Cardiology Flashcards
Screening age for AAA
65yr old male
Causes of AAA
Obesity Hypertension Hyperlipidaemia Smoking Connective tissue disorder
Management of AAA
Treat underlying conditions
Indications for surgery:
Rupture
Symptomatic
>5.5cm or increasing >1cm per year
ACEi side effects
Dry cough
Hyperkalaemia
First dose hypotension (expect upto 30% increase in serum creatinine and K+ of upto 5.5mM
Angioedema
Two fates of a fatty plaque
Can narrow the CA and lead to reduced blood flow
Can rupture and a piece break off to occlude the artery
ACS signs and symptoms
Central crushing chest pain radiating to the jaw and shoulders
Can be silent in diabetics or elderly
Also dyspnoea, sweating, N+V
ACS investigations
ECG
Cardiac markers
Management of ACS
Morphine
Oxygen (if <94%)
Nitrate
Aspirin (300mg)
Secondary prevention: ACEi Statin B-Blocker Aspirin Second anitplatelet may be appropriate (clopidogrel)
If present within 12hrs of symptoms and can deliver PCI within 120 mins then should deliver PCI (give praugrel if not on any other anticoagulants otherwise give clopidogrel- dual anti platelet therapy) otherwise fibrinolysis with an anti thrombin drug (give ticagrelor).
Features of acute pericarditis
Sharp chest pain Worse on inspiration Relived on sitting forward Pericardial rub Tachypnoea Tachycardia
Causes of pericarditis
Viral infection Trauma Smoke inhalation Hypothyroidism Malignancy Connective tissue disorder TB Post MI
Management of acute pericarditis
Rest and treat underlying cause
NSAIDs unless contraindicated then use colchicine
Adenosine
Used to treat SVT
Should not be used in asthmatics (bronchospasms)
Leads to transient block of the AV node therefore reduces hyperpolarisation. Short t1/2 of 8 seconds therefore should be given via IV access
SE: Bronchospasms Chest pain Transient flushing Can enhance conduction of accessory pathways i.e. WPW syndrome
Stable Angina
Treat with Aspirin, Statin and GTN spray.
First line treatment is either a CCB or BB. If CCB (verapamil or diltiazem). If not working then increase to max tolerated dose. If not working then add either a CCB or BB, depending on which one you didn’t start with. In this case the CCB should be nifedipine. If can’t handle dual therapy switch to mono therapy with long-acting nitrate, ivabradine etc
Aortic dissection and RF
Tear in tunica intima
RF: HTN Collagen disease (Marfans, Ehlers-Danlos) Turners syndrome Pregnancy Bicuspid valve
Aortic dissection features and classification
Features:
Severe chest pain, tearing and radiating to the back
Deficit in pulses (femoral, brachial, radial)
HTN
Specific arteries affected will have different effects; cardiac-angina, spinal-paraplegia, distal aorta- lower limb ischaemia
ECG non specific usually
Commonly Type A (2/3) ascending aorta Type B (1/3) descending aorta
Aortic dissection investigation and management
CXR- wide mediastinum CT angiography will show false lumen (conduct if pt stable) Transoesophageal echo (if unstable pt)
Treatment:
Type A with surgery once stable BP of 100-120 systolic
Type B with conservative management, rest and anti-hypertensives
Complications of back tear- inferior MI, aortic incompetence
Complications of a front tear- unequal pulses/BP, renal failure, stroke
Aortic regurgitation
Diastolic decrescendo murmur
+ve quinkes sign
Collapsing pulse
Causes include RF, biscuspid valve, collagen disorders, HTN
Aortic stenosis
Murmur, dyspnoea, chest pain and syncope. Also slow rising pulse
Causes include senile calcification, bicuspid valve and post RF.
Monitor if asymptomatic, but if symptomatic or severe then need a valve replacement
Types of AF
First onset
Paroxysmal- Self resolving within 24hrs-7 days
Persistent- Needs medical intervention, lasting greater than 7 days
Permanent- Cannot resolve with medical intervention.
NB- get dyspnoea, palpitations and chest pain.
Treatment of AF
Rate control- In most cases.
Treat with CCB(diltiazem)/BB as a monotherapy or a dual therapy of CCB/BB/digoxin.
Rhythm controls- In cases of existing heart problems, first onset AF, easily reversible cause.
Treat with electrocardioversion if haemodynamically unstable. Otherwise treat with either electrical or pharmacological (amiodarone or fleiclanide if no structural heart problem)
NB if presents within 48hrs then no need for anticoagulants but if >48hrs need anticoagulants 3 weeks prior cardioversion.
Need to anticoagulants looks at CHADSVASc.
If giving warfarin look at HASBLED for bleeding risk >3 is increased risk.
AF followed by stroke
Give warfarin or thrombin as choice of anticoagulation.
If no heamorrhage then anticoagulate after 2 weeks.
Rate control catheter ablation
Can undergo ablation of the areas where extra signals are being sent.
Need to anticoagulate 4 weeks prior and follow on with lifelong anticoagulants to reduce the risk of stroke.
Complications include stroke, cardiac tamponade and pulmonary valve stenosis.
Atrial flutter and management
SVT- Rapid depolarisation of the atria
Sawtooth appearance, can have a rate of 150bpm or greater depending on the ratio.
Treat same as AF; less responsive to the medication but very sensitive to the electro cardioversion, therefore lower energy levels required.
Can ablate the tricuspid valve isthmus as a cure
Atrial myxoma
Most common form of primary cardiac cancer, commonly affecting the left atrium.
Dyspnoea, fatigue, weight loss, clubbing and pyrexia.
Also emboli, AF
Atrial septal defects
Usually congenital defects found in adulthood with a high mortality rate.
More commonly osteum secundum than osteum primum. Ejection systolic murmur, paradoxical embolism
AV Block
1st degree- PR interval>20ms
2nd degree-
Type 1- increasing PR until QRS drop
Type2- constant PR with a random QRS drop
3rd degree- complete, no relationship between PR and QRS
BNP
Made mainly by the left ventricle in response to strain, high levels can also indicate disorders of the LV
Vasodilator
Marker for HF- if low then unlikely HF=> use as first line diagnostic test
Diuretic and natriuretic
Suppresses sympathetic and RAAS pathway
Increases with; LVH, ischaemia, tachycardia, sepsis, COPD, increased age, DM etc
Decreases with obesity, diuretics, ACEi, BB, ARBs
Cardiac enzymes and markers
Myoglobin is the first to rise
Troponin will be a marker for MI but will be present for upto 10 days
CK-MB is CK specific to the myocardium. Will resolve within a day therefore if still high can indicate a reinfarction
Cardiac tamponade
Increased fluid build up and pressure in the pericardium
Becks triad- Hypotension, increased JVP and muffled heart sounds
Also get paroxysmal pulse (large BP drop on inspiration), dyspnoea, tachycardia absent Y-descent in JVP.
Treat with immediate caridocentesis
Get ECG electrical alternans- switching between tall and short QRS.
In resitrictive pericarditis get present X and Y in JVP. No electoral alternans also
Choking
Mild- Can speak
Severe- Can’t speak, silent cough, wheezy etc
Mild- encourage coughing
Severe and conscious- 5 back blows, if unsuccessful then 5 abdominal thrusts, repeating this cycle until successful.
Sever and unconscious- call for ambulance and start CPR.
Clopidogrel
Indications- ischaemic stroke, PAD
Less effective if used with PPIs
Coarction of the aorta
Narrowing of the descending aorta, more common in males.
Infancy-HF
Adult- HTN
Radiofemoral delay
RF:
Turners syndrome
Bicuspid aortic valve
Berry aneurysms
Complete heart block
Syncope
Wide pulse pressure
HF
Bradycardia
Constrictive pericarditis
Same causes as acute pericarditis, more likely TB.
Dyspnoea
Increased JVP with X and Y present
Signs of RSHF
CXR will show pericardial calcification
Dabigatran
Alternative AC to warfarin which doesn’t require any monitoring.
Uses include prophylactic for DVT post TKR or THR.
Also prophylaxis for stroke in non-valvular AF pts with CHADSVASc RF.
Side effects include haemorrhage, dose should be altered in CKD patients.
Reverse with idarucizumab
DM- HTN
Should aim for BP <140/90
Use ACEi as renoprotective in DM
Don’t use BB as they can increase insulin resistance, decrease secretion and impair autonomic response to hypoG.
Dilated cardiomyopathy
Idiopathic During pregnancy HTN IHD Inherited- Duchennes muscular dystrophy
Leads to dilation of all four chambers, especially left ventricular- leads to predominantly poor systolic function
ECG axial deviation
Left- LBBB WPWS- right accessory pathway Inferior MI hyperK ASD- osteum primum
Right- RVH WPWS- left accessory pathway PE Cor pulmonale ASD- osteum secundum
Bi/Tri fasicular block
Bifasicular- L/RBBB + hemiblock (axial deviation)
Trifasicular- Bifasicular + heartblock
NB
LBBB- W in v1 M in v6
Causes include: IHD, HTN, aortic stenosis. If new then think ACS.
RBBB- M in v1 W in v6
Causes include: normal variant, PE, MI RVH
Digoxin ECG changes
ST depression- scooping
Inverted/flattened T waves
Short QT
Arrhythmias
ECG hypoK
U waves (after QRS)
Small/absent, usually inverted T waves
Long QT
ST depression
ECG hypothermia
J hump after QRS
Bradycardia
ECG MI
Talk t waves first
ST elevation
Inverted T waves
Pathological Q waves
Atrial enlargement
Right- P wave increased height and amplitude
Left- P wave increased amplitude and bifid
ECG T-wave changes
Tall- hyperK and MI
Inverted- MI, digoxin toxicity, PE, subarachnoid haemorrhage
Acute HF
Causes
Investigations
Causes:
Either de novo- less common, due to an increase in cardiac filling and pressure usually caused by an MI. Will lead to hypoperfusion and and pul oedema. Other causes of de novo include viral myopathy or toxins.
Or decomprnsated HF- more likely, have a history of HF. Due to structural or functional changes caused by ACS, hypertensive crisis, valvular changes or acute arrhythmias.
Investigations:
Look for other causes- BT (anaemia? Electrolytes?), CXR (pul causes?), echo (valvular?) or BNP
Acute HF treatment
O2 IV loop diuretics Opiates Vasodilators (nitrates) CPAP (sleep apnoea)
Consider discontinuing BB short term.
Chronic HF
Presentation
Treatment
Presentation:
Dyspnoea, orthopnoea, PND, cough (pink frothy sputum), bi basal lung crackles.
RS- Raised JVP, hepatomegaly and leg oedema
Treatment:
Usually oral loop diuretics (furosemide)
First line:
ACEi or BB (bisoprolol)
Second line:
Aldosterone antagonist (spironolactone)
Need to be wary of hyperK esp if used with ACEi
Third line:
Before starting need to refer to specialist.
May initiate digoxin
Heart sounds auscultation
P- Left sternal border, 2nd ICS
A- Right sternal border 2nd ICS
T- Left sternal border 4th ICS
M-Left, medial to mid clavicular line, 5th ICS.
Hypercalcaemia
Bones, stones, groans and psychic moans, thrones, tones.
Painful bones Renal stones Abdominal groans Psychic moans Thrones- Constipation/ frequent urination Tones- Muscle weakness, hyporeflexia
Hypertension investigations
Usually asymptomatic unless very high BP in which case get seizures, headaches and visual disturbances
Look for end organ damage:
Fundoscopy
Urine dipstick
ECG
Also:
U+E
HbA1C
Lipids
Management of hypertension
First line:
<55yrs or T2DM- ACEi or ARB
>55yrs or Afro-Caribbean (non T2DM)- CCB
Second line:
A+C or A+D (thiazide like diuretics)
Third line:
A+C+D
After this:
k+<4.5 spironolactone
K+>4.5 a/B blockers
Also consider lifestyle modifications, low salt diet
Diagnosing hypertension
Most accurate to use 24hr BP monitoring, but use Home BP or ambulatory BP monitoring.
> 140/90 (clinic) then offer ABPM or HBPM:
> 135/85 - stage 1 hypertension- treat if <80yrs and has end organ failure, renal/CV disease, QRISK>10%
> 150/95- stage 2 hypertension- treat all cases
HTN stages
Stage 1- 140/90 (clinic), 135/85
Stage 2- 160/100 (clinic) 150/95
Stage 3- >180 or />120
Causes of HTN
Can be primary (unknown specific cause)
Or secondary:
Commonly primary hyperaldosteronsim
Also
Renal: GN, RAS, APKD, pyelonephritis
Endocrine: Phaeochromocytoma (need to refer if suspecting this), primary hyperaldosteronism, Cushings, acromegaly
Drugs: Steroids, NSAIDs, COCP
Others: Pregnancy, coarction of the aorta
Infective endocarditis
Think if fever and new murmur, usually affecting the mitral valve
RF- previous episodes of IE, RF, prosthetic valves, IVDU (tricuspid affected mainly)
Caused mainly by staph aureus, unless have in dwelling line or had prosthetic valve surgery
Diagnose with 2 positive blood cultures showing organisms typical of infective endocarditis.
Treat with flucloxacillin- effective against staph
Give prophylaxis if previously infected pt develops an infection
Surgery indicated if: not responding to Abx, severe valvular incompetence or aortic abscess
Signs of inhaled foreign body
Cough
Stridor
Dyspnoea
Palpitations
Causes include arrhythmias, anxiety or becoming more aware of heart beat.
Tests- run an ECG, unlikely to see any changes in a few seconds so ask pt to take a Holter monitor (keeping a diary of when they felt palpitations and comparing to the rhythm strip)
If this is not useful can consider an external/implantable loop recorder.
Also do TFTs, U+Es (low K+), FBC
Mitral regurgitation
Pansystolic murmur, radiating from the apex to the axils
Usually asymptomatic but when more severe and get LVH then symptoms of HF
Causes: RF, mitral valve prolapse, congenital, IE, post MI.
ECG- may show atrial enlargement. CXR- may show caridomegaly. Diagnose with echo.
Treatment- medical management if acute, repair is better than replacement. Replace in acute severe regurgitation.
Mitral stenosis
Mid-late diastolic murmur heard better on expiration. Malar flush and AF.
RHEUMATIC FEVER!!!
CXR shows atrial enlargement
Use echo.
Complications of MI
Cardiac Arrest (following VF) Pericarditis Chronic HF Cardiogenic shock Left ventricular aneurysm VSD Tachyarrhthmias (VF) Bradyarrhythmias Acute mitral regurgitation
Myocarditis
Suspect in young pt presenting with chest pain
Look for cardiac enzymes, inflammatory markers and BNP
Manage by treating underlying cause (Abx) and offering supportive treatment.
Indications for temporary pacemaker
Trifasicular block before surgery
Post anterior MI- type2 or complete heart block
Symptomatic/haemodynamically unstable bradycardia
Orthostatic hypotension
Drop in BP by 20/10 when standing
Presyncope
Syncope
Treat with antihypotensives; flu for peristome or midodrine
PE presentation
Dyspnoea Pleuritic chest pain Haemoptysis Tachypnoeic Tachycardic Usually resp examination unremarkable may hear some crackles
PE investigations.
ECG- Sinus tachycardia, S1Q3T3 (s and a q large, t inverted- only on some cases find this pattern)
Need to do the rule out criteria to rule out a PE
If can’t rule out a PE then do the Wells score
If >4 need to do a CTPA, give DOACs whilst waiting for the diagnosis confirmation. If +ve then continue DOAC treatment, if -ve then conduct a proximal leg vein ultrasound if DVT suspected.
If <4 then do a d-dimer, if +ve then do CTPA and give DOACs whilst waiting for diagnosis. If this comes back -ve then stop DOACs.
PE management
Prescribe DOACs unless they have me severe renal impairment or APLS in which case give LWMH followed by Vit-K antagonist (Warfarin)
PE can either be provoked or unprovoked.
Provoked- Give DOACs for 3 months total
Unprovoked- Give DOACs for 6 months total- whilst monitoring the HASBLED risk.
If massive PE/haemodynamically unstable then consider thrombolysis as first line treatment.
Rheumatic Fever
Immunological reaction to a strep pyogenes infection (within 2-6 weeks)
\+ve throat swap Erythema marginatum Polyarthritis Pyrexia Raised CRP/ESR
Management:
Oral penicillin
NSAIDs
Statins
ADR- myalgia, rhabdomyolysis, liver impairment.
Contraindicated in pregnancy and with macrolides.
Uses:
Established CV event (Stroke, TIA, AF, PAD, ACS)
QRISK>10%
DM for over 10 years, over the age of 40yrs or with established nephropathy.
Primary prevention: Atorvastatin 20mg
Secondary prevention: Atorvastatin 80mg
SVT
Acute management:
Valsalva manoeuvre
IV Adeonsine (6mg->12mg->12mg)
Electrical cardioversion
Prevention:
B-blockers
Radio frequency ablation
Syncope
This is the transient loss of consciousness with a rapid onset, short duration and full spontaneous recovery.
Reflex: (most common)
Vasovagal- emotions, ‘fainting’, stress, pain
Situational- cough, micturition
Carotid sinus syncope
Orthostatic:
Primary autonomic- Parkinsonism, LB dementia
Secondary autonomic- DM nephropathy
Cardiac:
Arrhythmias
Structural- valves, MI
Other- PE
Look at postural drop in BP
Thiazide diuretics ADR
Dehydration HypoK/Na HyperCa Gout Impotence Impaired glucose tolerance
Takayasu’s arteritis
Vascular is of the large vessel, common in Asian and female. Occlusion of the aorta: Absent limb pulses Intermittent claudication Difference in BP across upper limbs Carotid bruit
Manage with steroids
Thrombolysis
Give to convert plasminogen into plasmid therefore leading to fibrin breakdown.
Alteplase, streptokinase
Risk of bleeding and hypotension
Tricuspid regurgitation
Pan systolic murmur
Pulsation hepatomegaly
Left parasternal heave
Causes: RV infarction Rheumatic heart disease Infective endocarditis Pulmonary hypertension (COPD)
VSD
More common with chromosomal disorders I.e. Downs, Edwards
Congenital infections
Or acquired I.e. post MI
VSD may be small and asymptomatic in which case they close spontaneously.
Can also be larger and symptomatic- Require treatment (present with HF), nutritional support and surgical repair.
Post natal presentation: Failure to thrive, HF symptoms, pan systolic murmur.
Complications: Aortic regurgitation, infective endocarditis, RSHF, pulmonary hypertension
Ventricular tachycardia
Can be monomorphic- common, post MI. Or polymorphic- I.e. Torsades de pointes (VT with long QT)
Need to treat since can progress to VF and then cardiac arrest.
Management:
If signs of haemodynamic instability present then need elctorcardioversion.
If not present then medical treatment; amiodarone (central line) or lidocaine. If not responding then synchronised cardioversion.
Do not use VERAPAMIL
If drug therapy does not work then may need implanted defibrillator
Warfarin
Inhibits the conversion of Vitamin K therefore reduces clotting
Used in VTE target INR<2.5, 3.5 for recurrent episodes
Used in AF target INR<2.5
Also used in mechanical heat valves
Potentiated by liver disease, P450 inhibitors, drugs displacing warfarin from albumin (NSAIDs), cranberry juice
Bleeding risk with Warfarin
Anything INR>5 need to consider stopping warfarin and giving Vitamin K.
Greater INR- greater bleeding risk
WPWS
Congenital accessory pathway between the atria and the ventricles, if not treated then the AF can develop quickly into VF.
ECG:
Short PR
Axis deviation
Wide QRS with delta wave (upstroke)
Treat with radio frequency ablation of the accessory pathway. Medical- sotalol (avoid in coexisting AF), amiodarone or flecainide.
