Cardiology Flashcards
How to work out rate in ECG
300/ Number of squares in R-R interval
how long should p wave be?
120-200ms
Prolonged PR interval indicates
AV block
Shortened PR interval indicates ? What other feature of this condition do you often see on ecg
atrial impulse to ventricles quicker i.e. accessory pathway
associated with delta wave (slurred QRS upstroke) in Wolff Parkinson White
QRS normal length ?
80-120ms
Where is the j point
where S waves meets ST segment
When is ST elevation significant?
> 1mm in 2 or more limb leads
or >2mm in 2 or more chest leads
What is the t wave?
ventricular repolarisation
When is a t wave “tall” what could this mean?
> 5mm in limb AND >10mm in chest
associated hyperacute STEMI and hyperkalaemia
Inverted T wave is normal where?
V1 and lead III
Inverted t waves association?
ischaemia, PE, BBB
What is sinus bradycardia
<60bpm
every P wave is followed by a QRS
Physiological causes of sinus bradycardia?
Pathological?
Physiological: athletes, young due to *high resting vagal tone (vagal activity is continuous)
Pathological: acute MI, drugs (BB, dig, amiodarone), hypothyroid, hypothermia, sick sinus, raised ICP
When do you treat bradycardia
<40bpm / symptomatic
Mx of symptomatic bradycardia
IV atropine - anticholinergic, i.e. muscarinic antagonist, reduces vagal tone
Temporary pacing wire
What is sick sinus syndrome? Causes ?
Result of dysfunction of SA node with impairment of ability to generate impulse
Normally idiopathic fibrosis of node
ischaemia
digoxin toxicity
Causes of AV block
MI/ischemia (inferior)
SLE
myocarditis
(lyme disease endocarditis, degeneration of HIS-PURKINJE, drugs (digoxin, BB, CCB))
1st degree heart block is?
PR > 0.2s, PR constant, every P followed by QRS
2nd degree heart block?
Intermittent failure of conduction from atria to ventricles. Some P are not followed by QRS
Mobitz type I (Wenckebach) failure at level of AV node.
PR interval progressively lengthens and is then blocked.
Mobitz type II intermittent failure of P wave conduction.
PR interval is constant + prolonged. Fixed PR interval, dropped QRS waves2:1 block or 3:1 block
What is 3rd degree heart block? Usual cause?
Complete failure conduction atria to ventricles
myocardial fibrosis
Name 3 causes of RBBB
Rheumatic heart disease
RVH
IHD, myocarditis, cardiomyopathy, degenerative disease conduction system
Name 2 changes on ECG of RBBB
MarroW
QRS > 0.12s
Secondary R wave in V1, V2 - RSR’ [Seconary R in RBBB]
Deep, wide slurred S wave in I, V5, V6
LBBB associated conditions. Name 2
Coronary artery disease, hypertensive heart disease, dilated cardiomyopathy, anterior infarction
Name 2 ECG changes in LBBB
WilliaM
Wide QRS > 0.12s
Absent Q in V5, V6
Broad R in I, V5, V6
Deep S in V1, V2 [Long S in LBBB]
Ix in brady?
12 lead ECG
electrolyte imbalance
UE, glucose, Ca, Mg, TFT, toxicology
Mx of brady
Treat cause - correct electrolytes / stop negative chronotropes
IV atropine 0.5mg (may repeat up to 3mg)
Poor response - transcutaneous pacing
\9May also try glycopyrrolate (antimuscarinic), glucagon (if due to BB or CCB))
Temporary or permanent pacing (esp @heart block, sick sinus)
What Sx do you get with sinus tachy and why?
In diastole coronary blood flow increases. As HR increases diastole shortens.
Decreased flow to heart with increased ventricular rate = angina type symptoms, chest pain, faintness, SOB
Definition and Some causes of sinus tachy
Every P followed by QRS, rate over 100
Physiological: exertion, anxiety, pain
Pathological: fever, anaemia, hypovolaemia
Endocrine: thyrotoxicosis, phaeo
Pharmacological: sympathomimetic, adrenaline, alcohol, caffeine, salbutamol
Ix in sinus tachy
12 lead ECG, cardiac enzymes, FBC (anaemia), TFT
Mx acute regular sinus tachy
Mx ongoing sinus tachy
Vagal manoeuvres: carotid massage (young pt due to stroke risk),
*vasalva manoeuvre (forceful exhalation against closed airway with nose pinched),
facial immersion in cold water
Ongoing:
BB
or non-dihydropyridine CCB (diltiazem, verapamil)
Eg of some SVTs
AF / fibrilation
Sinus tachy
AV re-entry tachy ….
What is the most common cause of paroxsysmal narrow complex tachy cardia (SVT) ? Usual onset?
AV nodal re entry tachy
late teens / 20s
ECG of SVT? Name 2 things
Regular rhythm, narrow QRS, rate 130-250
Retrograde atrial conduction: inverted P waves in II, III, AVF (inferior)
Atrial and ventricular depolarisation together - P waves buried in QRS
Mx of AVNRT (its an SVT)
1/2nd line?
prophylaxis?
curative?
First line: Vagal maneuvers may stop as transiently block AV node
Second line: *Adenosine (for junctional) can acutely stop as transiently blocks AV node. Feel like death.
Prophylaxis: one of the above or a BB
Curative: radiofrequency ablation
What is the delta wave seen in WPW ?
Slurred upstroke of the QRS
Mx of WPW
Acute?
Prophylaxis?
Currative?
Vagal maneuvres ± adenosine
Prophylaxis: drug for AV node and accessory: flecainide (1c) or sotalol (3)
Curative: radiofrequency ablation
Main complications of narrow complex SVT?
MI
HF
Mx of complications of Narrow SVT
If BP<90, chest pain (MI), heart failure, heart rate >200
DC cardioversion with general anaesthetic
± IV amiodarone (150mg IV over 10 mins)
Rhythm in AF
Irregularly irregular ventricular rhythm
Paroxysmal = spontaneous termination within 7 days Persistent = 7 days to one year Permanent = over a year
Risk factors:
- old age
- family history
- male
- obesity
Causes:
- Ischaemia - MI
- infection - myocarditis, endocarditis
- structural - mitral stenosis or any valvular disorder
- hyperthyroid
- hyper K
Symtptoms:
- palpitations
- syncope
- dizziness
- chest pain
- fatigue
- SOB
Signs:
- hypotension
- irregularly irregular pulse
Main complications of AF
Rapid chaotic atrial firing causes stagnation of blood in atria leads to thrombus formation and risk of embolism leading to increased risk of stroke
Reduction of cardiac output (esp in ex) may lead to heart failure
Mx of AF
Rate control:
First line: standard BB or rate limiting CCB (diltiazem, verapamil)
Dual therapy add digoxin or two of above (**ONLY DILTIAZEM)
Rhythm control
Persist over 48 hours offer electrical cardioversion (DC) (transoesophageal)
Consider amiodarone for 4W before + 12M after
Anticoagulate
When can you not use fleicanide for AF?
Ischemic / structual cause
What to do if drug Mx fails in AF?
left atrial catheter ablation (if paroxysmal) or pace and ablate (if permanent) (AV node)
What is meant by pharmacological cardioversion
IV amiodarone
ECG of atrial flutter
Atrial rate 300 - no p waves *F waves
Undulating saw-tooth Flutter waves
Regular ventricular rhythm 150bpm (2:1 and 4:1 common)
Causes of Atrial flutter
Name 2
CAD, HTN, hyperthyroid, obesity, alcohol, COPD
Ix in atrial flutter
TFT, FBC (anaemia precipitates HF), UE (potassium), renal func, LFT/coag for warfarin
Imaging: echo for underlying cardiac function
Mx of atrial flutter
Rhythm control: cardioversion or medications
- DC cardioversion (if >48hours ensure adequate anticoag)
- Or IV amiodarone, sotalol, fleicanide
Mx of recurrence of atrilal flutter
radiofrequency catheter ablation
Management of broad complex tachy?
what to monitor?
If unstable?
Support ABC, O2 and venous access
Monitor ECG, BP, sats
Identify and treat reversible cause e.g. electrolyte abnormalities potassium
Unstable:
DC schock
Or AMIODARONE 300mg IV over 10-20 mins
What should you consider long term and why for VT
It is usually due to damage so requires maintenance anti-arrhythmics (BB/CCB)
or consider ICD implantable cardioversion defibrillator
What does torsades de points look like on ECG?
Like a sound wave
(In sinus:
Prolonged QT and prominent U wave
In tachycardia:
Varied axis and varied amplitude QRS)
What may happen to torsades if untreated?
Deteriorate to VF
Mx torsades?
IV magnesium sulphate
What does VF look like on ECG?
Chaotic (varying amplitudes)
No identifiable P, QRS, T
Rate 150-500
Mx of VF acute? long term?
Defibrillation
Long term:
BB and ICD (implantable cardioverter defibrillators)
Mx of brugada?
ICD implantable cardioverter defibrillator
What is the brugada sign?
Coved ST segment elevation >2mm in >1 of V1-V3 followed by -ve T
ECG finding in PE
*Sinus tachycardia - main finding
S1Q3T3 - deep S, deep Q wave in 3, deep T wave in 3 - only 10%
ECG of hypothermia
brady
```
J wave
Late delta wave, positive deflection at junction of QRS and ST segment
~~~
What is amiodarone used for?
For tachyarrhythmias (AF, AFl, SVT) when other drugs or electrical cardioversion don’t work
Some adverse affects of amiodarone? name 2
Hypotension during IV infusion.
Chronic use lungs (pneumonitis), heart (AV block), liver (hepatitis), skin (grey discolouration), thyroid (long half life - hypothyroidism / thyroid crisis)
Adenosine use?
First line diagnostic and therapeutic in SVT (inc junc)
What is important thing about adenosine
Pt feels like they gonna die for a bit
Blocks SA and AV node - causes bradycardia and asystole - doom feeling
May induce bronchospasm in asthma or COPD
What to do when giving adenosine
must always monitor with continuous ECG
Digoxin uses?
Reduce ventricular rate (AF, AFl) - after CCB or BB
Severe heart failure - 3rd line
Important to remeber with digoxin
low theraputic index
which drugs have bad interactions with digoxin
Loop + thiazide diuretics cause hypokalaemia - toxicity
Amiodarone, CCB, spironolactone all increase plasma digoxin - toxicity
SAC those drugs if you’re gonna use them with digoxin you must be LOOPY
How do you monitor for digoxin toxicity?
What target level in blood?
Monitor symptoms (or vent rate) + ECG + renal dysfunction + hypokalaemia
(Sx - Nausea, vomiting, diarrhoea, dyspnoea, confusion, dizziness, headache, blurred vision)
Target blood conc
Target 1.0-1.5nmol/l
Above 2.0nmol/l suggests toxicity
ST-segment depression - reverse tick sign
CCBs uses
Rate control in SVT inc AF +AFl
Why should you not give CCB with BB
both negatively inotropic and chronitropic so may cause HF, bradycardia + asystole
When ar BBS used 1st line?
IHD reduce angina
CHF improve prognosis
AF reduce rate and maintain sinus rhythm
SVT to restore sinus rhythm
SE of BBs
Fatigue, cold extremities, headache, impotence
When are BBs CI ? how to mitigate?
Asthma - B2 blockade causes bronchospasm, usually safe in COPD
Choose a B1 selective (ABM, atenolol, bisoprolol, metoprolol), rather than non-specific (propanolol)
Where to listen for heart valves
Mitral area - apex midclavicular, 5th IC
Tricuspid - inferior right sternal (4th IC)
Pulmonary - left 2nd IC next to sternum
Aortic - right 2nd IC next to sternum
What position are mitral murmurs best heard?
@apex + radiate to axilla, heard best in left lateral position
MR murmur
pansystolic
MS murmur?
Loud opening snap S1 and mid-diastolic murmur
How to differentiate between MR / TR
Both pansystolic but TR does not radiate to axilla
PS murmur ? Interesting fact?
Crescendo-decrescendo systolic (louder then softer).
disappear on inspiration
PR murmur
early diasolic
When are aortic murmurs best heard?
holding breath
AS murmur?
Crescendo-decrescendo systolic
Aortic regurge best heard?
Early diastolic best heard leaning forward on breath hold (pulmonary diappears)
Usual cause of AS
Senile calcification
triad of SX in AS
chest pain (predisposes to chest pain),
heart failure (obstruction -> LV hypertrophy -> LV failure),
syncope (insufficient blood)
o/e AS?
Slow rising pulse
Narrow pulse pressure (diff between syst and dia)
LV hypertrophy -> apex thrill
Crescendo-decrescendo early systolic murmur heard at R2IS transmitted to carotids
What Ix confirms Dx of AS? other Ixs?
Echo
ECG
CXR
Mx of AS ? what if not fit for sugery?
Avoid heavy exertion, modify RF for CAD
If symptomatic - prompt valve replacement - first line
If not fit for surgery
Second line - balloon valvuloplasty - risk of re-stenosis
TAVI - transcatheter aortic valve replacement
Complications of mechanical heart valves
Predisposition to infective endocarditis
Small emboli
Decompensation - increased pressure in pulmonary - CHF
How to prevent IE with new heart vlaves
ABX prophylaxis
Target INR in valve replacement
Anticoagulate mechanical heart valves
Target INR 2.5-3.5 for aortic
Causes of AR
Bicuspid rheumatic fever IE collagen Marfans / ehler danlos / turners
How does AR present?
SOBOE/non specific or symptoms of left heart failure (orth, paroxysmal nocturnal dyspnoea)
Seen o/e AR?
Early diastolic murmur as R2IS sitting forward in expiration not well transmitted to carotids
Collapsing water hammer pulse
Wide pulse pressure
What might be seen on CXR of AR?
signs of hf due to volume overload
AR is monitored regularly. What is the drug mx of AR. If HTN/HF? Marfans?
With HF or HTN - ACE-I or A2RB
With Marfan’s - BB to slow aortic root dilatation
Mx if SX in AR / deterioration of LV function
valve replacement
Normal size of mitral? when is MS servre?
4-6cm2, severe if 1cm2
What sx can present due to a large LA in MS
hoarseness
dysphagia
O/E of MS
Malar flush (CO2 retention), raised JVP, RVH - laterally displaced apex/RV heave (4th intercostal tricusp), signs of RHF (hepatomegaly, ascites, peripheral oedema)
Mid-late diastolic murmur best heard in left lateral
Loud S1 with opening snap
Seen on CXR of MS if progressing to RHF
LA enlargement, interstitial oedema (Kerley A/B lines), prominent pulmonary vessels
MR Mx if signs of LV dysfunction / AF?
Surgery
how often do you monitor MR
6/12
whatt causes rheumatic fever
Group A beta haemolytic streptococci (pyogenes)
When does rheumatic fever occur? and what is affected?
2-4 weeks post streptococcal pharyngitis or skin infection
Joints, skin, heart, nervous system
What blood test can provide evidence of strep infection
antistreptolysin O titre
or DNase B titre
Which criteria used for rheumatic fever
jones
Ix rheumatic fever
Evidence of streptococcal: throat culture, antistreptococcal antibodies (ASO, *anti-DNase B) rise during first month. Check 2 weeks apart for a rise
ECG: PR, ST elevation (saddle shape) suggests pericarditis
CXR - ?heart failure
FBC (WCC), ESR, CRP
Doppler echo for carditis
Mx of rheumatic fever. how to eradicate strep? If HF? supress inflammation? if they have chorea?
Enforce bed rest till inflam markers normal
Eradicate strep - single IV benzylpenicillin + oral penicillin
Treat HF: diuretics, ACEI and digoxin
Suppress inflammation: NSAIDs
For chorea: self-limiting, may suppress with haloperidol (beware EPSE)
Fever + new murmur is what
= endocarditis until proven otherwise
IE RFs
Valve: disease, replacement
Congenital structural heart
Previous IE
Hypertrophic cardiomyopathy
IVDU
Most common pres of IE? Name 3 signs
*Majority are fever + chills + poor appetite + wt loss
FROM JANE
Fever > 38 + tachycardia
Roth’s spots - eyes, retinal haemorrhage with pale centre
Osler’s nodes - painful red blisters @ terminal phalanges and toes
Murmur - Tricuspid with s.aureus
Janeway lesions - painless red maculae on thenar eminence
Anaemia/Arthritis: subacute = asymmetic > 3 jts, acute = septic monoarticular
Nail haemorrhage - splinter - red and linear
Embolic phenomena e.g. stroke
Which bug is most common for IE? and which murmur is classic from it?
s aureus
tricuspid
[strep viridans is next most]
Main complications of IE
MI / pericarditis
glomerulonephritis
stroke / embolic
Ix in IE
FBC (WCC, anaemia), ESR/CRP, RF
Transthoracic echo within 24 hours
Blood cultures (subacute or chronic = 3 sets from peripheral sites with 6hrs between them, acute = start ABX then take 2 within 1 hour)
CXR
ECG
How long are you gonna give IV ABx for IE? which for staph / strep?
MRSA?
4 weeks
staph - fluclox
srep - benpen
MRSA - vanc
General Ix for cardiomyopathy
Bloods: FBC, ESR, U+E, LFT, cardiac enzyme, TFT
CXR
ECG: usually abnormal
Transthoracic doppler echocardiography: can confirm Dx of hypertrophy and exclude valvular
MRI: to distinguish constrictive and restrictive disease
HF CXR features
ABCDE (alveolar oedema - bat wing, kerley B - interstitial, cardiomegaly, dilated upper lobe vessels, pleural effusion
what is the Most common cause of sudden cardiac death in young people and athletes and what kills them?
hypertrophic cardiomyopathy
arrythmia / LV outflow tract obstruction
what usually causes myocarditis
coxackie virus
Ix for myoocarditis.
FBC - leukocytosis, ESR or CRP (75%), Cardiac enzymes: CK, TrI, TrT
+ve Viral serology
*Gold standard - endomyocardial biopsy
ECG: ST elev/dep + T wave inversion
CXR: normal cardiac silhouette but other signs of heart failure
typical sx of HF
breathless, fatigue, ankle swelling
typical signs of HF
tachycardia, tachypnoea, pulmonary rales, pleural effusion, raised JVP, peripheral oedema, hepatomegaly
What EF is usual cut off for HF
<40%
differenece between LHF / RHF in presentation
RHF: peripheral oedema, abdo distension (ascites), facial engorgement, pulsing in neck and face (tricuspid regurg)
LHF: dyspnoea, fatigue, cold peripheries, muscle wasting, orthopnoea, PND, nocturnal cough - pink frothy sputum
If previous MI and new HF what Ix and when?
2 week wait for specialist and doppler echo
LV func, diastolic func, LV thickness, valvular disease
General Ix for HF
BNP - if high -> 2 week wait for echo
ECG
FBC, UE, Cr, LFT, glucose, fasting lipids, TFT, consider cardiac enzymes
CXR
ejection fraction
Acute Mx of HF ?
when stable?
Monitor what?
when to follow up?
A-E
Oxygen + IV diuretics (furosemide) [F for failure, O is a heart]
± NIV (only if severe dyspnoea + acidaemia) or IV (if resp failure or reduced conc)
Monitor ECG and ABG, catheterise them!!!
When stable: BB (bisoprolol or metoprolol) + ACEI (or ARB) + aldosterone antagonist (spironolactone)
*monitor renal function, electrolytes, HR and BP for diuretics and BB
Follow up in 2 weeks
Chronic HF mx (no LV dysfucntion)
Lifestyle (ex, smoking, alc, diet), patient education, depression
Annual influenza vaccination, pneumococcal vaccination (once only) - prophylactic
Inform DVLA, air travel likely ok
Manage comorbities: HTN, prevention MI, diabetes
Anticoagulants + statins
Mx LV dysfunction in HF 1/2/3 line?
If Hx of ventricular arrhythmia?
ACEI + BB (start low and increase dose)
Add Aldosterone antagonist (spironolactone), ARB or hydralazine with nitrate - monitor K+
Third line: digoxin or ivabradine
Implantable cardioverter defibrillator [if previous ventricular arrhythmia]
4 stages of atherosclerosis
1 fatty streak
2 intimal hyperplasia
3 fibrous cap
4 plaque formation
How do statins work?
hmg-coa refuctase inhibitors
when might you prescibe statins
QRISK2 > 10% (10 year risk) - primary prevention if <84
History of CVD
Familial hypercholesterolaemia
Anyone over 85
statin SEs
myalgia (stiff, weakness, cramps)
What should you monitor with statins
LFTS
2 modifiable and 2 unmodifiable RFs for HTN
Modifiable: smoking, weight, alcohol, stress, exercise, dietary salt
Non-modifiable: old, fam Hx, ethnicity, gender
name 3 secondary causes of HTN
Renal disease: intrinsic (75%) i.e. glomerulonephritis, polyarteritis nodosa, systemic sclerosis, PCKD, or renovascular renal artery stenosis -> increased renin by decreased perfusion
Endocrine: cushings, conns, thyroid, phaeo, acromegaly, hyperparathyroid
Coarctation aorta
Pre-eclampsia and pregnancy
Drugs - decongestants, COCP, steroids
how to calculate BP
CO X TPR
Some end organ damage in HTN . NAME 3
Brain - Encephalopathy: seizure, vomiting, nausea
Dissection - delayed/weak femoral pulses
Pulmonary oedema - heart failure
Nephropathy - proteinuria ± loin bruit
Eclampsia
Papilledema
Retinopathy (hypertensive)
what might be seen on retinopathy of HTN
Grade 1: tortuous retinal arteries + silver wiring
Grade 2: AV nipping
Grade 3: flame haemorrhages and cotton wool spots
Grade 4: papilloedema
Htn general Ix
Urine dipstick (protein + blood), serum Cr and electrolytes (K+ low = Conn’s, Ca+ high = hPTH) , renal USS
12 lead ECG (LVH or heart failure) + echo
Fundoscopy
Lipids and FBG
What Ix in HTN for 2ndary cause
Neuroendocrine tumors?
Coarcation
Thyroid
Cushing
Hypokalaemia
Renal artery stenosis
Phaeo
24 hr VMA -Vanillylmandelic Acid (for neuroendocrine tumors)
MRI / echo - coarcatation
TSH
Urinary free cortisol and dexamethasone suppression test - cushing
Renin/aldosterone levels - hypoK
MRI renal arteries
24hr mepinephrines
HTN pharmacological mx
<55 - ACEi /ARB
>55 CCB (amlodipine)
Dual therapy
add indapamide (thiazide like diuretic)
resistant add spironolactone (if low potassium) or increase TLD (if high potassium
common se of amlodipine
ankle swelling
Target BP in HTN
<140/90
Ischemia and arteries / leads on ECG
Anterior leads
v3/v4 - LAD
Lateral leads
1 V5, V6 - circumflex
Inferior leads
II, III, aVF - RCA
Septal leads
V1,V2 LAD
What should you do with all new angina ?
Refer to Rapid Access Chest Pain Clinic for confirmation of Dx and severity assessmentUrgently - within 2 weeks
DDx angina
Pain over 5 mins - MI
Acute pericarditis - worse on inspiration, lying flat, swallowing
MSK - worse on mvmt
GORD
Pleuritic pain - sharp pain on deep inspiration, ?pneumonia or PE
Ix in anginaa
ecg - can see ischemic changes with excercise stress test
-ST flattening / inversion
FBC (anaemia),
FBG (diabetes),
FBChol/triglycerides,
LFT (baseline before statin)
\U+E (renal func),
TFT (increased work, hypo assoc cholesterol)
key non pharmacological mx of stable angina
modify Rfs
patient education
pharmacotherapy of stable angina
GTN
1st
BB or CCB
2nd combine - only amlodipine as CCB
3rd Add ivabradine
Reduce caridac RFs
- aspririn / clopidogrel
- could give statin
What if angina cant be controlled by pharmacology
CABG / PCI
Ix in ACS
ECG - What does ST elevation / depression suggest?
Pre existing CAD?
Name 2 cardiac enzymes?
When are they most sensitive - how long do they last?
2 other Ix?
12 lead ECG
ST elevation - transient = angina, fixed = acute infarction
ST depression or T wave inversion = unstable angina or NSTEMI
Pre-existing CAD = LVH, Q waves
T wave inversion = previous MI,
Pathological Q waves = ongoing or old MI
Cardiac enzymes: troponin T, troponin I, CK-MB (creatinine kinase), AST, LDH, CK
troponins most sensitive (3-6 hours post infarct - max at 12-24 hours, persist 14 days) *test troponins at 6 and 12 hours
[CK-MB is cardiac specific, troponins are a marker for cardiac necrosis but also marker for skeletal muscle injury]
Bloods: FBC (anaemia and baseline for anticoagulants), blood glucose (hyperglycaemia is common = poor prog), renal function, electrolytes, lipids, TFT
Imaging: CXR (complications of ischaemia i.e. pulmonary oedema etc. , or PE, pneumothorax, TAA), TTE wall motion abnormalities
mx for all ACS
Resuscitation: ABCDE (IV fluids)
Pain: GTN + intravenous opioid with antiemetic (morphine + metoclopramide)
Dual antiplatelet: loading dose *300mg aspirin + ticagrelor 180mg
Assess O2 sats: give high flow O2 if <94%
Monitor with 12 lead ECG
—-> PCI if within 120 mins vs fibrinolysis
What scale is used to assess 6 month mortality post acs? what to do if risk is over 1.5%?
Over 3% ?
surgical option?
GRACE
<1.5%
loading dose 300mg clopidogrel and continue for 1year
<3%
coronary angiography
PCI / CABG
Mx of STEMI
MONA
Morphine, Oxygen, Nitroglycerin and Aspirin
ECG
GRACE
Reperfusion - either PCI [if within 120mins] / fibronolysis
Eg of drug used for fibronolysis
altepase
streptokinase
key non pharma changes forpost acs
Discuss secondary prevention, lifestyle changes, smoking cessation
Whats given post MI ? what do you monitor?
ABSeeD
ACEI,
BB,
statin,
dual antiplatelet (aspirin + clopidogrel),
monitor BP, monitor renal function, assessment of LV function
Aspirin action = inhibits COX irreversibly
Driving post ACS?
4 weeks off driving,
1 week if treated by angioplasty
What is dresslers syndrome?
Post ACS
late pericarditis, inflammatory reaction in response to necrotic tissue
occurs at *2-8 weeks - severe chest pain, worse supine, *left ventricular thrombosis in 20% post infarct and 60% if large anterior
name 3 coplications post MI
DEPARTS + fails
Death, dresslers Electrical: tachy + bradyarrhythmias Pericarditis (acute), papillary muscle rupture Aneurysm -> persistent ST elevation Re-MI / rupture - tamponade Thrombus - stroke Shock - cardiogenic VSD Heart failure - pulmonary oedema
Unresponsive cardiac arrest
999
A+B (if breathing turn to recovery)
C - CPR 30:2, when airway secured = uninterrupted compressions and ventilate at 10/min
D defibrillator: AED automated external defibrillator
Complete 2 minutes of CPR between debif attempts
After 3rd shock give adrenaline + amiodarone
2 minutes CPR
Adrenaline
2 minutes CPR
Adrenaline
Name 2 causes of pericarditits
Viral: *coxsackie, EBV + staphylococcal/haemophilus... Rheum: *SLE, sarcoid + …. Post MI: *Dressler’s 24-72 hours Drugs: hydralazine Other: *uraemia
What causes granulomatous pericarditis
TB, sarcoid, fungal, RA
What things aggrevate pain in pericarditis? relieve?
- Aggravated by inspiration, cough, swallow, lying flat
* Relieved by sitting up and lying forward
O/E acute pericarditis
pericardial friction rub
Tachypnoea, tachycardia, fever
If tamponade -> becks triad 3xD Decreased heart sounds (muffled) Distended jugular veins Decreased arterial blood pressure
what is becks triad ?
Hypotension, elevated systemic venous pressure (JVP), muffled heart sounds
Ix in pericarditis
serial ECGs
CXR
(globular heart if >250ml)
FBC (WCC), ESR/CRP (raised) U+E (uraemia?) cardiac enzymes (if MI)
Echo - if suspect effusion or tamponade
mx stable pericarditis
Stable: rest + treat cause + NSAIDs (naproxen) ± PPI, (if uraemic consider dialysis)
When to admit pericarditis
if fever, evidence tamponade, a large effusion (echo free space > 20mm), on warfarin, trauma, fail to respond NSAIDs
Pericarditis with falling blood pressure what should you suspect ? Mx?
suspect cardiac tamponade - immediate peircardiocentesis with echo
Mx of reccurent pericarditis
colchicine in addition to NSAIDs
What is cardiac tamponade
Collection of blood/fluid/pus/gas in the pericardial space. A large volume will result in reduced ventricular filling leading to haemodynamic compromise
mx of tamponade
O2 + volume expansion + increase venous return (legs up) + inotrope (dobutamine) + pericardiocentesis
presentation of peripheral arterial disease
Intermittent claudication
Cramping pain in calf, thigh, buttock on walking. Symptoms worse uphill. Relieved by rest. Rest time, claudication distance.
Ischaemic rest pain
Severe unremitting pain in foot, stops from sleeping, relieved by dangling or foot on cold floor
o/e lower limb ischemia
absent reduced femoral pulse
trophic changes - pale,cold, hairless, skin change
ulcers
Buerger’s angle 20 degrees = angle to which leg must be raised before it becomes pale
cap fill prolonged
Name 2 DDx of lower limb ischemia
Sciatica, spinal stenosis, DVT, entrapment
Ix for lower limb ischemia
BP, FBC (amaemia aggravates), ESR (giant cell arteritis), thrombophilia screen, FBG, lipids, ECG (CAD), renal function, urine dip
Doppler ultrasonography (dublex) to calculate ABPI
What ABPI for mild/mod/severe PAD
<0.9 = mild PAD, <0.8 = mod, <05 = ischaemic rest pain
1 is normal
6 ps of acute limb ischemia
: pale, pulseless, pain, perishingly cold, parasthesia, paralysed
mx of acute lower limb ischemia
Requires re-vasc in 4-6 hours with *immediate heparinisation
Complications of PAD
Acute limb ischemia
infection
poor healing
gangrene
General Mx of PAD
Modify Rfs
Smoking, exercise, weight
Statins
ACEI
Manage Diabetes / HTN
Antiplatelet - clopidogrel
manage pain
What imaging if you are considering revascularisation of PAD ?
Duplex USS ± CT angiography
What is aortic dissection
Intimal tearing lead to disruption of media provoked by intramural bleeding. This leads to separation of the layers and formation of a false lumen
What simple Ix in aortic dissection for a key sign
BP may be different in both arms
What do you need to differentiate aortic dissection from and why?
Differentiate from MI as thrombolysis will be fatal with dissection
Imaging for aortic dissection/?
CXR - widened mediastinum, cannot exclude dissection
TTUS - site and extent of dissection
MRI for diagnosis and identification of other vessels
Aortic dissection complications
Rupture + multi-organ failure + cardiac tamponade + hypotension
Mx aortic dissection
Analgesia (morphine) and oxygen
ICU
Manage HTN aggressively - aim 100-120SBP
IV beta blockers (labetalol) to reduce ventricular contraction
IV nitroprusside (emergency vasodilator
Surgical repair
Sx of thoracic aortic aneurysm ?
Symptoms due to local compression: hoarseness, cough, stridor, dyspnoea, SVC obstruction, dysphagia
Sx if TAA ruptures
SHIT GON HIT THE FAN - Dude who binned it in ICE
acute pain + collapse/shock + aneurysm erosion into local structure: haematemesis (aorto-oesophageal fistula), haemoptysis (aorto-bronchial), haemothorax, cardiac tamponade
Ix in TAA acute?
chronic?
Acute: FBC, clotting, renal/liver, cross-match,
ECG,
CT contrast,
MR angiography
Chronic: FBC, ESR/CRP, LFT/amylase, ECG, LuFT, USS, *TTE, *AUS (for AAA) CT angiography, MR angiography (for cause, infective, inflammatory, pancreas (DDx))
Mx of TAA ? In who?
Surgery: *graft insertion or TEVAR (thoracic endovascular aneurysm repair)
if symptomatic *regardless of size
or Marfans
Ascending > 5.5cm, descending >6cm
What would you do for pt with marfans and TAA
lifelong BB, regular imaging of aorta and restriction physical activity
Ix AAA? What sign could indicate imminent rupture?
FBC, clotting, renal, liver, crossmatch, ESR/CRP
ECG, CXR
*USS for initial assessment
CT for more anatomical detail, evidence of mural thrombus - *crescent sign - indicates blood within thrombus - imminent rupture
MRI angiography
Mx of AAA
Regular USS monitoring
smoking, HTN, statin, antipt, low dose aspirin
Inform DVLA at *over 6cm
Elective surgical repair if >5.5cm or rapid expansion >1cm/year or symptomatic
- Open Or
- EVAR
Triad of features in AAA rupture
flank/back pain, hypotension, pulsatile abdominal mass
Ix of AAA rupture
FBC (Hb will be normal, high WCC), group and save/crossmatch, baseline U+E
USS / FAST scan
[CXR, AXR (75% are calcified)]
ECG for MI
Mx AAA rupture
Large bore IV access
Group and crossmatch, order 4-6 units blood, FFP, Pt
Immediate theatre
Secure proximal aortic control
Prosthetic graft repair and stem bleeding - EVAR
(they probs gonna die tho)
Types of shock
Hypovolaemic - loss of blood/fluid - decreases CO
-Blood loss - haemorrhage, fluid loss - dehydration/burns/pancreatitis
Cardiogenic - heart unable to pump enough blood for body - decreases CO
Distributive
- Septic - decreases systemic vascular resistance, decrease SVR - Anaphylactic - intense allergic reaction leading to massive release of histamine and other vasoactive mediators - decrease SVR - Neurogenic - spinal cord injury, epidural, spinal anaesthesia causes decreased SVR
What kills patients in shock?
coagulopathy, hypothermia, metabolic acidosis
Which organs are specifically at risk in sepsis?
Kidney (acute tubular necrosis),
lung (ARDS),
heart (MI),
brain (confusion, irritability coma)
Ix in hypovolaemic shock?
Hb, UE, LFT, group and crossmatch, ABG + lactate, monitor urine
What is meant by compensated hypovolaemic shock?
baroreceptors result in increased myocardial contractility, tachycardia and vasoconstriction.
->Maintain BP. Release vasopressin, aldosterone, renin
Mx of hypovolaemic shock
Raise legs
ABCDE
Crossmatch + blood for Ix as previous + catheter + ABG
Airway + high flow O2 + 2 large bore IV cannula
Fluid resus saline or Hartmann’s 500ml over 15 mins *may give 2l total then escalate
If haemorrhagic shock give blood as soon as possible O-ve
Pain relief - pain increases metabolic rate and increases ischaemia IV opiates
Surgery to stem blood loss: e.g. REBOA after resus
Usual cause of cardiogenic shock
acute MI
What things do you need to monitor in cardiogenic shock
cardiac monitoring,
BP - art line,
venous pressure - CVC,
urinary catheter
Mx cardiogenic shock
ABCDE
fluids
O2
Pain relief *IV morphine
cardiac inotropes *dopamine or dobutamine
Revascularisation
Anaphylaxtic shock mx
ABCDE
Lie flat
high flow O2 [/Intubate]
IM adrenaline
IV fluid challenge (500ml in 5 mins)
IV chlorphenamine (antihistamine) + hydrocortisone
Bronchodilators: salbutamol IV or nebulized,
ipratropium inhaled, aminophylline IV
3 key signs of septic shock
SOFA score (2 or more is not good)
HAT
Hypotension - < 100mmHg
Altered metal state - GCS < 15
Tachypnoea - >=22
Mx of sepsis
Blood cultures + septic screen, U+E Urine output - monitor hourly Fluid resuscitation Antibiotics - tazocin? gent? according to local guidelines Lactate, ABG/VBG Oxygen to correct hypoxia
Bar buffalo what other Ix might you do in sepsis
FBC, UE, urine dip, LFT, glucose, *clotting inc D-dimer and fibrinogen for DIC, CXR, AUSS - find the infection
Complications of spesis
DIC, renal failure, cardiorespiratory failure
amiodarone side effects
prolong QT
pseudohypothyroidism
hyperK Mx
calcium gluconate
Actrapid [insulin] with dextrose
salbutamol nebs
calcium resonium - for long term
3 ECG hyperK
tall tented T
broad QRS
flat P
[prolonged QT]
2nd Heart block mx
Unstable
atropine
-trancutaneous pacing if doesnt work
Stable
Treat cause -eg hypothyroid / pericarditis
Pacing if needed
3rd degree mx
Pacing
unstable = transcutaneous / venos pacing
stable - dual chamber pacing
ST elevation in all leads cause?
pericarditis
SAH
Short term vs long term PE
Short LMWH D dimer Wells CTPA , V/Q scan
Warfarin / NOAC 3-6months
Further Ix after cute Mx of PE
1-3 Day ECG
Abdo pelvis thorax CT - Rule out malignancy
What is an NSTEMI
Elevated troponin, inverted / depressed T waves
What Ix post management of ACS
Echo
[could also check HbA1c for diabetes]
Acute HF mneumonic
LM[N]OP Loop diuretic Eg furosemide Morphine [Nitrates] - No longer Oxygen Posture
CPAP
How does furosemide work
works on the ascending loop of henle to competitively inhibit the Na-K-2CL cotransporter
PCI vs fibrinolysis
PCI = has to be within 120 minutes of the time that fibrinolysis could be given in.
Risks of angiograms
bleeding, infection, trauma to structures, failure, heart attack
Reasons for raised troponin
MI, unstable angina, trauma to heart, any of the iris’s around the heart, CKD, sepsis
Capture beat
normal beat within VT
What are the 8 shockable rhythms
How often do you give adrenaline in
Pulseless VT, VF,
1/10,000 by IV injection repeated every 3-5 minutes
What are the reversible causes of cardiac arrest
tension penumothorax
tamponade
thormbosis
toxins
haemorrhage
hypothermia
hypokalaemia/hyperkalaemia
hypoxia
