Cardiology Flashcards
What is atherosclerosis ?
chronic inflam + activation of immune system => lipid deposition in artery walls => fibrous atheromatous plaques => stiffening, stenosis + rupture
what size vessels does atherosclerosis affect ?
medium and large
what is a thrombus in fast flowing arteries mainly made of ?
mainly formed of platelets
name modifiable CVD RF ? (8)
- high cholesterol
- smoking
- alcohol
- poor diet
- poor sleep
- sedentary lifestyle
- stress
- obesity
name non-mod CVD RF ? (3)
- increasing age
- FHx
- Male
what is primary prevention for cardiovascular disease ?
QRISK > 10% => statin (atorvastatin 20mg at night)
How do statins work ?
reduce cholesterol produced by liver by inhibiting HMG CoA reductase
statin SE ? (4)
- myopathy
- rhabdomyolysis
- T2DM
- haemorrhagic stroke
secondary prevention for CVD ?
4As
- Antiplatelet (aspirin, clopidogrel)
- Atorvastatin
- atenolol/bisoprolol
- ACEI
stable angina pathophys ?
caused by atherosclerosis affecting coronary arteries => insufficient supply of blood to meet demand => chest pain
how to differentiate between stable and unstable angina ? (2)
stable when: sx only come with exertion + always relieved by GTN
what is the definitive Ix for stable angina ?
- cardiac stress testing (with ECG)
- coronary angiogram
stable angina Mx ? (3)
3 steps
- immediate sx relief (GTN spray)
- long term sx relief (BB or CCB - verapamil, diltiazem)
- secondary prevention (4As)
what would you consider revascularisation in a patient with stable angina ?
(PCI or CABG plus DAPT for 1 yr - clopi and aspirin)
- when optimal med therapy proves inadequate or if ERR bad
what are the 3 types of ACS ? what tissue affected? ischaemia or infarction ? troponin levels
- unstable angina (sub endo ischaemia): trop -ve
- NSTEMI (sub endo infarct): trop +ve
- STEMI (transmural infarct): trop +ve
what do all ACS have in common ?
all share plaque rupture, thrombosis and inflammation
describe ECG changes in STEMI ? (4)
- ST elevation
- Tall T waves
- New LBBB
- Pathological Q walves
describe ECG changes in NSTEMI/unstable angina ?
- ST depression
- T wave inversion
- non-specific
- Normal !
what blood test would you specifically get in suspected ACS ?
troponin
- get 2 samples few hrs apart to see increase (or trend)
what could cause a raised troponin ? (5)
(released when myocardial cell damage)
- Myocarditis
- Pericarditis
- MI
- ventricular strain
- PE
more
What is immediate Mx of ACS ?
MONA
- IV morphine (+antiemetic - metaclopromide)
- Nitrate
- aspirin 300mg
(give oxy if sats < 95%)
STEMI Mx ? (after initial Mx) time frames ?
- PCI within 2 hrs of presenting
- thrombolysis > 2 hrs (streptokinase, alteplase)
(or CABG)
ongoing mx of ACS ? generally (3)
- echo to assess LVF
- cardiac rehab
- secondary prevention
what is secondary prevention after ACS ?
6As
- Aspirin
- Another antiplatelet (ticagrelor/clopi)
- Atorvastatin
- ACEI (ramipril)
- Atenolol (or other BB)
- Aldosterone antagonist
what are the complications of MI (STEMI/NSTEMI) ? (5) which most liekly in first 24 hrs *
DREAD
- Death
- Rupture syndromes
- oEdema (HF) *
- Arrhythmias *
- Dresslers
what is rupture syndromes ? name some, think about anatomy
(Complication of MI)
- LAD occlusion => intra-ventricular infarct => VSD => murmur + HF
- RCA occlusion => papillary muscle infarct => acute MR
- big LAD occlusion => free wall infarct => free all rupture => cardiac tamponade
how does MI cause HF ? Mx ?
HF/oEdema
- LAD occlusion => LV infarction => pulm oedema + reduced EF => reduced CO => hypotension => acute LVHF (+cardiogenic shock)
- Mx: oxy, diuretics, stop IV fluids
how does MI cause arrhythmias ? describe some
- RCA occlusion => AV node desctruction => heart block => bradycardia
- LAD/LCx occlusion => LV re-entrant circuit => VT => VF => cardiac arrest
what is dresslers syndrome ? complication of what ? how long after ?
14 days post MI
- pericarditis as a result of injury to pericardium
(localised immune response => inflam of pericardium)
dresslers syndrome Mx ?
- ECG
- NSAIDs (aspirin, ibuprofen)
- or if more severe: steroids
name some indications for permanent pacemaker ? (4)
- complete AV node block
- mobitz type II
- persistent AV block after anterior MI
- symptomatic bradycardia
What is an arrhythmia ?
abnormal heart rhythms caused by interruptions to normal electrical signals that coordinate heart contraction
what can braqdyarrhythimas be split into ? what HR ?
- sinus Brady
- AV node block
(HR <60)
sinus Brady pathophys ?
usually San dysfunction => reduce SA node firing => reduce electrical signals to atria and ventricles
causes of sinus bradycardia ? think drugs (4)
- Beta blocker
- CCB (verapamil, diltiazem)
- digoxin
- hyperkalaemia
(increase vagal tone - PSNS)
what can cause AV node block ?
inferior MI => AV node ischaemia => A node destruction => reduced nodal conduction
describe the different types of Heart block ?
- First degree (prolonged PR interval)
- Second degree Mobitz I (wenkebach) (PR intervals gradually elongate until a P wave is completely blocked)
- Second degree Mobitz II (PR interval is consistent but some P waves don’t conduct)
- third degree (complete AV dissociation)
Mx of unstable patient presenting with arrhythmia at risk of asystole ? (3)
- IV atropine
- Inotropes
- pacemaker
what is tachycardia ? what can it be broadly split into ?
HR > 100
- narrow complex tachy (QRS < 0.12s)
- Broad complex tachy (QRS > 0.12 s)
name some narrow complex tachycardias ? (4)
- sinus tachycardia (not an arrhythmia)
- SVT
- A Fib
- A flutter
what is SVT ? is it broad or narrow complex ?
supraventricular tachycardia: abnormal electrical signals from above ventricles
- electrical signals re-enter atria from ventricle => AVN => vent => self-perpetuating
(narrow complex tachycardia)
what two types does SVT include ?
- AVRT (atrioventricular re-entrant tachycardia)
- AVNRT (AV nodal re-entrant tachycardia)
SVT ECG changes ?
QRS followed by T then QRS then T (P waves buried in T)
what is WPW ? what kind of arrhythmia ?
congenital assessor conduction pathway (bundle of Kent) connecting A + V
- SVT - AVRT (narrow complex tachycardia)
What ECG changes does WPW cause ?
- short PR (<0.12)
- narrow QRS complex (>0.12)
- delta wave
SVT Mx ? (4)
- vagal manoeuvres
- adenosine
- verapamil or BB
- DCC
name some vagal manoeuvres ? (2)
- valsalva manœuvre
- carotid sinus massage
how do you manage narrow or broad complex tachycardia with life threatening features ?
synchronised DC cardio version under GA/sedation
- IV amiodarone if unsuccessful
what is broad complex tachycardia ?
HR >100
QRIS > 0.12s
Name some types of broad complex tachycardia ? most common ?
- Ventricular tachycardia (commonest cause)
- polymorphic ventricle tachycardia
what is prolonged QTc ? give reference ranges and explain pathophys ?
what does it increase the risk of ?
prolonged QTc: >440 men, >40 women
- prolonged repolarisiotn after heart muscle contraction => spontaneous depolarisation in some muscles => TdP (polymorphic vent tachycardia) => ventricular tach (=> cardiac arrest) or revert to sinus
causes of prolonged QTc ?
- long QT syndrome
- APs
- citalopram
- flecanide
- sotalol
- amiodarone
briefly explain Mx for narrow context tachycardias:
- sinus tachycardia ?
- Atrial flutter ?
- Atrial fibrillation ?
- SVT ?
- sinus tachycardia: treat underlying cause (stress, infection)
- AF/Aflut: Rate + rhythm control
- SVT: vagal manœuvre + adenosine
briefly explain Mx for broad complex tachycardias:
- ventricular tachycardia ?
- polymorphic ventricular tachycardia ?
- vent tachycardia: IV amiodarone
- polymorphic vent tachycardia (TdP): IV magnesium
there is a pulseless patient (cardiac arrest): what are the shockable rhythms ? (2)
- VT
- V Fib
there is a pulseless patient (cardiac arrest): what are the non-shockable rhythms ? (2)
- asystole
- pulseless electrical activity
what is atrial fibrillation ? and what arrhythmia category is it in ?
chaotic irregular atrial rhythm
- SVT (originates in atria)
and what bpm is af usually ?
300-600 bpm
name some of the cardiac and non cardiac causes of af ?
- cardiac causes: increase LA pressure (due to CHF, mitral stenosis or ischaemia - seen in 22% of MI patients)
- non-cardiac: hypoxia, electrical disturbances
how does increases LA pressure cause AF ?
increased LA pressure => atrial dilatation => atrial remodelling => re-entry circuits
what are the different types of AF ? (3) describe a bit
- paroxysmal (cardiac remodelling not complete): ep 30s - 48 hrs that self resolve
- persistent
- chronic: 7 days - 1 yr
paroxysmal AF Mx ?
pill in pocket approach (flecanide)
name and explain some complications of AF ?
- thromboembolisi: blood pools (usually atrial appendage) => stasis => thrombus => VTE/stroke/TIA/mesenteric ischaemia
- Acute HF: increase HR => reduce diastolic time => reduce CO => shock
- chronic tachycardia => dilated cardiomyopathy
what investigations for AF ?seen on ECG for AF ?
- irregularly irregular ventricular contraction
- absent P waves
- narrow QRS complex tachycardia (SVT)
what could be seen on echo in patient with AF ? (2)
- LA thrombus
- valvular disease
what are the 4 parts to AF control ?
- Rate control (first line)
- Rhythm control
- anticoagulate
- Ablation (if rate/ryhthm control not effective)
describe rate control in AF ? options (3)
- BB (bisoprolol)
- CCB (verapamil, diltiazem)
- digoxin (only in sedentary ppl as stops HR increasing even when exercising)
describe rhythm control in AF ? time frames
- if haemodynamically unstable or <48 hrs or anti coagulated for 3-4 weeks + TTE: DCC, then antiocoagulate for 4 weeks
- pharma cardioversion: amiodarone, flecanide (but can increase risk of TdP
describe the anticoagulation in AF Mx ?
CHA2DS2-VASc score >/=2 : anticoagulant
how does ablation work in AF Mx ? when consider ?
when rate/rhythm control not tolerated
- creates scar tissue to prevent re-entry
what is atrial flutter ? arrhythmia type ?
(SVT - narrow complex tachycardia)
- regularly occurring atria activity (>240 flutter waves/min)
describe he relevance of cavotircuspid isthmus to A flutter ?
in some patients electrical impulses cross isthmus slowly compared to rest of atrial tissue => develop re-entrance circuit
what is the classification of A flutter ? most common ? describe a bit
- isthmus dependant (most common): flutter circuit travels through CTI)
- isthmus indepedant
describe typical ECG findings in Atrial flutter ? (4)
- narrow complex tachycardia
- regular atrial activity at 300bpm
- low of isoelectric baseline
- saw tooth waves
A fib presentaiton ? (4)
- palpitations
- sob
- dizziness
- syncope
Atrial flutter Px ?
- worsening HF + pulmonary symptoms
- palpitations
- fatigue
overview of atrial flutter Mx ?
- haemodynamically unstable: emergency electrical cardioversion
- stable: same as AF (rate + rhythm control + anticoagulation)
What is Heart Failure ?
inability o heart to meet tissues demands
how does excessive preload affect ventricle ?
=> vent dilatation
how does excessive afterload affect ventricle ?
=> vent hypertrophy
what is systolic HF ?
inability of ventricle to contract normally
what is diastolic HF ?
inability of ventricles to relax + fill normally
LHF Sx ? (5)
- dyspnoea
- poor exercise toarence
- orthopnea
- PND
- fatigue
how do you distinguish systolic and diastolic HF ? explain this pathophys
ejection fraction
- Systolic HF: due to drop in LV contractility => reduced LVEF (<40%) => reduce CO
- Diastolic HF: due to increased afterload => hypertrophic LV => reduce CO with preserved LVEF (HFpEF)
name some causes of systolic LHF ? (3)
(things that drop LV contractility)
- MI
- cardiomyopathy (often dilated)
- IHD
name some causes of diastolic LHF ? (4)
(things that cause increased afterload)
- chronic HTN
- aortic stenosis
- ventricular hypertrophy
- tamponade
explain pathphys of RHF ? cause ?
due to reduced contractility => dilated RV => reduced RV EF
- caused by MI
explain pathophys of diastolic RHF ?
- anything that increased afterload (pulmonary hypertension) => RV hypertrophy
complications of LHF ?
- pulm congestion
- cariogenic shock
explain how LHF causes pulmonary congestion ?
blood congests back form LV to LA => pulm veins => increase pulm wedge pressure => fluid leak + pulm oedema => dyspnoea (PND + orthopnoea)
explain how LHF causes cariogenic shock ?
massive CO reduction => reduced systemic perfusion => increase SVR (to compensate for low BP) => vasocontrciton + cold peripheries
complications of RHF ?
increases CVP => raised JVP + raised peripheral oedema + ascites + hepatomegaly
HF investigations (4)
- CXR
- NT-pro BNP
- Echo: systolic (HFrEF), diastolic (HFpEF)
- NYHA classification
how does BNP affect Hf Mx ?
determines when seen
>2000mg/l => wishing 2 weeks
- also measure of prognosis
what are the CXR changes seen in patient with HF ?
ABCDE
- Alveolar oedema
- Kerley B lines
- Cardiomegaly
- Dilated upper lobe vessels
- Pleural Effusions
Acute HF Mx ?
Pour SOD
- Pour away (stop) IV fluids
- Sit up
- Oxygen
- Diuretics (furosemide)
long term HF Mx ? step wise (4)
- ACEI (ramipril) or ARB
- Add BB (bisoprolol) or SGLT-2 inhibitor
- add aldosterone antagonist (spironolactone)
- furosemide for oedema
(procedural: surgical procedure for valvular disease)
What counts as high blood pressure ?
> 140/90 in clinic or >135/85 with ambulatory or home readings
what is most common cause of hypertension ?
95 % primary hypertension (essential hypertension)
- developed on its own
list the secondary causes of hypertension ? which most common
ROPE
- Renal disease (most common), like glomerulonephritis
- Obesity
- Pregnancy
- Endocrine (Cushings/conns)
what is malignant hypertension ? what value ? px ? prognosis ?
> 200/130
- px: headache, visual disturbance, papilloedema
- untreated 90% die in 1 yr
what is HTN a big RF for ? what else ?
biggest CVD RF
- IHD, CVA, hypertensive retinopathy, nephropathy
how is HTN diagnosed ?
if clinic reading between 140/90-180/120 then ambulatory BP or home readings to confirm diagnosis
describe the HTN staging ? systolic and diastolic
- stage 1 (>140/90)
- stage 2 (>160/100)
- stage 3 (>180/120)
describe stepwise HTN Mx ?
Step 1: <55 and not black: ACEI or ARB (if ACEI intolerant)
- >55 or black: CCB (amlodipine)
Step 2: A/ARB + CCB
Step 3: A/ARB + CCB + Diuretic (indapamide)
Step 4: A/ARB + CCB + D + additional (Sprinolactone, BB)
describe blood flow in mitral regurgitation ? during which heart phase ?
back flow of blood form LV => LA (during systole)
what are the causes of mitral regurgitation ? (5)
- annular calcification (elderly)
- rheumatic fever
- IE
- MV prolapse
- EDS
what can mitral regurgitation cause ? describe pathophys ?
LV volume overload => dilatation => progressive HF
- compensatory mechanisms (LA enlargement, LV increase contractility)
mitral regurgitation Px ? (5)
- dyspnoea
- fatigue
- palpitations
- asymptomatic
- sx of causative factor (infection, EDS)
what is the most important Ix for heart murmurs ?
do an echo for all of em
what would be seen on these Ix in mitral regurg
- CXR
- Echo
- CXR: LA enlargement, central pulmonary artery enlargement
- Echo: estimation of LA, LV size + function
what heart on auscultation of mitral regurgitation ? heard loudest where ?
- pan systolic murmur
- heard loudest in mitral area (5th ICS, L MCL)
Mitral regurgitation Mx ?
- vasodilators (ACEI)
- BB
- antiocoagulants
- if valve badly destroyed then valve replacement + life long warfarin
what is rheumatic heart disease ? caused by what pathogen ?
caused by group A beta haemolytic streptococcus infection (often in children) that affects + damages heart valves => MR
what is mitral stenosis ? during which phase of cardiac cycle ?
obstruction of LV inflow during diastole
what murmur associated with mitral stenosis ? what other sign ?
- mid-diastolic murmur
- malar flush (due to reduced CO)
describe aortic stenosis ? and the compensatory mechanisms ? (pathophys)
(congenital or acquired, disease of the ageing)
- as borrowing increases => restricts blood flow between LV + aorta => initially compensated by hypertrophy (to maintain pressure for CO)
- when this fails: LV function declines + symptoms develop
aortic stenosis px ?
- exertion syncope
- angina
- dyspneoa
(typically in an old person)
(can cause sudden death !!)
aortic stenosis murmur on auscultation ? where loudest ?
what signs associated ?
- ejection systolic murmur (loudest aortic area) loudest 2nd ICS at right sternal border
- slow rising carotid pulse (narrower so harder for blood to get through), decreased amplitude (takes longer for smaller amount of blood to get through)
aortic stenosis mx ?
- good dental hygienist (poor dental health increases risk of bacterial infection in blood stream)
- IE prophylaxis
- aortic valve replacement (if symptomatic prognosis is port without surgery)
what is aortic regurgitation ? during which phase of cardiac cycle ?
leakage of blood from aorta => LV during diastole
aortic regurgitation murmur on auscultation ?heard loudest where ? what sings ?
- early diastolic murmur (2nd ICS, R sternal border)
- signs: collapsing pulse + hyper dynamic apex beat
what congenital conditions is pulmonary stenosis associated with ? (3) what murmur
- Turner
- ToF
- Williams
(ejection systolic murmur)
patient presents with fever + new murmur. this is what until proven otherwise ?
endocarditis until proven otherwise
what is infective endocarditis ?
infection of heart valves (or other endocardial lined structures - septal defect, pacemaker)
- like bad infection (shivers + sick) + showers of infectious maternal into blood stream
what pathogen most likely in IE ? in drug users ? in prosthetic valves ?
- viridens group step (dental)
- s.aureus (IV drug users)
- staph epidermis (prosthetic valves)
IE Px ?
(depends on site and organism)
- systemic infection
- embolisation (=> stroke, MI, kidney dystfunction)
- valve dysfunction (HF, arrhythmia, murmur)
what signs might you see in IE ?
- splinter haemorrhages
- jaenway lesions
- oilers nodes
- Roth spots
- heart murmur
what is used to diagnose IE (what tool) ? what investigations would you do ?
modified duke criteria
- blood cultures: 3 sets at different times form different sites)
- echo (TTE/TOE) may show vegetations
- FBC, U+E, CRP
IE Mx ?
- IV Abx (choose drug depending on bug) for 6 weeks !
- surgery to get ride of infected lateral (not always)
- prevention (good dental hygiene)
describe the pathophysiology of dilated cardiomyopathy ? causes what in the end ?
reduced contractility => reduce CO => reduce BP => increase SVR (to compensate low BP) => increase preload => overloads the weak heart => dilates => HFrEF
causes of dilated cardiomyopathy ? (5)
(all cause reduced contractility)
- alcohol
- cocaine
- chagras
- coxsackie B
- takotsubos
what is takatsubo ?
rapid onset (stress) induced LV dysfunction, mimic MI
- tends to resolve spontaneously with time
what is HOCM ? what does it cause ?
(hypertrophic cardiomyopathy)
- genetic mutation (usually autosomal dominant) => inter-ventricular septum hypertrophy => LV outflow tract obstruction => HFpEF
(leading cause of sudden cardiac death in young!)
HOCM complications ? (5)
- HF
- MI
- arrhythmias (a fib)
- sudden cardiac death
- MR
HOCM Px ? O/E ?
- asymptomattic
- sob
- fatigue
- dizziness
- chest pain
- palpitations
- HF sx
O/E: ejection systolic murmur at lower left sternal border (louder with valsalva)
HOCM Mx ? (3)
aim to reduce ventricular contractility: BB or verapamil
- surgical myomectomy
- avoid intense exercise
what is pathophys of hypertrophic cardiomyopathies ?
hypertrophy => thick interventiruclar septum => reduce atria + ventricle size => almost closing in on itself at end of systole => decrease cardiac output
what is myocarditis ? causes ? (2)
inflam of myocardium, often associated with pericardial inflammation
- causes: idiopathic (about 50%), infective (viral, bacteria)
myocarditis px ? similar to what ?
- similar to ACS Px
- HF
- palpitations
- tachycardia
myocarditis Ix ? gold standard ?
- ECG (ST changes and T wave invention, AV block)
- end-myocardial biopsy (gold standard)
myocarditis Mx ? risk of what ?
supportive, treat underlying cause
- risk of developing dilated cardiomyopathy
what is pericarditis ? causes ? (3)
inflammation of the pericardium
- cause: viral (common), underlying systemic (SLE), traumatic/iatrogenic (increasingly important - caused by previous procedures)
pericarditis clinical presentation ? (3) some strange ones too. what is important differential ?
- severe and sharp chest pain: pleuritic (worse with inspiration, received by sitting forward, worse supine (this rarely seen in IHD))
- pain in shoulder + hiccups (phrenic nerve)
- hoarse voice (recurrent laryngeal)
(usually flowing seven preceding illness: fever, rash, joint pain)
(need to distinguish from ischaemic chest pain)
describe how to diagnose pericarditis ? (4)
(2/4)
- chest pain
- pericardial effusion (seen on echo)
- ECG changes
- pericardial friction rub
describe ECG changes in pericarditis ? (2)
- widespread ST elevation, PR depression
what causes pericardial rub ?
pericardium inflammation => friction => sand paper sound
pericarditis Mx ? if tamponade ?
- NSAID (ibuprofen) + colchicine + PPI (omeprazole)
- if tamponade: urgent percardiocentesis
What is pericardial effusion
where excess fluid collects within pericardial sac (acute or chronic)
- can fill entire pericardial cavity or localised section
describe the contents of the two types of pericardial effusion ?
- transudates (low protein)
- exudates (high protein, associated with inflam, blood, pus)
pericarditis pathophys ?
extra fluid in potential space (pericardial cavity) => inward pressure on heart => harder to expand during diastole
describe pathophys of pericardial tamponade ?
pericardial effusion is large enough to increase intrapercardial pressure => squeeze heart => reduce filling during diastole => reduce CO during systole
causes of pericardial effusion ?
- (high venous pressure => reduced pericardial drainage): congestive HF, pulm HTN
- pericarditis: infection (TB, HIV), autoimmune (SLE), injury (MI)
pericardial effusion px ?
- chest pain
- sob (worse lying flat)
- fullness feeling
- hiccups (compression of phrenic nerve)
- dysphagia (compression of oesophagus)
- hoarse voice (compression of recurrent laryngeal)
pericardial effusion Ix ?
- ECG
- fluid analysis (bacterial culture, viral PCR)
- TTE
- CXR (enlarged cardiac silhouette)
pericardial effusion mx ?
- treat underlying cause (infection) and drainage of effusion
- if pericarditis: NSAID + colchicine + PPI
- draining: needles pericardiocentiusis, surgical drainage
explain pathophys of chronic pericardial effusions ?
chronic pericardial effusion allows adaptation of parietal pericardium (rubber stretches) => rarely causes tamponade (compression of the heart)
what is AAA ? over what size ?
abdominal aortic aneurysm: dilation of the abdominal aorta (>50% of original diameter)
- usually become aware when it ruptures (life threatening bleeding - 80% mortality)
describe AAA screening
all men at 65
AAA px ?
- asymptomatic
- non-specific abdo pain
- pulsatile mass
- incidental finding
AAA Dx ? what are the different sizes and what do you do ?
- ultrasound
- < 3cm: normal
- 3-4.4cm: small aneurysm, rescan in 12 months
- 4.5-5.4: medium aneurysm, rescan in 3 months
- > 5.5 large aneursym, refer to vascular surgery to be seen wihtin 2 weeks
AAA Mx ?
- treat reversible RF (smoking, HTN)
- elective repair (if symptomatic or large)
- screening and surveillance
how does ruptured AAA present ? Mx ?
px: severe abdo pain radiating to back, haemodynamic instability, pulsatile + expansive mass, collapse, LOC
- Mx: surgical emergency
What is aortic dissection ? between which layers
it is when a break of tea forms in the inner layer of aorta => blood flows between layers of th wall of aorta (between intima + media)
what are the 2 types of aorta dissection ?
stanford system classification
- A (ascending aorta)
- B (descending) (ascending not involved)
aortic dissection presentation ?
- Ripping tearing chest pain (anterior => ascending, posterior => descending)
- hypertension
- radial pulse defecit
- diastolic murmur
- focal neurological defects
aortic dissection Mx ? for which classification ?
surgical emergency (high mortality)
- analgesia (morphine)
- BP + HR control (BB, verapamil)
- surgical intervention: if standard type A of complicated type B
what is peripheral arterial disease ?
borrowing of arteries applying limbs + peripheries => reduced blood supply
- common (>20% in over 80 yo)
what is intermittent claudication ? describe pathophys
muscle pain due to lack of oxy - triggered by activity, relieved by rest
- lactic acid build up + anaerobic metabolism leads to K build up => leg pain (cramps, achey pain, usually calf, thigh, buttox)
what is critical limb ischaemia ? px ? (3)
inadequate blood at rest
- pain at rest > 2 weeks
- non-healing luvers
- gangrene
critical limb ischaemia Mx ?
emergency and may require open surgery of angioplasty
what test can be done to elicit signs of PAD ?
buergers test
- supine, leg at 45 degrees: pallor of leg suggests PAD
Ix for PAD ? first line ?
- duplex US (first line)
- ABPI
- angiography
- donation classification for PAD
intermittent claudication Mx ? (4)
- lifestyle changes (reduce risk factors, optimise med treatment)
- exercise training
- naftidrofuryl oxalate (peripheral vasodilator)
- bypass surgery
what is acute limb ischaemia ? Mx ? (3)
rapid onset of ischaemia in limb due to thrombus
- Mx: end-vascular thrombolysis, bypass surgery, amputation
post MI complication: how would VSD present ?
- acute HF
- with a pan-systolic murmur
post MI complication: how would acute MR present ?
- acute hypotension and pulmonary oedema
- early/med systolic murmur
- more common with infer-posterior infarction
post MI complication: how would left ventricular free wall rupture present ?
(occurs around 1-2 weeks afterwards)
- acute HF (secondary to cardiac tamponade - raised JVP, pulses paradoxes, diminished heart sounds)
post MI complication: how would left ventricular aneurysm present ?
- persistent ST elevation and LV failure
post MI complication: how would dresslers syndrome present ?
2-6 weeks post-MI (pericarditis)
- fever
- pruritic pain
- pericardial effusion
- raised ESR
