Cardio Flashcards
1
Q
risk factors aortic dissection
A
FAT CASH
- family hx
- atherosclerosis
- takayasu
- connective tissue disease
- smoking
- HTN
2
Q
aortic dissection pathophys, path and classification
A
pathophys
- risk factors weaken vessel wall
- cystic medial degeneration
- > loss of elastic fibres
- > loss of extracellular matrix
- > increase in GAGs
- laplaces law
- > wall tension proportionate to radius and pressure
- > inversely proportional to wall thickness
- > cycle of wall degeneration and increasing stress
- intimal tear
- > creation of false lumen within laminar plane of media
- extension
- > retrograde or anterograde
- occlusion
- > static with obliteration of branching vessel by haematoma on same side
- > dynamic during diastole when true lumen collapses and intimal flap closes over ostium on opposite side
path
- stanford classification
- > A = involves ascending +/- descending and thoracic
- > B = does not involve ascending (usually distal to left subclavian)
- microscopic
- > cystic medial degeneration
- > haematoma within laminar planes of media
3
Q
aortic dissection investigations
A
ECG
FBC -anaemia with haemorrhage EUCs -ischaemia = elevated BUN LFTs -ischaemia = transaminitis lactate -ischaemia blood type and cross match trops d-dimer -sensitive but non specific
CXR
-widened medistinum
CTA
-intimal flap
TOE
-if CTA unavailable or in ED
4
Q
hx and exam AAA
A
hx:
- ruptured triad
- > back/abdo pain
- > pulsatile mass
- > hypotension
- focused on assessing risk factors
- development
- > hyperlipidaemia
- > connective tissue disease
- > COPD
- > hypertension
- expansion
- > cardiac or renal transplant
- > severe cardiac disease
- > stroke
- > older age
- rupture
- > female sex
- > previous cardiac or renal transplant
- > hypertension
- smoking
- > risk factor for development/expansion/rupture
- family hx
exam
- pulsatile and expansile mass
- peripheral pulses
- > evidence of ischaemia or emboli?
- additional aneurysms
- eccymoses
- > cullens
- > grey turners
- > fox’s (thigh)
- > bryants (scrotum)
- fevers
- > suspicion for infective AAA
5
Q
investigations AAA
A
ABG
-acidosis
FBC -anaemia ->haemorrhage -leukocytosis ->infective/inflammatory AAA EUCs -acidosis -AKI LFTS -shock and end organ damage Coags Trops D-dimer -associated with aneursym diameter ESR -infective/inflammatory AAA
Ultrasound
- high sensitivity and specificity
- thresholds
- > diameter 1.5x normal
- > 3cm
Consider
- MRA/CTA
- > surgical planning
6
Q
AAA/dissection ddx
A
Pain (RAPID MEDS)
- ruptured viscus
- AAA
- pancreatitis
- infarct (MI)
- dissection
- mesenteric ischaemia
- embolism
- diverticulitis
- stones
Mass for AAA
- lymphoma
- lymph nodes
- > lymphadenopathy
- > mets
- abscess
- hernia
7
Q
AAA treatment
A
ruptured
- surgical repair
- > endovascular (lower mortality than open)
- > open
- medical support
- > ABCD
- > blood products
- > ICU
symptomatic
-requires surgery regardless of size
small asymptomatic
- no improvement in mortality with immediate surgery
- surveillance
- > every 6-12 months
- medical management
- > cease smoking
- > cardiovascular risk factor control
large asymptomatic
- surgery indicated
- > greater than 5.5cm in men
- > greater than 5cm in women
8
Q
lipid targets
A
*every reduction reduces events
LDL
- primary prevention = 2mmol/L
- secondary = 1.8 mmol/L
HDL
-1mmol/L
non-HDL
-2.5mmol/L
Total cholesterol
-4mmol/L
Triglycerides
-2mmol/L
9
Q
investigations APO
A
ECG -arrhythmias ABG -hypoxia -acid/base -electrolytes PEFR -ddx cardiac vs pulmonary Ultrasound -B lines
FBC -anaemia -leukocytosis EUC -eGFR -electrolytes CMP -arrhythmia BNP/NT-BNP -elevated in exacerbation CCF -specific and sensitive Troponins -subendocardial ischaemia with LV pressure TSH D-dimer -strong negative predictive value
CXR
- cardiomegaly
- butterfly
- air bronchogram
- effusion
- ddx’s
Echo
- LV size and wall thickness
- LV function
- estimate EF and pulmonary wedge pressure
10
Q
ddx APO
A
Exacerbation of CCF (A Reduction In Cardiac Output) arrhythmias -AF regurgitation -mitral (endocarditis, myxoma, papillary rupture) -aortic (endocarditis, dissection) infarct/ischaemia crisis (hypertensive crisis) overload (renal, drugs, fluids)
Dyspnoea (DICTAATE)
- reconditioning
- infection/inflammatory (pneumonia, bronchiectasis, bronchitis, ILD)
- COPD/asthma
- tumour (effusion)
- anaemia
- ascities
- thyroid dysfunction
- embolism (pulmonary)
11
Q
dukes modified criteria
A
Pathologic:
- pathologic lesions (on histology)
- > vegetation
- > intracardiac abscess
Clinical:
- Definite
- > two major
- > one major + three minor
- > five minor
- Rejected
- > symptoms resolve <4 with antibiotics
- > no histo in surgery or autopsy <4 of antibiotics
12
Q
major clinical dukes criteria
A
- Positive culture
- > typical organisms from 2 seperate blood cultures
- > persistently positive blood culture
1) 2 cultures taken >12 hrs apart for typical or
2) 3/3 or 2-3/4 cultures for skin flora
3) single positive culture for Coxiella or
4) positive Q fever IgG antibody titre - Evidence of endocardial involvement
- > positive echo
1) oscillating intracardiac mass
2) abscess
3) new partial dehiscence of prosthetic valve - > new valvular regurg
13
Q
minor criteria dukes
A
1) predisposition
- typical heart condition
- IVD
2) fever
3) vascular phenomena
- major emboli
- septic pulmonary infarcts
- mycotic aneurysm
- intracranial haemorrhage
- conjunctival petechiae
- Janeway lesions
4) immunologic phenomena
- GNP
- oslers nodes
- roths spots
- rheumatoid factor
5) microbio evidence
- positive culture not meeting major criteria
- serologic evidence of typical organism infection
14
Q
IE ddx
A
PAALMER
- PE (ddx’s: EMPPATHIC)
- Atrial myxoma
- Autoimmune/vasculitis (eg. rheumatoid or scleroderma)
- Libmann saccs
- > malignancy (lung, colon, pancreatic)
- > SLE
- > antiphospholipid
- MI with mural thrombus
- Emboli (cholesterol)
- Rheumatic heart disease
15
Q
CXR findings IE
A
PE signs -hamptoms hump -westermark sign Septic emboli -cavitating nodules CCF -cardiomegaly -batwing/butterfly -airbronchogram -effusion DDx's
16
Q
investigations IE
A
ECG
-heart block
Urinalysis
-GNP
Blood cultures -before antibiotics -3 sets -3 sites -first and last >1hr apart FBC EUC RF Complement ESR
Echo (TTE/TOE) -oscillating mass -abscess -partial dehiscence of prosthetic valve -new regurg CXR -septic emboli -caviating infiltrate -cardiomegaly CT chest/abdo/pelvis -systemic emboli ->infarct ->abscess
Consider
-MRI brain
17
Q
pathophys MI
A
Ischaemia effects (atherosclerosis)
- metabolism of fatty acids reduced, anaerobic glycolysis increased
- decreased production ATP
- decreased pH with lactate formation
- impaired K/Na pump and membrane integrity leads to increase in K efflux and Na/Ca influx
- regional failure of normal relaxation (decreases blood flow further), failed contraction (decreased supply)
- relatively poorer perfusion to subendocardium compared to subepicardium
- <20 mins = reversible
- > 20 mins = permanent necrosis
18
Q
distribution of STEMI
A
- LAD = approx 40%
- RCA = approx 1/3
- circumflex = approx 1/4
19
Q
Heart rupture in MI
A
Left ventricular free wall
- 1% of MI
- most common anterior left ventricle
- early (<72 hrs) and late (<2 weeks) presentation
- fibrinolytic therapy can accelerate rupture
- presents with haemopericardium and tamponade (Beck’s triad: hypotension, muffled heart sounds, elevated neck veins + electrical alternans) –> PEA
- mortality rate = 25%
Interventricular septum
- less common than free wall
- major risk factor is wrap around LAD
- hypotension, biventricular heart failure and harsh pan systolic murmur +/- thrill
- 50%
Papillary rupture
- LV
- hypotension, pulmonary oedema, LV heave and pan systolic murmur
20
Q
short and long term complications MI
A
Short (BIRD)
- bradycardia/block (1st and 2nd) in RCA and complete in LAD
- infarct/ischaemia (recurrent)
- rupture (free wall, ventricular septum, papillary muscle)
- dresslers syndrome (pericarditis)
Long (PACT)
- psychological (depression)
- arrhythmias (VT, VF)
- CCF
- thrombosis (mural –> systemic embolism)
21
Q
management CCF and APO
A
CCF:
Non Pharm: education -condition -drugs daily weights fluid restriction (1.5L) salt restriction exercise heart failure program -heart failure nurse dietician -anorexia
Pharm:
- ACEI and beta blockers
- swap with ARBs or aldosterone antagonists
- supplement with loops
- monitor and maintain iron
APO:
- furosemide IV
- high flow oxygen or CPAP
- add nitroglycerol
- dobutamine
- morphine
22
Q
Blood pressure ranges and targets
A
Range
- normal = <120 SBP, <80DBP
- prehypertension = 130-40 SBP, 80-90 DBP
- HTN = >140 SBP, >90 DBP
Effects
- linear increase in cardiovascular events
- linear increase in mortality above SBP 115
Targets
- general = <140/90
- high CVD absolute risk + SBP > 130 = SBP <120
23
Q
non pharm treatment of HTN
A
Complement pharm, not replace
- Exercise (aerobic)
- weight loss
- alcohol restriction
- salt restriction
- healthy diet
24
Q
pathology in HTN
A
Vessels
- arterial stiffness is a cause and consequence of HTN
- > ion transporter dysfunction (increased Na/H exchange)
- > increased Na entry
- > increased Na/Ca exchange ->increased contractility
- > increased pH -> increased contractility for Ca concen
- endothelial vasoactive dynsfuntion
- > NO (dilate)
- > endothelin (constrict)
- enhanced atherosclerosis
Heart
- most common cause of death in HTN
- LV hypertrophy –> CCF (HFrEF/HFpEF) + arrhythmias + MI
- CAD + microvascular disease -> MI
Brain
- stroke
- > HTN greatest risk factor (direct relation over age 65)
- > vascular dementia
- beta amyloid deposition
- > cognitive impairment
- > alzheimers
- autoregulation = 50-150mmHg
- > hypertensive encecphalopathy
Kidney
- atherosclerosis of afferent arteriole
- > ischaemia in glomerulus
- > loss of autoregulation -> transmission of high pressure to glomerulus -> hyperfiltration and hypertrophy -> glomerulosclerosis
- progresses to ischaemia of tubules and atrophy + focal necrosis of glomerular tuft
- > proteinuria
25
Q
acute management STEMI
A
Determine pathway
- confirm diagnosis (STEMI/NSTEMI)
- risk stratify
General management
- ACCU
- 2x IV canula
- O2
- Cardiac monitoring + ECG
- Routine bloods
- CXR
- nitroglycerine
- beta blocker (atenolol/metoprolol)
- morphine
STEMI -dual antiplatelet (aspirin + P2Y12 inhibitor) -LMWH or UFH re-perfuse -within 12 hours -PCI reduces mortality/recurrence and stroke compared to fibrinolytic PCI (balloon angioplasty/stenting) -within 90 minutes Fibrinolytic -alteplase or tenecteplase -within 30 mins consider contraindications
NSTEMI
- aspirin (without P2Y12 until after surgery)
- LMWH or UFH
- consider GpIIaIIIb inhibitor
- high risk -> coronary angiography and revascularisation (stenting/bypass)
- evidence supporting early intervention (eg. within 2 hours very high risk)
26
Q
Complications IE
A
CAMPER
Cardiac
- CCF
- perivalvular abscess
- > heart block
- intracardiac fistulae
- pericarditis
Aneurysm
-mycotic aneurysms
MSK
- septic arthritis
- vertebral osteomyelitis
Pulmonary
- infarct
- abscess
- effusion
- pneumonia
- pneumothorax
Embolic
- brain
- > haemorrhage/ischaemic stroke
- > abscess
- > meningitis
- spleen
- > infarct
- > abscess
- peripheries
- > paralysis
Renal
- infarct
- abscess
- glomerulonephritis
- nephrotoxic drugs
- AKI
27
Q
risk factors IE
A
CARDITIS
- congenital heart disease (eg. bicuspid aortic valve)
- age >60
- recurrence
- degenerative heart disease (rheumatic heart disease, prosthetic valve, mitral valve prolapse)
- IV drug use
- teeth (dental procedure, poor dentition)
- IVC/implantable cardiac device
- sex (male)
28
Q
IE pathophys
A
Undamaged endothelium is resistant to infection and thrombus formation
1) Direct infection by highly virulent organisms
- staph aureus
- fibronectin binding protein
- >adhesin: binding to fibronectin and fibrinogen
- >invasin: facilitates entry into endothelial cells
2) Endothelial injury due to high velocity blood jets or on the low pressure side of valve defect
- formation of platelet fibrin thrombus
- >acts as nidus
- >becomes colonised during transient bacteraemia
Growth of vegetation
- proliferation of bacterium
- > within cells
- > within fibronectin matrix
- release of tissue factor from endothelium and macrophages
- > platelet deposition
- > activation of extrinsic pathway
Layers of growth
- organisms deep in vegetations are metabolically inactive
- > resistance to antimicrobials
- outer layer is proliferating and shed continuously
- > emboli of vegetation fragments (local immune response)
- > deposition of immune complexes
29
Q
hx and exam IE
A
Hx: risk factors fever/chills/malaise/night sweats anorexia/weight loss arthralgia/myalgia/back pain abdo pain chest pain/palpitations dyspnoea/orthopnoea/PND meningism/stroke/headache haematuria/oliguria
Exam petechiae (cutaneous/mucosal) splinter haemorrhage janeway polyarthritis osler roth spots dentition focal neuro signs murmur effusion/diminished breath sounds splenomegaly vertebral pain
30
Q
Arrhythmia treatment
A
Regular and Narrow Tachy
- ddx
- > sinus tachy/SVT/atrial tachycardia/atrial flutter
- sinus tachy
- > treat underlying cause
- SVT
- > DC cardioversion if unstable
- > consider vagal maneuvers then adenosine if stable
- atrial tachycardia
- > DC cardioversion if unstable
- > if stable, beta blockers/non dihyrdropyridine CCB
- atrial flutter
- > treated liked AF
Irregular and Narrow Tachy
- ddx
- > AF/multifocal atrial tachy/atrial flutter variable conduction
- AF
- > unstable = DC cardioversion
- > stable = beta blockers/non dihydropyridine CCB
- > consider need for anticoagulation
- multifocal atrial tachy/atrial flutter variable conduction
- > usually underlying cardiac/pulmonary path
- > usually stable
- > treatment focused at addressing cause
Regular and Wide Tachy
- ddx
- > VT (until proven otherwise)
- VT
- > unstable = DC cardioversion
- > stable = amiodarone or lidocaine
Irregular and Wide Tachy
- ddx
- > polymorphic VT/VF
- polymorphic VT
- > unconscious = DC cardioversion
- > conscious with baseline long QT (torsades) = magnesium sulfate
- > conscious with normal baseline QT (post MI) = cardioversion if unstable, beta blockers if stable
- VF
- > ALS
Bradycardia
- only treat if shocked
- atropine while preparing for temporary pacing
- > atropine = 0.5mg
- > pacing = transvenous or transcutaneous
- consider dopamine or adrenaline if unsuccessful
