Cardio Week 4 Flashcards
where does right and left coronary arteries arise from
base of aorta
where does most coronary venous blood drain
via coronary sinus into right atrium
what is the intrinsic ways in which O2 is supplied to coronary arteries
decreased PO2 causes vasodilation, metabolic hyperaemia matches flow to demandAdenosine (ATP) also potent vasodilator in attempt to increase blood/O2 supply
what is the extrinsic ways in which O2 is supplied to coronary arteries
sympathetic stimulation of heart results in dilation despite constrictor effect (over ridden by metabolic hyperaemia as result of HR and SV) and circulating adrenaline causes vasodilation
when does peak coronary blood flow occur
diastole (due to high pressures in left ventricles and subendocardial vessels not compressed)thus shortening diastole - decreased coronary flow
the grey matter consists of most of brains neurone cell bodies. What happens during hypoxia
loss of consciousness after few seconds of ischaemia and irreversible damage in 3 minutes
which two structures anastomose to form circle of willis (major cerebral arteries arise from here)
basilar (formed by two vertebral arteries) and carotid arteries
what is the adaptation to cerebral circulation if MABP rises/falls
rises - vessels constrict to limit blood flow
when does autoregulation of cerebral circulation fail
if MABP falls below 60mmHg or rises above 160mmHg (below 50 - confusion, fainting, brain damage)
what is the value for normal intracranial pressure (ICP)
8-13mmHg
how to calculate cerebral perfusion pressure (CPP)
MAP - ICP increased ICP (injury or tumour) decreases CPP and cerebral blood flow
what is the blood brain barrier permeable to
O2 and CO2
how does glucose cross BBB
facilitated diffusion using specific carrier molecules since brain has obligatory requirement for glucose
what is BBB exceptionally impermeable to and what does this help protect brain from
hydrophillic substances such as ions, catecholamines, proteins etc - protect from fluctuating levels of ions etc in blood
how is the pulmonary circulation protected from pulmonary oedema
absorptive forces exceed filtration forces
what is the result of hypoxia on the pulmonary circulation
causes vasoconstriction (opposite to systemic) in order to divert blood from poorly ventilated areas of lung
what happens to skeletal muscle circulation during exercise
local metabolic hyperaemia overcomes sympathetic vasoconstrictor activity and adrenaline causes vasodilation
what is the advantage of large veins in limbs lying between skeletal muscle
contraction of muscle aids venous return
what is the cause of varicose veins
blood pools in lower limb veins if venous valves become incompetent - doesnt lead to reduced CO due to chronic compensatory increase in blood volume
what is cardiomyopathy
any disease of cardiac muscle that often results in changes of chambers or thickness
what is dilated cardiomyopathy
big heart (2-3x normal), heart is flappy and floppy
what is causes of dilated cardiomyopathy
genetics, toxins, booze, nutritional deficiency, doxorubicin (chemotherapy), cardiac infection or pregnancy
what is the clinical features of dilated cardiomyopathy
general picture of HF, lowered exercie tolerance, SOB and chest pain
what is hypertrophic cardiomyopathy
big solid heart, diastolic dysfunction since heart cannot relax so eventual outflow obstruction
what is causes of hypertrophic cardiomyopathy
genetic (beta myosin heavy chain, myosin binding protein C and alpha tropomysin)
what are the signs of hypertrophic cardiomyopathy
bulding IV septum, outflow tract obstruction, LV luminal reduction, disorganised myofibrils (swirls) - can cause sudden death in athletes
what is restricted cardiomyopathy
causes lack of compliance - stiff heart, doesn’t fill well so diastolic dysfunction but can look normal and there is biatrial dilation as result of back pressure
what is the causes of restricted cardiomyopathy
deposition of something in myocardium (iron, amyloid, sarcoid, tumours and fibrosis)
what is amyloidosis
abnormal deposition of an abnormal protein, have tendency to form beta pleated sheets and body cant get rid of it
what does amyloidosis look like in heart
paleness and expansion but it is also pan systemic (effects different systems eg renal)
what is amyloid
a pink waxy material, stains positively for congo red, exhibits apple green birefringence
what is arrhythmogenic right ventricular dysplasia (type of cardiomyopathy)
genetic disease, right ventricle becomes replaced by fat, not contractile to prone to arrhythmias and therefore sudden death
what is myocarditis
inflammation of heart - thickened beefy myocardiun
what are the main viral causes of myocarditis
coxsackie A and B
what are non infectious causes of myocarditis
after infection eg rheumatic fever, after strep throat, after drug or systemic lupus erythermatosus (SLE)
what is rheumatic fever
classic mitral stenosis with thickening and fusion of valve leaflets, short and thick chord tendinae
what is pericarditis
inflammation of pericardial layers
what are infectious causes of pericarditis
ECHO virus, bacteria (extension from elsewhere - pneumonia), fungi (post transplant) and TB (caseous material in sac)
what is non infectious causes of pericarditis
immune mediates (rheumatic fever), idiopathic, uraemic (renal failure) post MI (dresslers syndrome) and SLE
what are complications of pericarditis
pericardial effusion, tamponade, constrictive pericarditis, cardiac failure, death
what is endocarditis
affects heart lining but generally refers to inflammation of valves
what are causes of infectious endocarditis
can occur normally in valves, virulent organisms, bacterial or fungal, IV drug abuse and septicaemia
what are causes of non infectious endocarditis
rheumatic fever, SLE, non bacterial thrombotic endocarditis, carcinoid heart disease
who does endocarditis usually effect
people with abnormal valves eg previous rheumatic heart disease or prosthetic valves, congenial defects, MV prolapse or calcific disease
what is the pathology of endocarditis
aggregates of organisms on heart valves called vegetations, bacteria excite acute inflammation and bacterial and inflammatory cells produce digest valve leaflets
what is the microbiology of endocarditis
HACEK (haemophilus, actinobacillus, cardiobacteria, eikenella, kingella) IV drug users (candida, staph aurerus) and prosthetic valves (epidermidis)
what is the complications of endocarditis
arrhythmia, acute vascular incompetence, high output cardiac failure, abscess, fistula
what is the systemic manifestations
olsers nodes, laneway lesions, roth spots, splinter haemorrhages, septicaemia, systemic septic emboli (brain, kidney, spleen), mycotic aneurysms
what are carcinoid tumours
neoplasms of neuroendocrine cells (see them in any mucosa) and release hormones
what markers do carcinoid tumours produce
excess 5HIAA, serotonin, histamine, bradykinin
what is the consequence of carcinoid tumours
flushing of skin, nausea, vomiting, diarrhoea, ride sided cardiac valve disease
what is the most common tumour of the heart
atrial myxoma, can cause ball/valve obstruction, may cause tumour emboli, may develop endocarditis and is associated with systemic fever and malaise - IL6
what is the clinical signs of angina
pressing, squeezing, heavy pain, radiation to arms and jaw, exertion, stress, cold wind, after meals, relieved by rest or GTN
what is differential diagnosis of chest pain which can be associated with GI tract
reflux - burning, provoked by foodpeptic ulcer pain - epigastic, point of finger gestures relieved by antacids oesophageal spasm biliary colic
what is differential diagnosis of chest pain which can be associated with MSK
injury - tender, prolonged, exacerbated by moving nerve root pain
what is other differential diagnosis of chest pain
pericarditis (central, posture related) or pleuritic pain (focal, exacerbated by breathing, sharp, catching)
what chest pain can be counted as emergency
MI (ongoing), pulmonary embolus (breathless, dull - may also be pleuritic) and dissection of aorta (tearing, excruciating, severe then eases)
what is perfusion imaging
non invasive test that shows how well blood flows through heart muscle - show areas of less blood flow cons - radiation, false readings
what is CT angiography
non invasive, uses x-ray to visualise arterial and venous vessels though body
what is an angiography
invasive, sheath inserted into artery, catheter advanced from wrist/groin to coronary ostium, X ray contrast injected to outline coronaries
give a quick summary of drugs used in CHD
aspirin - anti platelet B blocker - slow HR, reduced O2 demand statin - reduce cholesterol ace inhibitor - reduces BP
what vessels are used in coronary artery bypass (medial sternotomy)
long saphenous vein, internal mammary artery
what are potential complications of coronary artery bypass
death, stroke, MI, AF, infection, cognitive impairment, sternal malunion, renal failure, failure to recover
which patients are suitable for both CAB and PCI
multi vessel disease, diabetes, left main disease, co-morbidities
what is percutaneous coronary intervention (PCI)
cardiac catheterisation which is insertion of catheter and injection of contrast dye into coronary arteries - used to open narrowing arteries or those blocked by plaque
how does PCI work
guidewire down vessel, balloons threaded over wire,, stents implanted
how is STEMI treated with revascularisation
primary PCI
how is acute coronary syndrome treated with revascularisation
angiography with a view to revascularisation
how is chronic stable angina treated with revascularisation
revascularisaion for severe symptoms or high risk (CABG vs PCI should be determined by discussion)
what is the definition of a aneurysm
dilation of a vessel by more than 50% of its normal diameter (1.2-2.0cm normal aortic)
what is true aneurysm
vessel wall is intact (all 3 layers)
what is false aneurysm
there is breach in vessel wall (surrounding structures act as vessel wall)
what are the different shapes of aneurysms
saccular (bubble on top), fusiform (within vessel) and mycotic (arises secondary to infectious process involving all 3 layers - common in IV drug users)
what causes the medial degenerations which result in aortic abdominal aneurysm
regulation of elastin/collagen in aortic wall, aneurysm dilation, increase in aortic wall and progressive dilation
what is the risk factor for AAA
age, gender (6:1 men to women) smoking, hypertension
what is signs of symptomatic (25% of AAA) AAA
pain (mimic renal colic), trashing, rupture
what occurs during AAA rupture
sudden onset of epigastic/central pain, may radiate through to back, collapse, 75% not make it to hospital
what may AAA look like upon examination
may look well, hypo/hypertensive, pulsatile, expansile mass which may be tender, transmitted pulse
when would you intervene in asymptomatic AAA
> 5.5cm AP diameter as this is when risk of rupture rapidly increases
what does a duplex ultrasound do in AAA
used in asymptomatic for surveillance of diameter and involvement of iliac arteries - only tells us there is AAA not its exact diameter
how is CT scan used in AAA
IV contrast in arterial system - lets see aneurysm morphology - shape, size, iliac involvement (only imaging to identify ruptured AAA)
how is an open repair of an AAA undertook
laparotomy, clamp aorta and iliacs, use dacron graft (polyester)
how is an endovascular aneurysm repair (EVAR) undertook
exclude AAA from inside vessel, inserted via peripheral artery, X ray guided, modular component - needs life long follow up
what is acute limb ischaemia
sudden loss of blood supply to limb due to occlusion of native artery or of bypass gradt
what is the clinical features of ischaemia
pain, pallor (pale then mottled), paraesthesia, paralysis, pulseless, perishingly cold
what happens after 0-4 hours of ischaemia
white foot, painful, sensory motor deficit - salvageable
what happens after 4-12 hours of ischaemia
mottled, blanches on pressure - partially reversible
what happens after >12 hours of ischaemia
fixed mottling, non blanching, compartments tender/red, paralysis - non salvageable
what is the management of acute limb ischaemia
ABC, FBC (U/Es, coag +/- troponin), ECG, CXR, anticoagulation
what triad leads to tissue ulceration, necrosis and gangrene in diabetes
diabetic neuropathy, peipheral vascular disease and infection
what may diabetic foot sepsis be a result of
simple puncture wound, infection from nail plate or from neuro-ischaemic ulcer
NOTE
learn compartments of foot
what are the clinical findings of diabetic foot sepsis
pyrexia, tachycardia, tachypnoeia, confused, kussmaul breathing
what are the local signs of diabetic foot sepsis
swollen, tenderness, ulcer with puss extruding, erythema (redness), patches of necrosis, crepitus in soft tissue of foot
how is diabetic foot sepsis managed
treated as vascular surgery emergency also antibiotics taking into account polycrobial nature of diabetic foot infection
what is the aftercare of diabetic foot sepsis
diabetic foot problems can be prevented with adequate education, foot assessment and pressure offloading footwear
how is chronic ischaemic disease developed
damage to artery wall (smoking, BP, glucose, cholesterol) and plaque formation
what is intermittent claudication
muscle ischaemia on exercise - angina of the legs
how can intermittent claudication be tested for
ankle brachial pressure index!!, also duplex ultrasound, CT angiography (invasive) and catheter angiography
what does the results of ABPI tell us about claudication
normal - 0.9-1.2claudication - 0.5-0.85severe - 0-0.45
what is the slow progression treatment of intermittent claudication
smoking, lipid lowering, anti-platelets, hypertension, diabetes, lifestyle issues
what drugs used in intermittent claudication
cilostozol, pentoxifylin
what is involved in an inflow bypass
anatomic or extra anatomic using prosthetic (Dacron, ePTFE) or own vein
what causes critical limb ischaemia
if claudication doesn’t stop - can progress to this
what is pain at rest a sign of
toe/foot ischaemia (lying and sleeping)
what is ulcers and gangrene a sign of
severe ischaemia and damage (trauma and footwear)
what is the findings of a clinical examination in critical limb ischaemia
cool to touch, absence of peripheral pulses, colour change, worse at night
where does a DVT normally form
venous valve pockets and other sites of presumed stasis
what does a distal vein thrombosis refer to
DVT of calves
what does proximal vein thrombosis refer to
DVT of popliteal vein or femoral vein
what causes a hypercoaguable state
malignancy, pregnancy, oestrogen therapy, inflammatory bowel disease, sepsis, thrombophilia
what causes endothelial injury
venous disorders, venous valvular damage, trauma/surgery and indwelling catheters
what causes circulatory stasis
left ventricular dysfunction, immobility or paralysis, venous insufficiency or varicose veins, venous obstruction from tumour, obesity or pregnancy
what causes provoked VTE
surgery, hospitalisation (reversible) or cancer (irreversible)
what is the consequences of VTE
fatal, reoccurrence, post thrombotic syndrome (pain, oedema, eczema, varicose veins, venous ulcerations) or chronic thromboembolic pulmonary hypertension (initially asymptomatic followed by dyspnoea, hypoxaemia, right heart failure)
what is the test of exclusion in PE
D dimer - breakdown product of cross linked fibrin - valuable first line screening test for suspected VTE with low Wells scoreif undetectable - excludes PE
what Wells score makes PE likely
> 4
what is the first line of imaging in suspected VTE
CT angiogram
what other tests can be used
CXR (normally in PE) and V/Q scan (mismatched perfusion defects - small PEs and pregnancy)
what is the pharmacological interventions of DVT and PE
anticoagulation (prevent clots), thrombolysis (destroy clots) and analgesia (pain relief)
what is the mechanical interventions of DVT and PE
graduated compression stockings (prevent post thrombotic syndrome for 2 years) and IVC filters (proximal DVT or PE who can’t have coagulation or who can but it keeps reoccurring despite target INR or LMWH - con they often thrombose)
what specific drugs are used in DVT and PE
apixaban, rivaroxaban, dabigatran and endoxaban and frogmen (esp for DVT caused by cancer)
when should thrombolysis be considered for DVT
symptomatic ileofemoral DVT symptoms less than 14 days duration and good functional status, life expectancy of 1 year or more and low risk of bleeding
when should thrombolysis be considered for PE
consider pharmacological systemic thrombolytic therapy for patients with PE and haemodynamic instability, do not offer for stability
what is a haemorrhagic stroke
bleeding occur inside or around brain tissue
what causes haemorrhagic stroke
raised BP and weakened vessel wall due to structural abnormalities like aneurysm, arteriovenous malformation (AVM) or inflammation of vessel wall (vasculitis)
what is ischaemic stroke (common)
clot blocks blood flow to brain - can be thrombotic, embolic or hypo perfusion (due to reduced flow of blood due to stenosed artery rather than occlusion of artery)
what are the non modifiable risk factors for stroke
age, family history, gender, race and previous stroke
what is the potentially modifiable factors for stroke
hypertension, hyperlipidaemia, smoking, history of TIA (temporary occlusion), AF, diabetes, congestive HF, alcohol excess, obesity, physical inactivity and poor socioeconomic status
narrow window treatment of ischaemic stroke
thrombolysis or thromboectomy
how to prevent next stroke if its atheroembolic or due to thrombus
antiplateles, statins for high lipids, diabetes and hypertension management
how to prevent next stroke if its due to AF
anticoagulate ASAP via warfarin or direct oral anticoagulants (inhibit factor X and thrombin)
what is a surgery used to manage stroke
haematoma evacuation - relief of raised intracranial pressure of carotid endarterectomy
what imaging is used in stroke
CT brain +/- angiography - only way to differentiate between ischaemic and haemorrhagic stroke
what is an atheroembolism
embolism from a thrombus forming on a atherosclerotic plaque - platelet rich clots - and infarcts in same side of carotid artery carotid scanning, CT/MR angiography of aortic arch
what is a cardioembolism
embolism from clot formed in heart (usually left atrium) - clotting factor rich clots - infarcts bilaterally ECG (AF and LVH) or ECG bubble contrast study to look for interatrial connection
what should you question in a haemorrhagic shock
young - investigate for underlying aneurysm and AVNmultiple haemorrhages - question vasculitis, moya moya disease, cerebral amyloid angiopathy
