Vascular Flashcards
Pathogenesis of Atherosclerosis plaque
Mechanical sheer streets lead to damage to endothelium from HTN, increased LDL’s, toxins from smoking leads to inflammation of the tunica intima and LDL deposition. The deposition of LDL leads to an inflammatory response and recruitment of macrophages due to cytokine production. Macrophages in turn phagocytose the LDL transforming into lipid laden foam cells. Further irritation leads to TGFb and other cytokines production which promote SM proliferation to form a fibrous cap over the lipid core
PC of atherosclerosis
Stenosis - claudication, angina, mesenteric ischemia, renal artery stenosis - HTN/CKD
Plaque rupture - Stroke/TIA, MI, acute limb schema
Plaque thrombus formation
1 - Endothelial injury exposes the connective tissue matrix beneath, platelets adhere to the collagen fibres forming a thrombus
2 - Deep endothelial fissuring allows blood to enter the plaque, the mix of macrophages, LDL’s and tissue factor is highly thrombogenic and leads to an expansive thrombus in the plaque
Peripheral arterial disease
Most asymptomatic only 7% require intervention. Due to atherosclerosis of the aorta-iliac vessels. If a pt has PVD they have CAD!
Limb ischemia PC
Stage I - asymptomatic
II - intermittent claudication (relieved by rest)
III - rest/night pain a sign of critical ischemia
IV - gangrene
Can present with cold extremities, hair loss, eczema,
arterial ulcers - deep punched out, over pressure points
Burgers test +ve
Acute limb ischemia
Embolic event leading to occlusion. 6 P’s
Pain pulseless, parathesia, paralysis, perishling cold and pallour
ABPI
Ankles brachial pressure index.
>1.30 = calcification of vessels
0.71-0.90 = mild PAD
<0.4 = severe PAD
Coronary Artery disease risk factor
Modifiable - smoking, HTN, cholesterol levels - HDL and triglycerides, DM, obesity and exercise, hyper coagulability, COCP
Non modifable - age, male sex, afro-carribean, FHx
Myocardial ischemia
Reduced blood flow - atheroma, thrombus, embolus, arteritis,
Reduced oxygenation of the blood - anaemia, hypotension, hypoventilation
Increased demand - hypertrophy of cardiac muscles, increased cardiac output (hyperthyroid)
Metabolic syndrome
3/5 of the following: insulin resistance (DM), HTN, central obesity, hyperlipidemia - high TG, low HDL
Angina PC
PC crushing centra/retrosternal chest pain brought on by exertion, stress or cold relieved by GTN or rest. May radiates to the jaw or left arm
Cardiac Chest Pain
MI central crushing, high troponin, ST changes ECG, PMHx or risk factors!
Angina relieved by rest or GTN
Pericarditis pleuritic pain better on sitting forward, saddles shaped ST changes globally on ECG
Dissection tearing retrosternal pain often accompanied by hypotension, unequal BP in arms, neurological sequale
Respiratory Chest Pain
PE sudden onset SOB, sinus tachy, +/-haemoptysis, risk factors/DVT
Pneumothorax sudden onset SOB, hyperresonant to percussion, absent breathe sounds
Pneumonia fever, SOB, green/purulent sputum, crackles on auscultation, CXR - shadowing
Gastro Chest Pain
GORD/PUD retrosternal pain, worse on large meals or lying down
Gallstones - PMHx, fat, female, forty, fertile, classic bilary colic pain worse after eating
Pancreatitis - severe epigastric pain, vomiting, nausea, diarrhoea, jaundice, high amylase
Other Chest pain
Anxiety - hyperventilation, stressed, tight chest
Boerhaave taer - rupture oesophagus
MSK - costochondritis/fracture specifically localised pain, worse on inspiration, ?trauma
Definition of MI
Universal definition of myocardial infarction =
troponin >99 centile and symptoms/ECG evidence of ischemia or necrosis
Risks of Obesity
1x GORD,PCOS, infertility, Cancer
2x CHD, HTN, OA, gout
3x T2DM, OSA, dyslipiemia
Type I MI
Related to atherosclerotic plaque rupture from ulceration, fissuring leading to intraluminal thrombus
Type II MI
Imbalance in o2 delivery to myocardium may be seen in tachyarrythmias, anaemia, respiratory failure
Type III MI
Post mortem diagnosis of sudden cardiac death
Type IV and V MI
IV - due to PCI (trop 5x) or stent thrombosis
V - due to CABG (trop 10x URL)
Stable angina Mx
Lifestyle advice, treat HTN, DM and give statins
Short acting GTN spray for symptomatic relief
- Used Blocker or CCB
- If continue to be symptomatic/significatn stenosis offer revascularisation
PCI - single vessel + suitable anatomy
CABG - multi vessel, DM
ACS
i) STEMI
ii) NSTEMI
iii) Unstable angina - crucially = ischemia not infacrtion so no increase in trop
PC ACS
Severe sudden onset retrosternal chest pain radiating to jaw/ left arm. No relief by GTN or rest. N/V, sweating and palpatiatons
O/E ACS
tachycardia (bradycardia if RCA occlusion due to SAN/AVN supply
apex displacement, S4 gallop
hypotension, new pan systolic murmur - VSD rupture
mitral regurg = papillary muscle rupture
Signs of other pathology - aortic dissection unequal BP
Atypical MI
DM or elderly can present with SOB, abdo pain completely asymptomatic
Leads on the ECG
Inferior leads - II,III and avF = RCA
Anterior leads - V1-V4 = LAD
Lateral - V5,V6, I and avL = L circumflex
ECG signs in ACS
ST elevation or depression - T wave inversion - Pathological Q waves (1mm wide, 2mm deep)
Troponin T
Expressed in cardiac and skeletal muscle responsible for coupling sarcomeres when high intracellular Ca2+, binds to tropomyosin to position actin
Causes of raise trop
sepsis, PE, rhabdomyolysis, LVF, AF, post op, pericarditis, myocarditis, cardiomyopathy
ACS diagnostic troponin
> 99URL = diagnostic. 2nd troponin post 3hrs
- different in 10mg/l or 20% rise
GRACE Score
Predictor of death/MI 6months post discharge.
Uses age, HR @ presentation
Findings during stay = SBP, Hx of CCf or MI,cardiac enzymes, ST depression, PCI and creatinine level
NSTEMI Mx
Loading dose of aspirin 300mg and ADP receptor antagonist i.e. clopidogrel or ticagrelor
- These acts anti platelets
LMWH/fondaparinaux to anticoagulate
Morphine for pain
GRACE score or clinical picture dictates PCI intervention if deemed need PCI should occur within 72hrs
STEMI Mx
Morphine, aspirin 300mg, clopidogrel/ ticagrelor, LMWH o2 high flow
PCI within 2hrs
Fibrinolysis
Only if unable to reach PCI centre.
PCI to fibrinolysis
Recent surgery, GI bleed, aortic dissection, Hx bleeding disorders, haemorraghic stroke, ischemic within 3months,
Post hospital discharge MI
Lifestyle - cardiac rehab, dietician input, stop smoking, reduce alcohol, BMI <25, physically active
Medical - antihypertensives, control DM, aspirin 75mg od, clopidogrel, statins, ACEi
Complications of MI
Heart failure
Myocardial rupture of LV free wall often fatal event leads to haemodynamic collapse and cardiac arrest
VSD gives a pansystolic murmur
MR due to severe LV dysfunction leading to annular dilation, MI of inferior wall leading to papillary dysfunction, Infarction of the papillary muscle = sudden onset HF and cardiogenic shock
Dresslers 6-8wks post MI self limiting pericarditis
Arrthymias are v common
Hypertension diagnosis
Anyone with SBP >140/90 is offered ABPM to confirm the diagnosis
Complications of HTN
Heart - MI, LV hypertrophy due to increased afterload from high PR. Can lead to hypertensive cardiomyopathy and HF
Brain - Stroke/TIA, vascular dementia, hypertensive encephalopathy
Renal - hypertensive nephropathy. Thickening of arteriole walls leads to reduced blood flow, tubular atrophy and interstitial fibrosis and glomerular ischemia = ESRF
Hypertensive retinopathy, PVD
Hypertensive encephalopathy
Rare due to cerebral blood pressure >200/130 spasm of cerebral vessels leads to ischemia
PC occurs approx 36hrs post BP increase, severe headache, reduced GCS, impaired cognition and neurological signs
Hypertensive retinopathy
I = vasospasm, increased arteriolar tone narrowing retinal arteries - silver wiring (tortuous and increased reflective) II = sclerosis and intimal thickening AV nipping III = disruption of blood-retinal barrier SM and endothelial dysfunction. Cotton wool spot (ischemia), hard exudates(lipids) and dot/blot haemorrhages
1 HTN
Essential HTN (90%) due to increasing age, males, obesity, high salt, FHx, lack of exercise
2 HTN
Always think if treatment resistant, young
Endo - Conns, acromegaly, cushings, phaechromocytoma
Renal - Anything that leads to ESRF, renal artery stenosis, ADPKD,
Vascular - coarctication
Drugs - cocaine, epo, steroids, caffeine, nicotine, NSAIDs
OSA and white coat HTN
RAS
Angiotensinogen produced by liver in response to low BP, activated by renin (produced by juxtaglomerularappartus hypoperfusion)
This produces angiotensin I which is cleaved by ACE to angiotensin II.
Actions of angiotensin II
Vasoconstrictor - binds to At1 receptors on endothelium to inhibit bradykinin synthesis, therefore NO
Aldosterone secretion from adrenal = Na+ retention and K+ excretion
ADH production from post pituitary = aquaporin insertion @ collecting duct therefore h20 reabsorbed
Phaechromocytoma
PC headaches, severe HTN, sweating and palpitations
linked to MEN2 and von hippel lindau. Inv = high plasma/urine metaepinephrines
Cushings syndrome
PC wt gain, central obesity, proximal myopathy, high glucose, facial plethora, striae, hirsutism
Inv - 24hr urinary cortisol, morning cortisol, low dose dexamethasone, plasma ACTH
HTN due to cortisol having affinity for aldosterone receptors
Hyperaldosteronism
1 = Conn's or adrenal hyperplasia 2 = LVF, cirrhosis, cor pulmonale all lead to high renin
Aldosterone:renin need to identify which
Conn’s
PC HTN, muscle weakness, fatigue, headache, low K+, high Na+, high serum aldosterone:renin
May need adrenal vein sampling
Renal artery stenosis
May be linked to fibromuscular dysplasia esp young females, may = gradual decline in renal function or abrupt flash pulmonary oedema. Abdo bruit
Inv - MR angiography
Liddle syndrome
Hyperactivity of ENaC. AD leads to high levels of ENaC channels present and activated in the collecting duct hence hypernatremia and HTN
hypokalemia, metabolic alkalosis due to increase bicarb retention
Mx = K+ sparing diuretic
AME - apparent mineralocorticoid excess
AR condition due to deficiency in 11B dehyrdoxysteriod dehydrogenase preventing cortisone to cortisol. This leads to cross reaction and simulation of aldosterone receptor
Inv = urinary cortisol:cortisone
Classification of HTN
I = >140/90 in clinic or 135/85 on ABPM II = >160/110 in clinic or 150/95 on ABPM III = >180 EMERGENCY
Acute stroke imagine
CT. Haemorrhage = white, Ischemia = grey
Early signs of ischemic stroke on CT
loss of grey white matter differentiation, lack of definition of lentiform nucleus
Carotid imaging
Carotid duplex USS used to screen for carotid stenosis
Pericarditis PC and Mx
Inflammation of the pericardium. sharp chest pain made better on leaning forward, radiates to trapezius, may have fever, dry cough, AKI
Mx = self limiting NSAID’s if large pericardial effusion pericardiocentesis
O/E Pericarditis
ECG - globally saddled shaped ST elevation, flattened t waves,
Huge troponin often 1000’s
Pericardial rub
CXR = globular “water bottle” heart
Complication of pericarditis
Pericardial effusion which can lead to tamponade
Causes of pericarditis
Viral - coxsackie, influenza, mumps TB, Bacterial (strep, staph, Hib) Post MI - dresslers Ureic pericarditis AI - SLE, RA, systemic sclerosis
Consider familial hypercholestrolemia
total cholesterol > 7.5mmol or FHx premature coronary disease
Aortic dissection
Tear in the tunica intima allows blood to enter inbetween the intima and media forming a false lumen which can compress vessels coming off the aorta as it expands.
PC aortic dissection
PC = sudden onset severe chest pain, radiating to the back. hypotension, vomiting and sweating
O/E = hypotension - difference in-between arms
Complications
- Ascending = AR,MI, tamponade, neurological defect
- Descending = AKI, acute mesenteric ischemia, acute limb ischemia
Causes of aortic dissection
HTN, coarctation, Marfans and Ehlers damlos. Turners and Noonans
Pathogenesis of dissection
Normally @ aortic arch or 2cm above aortic root
I = ascending and descending
II = only ascending aorta
III = descending aorta only
Invx dissection
CXR = widened mediastinum. TOE = gold standard, ECG and troponin to rule out MI
Number needed to treat
NNT = 1/ARR
Q RISK 2
Predicts a persons 10yd cardiovascular risk. Anyone with risk >10% needs statins, HTN contract and advice about exercise, diet, smoking and BMI
Measuring the JVP
Used as no valves between the internal jugular vein and the RA. Hence is an indicator of RA pressure
S3 and S4
S3 - due to rapid ventricular filling present in HF
S4 - associated with atrial contraction
If heard together = gallop rhythm
Cardiac tamponade
Build up of fluid in the pericardium leading to compression of the heart. Causes = trauma, pericardial effusion,retrograde aortic dissection.
PC and O/E of tamponade
Cardiogenic shock - SOB, hypotension, cold peripheries
O/E = Beck’s triad - muffled heart sounds, low BP and JVP distention, rapid weak thready pulse, cool clammy mottled skin due to vasoconstriction and hypoperfusion
pulsus paradoxus - drop in BP >10mmHg on inspiration
Inv and Mx tamponade
ECG may show electric alternans - alternation of QRS complex amplitude between beats
Echo = diagnostic
Mx = pericardiocentesis via 5th ICS or xipisternal
Signs of hyperlipidemia
Xanthelasma - cholesterol deposits on eyelids/ under the eyes
Corneal arcus - cholesterol deposit around cornea
Tuberous xanthoma - orange streaks of cholesterol on palms
Tendon xanthomas- nodules @ achilles tendon or digital extensors
In hypertriglyceridemia = pancreatitis and eruptive xanthoma
Lipid physiology
Lipids are insoluble in water and so are transported in the bloodstream as macromolecular complexes. The central lipid core is surrounded by a coat of phospholipids. These apoproteins transform the lipid into a lipoprotein. There are 5 main types of lipoprotein separated by their relative size and density
Chylomicrons
Triglyceride rich allowing transport of lipids from the intestine to the adipose, cardiac and skeletal tissue. Lipoprotein lipase present in these tissues hydrolyses the triglycerides to fatty acids. The rememant chylomicron is taken up by the liver. ApoB48
VLDL
Synthesised by the liver contain endogenous triglycerides. Main energy source when fasting. Triglycerides are removed via apoprotein CII binding to the capillary endothelium. When depleted of TG = IDL
ApoB100
LDL’s
Main carrier of cholesterol delivering it to the liver and peripheral cells. Contains a single apolipoprotein B100 which allows it to bind to receptors on the surface of the hepatocytes. It is then internalised and degraded by liposomes
HDL’s
Nascent HDL produced by intestine and liver travel to peripheral tissues they transmutate into mature particles with the acquisition of phospholipids and A and C apoproteins they can then removed cholesterol from the periphery. ApoA1
Terminology of lipids
Cholesterol - structural component of cell membranes used to produce bile acids, steroid hormones and transport fat soluble vitamins (ADEK)
Triglycerides = glycerol and 3x fatty acids
Secondary hyperlipdemia
High triglycerides and VLDL = DM, CKD, alcohol and hypopituitarism, drugs - steroids, b-blockers, diuretics, HIV meds
High cholesterol = nephrotic syndrome, hypothyroidism, Cushings, choleostasis
Total cholesterol
Total cholesterol = LDL,VLDL, HDL and IDL approx 5.0 mol/l
Triglyceride levels
Not considered directly atherogenic but important to consider due to role in metabolic syndrome.
Can = pancreatitis or eruptive xanthoma in high levels
12hr fasting TG <1.7 mol/l
HDL levels
HDL - antiatherogenic molecule shown to be protective against CVD and atherosclerosis
LDL level
Calculated using Freidewald equation. Prolonged fasting state is needed so rarely used!
High levels linked to CVD and atherosclerosis
Non HDL cholestrol
Frequently used as fasting isn’t required
Familial hypercholesterolemia
1/500 people AD mutation in LDR receptor. This leads to reduced removal of LDL from the blood.
PC often asymptomatic, tendon xanthomas or corneal arcus. High LDL and total cholesterol
Codominance in familial hypercholestrolemia
Homozygous = 50% of 60y/o pt will die if untreated
Heterozygous = rare no LDL receptors leads to hugely elevated LDL leading to mass deposition in arterial walls. Death from IHD in childhood or adolescents
Diagnosis of familial hypercholesterolemia
1) Total cholesterol > 7.5mmol/l or LDL > 4.9mmol/l
+ 2)Tendon xanthomas or 1st degree relative
3)DNA evidence LDL mutation
Familial combined hyperlipidemia
High LDL and TG levels, Low HDL approx 1/200
Remnant (type III) hyperlipidemia
AR 1/5000 due to a mutation in apoplipoprotein E which prevents the normal metabolism of IDL, VLDL and chylomicrons. Hence accumulation of chylomicron remnants
PC = eruptive xanthoma, xanthum striatum palmare
Inv = v high TG, high total cholestrol
Familial hypertriglyceridemia
AD can be due to excessive VLDL production or defects in LPL and apoCII leading to vv high triglyceride levels >10mmol, with normal cholesterol
PC = eruptive xanthoma, pancreatitis, lipideamia retinals
very high CVD risk
When not to use Q risk 2
Pt with 1 lipid disorders, high risk CVD conditions such as DM, CKD - eGFR <60, 85+y/o
Amaurosis fungax
Sudden onset transient loss of vision usually lasts mins-hrs described as black curtain descending +/- fogging of vision
Causes of amaurosis fungax
Embolic/hameodynamic - atherosclerotic carotids, cardiac emboli (AF, myxoma), vasospasm, GCA, SLE, antiphospholipid syndrome, malignant HTN, post endoarchtectomy. bypass
Ocular - closed angle glaucoma, iritis/keratitis
Neurological - optic neuritis, papilloedema, migraine
Ocular ischemic syndrome
Chronic hypoperfusion to the eye due to severe carotid artery stenosis (90%)
PC - males 65+y/o dull pain over eyebrow, visual loss, often PMHx of DM, HTN
Mx - rule out vasculitis, stroke prevention and increase blood flow to retina
Causes of carotid bruit
Carotid artery stenosis, AS, hyperthyroidism
Carotid endoarchectomy
Diagnosed via duplex USS 1st line for pt with 50-99% stenosis
Reversible causes of a cardiac arrest
6H’s and 6T’s
6H’s
Hypoglycaemia,
Hypothermia - body temp <35 rewarming via bypass or irrigation of cavities
Hyper/hypokalemia - If K+ calcium gluconate, Neb salbutamol, IV insulin/glucose
Hypoxia - O2, tracheostomy if needed
Hypovolemia - IV fluids, tranfusion, find and stop the cause of bleeding. Surgical tamponade for varies/PPH
H+ acidosis often from prolonged hypoxia - glycolysis produces lactate. Sodium bicarb buffer
6T’s
Thrombosis = PCI
Tamponade = Pericardiocentesis stat. PC muffled heart sounds, distended neck veins, narrow pulse pressure, rapidly falling BP
Tension pneumothorax = needle thoracotomy 2nd ICS mid clavicular
Toxins = TCA’s, B-blockers, cocaine, aspirin
Trauma - Commotion cordis
Thromboembolism = Massive PE
Cardiac channelopathies
Congenital disorder caused by genetic mutations that affect the cardiac ion channels and electrical activity of the heart. Eg Brugada, long QT, CPVT
Ventricular fibrillation
Broad complex tachycardia QRS >0.12 ECG shows shapeless rapid oscillations with no organised complexes
Disorganised contraction of the heart leads to low CO and can = ischemia of heart muscle
Pulseless pt becomes rapidly unconscious leading to cardiac arrest
Mx = defibrillation stat
Long QT syndrome
Rare inherited cardia syndrome usually AD but can be AR. Channelopathy involving abnormal repolarisation of the heart giving different refractory periods in myocytes. These can propagate to neighbouring myocytes = re-entrant ventricular arrhythmia
Due to reopening of L-type Ca2+ channels @ plateau phase early after depolarisation.
Causes of long QT
Inherited = Romano ward (AD), Jervell-Lange-Neilsen (AR)
Acquired = hypokalemia, hypocalcemia, acute MI, bradycardia, DM, drug induced, hypothermia
Drug induced long QT
Fluoroquinolones: cipro Neuroleptics: phenothiazines, haldol Macrolides Anti-arrhythmics 1a/III: quinidine, amiodarone, sotalol TCAs Histamine antagonists
Types of inherited long QT
Type I = Provoked by exercise esp swimming
Type II = Provoked by emotion or acoustic stimuli
Type III = @ rest or asleep
PC long QT
Asymptomatic. Can present as syncopal episodes or incidentally
QTc >480mms. Worked out using Bazzetts formula
Inv for cardiac syncope
ECG crucial
Echo to identify structural abnormalities i.e. cardiomyopathy
Heart monitors
Heart monitors
ILR - implantable loop recorder small chip implanted under the skin that can record ECG for up to 3 years. It picks up event and notifies hospital switchboard
Halter monitor = pt wears a ECG recorder for 1-7 days
Torsades de pointes
QRS twisting at isoelectric line. QT prolongation required. This can degenerate to VF
Wolff-parkinson white syndrome (WPW)
Presence of an accessory pathway connecting atria and ventricles allowing electrical impulses to bypass the AVN leading to premature ventricular contraction
WPW ECG
slurred delta wave at base of QRS, shortened PR interval <120ms, wide QRS. Can lead to SVT
Mx = ablation of bundle of lent
Arrythmogenic RV cardiomyopathy
Usually presents in adolescent 80% with syncope and dyspnea. AD with variable expression. Increased incidence in italian males
Fatty infiltration confined to RV leading to atrophy of cardiomyocytes
Brugada syndrome
20% of cases due to mutation in gene encoding Na+ channels in cardiac myocytes. AD increase prevalence in males and south asian populations
Risk of sudden cardiac death and VF
Mx = ICD
ECG brugada
Provoked by flecanide administration
type I = coved ST elevation v1-v3 + RBBB
type II = saddle back ST change and biphasic T waves
Catecholaminergic polymorphic VT (CPVT)
Mutations in Ca2+ channels on sarcoplasmic reticulum. Seen in young people often syncopal episode or MI before 20y/o triggered by exercise or stress
Mx ICD
ECG arrythromgenic RV cardiomyopathy
T wave inversion v1-v3, RBBB,
Epsilon wave = terminal notch in QS due to slow intraventricular contraction
Commotio cordis
Blow to pericardial region @ critical time in cardiac cycle. Ascending T wave ventricular repolarisation
HOCM
Most common cause of cardiac death in young people. 1/500. AD condition mutations in B myosin heavy chain protein. Causes variable myocardial hypertrophy frequently involving the AV septum = LV outflow obstruction
PC HOCM
Asymptomatic - incidental ECG finding.
Chest pain, SOB and palpitations on exertion
O/E = double apex beat = s4, jerky carotid pulse due to rapid ejection and sudden LV outflow obstruction, ejection systolic murmur @ LL sternal edge
Inv and Mx HOCM
ECG - LVH, abnormal Q waves in inferolateral leads
Echo = diagnostic of asymmetric LV hypertrophy with septal involvement
Mx = ICD or amiodarone
Causes of sudden cardiac death
Coronary artery disease - Acute MI, IHD
Non coronary artery disease - HOCM, Brugada, Long QT, dilated cardiomyopathy, Valve disease and congenital heart disease
Dilated cardiomyopathy
Dilatation of the ventricular chambers and systolic dysfunction with preserved wall thickness
Causes of dilated cardiomyopathy
Familial = AD Acquired = SLE, pregnancy, myocarditis (cox-sackie, HIV, fungi, adenovirus) , alcohol, pregnancy
A Wave in JVP
Atrial systole
Large a wave - pulmonary hypertension and stenosis
Absent a wave - AF due to dysfunctional syncope
Cannon a wave - complete HB
Large v wave
Atrial filling against closed tricuspid valve
Raised JVP normal waveform
HF and fluid overload
Prinzmetal’s angina:
Refers to an angina that occurs without provocation, usually at rest, as a result of coronary artery spasm
• Occurs more frequently in women
• Arrhythmias (both VT and heart block) can occur during the ischaemic episode
Aortic stenosis
Syncope, SOB. Ejection systolic murmur radiating to the carotids
Causes of cardiogenic shock
MI, cardiac tamponade, arrhythmias, tension pneumothorax, aortic dissection
Signs and symptoms of RHF
PC = peripheral oedema, ascites, fatigue, wt loss, SOB
Signs = transudative pleural effusion, raised JVP, 3rd heart sound
Causes = 2ndardy to LHF, pulmonary hypertension, tricuspid or pulmonary stenosis, cor pulmonale
Signs and symptoms of LHF
PC = orthopnea, PND, fatigue and SOB
Simon Broom criteria
Total Cholesterol >7.5mmol/L or LDL >4.9mmol/L
+
Tendon xanthomas in the patient, first or second degree relatives
OR
DNA Evidence of LDLR mutation, ApoB100 or PCSK9 mutation
Causes of familial hypertriglyceridemia
Familial hypertriglyceridemia
Lipoprotein Lipase Deficiency and Apoprotein C-II deficiency Rare, presents in childhood. Severe hypertriglyceridaemia
Pancreatitis, retinal vein thrombosis, eruptive xanthomas
Mx dyslipidemias
high triglycerides = fibrates
high cholesterol = statins
combined = fibrates
Diagnosing HF
Previous myocardial infarction
arrange echocardiogram within 2 weeks
No previous myocardial infarction
measure serum natriuretic peptides (BNP)
if levels are ‘high’ arrange echocardiogram within 2 weeks
if levels are ‘raised’ arrange echocardiogram within 6 weeks
