and has AF >48 hrs)?
Acute onset of atrial fibrillation: if ≥ 48 hours - rate control initially, then if considered for long-term rhythm control, delay cardioversion until they have been maintained on therapeutic anticoagulation for a minimum of 3 weeks
How can sarcoidosis present?
acute: erythema nodosum, bilateral hilar lymphadenopathy, swinging fever, polyarthralgia
insidious: dyspnoea, non-productive cough, malaise, weight loss
ocular: uveitis
skin: lupus pernio - puple/ blue lesions on extremities eg nose
hypercalcaemia: macrophages inside the granulomas cause an increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)
can get Heerfordt’s syndrome (uveoparotid fever) there is parotid enlargement, fever and uveitis secondary to sarcoidosis
features of aortic stenosis?
murmur of aortic stenosis is a crescendo-decrescendo, high-pitched ejection systolic murmur, heard loudest in the second right intercostal space, which radiates to the carotids. If severe stenosis is present other examination findings may include:
narrow pulse pressure
slow rising pulse
a thrill palpable over the cardiac apex
a fourth heart sound (S4) indicative of left ventricular hypertrophy
a soft/absent S2
What is included in the GRACE score?
age
heart rate, blood pressure
cardiac (Killip class) and renal function (serum creatinine)
cardiac arrest on presentation
ECG findings
troponin levels
Type A vs type B aortic dissection?
Stanford classification
type A - ascending aorta, 2/3 of cases - sugrical mx - can affect aorta and cause murmur on presentation
type B - descending aorta, distal to left subclavian origin, 1/3 of cases - conservative mx
will have widened mediastium on XR and CT angio shows false lumen
features of klebsiella pneumonia?
more common in alcoholic and diabetics
may occur following aspiration
‘red-currant jelly’ sputum
often affects upper lobes
What is an atrial myxoma?
myxoma = tumour
Causes HF type sx
Abnormal HS
Familial inheritance assciated with CARNEY syndrome
What signs are heard in mitral regurgitation?
pansystolic murmur
at apex
raidtaes to axilla
louder on expiration
Absolute CI to thrombolysis for MI?
Prev IC haemorrhage
ischemic stroke <6m
cerebral neoplasm or AVM
major trauma/ surgery/ head injury in last 3 weeks
Aortic dissection
Active bleed
GI bleed
non-compressionnable punctures in last 24 hrs eg liver biopsy, LP
Differentiating obesity hypoventilation from OSA?
Both cause daytime sleepiness, hypoventilation at night and are linked to obesity
Obesity hypoventilation causes daytime hypercapnia
OSA will have epworth score over 10
Presentation of mesothelioma vs bronchial carcinoma vs asbestosis
bronchial carcinoma causes 95% of lung ca - causes haemopysis, consolidation and clubbing
mesothelioma - causes pleural effusion, pleural thickening, asbestosis exposure long time ago normally, usually palliate
asbestosis - type of ILD causing pulmonary fibrosis, will be honeycombing on CT
Mx of tension pneumothorax?
needle decompression - 2nd intercostal space, mid clavicular line, above the 3rd rib
What is Goodpasteurs?
Autoantibodies form against the basement membrane of the lungs and kidney
Get cough, SOB, haemoptysis, kidney injury
Anti-GBM antibodies found
Wegeners is similar BUT you get also nosebless and c-ANCA
NICE criteria for two week CXR?
Clubbing
Lymphadenopathy (supraclavicular or persistent abnormal cervical nodes)
Recurrent or persistent chest infections
Raised platelet count (thrombocytosis)
Chest signs of lung cancer
Two or more unexplained symptoms in patients that have never smoked
One or more unexplained symptoms in patients that have ever smoked or had asbestos exposure
The unexplained symptoms that the NICE guidelines list are:
Cough
Shortness of breath
Chest pain
Fatigue
Weight loss
Loss of appetite
STEMI management? in context of reperfusion therapy (PCI or fibrolysis) or medical mx?
PCI - Prasagrul + aspirin, offer clopidogrel + aspirin if on a DOAC or had previous stroke/ TIA
fibrinolysis - offer ticagrelor + apirin, offer aspirin alone of with clopidogrel if high bleed risk
medical - offer ticagrelor + apirin, offer aspirin alone of with clopidogrel if high bleed risk
Which respiratory conditions do NOT cause clubbing?
pneumonia
COPD
asthma
ms of PE causing haemodynamic instability?
give continuous unfractionated heparin infusion
consider thrombolytic therapy
What is cor pulmonale? Causes?
cor pulmonary overload of R ventricle due to pulmonary HTN
Causes = ARDS, PE, SCD, severe asthma acutely, chronic lung diseases, pulmonary vacular disorders, neuromuscular diseases, thoracic cage abnormalities eg kyphosis
When do you refer to sleep clinic urgently for ?OSA?
Urgently if symptoms such as excessive sleepiness are impacting on their role as a professional driver or safety-critical worker; or if OSAS can worsen the prognosis of a comorbid cardiopulmonary condition, if the person is pregnant, or undergoing pre-operative assessment for major surgery.
What is the best way to check lung function in chronic lung disease?
TLCO
What is aortic sclerosis
ejection systolic murmur, incidental, in older ppl, no other sx
How would you diagnose an empyema?
on pleural tap pH would be less than 7.2
What are the features of brugada syndrome? what do you do with it?
features: ST elevation in V1-V3, AD inheritance, impaired sodium channels, more prevalent in SE asian
Needs urgent cardio input for ICD
What are other causes of a raised troponin other than ACS? How long does troponin remain risen for post MI?
Other causes of raise in trop: post PCI, post heart surgery, peri/ myocarditis, aortic dissection, cardiotoxic chemo, catheter ablation, defib/ cardioversion, amyloidosis, HF, PE, AKI, sepsis, rhabdomyolysis, mismatch of oxygen supply + demand eg COPD, acute HF, tachyarrhythmia
Troponin can remain elevated for up to 2 weeks post MI, peak levels are at 18-24 hrs, start to rise at 2-4 hrs post MI
mx of 1st degree heart block?
if asx no further management needed, relatively common → caution using BB, dig and diltiazem as could prolong AV block
Which lung cancer is most associated with hypercalcaemia?
SCC
What is 1st line for HTN in >55? If this is not tolerated what do you do next?
1st line for >55 without diabetes or if afro-caribbean is CCB
If a CCB is not tolerated, for example, because of oedema, offer a thiazide-like diuretic, such as indapamide.
What cancer is asbestosis most likely to cause?
Asbestosis is most likely to cause lung cancer NOT mesothelioma
Can cause other cancers too
70 yr old, confused, pyrexia, rust coloured sputum, RR=26, creps R lower base, CXR shows consolidation ?cause
s.pneumoniae
What peak flows correspond to which classifications of astham attacks?
Pefr 50-75 = moderate, 50-33 = severe, <33 = life threatening
What might you find on ecg in hypercalcaemia
J wave
shortened QT
What is the most important ix for diagnosing pericarditis?
ECG
What are important points for checking a chest drain?
Chest drains should be kept below patients chest level to help with drainage, should rise and swing with respiration, are removed on expiration, should only be clamped when changing bottle as risk of pneumothorax, if air leak (continous bubbling) is noted - check chest tube, connecting tubage, drainage bottle + wound for loose connection/ tube dislodged. If disconnection occurs tube wont swing with inspiration, tube should be reconnected, ask patient to cough, air bubbles confirm is working and in right position
What does hyperresonant chest percussion show?
COPD (hyperinflation) or pneumothorax
caucasian young woman, painful red eye, 6 week dry cough ? cause
sarcoidosis
What does GRACE score (used for NSTEMI) >3% indicate
need for PCI in 72 hrs
