cardio Flashcards
what is pericarditis
inflammation of the pericardium - the sac which surrounds the heart
aetiology of pericarditis
- viral – cosackies, mumps, EBV, CMV, varicella, rubella, HIV, Parvo-19
- MI + Dressler’s, aortic dissection, uraemia, SLE, IBD
clinical features of pericarditis
- Classic triad of pericardial rub, chest pain, ECG changes
- Retrosternal/ precordial pleuritic chest pain worse lying flat or inspiration, coughing,
- Pain relieved by sitting forward, radiate to trap/ neck/ shoulder.
- Fever.
- Dry cough.
what are the pericarditis specific ECG changes
PR depression, widespread saddle ST elevation
Ix and Mx of pericarditis
ECG
- Refer to cardiology if tamponade pericardiocentesis
- If bacterial pericardiocentesis + systemic Abx (vancomycin + ceftriaxone)
- Treat cause
- NSAID + PPI
- Colchicine – used to prevent further pericarditis
what is accelerated hypertension
recent inc in BP to over > 180 and > 110 + papilloedema or retinal haemorrhage
clinical features of accelerated HTN
papilloedema
retinal haemorrhages
signs of end-organ damage - headache, fits, N+V, visual disturbances, chest pain, bleeding due to DIC, microangiopathic haemolytic anaemia
Investigation and treatment of accelerated HTN
medical emergency
same day referral for pt with accelaterd HTN with papilloedema/retinal haemorrhage
aim - reduce BP steadily over 24-48 hours - IV nitroprusside, labetalol or nifadipine
what is pericardial effusion
collection of fluid in the pericardial space
what are the different types of pericardial effusion?
transudate - fluid pushed through capillaries due to high pressure within them
exudate - fluid that leaks around the cells of capillaries due to inflammation
haemopericardium - blood
causes of pericardial effusion
pericarditis MI AKI/CKD malignancy nearby autoimmune conditions
clinical features of pericardial effusion
- Depend on speed and size of effusion
- Chest pain: relieved by sitting up and leaning forward and intensified by lying down.
- Light-headedness and syncope
- Palpitations
- Cough
- SOB
- Anxiety
- Beck’s triad of pericardial tamponade: hypotension, muffled heart sounds, jugular venous distention.
- Pulses paradoxus (significant drop in BP on inspiration)
ix and Mx of pericardial effusion
echo -diagnostic
refer to cardiology
treating underlying cause
pericariocentesis
what are the 2 shockable rhythms?
pulseless ventricular tachycardia
ventricular fibrillation
what are the 2 non-shockable rhythms?
pulseless electrical activity
asystole
what is the sequences of action in cardiac arrest
discover a patient unresponsive and not breathing normally –> call for help –> CPR 30:2 –> attach defib pads + airwya mx + IV access –> assess rhythm (pause CPR for rhythm analysis and pulse check)
what are the reversible causes of cardiac arrest
4Ts
- tamponade
- thrombosis
- tension pneumothorax
- toxins
4HS
- hypothermia
- hypoxia
- hypovolaemia
- hypo/hyperkalaemia/metabolic
what is acute left ventricular failure
- Left ventricle is unable to adequately move blood through the left side of the heart and out of the body.
- This causes a backlog of blood that increases the amount of blood in the left atrium, pulmonary veins and lungs.
- As the vessels in these areas are engorged with blood due to increased volume and pressure, they leak fluid and are unable to reabsorb fluid from the surrounding tissues.
- This causes pulmonary odema where the lung tissues and alveoli become full of interstitial fluid
- This results in lack of gas exchange and desaturation.
aetiology of acute left ventricular failure
iatrogenic - aggressive IV fluids in frail people with impaired left ventricular function
sepsis
MI - think if flash pulmonary oedema
arrythmias
clinical features of acute left ventricular failure
- rapid SOB
- looking unwell
- dry cough - due to irritation of pleura
- inc RR
- reduce O2 sat
- tachycardia
- 3rd HS
- bilateral pulmonary basal crackles
- hypotensions in severe cases
- cold and clammy due to peripheral shutdown
signs of underlying causes
- chest pain in ACS
- fever in sepsis
- palpitation in arrrythmias
if RHS failure as well
- raised JVP
- peripheral oedema
ix for acute left ventricular failure
ECG - arrythmias and ischaemias
ABG - low o2, high co2
bloods - FBC, U&Es, LFT, CRP, BNP, Trop
CXR - pulmonary oedema pictures - Kerley B line, cardiomegaly, dilated upper lobe vessels, pleural effusions
ECHO - main measure of left ventricular function is ejection fractions, <40 = LHeart failure
management for acute ventricular failure
A-E approach
PODMAN
Position pt - sit up oxygen Diuretics - furosemide 40mg IV + fluids restrction morphine - consider anti-emetics - consider nitrites - consider
other consideration
- nitrate (must have SBP > 90) - for MI, severe HTN, aortic regurg or mitral stenosis
- IV opiates to act as vasodilator
- CPAP if dyspnoea and acidaemia
- inotropes - those with potentially reversible cardiogenic shock
what are some causes of secondary hypertension
renal disease - glomerulonephritis, pylonephritis, PCKD)
endocrine disease - Cushing’s, Conn’s, acromegaly, hyperPTH, pheochromocytoma, hyperthyroidism
other
- pregnancy
- steriods
- coarctation
- OCP
what is chronic cardiac failure?
the ability of the heart to maintain the circulation of blood is impaired as a result of a structural or functional impairment of ventricular filling or ejection
aetiology of chronic cardiac failure
coronary artery disease and heart attack - most common cause
HTN
valvular disease - aortic stensois
AF
other - hyper/hypothyroidism, haemochromatosis, protein powder?
clinical features of chronic cardiac failure
SOB - on exertion, lying flat, nocturnal cough, PND
fluid retention - ankle, abdomen, weight gina
fatigue, dec exercise tolerance
light headed/Hx syncope
tachycardia
LHF
- SOB, pulmonary oedema, displaced apex, heaves, murmurs, gallop rhythm, basal creps
RHF
- fatigeu, SOB, anorexia, inc JVP, hepatomeglay, pitting odema, ascites
what is Vicrchow’s triad
altered flow - turbulence, stasis, varicose veins
altered vessl - HTN
hypercoagulable - nephrotic syndreom, trauma or burns, cancer , pregenancy, inc age, race, smoking, obese > 30
what medications are used in DVT prophylaxis?
LMWH
UFH if renal/low platalet
graduated comprssion stockings (not if PVD, ischaemia)
management of DVT
- Refer for same day assessment. High wells/ +ve D-dimer should try 4hr.
- Anticoagulate: LMWH (enoxaparin 1.5mg/kg/24h SC) (unfractioned heparin in renal failure guided by APTT) or Fondaparinux.
IVC filter if not possible to have LMWH
Following.
• Stop heparin when INR 2-3 or 24 hrs after.
• Warfarin/DOAC 3 months (provoked), 6 months (unprovoked) review and aim INR 2-3.
if cancer 6 months
aetiology of acute ischaemic leg
embolism - from AF, mural thrombus after MI, prosthetic and abnor valves, aneurysm, maliganat tumour, trauma - fat embolism in long bone fracture
thrombosis
Raynaud’s
compartment syndrome
aortic dissection
diabetes
investigation of acute ischaemic leg
examine limb - last palpable pulse
Doppler US
BLoods - FBC, U&Es, LFT, ESR, glucose, lipids, thrombophilia screen (esp antiphospholipid syndrome)
source of emboli - ECG, ECHO, aortic/femoral/popliteal US
management of acute ischaemic leg
• Initial
o urgent admission + analgesia
o percutaneous catheter-directed thrombolytic therapy
o emergency embolectomy if life threatening
o endovascular revascularisation
o amputation
o fasciotomy (cut fascia – relive pressure) (compartment syndrome)
• long term management
o Heparinisation after thrombolysis and surgery
o Aspirin
o lifestyle diet, exercise, HTN management, hyperlipidaemia management, smoking cessation
management of acute ischaemic leg
• Initial
o urgent admission + analgesia
o percutaneous catheter-directed thrombolytic therapy
o emergency embolectomy if life threatening
o endovascular revascularisation
o amputation
o fasciotomy (cut fascia – relive pressure) (compartment syndrome)
• long term management
o Heparinisation after thrombolysis and surgery
o Aspirin
o lifestyle diet, exercise, HTN management, hyperlipidaemia management, smoking cessation
what is superficial thrombophlebitis
a superficial vein, usually the long saphenous vein of the leg or its tributaries becomes inflamed secondary to a blood clot inside it
which vein is most suspectible for superficial thrombophlebitis
long saphenous veins
aetiology of superficial thrombophlebitis
varicose vein - trauma to a varicose vein accounts for 65-80% of presentations
IV cannula
prev superfiical thombophlebitis or DVT or chronic venous insufficiency
> 60 yrs old obesity smoking IVDY hpercoagulability states
clinical features of superficial thrombophlebitis
hard and painful to palpation - the vein feels like a hard cord if it is not varicosed and like a hard knot if it is varicosed
inflammed, erythema, warmth and welling of the skin
associated bruising
maybe some features of cellulitis (acute onset of red, painful, hot, swollen and tender skin) or an abscess
investigation for superficial thrombophlebitis
clinical diagnosis
doppler to rule out DVT
differential for superficial thrombophlebitis
DVT - generalied pain
cellulitis - systemic features
lymphangitis - red streaks from infected area to groin/armpit
erythem nodusm
lipodermatosclerosis - chronic venous insufficiency leading to hardened, tight, red or brown skin typcially affecting htye inner part of the calf and cuasing champagne bottle appearance
treatment for superficial thrombophlebitis
Treat pain with a simple analgesic -paracetamol/NSAIDs
Manage swelling and discomfort with compression stockings.
If very big anticoagulation tinzaparin or enoxaparin
what are some complication for superficial thrombophlebitis
septic thrombophlebitis
DVT/PE
varicose veins
what is cannula-related phlebitis
Inflammation of a vein following the insertion of a cannula
aetiology of cannula-related phlebitis
- Mechanical damage to the vessel wall/ foreign body irritation from the insertion of a cannula OR chemical irritation from the medicine
- Increased length of stay of cannula in-situ
clinical features of cannula-related phlebitis
- Redness
- Swelling
- Warmth
- Visible streaking at the site of the cannula
- Tenderness
- Rope/cord like structure which can be felt through the skin.
investigations of cannula-related phlebitis
diagnosis of clinical features
Mx of cannula-related phlebitis
- remove cannula
- treat pain- analgesia
- warm and cold compresses can be applied to areas to increase flow of blood around the area and reduce the swelling.
what is complete heart block?
3rd-degree heart block between the SA and AV node
what are some causes of complete heart block
inferior MI, IHD
cardiomyopathy
idiopathic degen of conducting system (lenegre’s or Leves disease)
inflam cardiac disease - SLE, myocarditis, RA
AV node blockign agents - B-blocker, CCB, digoxin
hyperkalaemia
what are the different types of complete heart block
nodal block - (intermittent delay at the AV node, narrow QRS) - good progress
infra-nodal block - (in or below the bundle of His, wide QRS) - bad progress
what is the heart rate of complete heart block like?
atrial > 75
ventricular rate > 45
clinical feature of nodal complete heart block?
mild fatigue, dizziness, reduced exercise tolerance, palpaitation
clinical features of intranodal complete heart block?
haemodynamically compromised, syncope, confusion, dyspnoea, severe chest pain, sudden death
investigation of complete heart block
ECG - P waves occur regularly at 75 bpm + unconnected with the rhythm of QRS complex
bloods - FBC, glucose, trop, U&Es, Ca, mg
ECHO - for structural abnor
management of complete heart block?
should follow the resus bradycardia algorithm
A-E assessment
check if any adverse features present? (shock, syncope, myocardial ischaemia, heart failure)
if yes - atropine 500mcg IV
and check if satisfactory response obtain?
long term mx
- ifAv block irresversible -
what defines postural hypotension?
a drop in systolic BP upon standing of > 20 mmHg
aetiology of postural hypotension
Venous pooling of blood • Severe varicose veins • Prolonged standing Reduced muscle tone • Prolonged bed rest Impaired vasomotor tone • Diabetic autonomic neuropathy • Shy-Dager syndrome Hypovolemia • Dehydration • Exsanguination e.g. gastro-intestinal bleed. Drug • Hypotensive agents • Tranquilliser • Phenothiazines • Levodopa Addisonian Disease • Addison’s disease • Hypopituitarism • Abrupt cessation of steroid therapy.
clinical features of postural hypotension
dizziness or syncope upon standing up (too fast)
relieved by sitting back down or lying down
blurring of vision
falls
INvestigation for postural hypotension
- Lying and standing blood pressure
* HR
management of postual hypotension
conservative management
meds
1st line - fludrocortisone
2nd - midodrine
what is aortic dissection
• Disruption of medial layer of aortic wall provoked by intramural bleeding separation of aortic wall layers formation of true lumen and false lumen +/- communication.
aetiology of the aortic dissection
- Most common cause = essential hypertension
- Marfan syndrome and ehlers danlos syndrome
- Bicuspid aortic valve • trauma
- infection
- Aortic manipulation to associated with cardiac surgery iatrogenic causes
what are the types of aortic dissection?
Standford
- Type A - involves the aortic arch and ascending aorta
- Type B - involve the descending aort
Debakey
- type 1 - both aortic arch and descending aorta
- type 2 - jsut the aortic arch
- type 3 - just the descending aorta
clinical features of aortic dissection
chest pain - sudden onset, sever on the chest or back, ripping/tearing/sharp, moving downward
o Signs related to haemopericardium – pulsus paradoxus, faint/absent heart sounds, distended neck veins and shocked.
o Signs related to aortic root dilatation – wide pulse pressure, diastolic murmur over the aortic area.
o Hypertension. (may also be hypovolemic if there is a massive haemothorax.
what is abdominal aortic aneurysm
Defined as a 50% increase in dilation of the aorta.
what are some fo the causes of AAA
coactation of the aorta marfan syndrome, Ehlers Danlos previous aortic surgery pregnancy trauma tertiary syphilis atherosclerosis > 65
clinical features of AAA
unruptured - asymptomatic, can be an incidental finding or epigastric pain to loin, grain.back, pulsate +expanile mass. can obstruct duodenum causgin vomiting or IVC casuing oedeam, DVT
ruputre - sudden pain in lower back or central abdo , can radiate to loin, groin . collpase (if hypovolaemic shock). grey turners
what are the investigations for AAA
abdo exam
USS abdo = gold standard
CT angiography if stable and consider for surgery
bloods - FBC, U&Es, LFT, G+S, crossmatch, crp
management of AAA
NICE guideline
if <5.5cm - monitor, treat RF
- if > 5.5cm/rapid growth >1cm a year/ rupture , will need surgical repair
the repair can be done through open lapratomy or endovascular aneurysm repair (EVAR via femoral artery)
what are some risk factor for AF?
PIRATE
P- pulmonary causes - obstructive sleep apnoea, PE, COPD, pnemonia)
I - chaemia/infarction/CAD
Rheumatic fever and mitral regurgitation
alcohol/anaemia
thyrotoxicosis/toxins
electrolytes/endocarditis
Sepsis/sick sinus syndrome
what is atrial flutter?
atria beat regularly, but faster than usual and more often than the ventricles, so you may have 4 atrial to every 1 ventricular beat
what are the 2 types of atrial flutter
typical - rhythm has its origins in the right atrium at the level of the tricuspid valve - saw tooth on ECG
atypical - atypical - origin is elsewhere in the right atrium or the left atrium
aetiology of atrial flutter
- Age
- Structural abnormalities of the heart e.g. left atrial dilatation.
- Previous heart surgery
- Pericarditis
- Thyroid disease/COPD.
- Alcohol, obesity
- Atrial fibrillation – those who are on long term suppression
how common is atrial flutter?
1/10th less common than AF
2nd most common arrhythmia
clinical features of atrial flutter
- Asymptomatic and incidental finding on ECG
- Mild symptoms: palpitations, irregular heartbeat, fatigue, dyspnoea, chest pain, dizziness
- Syncope
- Heart failure
- Irregular or regular pulse BUT tachycardia.
investigation of atrial flutter
ECG - saw tooth best seen in the inferior lead II, III, aVF with atrial rte of 240-340, variable AV conduction (commonly present with 2:1, 3:1)
bloods - TFT< FBC, ESR, UE, LFT
ECHO - assess underlying cardiac function and assess for structural abnor
management of atrial flutter?
same for AF
rate control if > 48 hours
rhythm control if <48 hours, DC cardioversion if unstable and < 48 hours. if > 48 hours the nanticoagulant for 3 weeks prior to cardioversion
prevention of thromboembolism
- use CHADS2VASC/HASBLEED
- warfarin or NOAC
aetiology of 1st degree heart block
physiological - during sleep, in athletes
cardiac causes - AV block or sinus node disease
non-cardiac causes - vasovagal, hypothermia, hypothyroidism, hyperkalaemia, lyme
drugs - beta-blocker, diltiazem, digoxin, amiodarone
congential
what is the most common cause of 1st-degree heart block?
amiodarone overdose
clinical features of 1st-degree heart block
• Asymptomatic: incidental finding on ECG. • Bradyarrythmias < 60 • Syncope • Dyspnoea • Chest pain, palpitation, N+V HTN (or less commonly low)
ix for 1st degree heart block
- ECG
- Trop
- If metabolic cause suspected check UE’s.
what are the ecg finding of 1st degree heart block
PR interval of greater than 0.2 (> 5 small squares)
each atrial activation leads to a ventricular activation with a 1:1 correspondence - just prolonged
management of first-degree heart block
typically no management at all
if bradycardia - go with the resus bradycardia pathway
what are the 2 types of 2nd degree heart block
Mobitz type 1 - Wenckebach - stepping back
- There is progressive prolongation of the P-R interval following each atrial impulse, until an atrial impulse fails to be conducted to the ventricles
Mobitz type 2 - There is intermittent failure of conduction of atrial impulses to the ventricles without progressive lengthening of the P-R interval, thus the P-R interval of conducted beats is constant. Ratio (2:1)
aetiology of 2nd degree heart block
- Physiological - during sleep, in athletes
- Cardiac causes - AV block or sinus node disease.
- Non-cardiac causes - vasovagal, hypothermia, hypothyroidism, hyperkalemia, Lyme
- Drugs - beta-blocker, diltiazem, digoxin, amiodarone in therapeutic use or OD
- Congenital
clinical features of 2nd-degree heart block
- Bradyarrythmias < 60
- Mobitz Type 1: asymptomatic, may experience mild headedness or dizziness, fainting.
- Mobitz Type 2: mild light-headedness or dizziness, fainting, chest, SOB, feeling very dizzy suddenly when standing up from a lying or sitting position- this is caused by having low blood pressure.
investigation for 2nd-degree heart block
ecg
trop
u&Es
management of 2nd degree heart block?
treat through the resus bradycardia algorithym
type 1 - no management of treat through the asystole part
type 2 - treat through the aystole part
permanent pacemaker for type 2 onward for sure, type 1 can be considered
pathophysiology of AVRT
Accessory bypass tract (Wolff Parkinson White syndrome) -involves tracts of conducting tissue that partially or totally bypass normal AV connections (bypass tracts).
They run most commonly from the atria directly to the ventricles. Triggered by atrial or ventricular premature beats.
what are the 2 different types of re-entrant supra-ventricular tachycardia
AVNRT - re-entry caused by nodal pathwyas
AVRT - the type of SVT where you have an abnor loop of electricity/re-enrant circuit between 2 pathways
pathophysiology of AVNRT
AV node: a reentrant circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. this creates a re-entrant loop
what is the classic ECG appearance of Woof-Parkinson White Syndrome/AVRT
Delta wave - upward slope of P wave
shortend PR interval - < 0.12
prolonged QRS
HR > 100
what is the classical ECG appearance of AVNRT
like SVT
- shortned QRS
- rate > 100
clinical features of re-entrant SVT?
20-40s
sudden episodes of palpitations that begin and terminate abruptly
attacks may last from few seconds to several hours
SOB, chest pain, dizziness, neck pulsation
severe tachycardia
ix for re-enterant SVT?
ECG = diagnostic
blood test - U&Es, TFT, trop, calcium, magnesium
management of re-enterant SVT?
vagotonic maneuvers eg holding breath and straining, dunking face in ice water pr coughing
IV adenosine
electrical cardioversion if unstable
prevention
- beta-blocker
- ablation - fore frequent recurrence
what is ventricular tachycardia?
broad complex tachycardia
risk factor of VT?
caffeine
cocaine
TCA
acidosis
symptoms of ventricular tachycadia?
symptoms of IHD or haemodynamic compromise
- chest pan
- palpitations
- dyspnoea
- dizziness
- sncope
- tachy, palor, shock, low GCS
investigation of ventricular tachycadia
ECG - HR > 120, wide QRS complex (>120m), no obvious p wave
FBC, U&Es, ca, mg, po4, troponin, glucose
level of therapeutic drugs eg Digoxin
CXR
ECHO
drug screen for cocaine
treatment of ventricular tachycardia
A-E assessment
go through the resus council tachycardia algorithm -amiodarone 300mg IV over 20-60 mins then 900mg over 24 hours
if adverse features - synchronized DC shock
aetiology of ventricular fibrillation
MI
AF
digoxin toxicity, TCA
management of ventricular fibrillation
shockable - 1 shock, resume CPR for 2 mins - assess rhythm
IV adrenalien 1:1000 1mg
IV amiodarone
aetiology of mitral regurgitation
primary - valve causes ventricular damage
- rheumatic fever - following a throat infection, fever + joint swelling
- infective endocarditis
- mitral valve prolapse
secondary - ventricule casues valve damage
- cardiomyopathy
- CHD
- AF
what are some symptoms of mitral regurgitation
mild maybe asymptomatic
acute - pulmonary oedema, dizziness, fatigue, chest pain, palpitation
chronic - SOB, LHF (dyspnoea on exertion, orthopnoea, PND)
signs of mitral regurgitation
pan systolic murmur at apex radiating to the axilla
displaced apex beat
development of LHF as enlarged left atrium and ventricular can no longer cope with inc volume
Ix of mitral regurgitation
ECG - AF, left ventricular hypertrophy (tall QRS complexes)
CXR - left atrial and ventricular enlargement
ECHO - enlarged left atrium and left ventricle with abnormal mitral valve.
doppler - size/site of regurgitation
BNP - for heart failure
management of mitral regurgitation
acute - medical stabilisation with diuretics and vasodilator (reduce the afterload) and so less regurgitation volume
medical
- treat AF
- LFT - diuretics and ACEi + aldosterone agonist
- prophylaxis abx for infective endocarditis
surgical
- mitral valve replacement
what is the most common cause of mitral stenosis
rheumatic heart disease - most common 99% of cases
aetiology of mitral stenosis
rheumatic heart disease = most common 99% of cases
degenerative calcification
infective endocariditis
amyloid deposition
congenital mitral stenosis
SLE, RA
symptoms of mitral stenosis
asymptomatic for years progressive dyspnoea - main symptoms orthopnoea PND AF haemoptysis - rupture of a bronchial vein due to left atrial pressure systemic emboli - MI RVF - ascites
what are some signs of mitral stenosis
mid-diastolic murmur (low picthc) –> best heard with bell at apex with patient rolled to the left holding breathing after expiration
Malar flash
AF common
raised JVP
laterally displaced apex beat
raised pressure in left atrium transmitted to pulmonary vessles
right ventricular heave
RV failures - hepatosplenomegaly, ascites, due to LHSHF which put strain on RHS
investigation of mitral stenosis
ECG - AF, left atrail enlargement - tall QRS waves
CXR - left atrial enlargement, pulmonary oedema
ECHO - left atrial enlarement
treatment for mitral stenosis
medical therapy
- diuretics and vasodilators (nitrates) - lessen pulmonary venous pressure
- AF management - beta-blocker/calcium antagonist/digoxin, anticoagulant
- prophylactic abx for rheumatic fever
surgical
- percutaneous mitral commissurotomy PMC
- balloon valvuloplasty
- open mitral valve replacement
what is aortic stenosis
obstruction of blood flow across the aortic valve due to pathological narrowing
aetiology of aortic stenosis
snile calcific aortic stenosis - most common cause
bicupsid valve
childhood hx of rheumatic disease
what is the most commonly affect valvular disease
aortic stenosis
clinical features of aortic stenosis
usually on exertion
triad of symptoms - syncope, angina, dyspnoea
-palpitations
examination finding of aortic stenosis
ejection systolic murmur - S2 is often diminished
pulse - slow rising
BP - narrow pulse pressure, but normal
Left ventricular heave - hypertrophy as more force is needed
aortic thrill
best heard over the aortic valve area with radiation to the carotid and apex
what are the ecg finding of aortic stenosis
LVH, left anterior hemiblock (LAD)
LBBB - cardiomyopathy//LV strain
investigation for aortic stenosis
ECG
CXR - calcific aortic ring, cardiac enlargement, post stenotic dilatation of the aorta
ECHO - diagnostic –> thickened, calcified valve, LV hypertrophy
Doppler echo - site/severity of AS
BNP
management of aortic stenosis
if asymptomatic
• Monitor + advise against competitive sports.
• Lifestyle changes and symptoms control e.g. BP/HF.
if symptomatic
- aortic valve replacement
- TAVI (transcatheter aortic valve implantation) - less complication than AVR
- balloon valvuloplasty - risk of failure
- prophylactic abx against bacterial endocarditis
aetiology of aortic regurg
bicuspid aortic valve - most common congenital cause
rheumatic fever
infective endocarditis
Collagen vascular diseases - marfan’s ehlers danlos
degeneartive aortic valve disease
clinical features of aortic regurg
early stages - asymptomatic
end stage
- dyspnoea
- orhtopnoea
- angina
- syncope.dizzy
- palpitations
exam finding of aortic regurg
high pitched early diastolic murmur - best heard when patient lean forward on expiration
pulse - collapsing water hammer
BP - wide pulse pressure (high systolic and low diastolic)
displaced apex beat to the left
corrigan’s sign - carotid pulsation
de Musset - head bobbing
Quincke’s - nail bed bobing
Investigation for aortic regurg
ECG - LVH
CXR - LVH, dilated ascending aorta, pulmonary oedema and cardiomegaly
ECHO - dilated left aortic root, reverse flow from aorta, LVH
management of aortic regurg
acute
- diuretic and vasodilator
chronic
- monitoring
- or medical
- ACE reduced BP -when surgery contraindicated/LV dysfunction post-surgery
- B-bloack - marfan’s prevent aortic root dilatioan
- prophylactic ABx against infective endocarditis
surgical
- AVR
- aortic root surgery
what is infective endocarditis
infection of the endocardium of the heart
what is the most common causative agent in infective endocarditis
staphoccous infection
- S aureus via vascular line
Streptococcus = 2nd most common
- S viridian via oropharynx
Enterococci - following instrumentation of bowel or bladder
what is the clinical feature of acute endocarditis
Acute - Staph A
- rapid onset
- infective organism damages normal valve
- clumps of bacteria form - septic emboli in circulation
- toxic presentation with metastatic infection
what is the clinical feature of subacute endocarditis
- Gradual onset
- Weakly infective organism damages defected valve.
- No septic emboli
- Mild toxic infection with not metastatic infection
RF for infective endocarditis
valvular heart disease - with stenosis or regurgitation
valvular replacement
structural congenital heart disease- septical defect or repaired defect
previous IE
hypertrophic cardiomyopathy
IVDU
invasive vascular procedure
clinical feature of infective endocaritis
fever + chills, reduced appetitse, weight loss
new-onset murmur
LHS - major systolic emboli anywhere in the body
RHS - prominent pulmonary symptoms and numerous septic embolic in lungs
Roth spot - red spot on retina with characterisitic white spot centre
Osler’s node - painful on tips of hands and toes
Jane way lesions - non-painful on palms and soles of feet
splinter haemorrhages
ROJS
- Petechiae (conjunctiva, hands, feet, chest, abdomen)
- Splenomegaly – long standing
- Haematuria- long standing and glomerulonephritis.
- Clubbing-longstanding.
- Arthritis- longstanding
- Arterial emboli
- Septic infarcts
investigation for infective endocarditis
bloods - FBC, U&Es, LFT, CRP/ESR
ECG/CXR
blood culture - 2 sets of bloods within 1 hour
transthoracic echo - repeat in 7 days
what is the diagnostic criteria of infective endocarditis
duke criterai
- requires 2 major criteria or 1 major and 3 minor to diagnose
major
1) +ve blood culture of IE
2) evidence of endocardial involvment –> ECHO evidence (intra-cardiac mass on valve or supporting structure, abscess, new partial dehiscence of prosthetic valve or new valvular regurgitation)
minor
1) predisposing heart condition or IVDU
2) fever > 38
3) vascular pheonoma - major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhage and Janeway’s lesion
4) immunological phenomena - glomerulonephritis, Osler’s node, Roth’s spot and rheumatoid factor
5) PCR - +ve broad-range PCR 16
6) echo findings consistent wit hIE but do not meet a majror criteria
management of infective endocarditis
IV Abx 4-6 weeks
native valve - empiriacal abx (amoxicillin and gentamicin)
prosthetic valve - empirical (vancomycin + gentamycin + rimgamicin)
surgical dariange of abscess if abx ineffective or valvular damage
pathophysiology of varicose vein
- Veins contain valves that only allow blood to flow one direction – towards the heart
- In the legs this means that as the leg muscles contract, they squeeze blood upwards against gravity
- When these valves become incompetent, the blood pools (drawn by gravity) in the veins and is not effectively pumped back to the heart
- The deep vs superficial veins have a connection called the “perforators” that allow blood to flow from the superficial veins to the deep veins
- When the valves are incompetent in these perforators, blood flows from the deep veins back into the superficial veins and overloads them
- This leads to dilatation and engorgement of the superficial veins
aetiology of varicose vein
primary - unknow, congenital valve absence
secondary
- obstruction (DVT, foetus, ovarian tumour, obesity)
- valve destruction - DVT, AV malformation, constipation, overactive muscle pumps (cyclist)
RF - prolong standing, FHx, OCP
symptoms of varicose vein
- “Legs are ugly”
- Pain
- Cramps
- Tingling
- Heaviness/ dragging sensation in legs
signs of varicose vein
oedema
ulcers
haemodersrin deposit - veins become leaky and blood starts to pool and being broken down (Haemodersrin - area of blackness)
thrombophlebitis and DVT
atrophie blanche - white scarring with red dot (capillaries)
varicose eczema - skin becomes dry and inflamed
lipodermatosclerosis - champagne bottle legs - skin and soft tissue become fibrotic causing tight narrowed lower legs
saphenex varix - dilation of saphenous vein at its confluence with the femoral vein
investigation of varicose vein
exam –> assess with pt standing up - palpaitae for tenderness or hardness
- feel for cough impulse at saphenofemoral junction - 4cm lateral and inferior to pubic tubercle to exclude
percussion test - tap SFJ and palpate for transmitted impulse at the varicose vein identified
auscultate for bruits
Trendelenburg test - • Ask the patient to lie down. Elevate the leg, and empty the veins by massaging distal to proximal.
• Using a tourniquet, occlude the superficial veins in the upper thigh. Ask the patient to stand.
• If the tourniquet prevents the veins from re-filling rapidly, the site of the incompetent valve must be above this level i.e. at the sapheno-femoral junction.
• If the veins re-fill, the communication must be lower down. Repeat at lower levels in the legs (knee and ankle)
dopper = diagnostic
management of varicose vein
treat underlying causes
educate - avoid longstanding, elevate legs, lose weight
stockings
endovenous ablation
• Radiofrequency (catheter inserted into vein and probe generated and then closed)
• Laser ablation (catheter inserted into vein and heated and then closed.
• Injection sclerotherapy –liquid foam (below the knee), obliterates the lumen and damages the endothelium
• Stripping- veins pulled out of leg
symptoms of chronic limb ischaemia
cramping pain in the calf (popliteak) or thigh (femoral) or buttock (iliac)
worse when walking on flat/hill
relieved by rest - intermitten caludication
change in leg - think, coolor, paler, ulceration, eczemam haemosiderin deposition gangree
ischaemic rest pain - nocturnal burning foot pain relieved by handing legs over the side of the bed
signs of chronic limb ischemia
- Absent femoral, popliteal, foot pulses.
- Punched out skin ulcers.
- Irregular borders
- Capillary refill > 15 secs
- Buerger’s test: raise leg to 45 degrees and look for pallor (+ve). Look for reperfusion by allowing the patient to sit with their legs over the edge
- Postural dependent colour change :pallor on leg elevation
- Calf wasting.
investigation for chronic limb ischemia
bloods - FBC, ESR, throbophilia screen, fasting glucose, lipid level
BP
ECG - CHD
patient <50 - homocysteine taken
doppler - gold standard - ABPI, normal =1, claudication 0.6-0.9, rest pain 0.3-0.6, impending gangrene < 0.3
DM = >1
duplex USS - site and degree of stenosis
what is fontaine classfication
I - ABPI > 0.9
II - ABPI 0.6-0.9
III - ABPI 0.3-0.5
IV < 0.3
management of chronic limb ischemia
ABCDES Atorvastatin 80mg • Blood pressure control • Clopidogrel 75mg • Diabetes control • Exercise training – first line intervention for claudication • Smoking cessation
surgical
- endovascular revascularistaion (stent)
- surgical reconstruction - bypass for dffuse disease
- amputation - last resort
peripheral vasodilator - naftidrofuryl oxalate - for those who can not have revascularisation and exercise fails to improve
