PY6030 The Cardio-Respiratory System 2 ANGINA: Tests:

Term 1 Chronic stable angina: Non-invasive:

Reversible imbalance between myocardial oxygen supply and demand. Anatomical: CT coronary angiography with/without Ca score (understand risk of MI)
CHEST PAIN: What makes it stable? Functional Stress Test (if CT angiography non-diagnostic): Stress echocardiography,
Possible causes of Chest Pain: Symptoms occur for more than 2 months with no changes in severity, character or triggers. nuclear myocardial perfusion scan, MRI perfusion scan or exercise ECG, In
 Angina/CHD What causes this imbalance?
 Peptic Ulcer Disease The oxygen demand is greater than what is supplied. Invasive angiography:
 Reflux Oesophagitis Main causes = can be serious. Usually induced, by exercise, emotion or stress but may Dr inserts catheter with dye.
 Pulmonary Embolism also be spontaneous.
 Biliary Tract Disease Differential Diagnoses:
Other possible causes: Why is there an imbalance? Musco-skeletal – chest wall tenderness?
 Aortic dissection The most common cause: Atheromatous plaque which builds up with age and is Pneumonia – cough, fever, sputum?
 Pericarditis exacerbated by poor diet. Atherosclerosis = build- up of lipids and fatty substances causing Pulmonary embolism – dyspnoea, lower limb DVT, pleuritic chest pain?
 Pneumonia thickening of arterial walls. This leads to obstruction of blood flow. Blockage of over 70% Pericarditis – worse when lying flat?, relieved by leaning forward?
 Fractured rib can lead to stable angina due to insufficient coronary blood flow following exercise. Other GORD – worse after eating?
 Musculoskeletal pain factors contributing to the imbalance:
 Oesophageal/peptic cancer  Coronary vasospasm – sudden intense vasoconstriction that causes occlusion of bv Refer:
 Lung Cancer (absence of atherosclerotic plaque – Prinzmental variant angina) If Pt is experiencing stable angina symptoms  rapid access chest pain clinic
 Asthma – as a result of severe breathlessness.  Microvascular dysfunction If Pt is experiencing unstable angina or sever, persistent chest pain  EMERGENCY
 Left ventricular hypertrophy
Hx TAKING:  Systemic disease – anaemia, thyrotoxicosis Tx Aims:
 Presenting Complaint (PC)  Haemodynamic factors – tachycardia and hypertension. 1. Prevention and relief of Sx,
This is what the Pt tells you is wrong. E.g Chest Pain Restore O2 supply/demand balance.
Prevalence: Angina is more prevalent in males (70%) and is more common in the elderly. GTN or angina attacks and drugs for angina prophylaxis
 Hx of PC
Gain info on specific complaint. Eg Use SOCRATES. Importance: Ischaemic heart disease (IHD) is the leading cause of death worldwide and 2. Slow atherosclerosis progression
stable angina in a common manifestation of IHD. Manage risk factors:
Angina can impact one’s quality of life. Lifetyle (diet, exercise, smoking cessation)
 Systemic Enquiry
Optimise management of co-morbidities
Info about other systems in the body not covered in Hx of PC.
Sx: Central/Lefts-sided chest ‘tightness’ may radiate to arm/jaw Drugs  statins, consider anti-platelet and ACEi
Main systems to cover: CVS, Respiratory, GI, Neurology, Renal, Musculoskeletal
Provoked by predictable and reproducible level of physical activity improve long-term prognosis.
and Psychiatry.
Relieved with rest or GTN spray
3. Improve long term prognosis
 Past MHx
Types of angina: Stenting or Bypass surgery can also be considered. In conjunction with anti-platelet
Gain info on Pt’s other medical problems.
Atypical angina – 2 of the above, Non-angina – 1 or none of the above therapy. For at least one year.
 FHx and SHx
Severity of angina can be classed. Coronary Bypass Graft:
Info on family history; Hx of diabetes or cardiac history.
Divert blood flow around clogged artery.
Find out more about the patient’s background. Do they smoke? Drink? If so how
many units/cigarettes? Is the patient taking any recreational drugs? Who lives with Canadian Cardiovascular Society classification of angina severity:
Class Severity of Symptoms Medications:
the Pt? Who handles their meds?
I Angina not triggered by ordinary activity but by strenuous or prolonged GTN – angina relief
exertion only. Do not combine rate-limiting/non-dihydropyridine
 Drug Hx
II Slightly affected by ordinary activity. Angina on walking or climbing stairs First line agents: CCB (diltiazem or verapamil) w/ beta blockers= HF
What medications are the patient taking? Strength, dose and how often?
rapidly, walking uphill or exertion after meals, cold weather and when  Beta blockers and bradycardia can occur.
SOCRATES:
under emotional stress. Lowers HR,
Description
III Notable limitation of ordinary physical activity. E.g. Angina on walking one contractility and BP. Also prolongs filling time
S Site of pain – Where is the pain located?
or two blocks or one flight of stairs. S/E: Fatigue, dizziness, bradycardia and bronchospasm
O Onset – When did it start? Was it sudden or gradual?
C Character – What was the pain like? Sharp? Burning? IV Inability to carry out any physical activity without discomfort.
 Ca – channel blockers
R Radiation – Does it radiate anywhere? Rate limiting CCB acts similarly to B-blockers.
A Associations – anything else associated with the pain? N+V? Sweating? Risk Factors of angina:
Unmodifiable Modifiable Co-morbidities S/E: dizziness, headache, fatigue and ankle swelling.
T Time Course – How long does it last? Does it have a time pattern?
E Exacerbating/Relieving factors – What makes it better/worse  Age  Obesity  Hypertension
Second line agents:
S Severity – Rate pain on a scale of 1 – 10 (10 being most painful)  Congenital  Smoking  Hyperlipidaemia
 Long acting nitrates (e.g isosorbide mononitrate)
heart defects  Inactivity  Diabetes
NO donor – inhibits contractions = vasodilation.
ASSOCIATED Sx:  Genetics  Stress
S/E: headache, dizziness, flushing and nausea.
Cardiac:  Hx of Heart
Dyspnoea (difficulty in breathing), Orthopnoea (shortness of breath when lying down), disease
 Nicorandil (K+ channel opener)
Ankle swelling, oedema and palpitations.  Male
 Ranolazine / Brand: Ranexa (Inhibitor of late Na current)
Diagnosis:
 Ivabradine (Inhibitor of the If/ heart’s pacemaker current channel that control SA
Respiratory: Initial assessment:
node – HR must be over 70bpm
Cough, sputum, wheeze, pleuritic pain, haemoptysis (coughing up blood), Dyspnoea 1. Clinical Hx and Examination
2. Blood test: glucose, lipids, full blood count, thyroid function tests
GI Symptoms: 3. ECG, CXR, Chest X-Ray
Heartburn, dyspepsia, wind, dysphagia, change in bowel habits, weight change Further tests based on risk satisfaction from clinical hx and risk factors. If probability is
less than 5%, further tests not usually needed.
If pain is severe Pt can experience N+ V.
 ACUTE CORONARY SYNDROME (ACS): What is a thrombolytic?  Tx and prevention of HF>
Unstable Angina, STEMI, NSTEMI  Enzyme that breaks down blood clot.  Prevent left ventricular remodelling.
 Alteplace, reteplase, streptokinase or tenecteplase  Nephroprotective.
ACS = Sx that result from acute obstruction of coronary artery.  IV administration. Contraindicated in Pt with bleeding risks.  Titrate dose up – increase to max tolerated dose.
Blockage – due to rupture of atherosclerotic plaque causing thrombosis in lumen, therefore  PCI can still be considered following thrombolysis. – if it is found that the clot is still  SE: dry cough, hyperkalaemia.
preventing blood flow to heart – myocardial cell damage. obstructing blood flow. = Pt should be referred to PCI within 24 hrs. Have angiography prior  Monitor Pt’s renal function and serum electrolytes. Monitor annually if target is
to stent. reached.
NSTEMI – incomplete blockage – occlusion occurred in small arteries.  Aspirin and Clopidogrel – recommended as Ticagrelor and Prasugel has limited studies on
STEMI – full blockage it. BETA BLOCKERS:
 Should be started asap. B-blockers decrease infarction size.
Pathology – Manifestation of atherosclerosis: Best anticoagulant – LMWH.  Caution: Pt with HF, hypotension, bradycardia and asthma.
1. Irritant – LDL, cholesterol, toxins and hypertension NSTEMI Management  Titrate up to max tolerated dose.
2. Damage to endothelium – LDL deposits are oxidised and triggers myocytes – Single dose of 300mg aspirin asap.  S/E: fatigue, coldness of the extremities, sleep disturbances
macrophage devours these lipids and become full and die = turning into foam cells. Antithrombin therapy:
3. SMC secrete fibrous cap – blocks plaque from rest of the blood  Fodapurinux – if angiography is not likely to happen witihin 24hrs. Give to Pt with CrCl of STATINS:
4. If this plague bursts = thrombosis due to platelet accumulation. less than 20ml/min.  Give high doses for plaque stabilisation.
Diagnosis:  Unfractioned heparin – if angiography is likely witihin 24 hours and if Pt has renal  Lower if:
STEMI NSTEMI UA impairment.  Drug interactions
Hx Chest pain Angina at rest >20 min Angina at rest for Assess individual’s risk of future adverse cardiovascular events using the GRACE score.  High risk of adverse effects
N+V with increasing longer than 20 min  Patient preference
Sweating frequency not relieved Increasing frequency Risk Assessment:  Cautions: in Pt w/ liver disease, high alcohol intake
by GTN No relief with GTN GRACE – estimates mortality within 6 months for patients with NSTEMI/UA.  AVOID GRAPEFRUIT
Occlusion Complete occlusion ECG normal or with ST Non – occlusive  Monitoring check lipids.
Severe cardiac damage depression and/or T thrombus >3% intermediate risk  >9% highest risk  S/E: myopathy (muscle weakness), rhabdomyolysis (rapid break down of damaged
inversion.  Dual antiplatelet therapy skeletal muscle fibres)
ECG ST elevation Normal Normal  Angiography within 96 hrs or asap  Advise patient to report muscle pain/tenderness or weakness.
Troponin* Highly elevated Slight elevation Normal  Glycoprotein iib/iia inhibitor given if chest pain persists.
*Troponin: GASTRO - PROTECTION:
 released in cell damage – specific to myocytes. There is also a cardiac myosin-binding 1.5to 3% = low risk  Lansoprazole 30mg OD – given to all Pt on dual antiplatelet.
protein C (cMyC) which is present in higher amounts than troponin but this is currently  Dual antiplatelet therapy  S/E: gastro disturbances and headache.
being studied.  Coronary angiography if ischaemia is experiences  Alternative – ranitidine 300mg bd.1
 Levels rise 3 – 24hrs after injury. ANTI COAGULANTS
 Levels can remain high after 2 weeks. Unfractioned  Only for Pt with renal impairment. OTHER CONSIDERATIONS:
Sx: heparin (UFH)  Has direct effect on thrombin. Pt who are hyperglycaemic  levels should be kept below 11mmol/L but avoid hypo.
 Pale and clammy  Causes thrombocytopenia (reduced platelet count) Dose adjusted insulin – monitor levels aswell
 Pulmonary oedema  Monitoring is required – activate partial thromboplastin time. aPPT
 Hypotensive / bradycardiac can also be tachycardiac LMWH  More predictable therefore no monitoring is required. If Pt is still hyperglycaemic after ACS --? HbA1c test before discharge and fasting blood
 N+V  Less thrombocytopenia. glucose should be checked around 4 days after ACS incident.
 Collapse, sweating, pallor (unhealthy pale appearance)  Titrated against body weight.
 Chest pain and SOB  Not given if Pt has poor renal function. CrCl <30ml/min. PHARMACIST INTERVENTIONS:
Fondaparinux  Good bioavailability. Pt should avoid NSAIDs. Atorvastatin 80
Immediate management – pre-hospital:  SubCut administration. Pt should be counselled, and informed of S/E as well as Beta Blockers
Resuscitation prn  T1/2 = 15 – 18 hrs  allows od administration interactions. Gastro - protection
MONA – Morphine, Oxygen, Nitrates and Aspirin 300mg  S/E: bleeding, anaemia.
 No association with heparin – induced thrombocytopenia Lifestyle:
Morphine: 5-10mg IV.  Smoking cessation
Consider giving Pt antiemetic to treat N+V. (E.g Cyclizine or metoclopramide)  Diet – healthy diet based on low salt intake, decrease in saturated fats and regular
ANTI PLATELETS
Oxygen: Give O2 if sats are less than 94% - O2 sat aim is between 94 – 98% intake of fruit and veg
Aspirin  300mg initially then decrease to 75mg.
Nitrates: Give if pt is not hypertensive. Give GTN sublingual or IV.  Exercise regularly at least 30 mins of moderate activity 5x a week.
 Caution: asthmatics and Hx of peptic ulcer
Aspirin 300mg: chewed or dispersible.  Stress management
 Take with or after food – risk of GI irritation/ulcers
Pt should also have a resting 12 lead ECG  Control comorbidities such as hypertension and diabetes.
Clopidogrel  Great at preventing stroke when used with Aspirin.
STEMI Management – Emergency reperfusion to restore coronary blood flow and minimise  300mg with 300mg Asp to be taken before PCI.
myocardial injury.  Interacts with omeprazole.
PCI – preferred.  Usually given for 12 month with dual therapy
Pt is eligible for PCI (percutaneous coronary intervention) within 90 mins from first medical Ticagrelor  Given with aspirin in patients who had an MI and who are at high
contact. After 90 mins, complications are higher. risk of a further event.
Before PCI, another anticoagulant and anti- platelet is given. – limit secondary thrombosis.  180mg stat and 90mg bd.
 Interactions: clarithromycin, digoxin and rifampicin.
Pt can also be given a glycoprotein iib/iia inhibitor to reduce the risk of immediate vascular Prasugel  60mg loading then 10mg od if pt is over 6okg
occlusion. Use is not common nowadays due to new antiplatelets such as ticagrelor or  5mg OD in pt who are under 60kg or over 75 years old.
Prasugel.  No significant interactions.

If Pt has no access to PCI within 90 minutes, give thrombolytic. Ideally should be done LONG TERM MANAGEMENT:
within 12 hrs. ACEi /ARBS
 Reduced mortality regardless of bp.
 ARRHYTMIAS & ATRIAL FIBRILLATION (AF): Risk Factors of AF:  N+V, taste disturbances are commonly experienced by reduced when dose is
Modifiable Unmodifiable reduced.
Cardiac Arrhythmia –  Age  High BP  Neurological Sx  tremor, ataxia. Usually occurs when loading dose is
abnormal rhythms of the  Congenital  Sleep apnoea – hypoxia can cause cell abnormalities – cells administered by improve when maintenance dose is started.
heart causing ineffective heart defects which are non- pacemaker cells generate an action
pumping / disturbance of the  Genetics potential DRONEDARONE:
electrical rhythm of the  Hx of Heart  Diabetes – high glucose levels can damage myocytes  Similar structure to amiodarone but considered as less effective. However, this
heart. disease  Obesity seems to be better tolerated with fewer S/E.
 Prior open-  Thyroid problems
Some arrhythmias are benign heart surgery  Exposure to stimulants FLECAINIDE 300mg/ PROPAFENONE600mg:
but some can be dangerous  ‘pill in the pocket’
 Stress
and require immediate  suitable for those with paroxysmal AF with no LVSD and IHD.
treatment to prevent cardiac  Systolic BP >100bpm and Diastolic >70bpm
CLINICAL MANIFESTATIONS (Symptoms):
arrest / haemodynamic  PATIENT ADVICE: Take if AF is lasting for >5min. Go to hospital if not resolved
 Palpitations and Irregular pulse
compromise. within 6-8 hrs or new Sx develop. MAX DOSE IS ONE IN 24HRS. Inform GP.
 Difficulty in breathing (dysponea)
 Shortness of breath and dizziness  Not for Pt with known IHD/ HF.
CLASSIFICATION OF ARRHYTHMIAS:  S/E: Flecainide: visual disturbances – blurred vision.
 Tiredness/ fatigue – due to insufficient blood flow = less O2 being delivered to
1. Heart Rate: Propafenone: constripation.
tissues.
Tachycardic – over 100bpm
 Patient may have syncope – sudden fainting
Bradycardic – less than 60 bpm RATE CONTROL
 Generalised weakness and poor exercise intolerance
Arrhythmia is not terminated but the ventricular response in controlled.
2. Origin: Common Tx for older patients or those with a long Hx of AF and those with persistent AF
Atria – Supraventricular MANAGEMENT:
NICE Guidelines  prevent thromboembolic events; relieve symptoms; restore and (cannot interfere w/ rhythm)
Ventricles – ventricular
maintain sinus rhythm and reduce and control rapid HR.  Identify underlying cause.
 1st Line:
3. Time Course: Rate control is preferred as maintaining sinus rhythm is difficult and drugs used to do BETA BLOCKERS (Class II) (excluding sotalol) or RATE LIMITING CCB (Diltiazem – off
 Paroxysmal – intermittent and terminates by itself this have plenty of S/E. label or verapamil)
 Persistent – Does not terminate when they occur. Requires electrical or DIGOXIN: Only consider monotherapy with digoxin for Pts with non-paroxysmal AF
pharmacological intervention. ≥ 2 episodes. RHYTHM CONTROL or ‘Cardioversion’ if they are sedentary. Mechanism of this is not completely understood. – said to
 Permanent – arrhythmia continues despite intervention. > 1 year Aimed at restoring and maintaining sinus rhythm. bind to Na/K/ATPase pump in myocyte.
Recommended for younger Pts / or those with new onset AF – prevention of life-long AF.
CARDIAC ACTION POTENTIAL:  Can be done pharmacologically for those who are medically stable. Give  2nd Line:
 Phase 4 – resting potential amiodarone or flecainide. Combination of two
Normally at -90mV. There is an equilibrium in ions  Flecainide – younger patients and those who DO NOT HAVE IHD.
entering and leaving the cell. Cells are waiting for  Amiodarone – more elderly patients at risk of IHD. Which one should be used?
stimulus to depolarise. NOTE: Amiodarone S/E include lung disease, can cause thyroid issues and corneal IHD HPT HF OTHER
-70mV – sodium channels open = depolarisation. deposits  photosensitivity. BETA ++ +/- ++ Thyrotoxicosis
 If Pt is medically unstable (chest pain, low BP, syncope and evidence of HF)  BLOCKER Post MI
 Phase 0 – Na+ influx Electrical  electrodes with pads CCB + ++ - not used as it COPD
reduces force of Bronchospasm
 Phase 1 – K+ efflux Vaughan – Williams classification: contraction
Sodium channels close – leakage of K+ out of cell. Class Drug DIGOXIN +/- +/- + Sedentary
1a - Na+ channel Quinidine Lifestyle(monotherapy)
 Phase 2 – Ca2+ influx blockers Procainamide
Plateu phase. Resulting in contraction due to Ca2+ entry/ This is when the cell contracts. How do they work?
1c – Na+ channel Propafenone
 Phase 3 – K+ efflux BETA BLOCKERS:
blockers Flecainide
*0-3 is called the refractory period.*  Inhibits sympathetic activation.
2 – B Blockers Beta- blockers
 Phase 4 – Resting potential allows ventricles to fill.  Decrease SAN activity = decreases sinus rate.
3 – K+ion channel Amiodarone
blockade Phase 3 Sotalol – has proarrhythmic effect - not be used in minor cases.  Decrease conduction velocity and inhibit abnormal pacemaker activity.
Atrial fibrillation is the common type of arrhythmia.
Dronedarone  Beta blockers can also increase refractory period and AP duration. = can block
No.1 cause for hospital admission regarding cardiac arrhythmia.
4 - CCB Verapamil arrhythmias.
Prevalence increases in older patients.
Diltiazem The choice of beta blockers can depend on the pt’s co-morbidities, local policy and cost.
AF = originates from the ATRIA.  form of supraventricular arrhythmia.
Pt w/ AF alone = atenolol 50-100mg od.
Long-term rhythm control: Pt with HF: Bisoprolol, carvedilol or nebivolol.  licensed for use in HF.
Atrial rhythm is irregular – HR 300 – 500 bpm = tachycardiac
Cardioversion
AV node slows down speed therefore ventricular rate is not as fast as atrial rate.
Pt w/ DM: Cardio-selective beta blockers (e.g atenolol, bisprolol, metoprolol and nebivolol)
CAUSES:
Beta Blockers is preferred.
Cardiac: Non-cardiac: Drugs S/E: bradycardia, cold extremities, sleep
Common.  AF usually Hyperthyroidism, acute E.g Beta 2 agonists Check Pt’s pulse and bp 1 week disturbances or nightmares (in these cases consider
2nd Choice:
occurs following damage to infections, e- abnormalities Thyroxine – tx for after each dose titration to switching to a water-soluble B-Blocker as this does
 Flecainide or propafenone – if Pt has no IHD or CHF
the heart e.g in MI / (Ca2+, Na+ and K+) hypothyroidism assess response to Tx. not cross BBB), fatigue, sexual dysfunction.
 Dronedarone – suitable if no LV systolic dysfunction or CHF
infarction Alcohol
Caffeine  Amiodarone – Suitable if Pt has LVSD or CHF.
AMIODARONE: Contraindications and cautions: Hx of obstructive airways disease, severe bradycardia,
 Long T1/2, uncontrolled HF, severe hypotension, frequent episodes of hypoglycaemia.
 Some cells that are not normally pacemaker cells sends electrical signals
 Slow onset but long duration of action
RATE LIMITING CCB (Diltiazem and verapamil): ANTICOAGULATION FOR STROKE PREVENTION IN AF (DR KHONG): TTR – Time in Therapeutic Range = check if Pt is taking enough warfarin. Poor TTR = more
 Binds to L-type Ca channels located on cardiac myocytes and cardial nodal tissue Stroke if a fatal consequence of AF. strokes and greater risk of bleeding. Strokes DO happen on warfarin.
(SAN and AVN). These channels are important in regulating influx of Ca2+ which
stimulates cardiac contraction. Prevalence of AF increases with age. Patients with AF have a greater risk of developing a DIRECT ORAL ANTICOAGULANTS (DOAC):
 CCB blocks Ca entry  decrease in myocardial force of contraction (-ve ionotropy) stroke (4-5x more likely) strokes as a result of AF are usually more severe. There are a number of new DOACs and they act on different parts of the coagulation
Decrease HR (-ve chronotropy) cascade.
Decrease conduction velocity within the heart (-ve dromotropy), particularly in the HPT is common cause of AF. A study carried out amongst Norwegian men over 35 years
AVN. showed that AF is related to BP. High BP = more likely to develop AF. HPT is also a major
 CCBs can decrease the firing rate of abnormal pacemaker sites within the heart but determinant of stroke risks in AF.
are also related to their ability to decrease conduction velocity which prolongs
repolarization, especially in the AVN. AFFIRM Study on Rhythm Control vs Rate Control:
 No survival advantage but there is a greater risk of hospitalisation with rhythm
Start w/ low dose and titrate up until AF is controlled. control – 80.1% vs 73% (p<0.001)
Diltiazem – not licensed for AF therefore use is off-  Rate control may be a safer Tx option.
Check the Pt’s pulse and BP 1 label.
week after each dose titration 60 -180mg tds. If MR is prescribed – specify brand as CHA2DS2 – VASc
to assess response to Tx. brands are not interchangeable. Quantifies risk of stroke.
CHA2DS2 – VASc criteria Score
Verapamil – doses 40mg – 120mg tds. Congestive HF / left ventricular dysfunction 1
HPT 1
S/E: Bradycardia, vasodilatory adverse effect, verapamil causes constipation, diltiazem Age (over 75) 2
causes dizziness, atrioventricular block, palpitations, GI disorders, erythema, and fatigue. Diabetes mellitus 1
Stroke / ischaemic attack / TE 2
CI and cautions: congestive HF, severe hypotension, caution with pregnant women and Vascular disease (prior to MI, peripheral artery disease or aortic plaque 1
women of childbearing age. Age 65 - 74 1
Sex category (Female) 1 Remember cascade and which part of the
DIGOXIN: cascade the drug acts on.
*>2 = High risk.
 Blocks the Na+/K+ pump. Mechanisms are unknown.
 Reduces SAN firing rate. = decreasing HR, -ve chronotropy) ORAL ANTICOAGULANTS:
 Conduction velocity of electrical impulses through the AVN. Trials of New Oral Anticoagulants:
WARFARIN:
Loading dose: 250 mcg to 750 mcg for 7 days. Dabigatran Rivaroxaban Apixaban
 Coumarin derivative
Maintenance dose: 125mcg to 250 mcg od. Brand Pradaxa Xarelto Eliquis
 Mechanism: Inhibits the reactivation of Vit K in the liver and therefore inhibits the
Dose should be adjusted according to renal function, initial lading dose and HR response. Clinical RE-LY ROCKET- AF ARTISTOTLE
formation of clotting factors. Specifically, II, VII, IX and X; Protein C and S.
 Protein C and S are anti thrombotic factors  complications with warfarin can also Trial
S/E: cardiac adverse effects usually associated with overdose, n+v, visual abnormalities. Therapeutic Thrombin Factor Xa Factor Xa
cause a thrombus. – paradoxical effect.
CI and cautions: supraventricular arrhythmias, caution with renal impairment, Target
 Warfarin is only effective if Pt’s INR is between 2 and 3 = therapeutic window.
hypokalaemia, elderly people. Dosing 150mg or 110mg bd 20mg od 5mg bd
Above this, Pt can suffer from haemorrhage/ ischaemic stroke.
 S/E: Bleeding, fetal warfarin syndrome, n+v, pancreatitis, diarrhoea and rash T1/2 8-7 hours 5-9 hours 9-14 hours
Interactions: TCAs, diuretics, St John’s wort. May increase plasma conc. Amiodarone, CCB Renal 80% 33% 25%
 Advatages: Can reduce stroke risks by 64%.
and spironolactone. Medicines can cause K+ loss. Metabolism
 Disadvantages:
 Can interact with food and other drugs. Hepatic 20% 75% 67%
Monitoring: Routine monitoring of serum is not recommended. Metabolism
 Requires regular monitoring
Consider checking levels if signs of toxicity occur such as confusion, nausea, visual  Unpredictable pharmacology (can also cause thrombus formation) NOTES: 150mg Similar risk of stroke  Decreases risk of
disturbances and anorexia or if poor adherence is suspected.  Pharmacokinetics:  Risk of stroke down by  Decrease in risk of stroke by 21%
Take blood samples 6 hrs after previous dose but ideally 8-12 hrs afterwards.  Readily absorbed but 97% is protein bound = inactive. 34% intracranial  Reduced risk of
 Metabolised by CYP450  Decrease in risk of haemorrhage by major bleeding by
Check blood chemistry (electrolytes, urea and creatinine) annually or frequently in  NOT FOR USE IN PREGNANCY – can distribute to the breast and can also cross intracranial 33% 31%
elderly people or for those with renal impairment. the placenta. haemorrhage by 74%  Risk of GI bleeding  Reduced risk of
 Drug Interactions:  Risk of major bleeding intracranial
ABLATION:
Inhibitors of CYP (+ve effect) Inducers of CYP (-ve effect) 110mg haemorrhage by
If drug Tx is unsuitable/has failed to control Sx – ablation can be considered.
 Alcohol (acute)  Carbamazepine  risk of intracranial 49%
Ablation  destroy abnormal sources or electrical impulses that may be causing AF.
 Allopurinol  Rifampicin haemorrhage by 69%
 Amiodarone  Alcohol (chronic)  risk of major bleeding
Consider a pacemaker and atrioventricular node ablation for people with permanent AF
with Sx of left ventricular dysfunction caused by high ventricular rates.  Omeprazole  Phenytoin
Advantages: Unresolved Issues:
 Phenytoin  Barbiturates
Pharmacology: Potential Issues:
ANTICOAGULATION:  Statins  Oral Contraceptives
 Predictable  Long – term safety
Inefficient blood flow = pooling. This can result is formation of thrombus.  Tamoxifen
 High specificity  Agents haven’t been compared against each
Pt with AF  5x more likely to suffer from a stroke.  Erythromycin
 Rapid onset of action other
 Ciprofloxacin
 Fewer drug interactions  Lack of antidote to cure bleeding issues
Reduce risk by Cardioversion OR anticoagulants (warfarin or DOAC)  Metronidazole
Practicalities
Drugs w/ high protein – binding affinity can compete with warfarin and
 Fixed daily dose Monitoring:
CHA2DS2 – VASc  if score ≥2 then patient needs an anticoagulant. displace it
 No need for monitoring  Adherence?
HASBLED  ≥ 3 indicated ‘high risk’ NSAIDs, Diazepam, Amitriptyline, Phenytoin, Propanolol,
Patient:  How to detect accumulation or overdose?
Chlorpromazine, Chlordizepoxide, Tolbutamide
 Good efficacy/ tolerable  Monitoring may be good for Pt reassurance
What are the consequences of AF?
Cardiac output is decreased and therefore can result in HF.  Minimal/no food interactions
 PROTECTING PATIENT’S AT RISK OF THROMBOEMBOLISM:  Ask for more info if needed  Plasminogen activators (streptokinase/alteplase/retaplase)
Thrombo = clot; Embolism = blockage  Lifestyle advice *refer to cardioresp prac*  Glycoprotein IIb/IIa inhibitor (abciximab/tirofiban)
 Heparin – unfractionated /LMW
Diseases that arise from thrombus formation in BV include stroke, MI, and venous HASBLED – assessing risk of bleeding:
thromboembolism. Commonly used in the UK. Plasminogen Activators:
HASBLED Criteria Score Plasminogen  plasmin = degrade fibrin and therefore breaks up clot.
Components of a blood clot: Hypertension 1  Streptokinase and alteplase have been shown to reduce mortality regardless of age
 Fibrin – stabilises the clot and stops it falling apart; forms a mesh that traps RBC. (more Abnormal Renal/ Liver function 1  Reteplase and tenecteplase -licensed for acute myocardial infarction.
important in clots that form in veins (slow moving blood) – although it still plays a role in Stroke 1  Trials have shown that the benefit is greatest in those with ECG changes that include
arterial blood clots.) Bleeding 1 ST segment elevation (especially in those with anterior infarction) and in patients with
 Platelets – type of blood cells that clumps; adds to mass of the thrombus (more Labile INR 1 bundle branch block.
important component that form in arteries.) Elderly (>65) 1  Alteplase should be given within 6–12 hours of symptom onset,
Drugs or Alcohol 1  Reteplase and Streptokinase within 12 hours of symptom onset, but ideally all should
2 classes of Antithrombotic drugs: be given within 1 hour
 Anticoagulants – slow down blood clotting – reduces fibrin formation Modifiable risks:  Tenecteplase should be given as early as possible and usually within 6 hours of
(E.g. heparins, fondaparinux, warfarin, dabigatran, rivaroxaban, edoxaban and apixaban) HPT, INR, medications and alcohol intake symptom onset.
 Antiplatelet – prevent platelet aggregation prevent thrombus formation  Alteplase, streptokinase and urokinase can be used for other thromboembolic
(E.g aspirin, clopidogrel, prasugel, ticagrelor and dipyridamole) Potentially modifiable: disorders such as deep-vein thrombosis and pulmonary embolism. Alteplase is also
Blood platelets are inactive until damage to bv or blood coagulation causes then to Anaemia, renal function, liver function, platelet count/function used for acute ischaemic stroke.
explode into sticky irregular cells and aggregate.  Urokinase is also licensed to restore the patency of occluded intravenous catheters
Non-modifiable: and cannulas blocked with fibrin clots.
Ag, Hx, Genetics, Liver disease
Glycoprotein IIb/IIIa Inhibitors (clopidogrel, prasugel, ticagrelor):
Reducing bleeding risks:  Prevents platelet aggregation and thrombus formation bu inhibition of GP iib/IIz
 Control BP receptor on platelet surface.
Antithrombotic therapy is associated with bleeding…
 Review benefits and risks of using anticoags AND antiplatelets  Used in combination w/ aspirin and unfractionated heparin for prevention or early MI
 Applies to both anticoagulants and antiplatelet.
 The risk of bleeding is greater during the first 90 days of oral anticoag therapy. in Pt w/ unstable angina/NSTEMI.
 Taking a combination of both (e.g in ACS treatment) can further increase this risk.
 GI bleeding – dark or bright red blood in stool or black stools associated with SOB and  Review DHx – interactions? (SSRIs also predispose Pt to bleeding)
 Consider a PPI – bleeding commonly occurs in the GI Heparin:
dizziness.
 Heparin binds to the enzyme inhibitor antithrombin III (AT).This activated AT then
 Bleeding in the brain (intracerebral haemorrhage) – sudden onset of severe headache,
Pharmacist’s Role and antithrombotic treatment: inactivates thrombin, factor Xa and other proteases thus inhibiting
loss of vision, slurred speech, trouble swallowing, loss of balance, sudden weakness or
 Inform Pt about antiplatelet and anticoagulants = help select appropriate Tx.  Unfractionated Heparin -short half life - stop with immediate affect
face arm and leg possibly on one side.
 Review the risks and benefits of continuing therapy. Patients should be aware of  Low molecular Weight Heparins(Dalteparin/Enoxaparin/Tinzaparin)-Longer half life
 Bruising is also common.
Abcimab and Tirofiban = bleeding risks.  LMW forming a complex with antithrombin (AT) catalysing the inhibition of several
stops fibrinogen bridge  Support – check if they’re adhering to Tx. activated blood coagulation factors: thrombin (factor IIa), factor IXa, Xa, XIa and XIIa.
 Optimise therapy to prevent emboli and Counselling normally takes 30 mins – a lot When is, it used and what are the factors which governs choice?
forming – stops
bleeds. – NMS Service of info. Make sure Pt understands – let  Treatment of DVT/ unstable angina and NSTEMI – prophylaxis against
coagulation. venous thromboembolism
them ask Qs during follow up .
What can affect Pt adherence?  Unfractionated – poor bioavailability and short half-life therefore LMWH -
Review suitability and scores  plan for
Clopidogrel, Ticagrelor  Patient perception of meds (warfarin is preferred
monitoring.
and Prasugel – works on also used as rat poison)
P2Y12 and stops ADP   Complexity of regimen – establish routine LMW Heparin:
inhibits coagulation.  Lifestyle factors – dietary, alcohol and travel  LMWHs have high absorption, high bioavailability, and long half-lives enabling once-
 S/E and tolerability issues. or twice-daily dosing with predictable dose-response relationships
 Psychological problems  These factors enable the LMWHs to be used without laboratory monitoring and at
 Cognitive impairment home for acute DVT management
 Studies continue to show that LMWH preparations effective as Unfractionated form
Promoting adherence:  VTE disease prophylaxis, management of acute VTE disease, unstable angina, and
 Within 7 days from initiation – Pt should be referred to qualified professional. NSTEMI
 1-10 days = primary care  Heparin-induced thrombocytopenia is less of a problem with LMWHs.
Where are antithrombotic initiated?  2-4 weeks = follow up Pt – they might have stopped taking it.  Use of LMWHs has resulted in cost benefits in the treatment of acute DVT/Unstable
 A&E for Pt with newly Dx PE/DVT  Follow up 3 months’ after Angina and NSTEMI as well as in prophylaxis against venous thromboembolism
 Cardiac/stroke wards/hospitals – Pt with new metallic heart valve with Pt Dx w/ AF or  Always check adherence when dispensing. NMS service utilise (improves adherence by
stroke or VTE.  you can get slow blood flow around metallic valve. They will be 10%) Measure Pt’s platelet count before Tx w/ LMWH or Heparin.
referred and followed up in an anticoagulation clinic.  Management: clinic appointments, MUR, blood tests – check scores and INR
 Pt Dx w/ AF – often have GP referral unless GP is trained to initiate anticoagulation HEPARIN-INDUCED THROMBOCYTOPENIA (HIT):
 Pt requiring primary/secondary prevention of IHD. Management during hospital admission:  Low platelet count (thrombocytopenia) due to heparin administration.
 Always check indication for warfarin – medicines reconciliation  HIT is caused by formation of abnormal antibodies against platelets.
Initiating Oral Anticoagulation:  Recalculate CHA2DS2-VASc and HASBLED scores  Doesn’t happen to a huge no. of Pt.
Explain to Pt:  Support Jr Doctors as they may be unsure.  Less of a problem in LMWH
 What an anticoagulant is and how it works  On discharge document and communicate dose and strength – refer to Pt’s usual clinic Give Argatroban instead.
 Go through warfarin/DOAC counselling checklist – *refer to CardioResp Practical book*  Document and communicate any changes to medication
 Give resources such as yellow book, leaflets and decision aids  Provide info leaflets to family/careers as well as Pt.
 Some Pt have more choices than other. For example, AF patients can take warfarin or * Familiarise with anticoagulation therapy – interactions and routine monitoring* ISCHAEMIA:
DOACs but Pt with metallic valve can only take warfarin. IV THROMBOLYTICS:
 Act on symptoms on bleeding Types of thrombolytic drugs used for MI: What is ischaemia?
Supply and demand imbalance. May be as a result of coronary artery occlusion, open heart  Bi- directional – can work in reverse mode REPURFUSION – Restoring blood flow:
surgery, cardiac transplantation, angina?  Na+ : Ca2+  23Na NMR shows no further increase in [Na]i
Forward mode – 3 in :1 out  Sodium channel – back to normal conductivity
To understand ischaemia, we need to understand the ionic homeostasis in myocardial cells. Reverse mode – 1 out : one in  Na+/K+ pump – rapidly become reactivated
 Electrogenic – activated by membrane potential during an AP  NHE – reperfusion removes extracellular acidosis.
In a cardiac myocyte, an ATPase pump moves 3Na+ ions out of the cell and 2K+ in.  Transports Ca2+ in during depolarisation and out during repolarisation Issue occurs  proton accumulation lead to proton leakage to extracellular space
Ischaemia leads to a drop in ATP levels and therefore the ionic haemostasis is affected.  Phosphorylated by PKA and PKC  reperfusion washes acidity in extracellular space  extracellular = normal but
intracellular = acidic  this leads to a large proton gradient  NHE works and
[K+]e accumulation in ischaemia Ca2+ Channels: therefore Na can accumulate inside the cell
 This is due to the fact that Na+ is not effluxed as a result of low ATPase activity.  Alpha 1 unit – pore forming S1 – S6 This is corrected by NCX working in reverse mode.
 30 mins of global ischaemia (interrupting entire blood flow to the heart) can induce  Auxiliary subunits = Beta, alpha2delta, gamma = open for modification by other  KB-R7943 is an inhibitor of the NCX channel BUT ONLY IN REVERSE MODE 
a 15-20mM increase in [K+]. molecules. affecting calcium influx. This is because calcium accumulation can be damaging to
 Using the Nernst Equation for K+ approximates the resting membrane potential  S5 and S6 are selective = only calcium can enter the cell cardiac myocytes.
which is around -85mV. BASAL  S1, S2, S3 and S4 = voltage sensors
 There are 7 isoforms CALCIUM ACCUMULATION:
Na+/K+ ATPase pump CaV 1.1 – 1.4  Can activate proteases that are calcium sensitive  break down of proteins in
 ATP dependent. CaV 2.1 – 2.3 cardiac cell.
 Main Na+ efflux pathway in cardiac cells. Increase in [Na+]i as a result of the  CaV 1.2 alpha 1c – found in  Depending on cytosol conc, there can be Ca2+ accumulation in mitochondria 
ATPase pump drives NCX to pump Ca+ in  contractility. ventricular myocytes. can activate mitochondrial permeability transition pore (MPTP)  collapse
 Has 3 alpha and 2 beta subunits. Sodium has different affinities for these subunits.  L-type Ca2+ channels have membrane potential and interfere with ATP synthesis
 The pump is regulated by PHOSPHOLEMMAN (PLM) which acts as an inhibitor. two forms depending on  Increase in Ca can also cause Ca2+ accumulation inside mitochondria – can
 If PLM becomes phosphorylated = inhibited. (The inhibitor becomes inhibited) activity – the largest is 240 combine with phosphates = calcium phosphate – insoluble  forms crystals 
 Inhibition of PLM speeds up the activity of the pump and therefore speeds up the kDA big. interfere with ATP synthesis
contractility. (NCX activity)  If a part is cleaved (loop in  CELL DEATH and IRREVERSIBLE INJURY
intracellular space) the channel is 190kDa in size.
Na+ Channels  Ca2+ channels are activated by depolarisation – open during Phase 0
 Alpha subunit forms a pore where sodium ions can enter.  Also has a ‘window’ current which is around -25mv to ~0mV
 Na+ channels have 4 domains each consisting of 6 transmembrane domains.
 Sodium channels have different isoforms found in different areas of the body: INTRACELLULAR SODIUM – BASAL CONDITIONS:
 Nav 1.1 – 1.3, 1.6 and 1.7 =
Neuronal There are multiple methods used to measure [Na]i:
 Nav 1.4 = skeletal 1. Radioactive 24Na – unsafe – not widely used
 Nav 1.5 = cardiac  encoded 2. Sodium selective microelectrodes – stab cells with 2 pieces of glass – difficult to do
by SCN 5 gene. 3. 23Na NMR – commonly used
 Studies have shown 1.1 and
1.3 is also found in cardiac Fluorescent dyes can also be used:
cells but 1.5 is predominant.  SBFI
 There are intra and extracellular  CoroNa Green – track Na in CYTOPLASM
loops which contain AA that can be  CoroNa Red – track Na in mitochondria
phosphorylated by protein kinases (A + C). This increases the conductance of
sodium through the cell meaning faster re-uptake. NAdr – can do this. Sodium influx occurs via many routes:
 TETRODOTOXIN (TTX): found in pufferfish – toxin which inhibit Na+ channels.  Sodium channels
TTX has a higher affinity for Na+ channels in the brain than in cardiac cells. Important in disease and are
 3Na+/Ca+ exchanger (NCX)
However, this toxin can still be fatal. studied commonly.
 Na+/H+ exchanges (NHE)
 Mutations in Na+ channels can cause a long QT syndrome – this can be dangerous  Na+/HCO3- symport
as it leads to arrhythmias and is characterised by sudden fainting. (QRS wave =  Na+/K+/Cl- co transporter
Ventricles contracting; T wave = ventricles relaxing)  2NA+/Mg2+ exchange
 Gates: Sodium channels have gates and are open depending on voltage. LIPOPROTEINS AND HEART DISEASE
30mins of ischaemia can increase [K+]e to ~25mM  using the Nernst equation Mitochondria:
the membrane potential increase from -85mV to ~-50mV  depolarisation.  NHE is more active here than in the cell. Physiology of Lipid metabolism:
SODIUM ‘WINDOW’ CURRENT = -60mV to -10MV = channels are open and are able  E- Transport chain (requires O2) – protons are effluxed therefore the mitochondrial 1. Fats from diet arrive in the small intestine as lipid droplets
to conduct sodium in the cell. matrix is more alkaline than the cytosol. 2. Lipid droplets are digested into micelles and absorbed into intestinal cells and
 Sodium conc. Is slightly lower compared to cytosol ~6nM. monoglycerides and fatty acids. Cholesterol is also absorbed
Na+/H+ exchanger (NHE1/SLC9A1) 3. Intestinal cells package fatty acids, monoglycerides, cholesterol and apoproteins
 Not energy dependent – stimulated by acidic pH. into cholymicrons. Chylomicrons consists of little proteins but is predominantly
 Inactive at physiological pH – quiescent. IN ISCHAEMIA: made up of lipids.
 Exchanges one H+ for one Na+  23Na NMR shows that [Na+]i can increase 3 -4 fold. Due to to increase in Na+ influx 4. Cholymicrons move to lympathic system before moving to bv. Go to liver but can
 9 isoforms and decrease in Na+ efflux. go to adipose tissues.
 involved in cell volume and cytoskeletal organisation.  Na+/K+ - decrease in ATP inhibits pump  accumulation of K+ outside the cell. 5. These deliver lipids and triglyceride to tissues and the remains go to the liver.
 In ischaemia, there is a lack of ATP due to incomplete glucose breakdown, shut  Na+ channel – Sodium window current due to accumulation of K+ in extracellular
down of e- transport chain.  proteins are not shuttled and ATP is not made. space. Membrane potential increases and sodium leaks inside the cells via sodium There are two types of lipoproteins:
 Protons accumulate = cells become acidic. channels. Triglyceride rich lipoproteins  VLDL – transport of fatty acids to body tissues.
Na+/Ca+ exchanger (NCX)  NHE – contributes to sodium accumulation within the cell. Cholesterol rich lipoproteins  LDL and HDL (pick up excess cholesterol and brings it to
 Important in controlling calcium. liver
 Sodium accumulation affects calcium balance inside the cell.
 The cardiac isoform is NCX1. Consists of 970 AA and 110 kDa. HDL: LDL:
 NCX works in reverse mode – Na+ efflux and Ca2+ influx.
 Has 9 transmembrane domains – responsible for ion exchange and transpo  HDL  protective effect for CHD  LDL – strongly assoiated w/
artherosclerosis and CHD –
  Lower HDL = high CHD risk  Tube passed through nasal cavity
 HDL is lowered by smoking, obesity and physical inactivity Pathophysiology:  pH measures 5cm above LOS
  Imbalance between defensive factors and aggressive factors:  Monitors every 4-6 seconds
Clinical Presentation:
Hx: On Examination: Oesophageal manometry – pressures monitored within oesophagus
 Diabetes  Xanthoma (fatty growths Barium swallow – determines cause of dysphagia, barium sulfate – shows up on X-Rays.
 Smoking – major risk factor under skin)
 FHx of IHD  BMI increase Surgery: If PPIs are not tolerated/ineffective.
 Previous CVD  High BP Laparoscopic Nissen fundoplication: common procedure
Upper portion of stomach wrapped around distal oesophagus, common S/E; dysphagia,
Classification: belching, bloating, flatulence.
Hyperlipidaemia can be inherited.
Treatment: PEPTIC ULCER DISEASE is also diagnosed via endoscopy (ulcers in stomach or duodenum)
Lifestyle changes:  Epigastric pain (pain below ribs, upper abdomen)
Check Pt:
 Alter eating habits: eat small meals, remain upright after meals, avoid bedtime usually postprandial (after dinner/lunch)
 Diabetes control,
snacks  Associated with Nausea, heartburn.
 Case of hypothyroidism?
Secondary causes  Change diet: avoid fatty foods, limit intake of chocolate, peppermint and alcohol.  Sx relieved with antacids
 Renal disease
Reduce citrus fruits and tomato-based products.
 Liver disease?  Pain may be relieved by food.
 Reduce weight
 Alcohol consumption?  Aetiology is same as GORD PLUS the presence of
 Wear lose fitting clothing H.pylori.
Tx:
 Smoking cessation
 Weight loss
 Change posture during sleep – elevate head and sleep on left side Helicobacter pylori:
 Lifestyle modifications; diet, increase exercise
 Gram –ve, associated w/ dyspepsia and GORD.
Antacids:  Common cause of ulcers.
Medication: Statins, Ezetimbe and Fibrate
 Sodium bicarb, calcium bicarb, magnesium/aluminium salts  Increases risk of GI cancers.
MOA:
 These act as a buffer for stomach acids.  80% of people w/ H. pylori are asymptomatic.
Statin: Inhibit HMG CoA reductase involved in making cholesterol
Can significantly decrease LDL levels by 24-50%, increases HDL by 6-12%  NOTE: Mg has laxative effect and aluminium can cause constipation.  Test: Urea breath test – swallow radioactive urea  detect CO2 exhaled
 Antacids with Al+Mg  reduce undesirable constipation or diarrhoea. Stool antigen test
Ezetimbe: Blocks cholesterol absorption Can decrease  Invasive test: rapid urease test; sample from mucosa and apply to slide w/ urea –
Alginate raft
Decreases LDL levels by 18% and increases HDL levels by 1% TG levels. Alginates: colour change if bac is present.
 Sodium alginate
Fibrate: increases lipolysis and elimation of TG rish particles by activing lipoprotein  Act by increasing viscosity of stomach contents Tx: PPI plus 2 a/biotics for ONE WEEK
lipase and reducing apoprotein C-3 activity which forms a protective raft

PCSK9i: PCSK9 regulates LDL receptors in response to cholesterol levels H2 receptor antagonist: SUMMARY:
Binds to receptors and allows LDL to enter cells.  Competitive antagonist of histamine at H2
 Alirocumab receptors in parietal cells.w
 Evolocumab
WHEN TO REFER:
Range: When Sx is severe or resitant to OTC Tx.
LDL levels – less than 100mg/dL or 0.7mmol/L to 1.4 mmol/L Tx example:
Possibility of cancer:  Lanzo 30mg every 12 hrs
 Aged 55 and over with NEW onset dyspepsia  Clarithromycin 500mg every 12hrs
 Dysphagia – difficulty in swallowing  Amo 1g every 8hrs.
 Jaundice
 Haematemisis – blood in vomit; malaena – black stool due to digested blood HEART FAILURE NOTES (FREESTONE)
DYSPEPSIA AND GASTRO-OESOPHAGEAL REFLUX DISEASE (GORD) Further Investigations:
Endoscopy:
DYSPEPSIA – collection of Sx, not a diagnosis in itself.  If Pt’s Sx is severe or suggestive of cancer – refer to endoscopy.
20-40% of the UK have dyspepsia; 68m Rx in UK per year.  GP advice: Four weeks of full dose H2 antagonist or four weeks of PPI Tx.
 Upper abdominal pain, discomfort  If Sx do not improve – send to endoscopy
Most people will experience these Sx  STOP drug Tx two weeks before endoscopy.
 Heartburn occasionally but not have the disease.
 N+V
 Gastric reflux LA classification of reflux oesophagitis:
Criteria – more than one episode/week Grade Description
If symptoms of gastro-oesophageal are severe/frequent and have significant impacts  A One or more mucosal lesions; max size 5mm.
reflux disease. B One or more mucosal breaks, max length >5mm but not continuous across
mucosal folds.
GORD – diagnosed on endoscopy/pH studies showing inflammation in oesophagus C Mucosal breaks between more than two mucosal folds but less than 75% of
circumference is involved.
Risk factors: D Mucosal breaks more than 75% of oesophageal circumference.
Genetic Demographic Behaviour
GI disease/Sx in immediate Pregnancy Smoking PPIs: Only 60-70% of patients take PPIs correctly
relative Age Alcohol There is poor compliance e.g. not taking it on an empty stomach.
BMI Drugs: anticholinergic, NSAIDs,
Aspirin, Oral steroids and nitrates Oesophageal pH monitoring:
 HYPERTENSION

Blood pressure: measurement of the force against the walls of the arteries as the heart
pump blood around the body; arterial BP.
Cardiac Output x Total Peripheral Resistance = BP
Measurement:
Indirect: sphygmomanometer and auscultating (listening)
with a stethoscope. The sounds are called Korotkoff sounds.

Directly: using an arterial cannula (only used in Critical Care

Areas and Operating Theatres)

BP Readings: Normal 120/80mmHg || High BP 140/90 mmHg

Systolic: ventricles are fully contracted;
blood pumped out; max pressure exerted in arteries during systole.
Diastolic: relaxation of ventricles; heart filling up; min pressure in arteries during diastole.

Pathophysiology:
 Investigation: CXR, ECG – sinus tachycardia, D-dimers (normal <0.3mg/l), troponin levels 67

Sx:
 Chest pain – worse when inhaling.
 Sudden SOB
 Tachycardia
 Coughing up blood
 Light-headedness
 Anxiety

Treatment and Prevention:

RESPIRATORY CONTENT
Types of HPT: Thrombolytic: streptokinase, reteplase, alteplase
Primary – no secondary cause. BP
is over 140/90 mmHg Blood thinner: taken for at least 3 months; Warfarin or DOAC.
Anticoagulation for low risk – LMWH and vitK antagonist = warfarin.
Secondary – due to another Warfarin: INR monitoring
medical condition; kidney DOAC: less monitoring. E.g apixaban, dabigatran, edoxaban and rivaroxaban. For Pt with
disease, diabetes, chronic drug poor renal function/hepatic function. Found to be less effective
usage.
Malignant Hypertension – leads to rapid organ damage if not treated properly. Usually as a Tx = attached
result of HF.

Isolated systolic HPT - systolic BP over 160mmHg and diastolic is less than 90mmHg.
Occurs in the elderly. Related to stiffening of arteries and loss of elasticity.

White coat HPT – when tested by HPC

Resistant HPT – cannot be reduced below 140/90 mmHg despite Tx.

Dx: Clinic BP is >140/90mmHg, offer ambulatory BP monitoring (BP monitored as you’re

going around).
Supine/seating BP reading in Pt who may have postural hypotension.
Measure BP on both arms if diff is >15mmHg repeat and if it still greater than 15mmHg =
use arm with higher reading.

Investigation: Test for proteinuria and haematuria, ECG, if no target organ damage –
measure BP in 7 days. Estimate CVD risk. QRisk

Look at BP Tx notes

Alpha blockers:

PE/DVT SGUL Chronic Obstructive Pulmonary Disease (COPD):

Virchow’s Triad: (Also known as chronic bronchitis or emphysema or both)
Must be balanced otherwise – individual may be predisposed to  Common chronic condition involving airflow obstruction that isn’t fully reversible.
venous thromboembolism.  Airway and parenchymal damage resulting from chronic inflammation.
 Progressive  develops overtime  more coughs, recurrent infections
Pulmonary embolism: a complication of deep vein thrombosis
(DVT). Blood clot from legs travel to lungs. Life threatening. Pathophysiology:
Follow Tx plan to stop enlargement of thrombus. Inflammatory response to inhaled irritants
Chemotactic factors – activation of immune cells by irritants
Endothelial injury: Oxidative stress – due to free radicals in tobacco smoke
Vascular damage; pelvic, hip, leg injury or surgery. Proteases break down lung tissue
Hypercoagulability: factors that affect blood clotting Remodelling of airways – loss of elastic recoil
Stasis of blood flow: Immobile? Long haul flight? Pregnancy, cardiac failure..
Clinical features:
Risk factors:
Wells Score: Well’s score for DVT = probability of DVT >3 score = high risk. Sx:
 Age
1-2 moderate risk; <1 = low risk  Exertional breathlessness
 Smoking – 10% to 20%
 Chronic cough
of smokers get COPD
Well’s Score for PE = >6 high risk of PE; 2-6 moderate; <2 = low risk
 Sputum productions – cannot be cleared due Spirometry confirmed Dx  assessment of airflow limitation w/ FEV exacerbation Hx (>2 *spacers can also reduce risk of oral thrush caused by steroids
to ciliary dysfunction – leading to hyper or >1 that lead to hospital admissions Ax of Sx and risk of exacerbations.  CAT and
expanded lungs. mMRC: Oral therapies:
 Wheeze mMRC and CAT – tells us about the Sx.  Carbocisteine / Acetylcisteine – mucolytics; consider in Pt w/ chronic productive cough
 Winter bronchitis mMRC 0-1 and CAT of <10 = less Sx  Azithromycin (associated w/ resistence) /Erythromycin– antibiotic – COPD Pt with
 No clinical features of asthma recurrent infections – not for Pt with heart issues as it can cause arrhythmias.
mMRC >2 and CAT of >10 = more Sx  Theophyline – Phasing out but still used – not recommended unless Tx was not
On examination: Sx is separate from risk = Pt can have high risk but less Sx. effective / bronchodilators not affordable. Caution: elderly, co-morbidities, interactions
Pt presents with ‘barrel chest’ – hyper inflated –  Prednisolone – steroid; for COPD 30mg – Pt shouldn’t be on this long term.
short shallow breaths High risk  GOLD 3/4 and exacerbation Hx of >2. Take in the morning as if taken at night, it can disrupt sleep.
Low oxygen sats (88-92% for COPD Pt), low BMI,
poor air movement when you listen to chest. Oxygen and non-invasive ventilation:
 Not everyone with COPD needs O2. Inappropriate use = resp depression
In comparison to asthma, Sx of COPD are GROUP A:  Carry out risk assessment – oxygen tank is flammable. – make sure patient and
experienced throughout the day and are not Give a bronchodilator, based on breathlessness severity. This can be short acting or long relatives DO NOT SMOKE.
reversible with SABA (short acting acting. Continue if Pt benefits. If not, try another class of bronchodilator.  If pO2 is 7.3% or less = qualified for home oxygen.
bronchodilators).  differentiation of the two  Studies show that oxygen does not help breathlessness.
conditions. GROUP B:  O2 is used for 15/16 hours a day.
Initial – bronchodilator. LABAs / LAMAS are better than SABAs. (taken prn?). If Pt has  Non–invasive  for Pt with elevated pCO2
Investigations: severe breathlessness – two bronchodilators as initial therapy can be considered.
Spirometry / Lung function test Other Tests: LABA or LAMA  persistent Sx LAMA + LABA COPD COMPLICATIONS:
Measure lung volume and capacities  Haemoglobin - Alpha 1 antitriptan and How to recognise COPD exacerbations:
 FEV1 Forced expiratory volume in one second inflammatory markers Pt in this group are likely to have co-morbidities so investigate these.  Worsening of symptoms – sustained – does not recover
 FVC – Force vital capacity  ECG – chronic lung disease  right heart  Increased sputum and/or change in sputum colour
Ratio of two – gives an idea of obstructive airways failure (cor pulmonale) GROUP C:  Coughing and breathlessness
disease  Phlegm – Pseudomonas, (blood – may be Long acting bronchodilators as initial therapy. LAMA was found to be better in prevention Management:
 Ratio 70% or 0.7 cancer) of exacerbation therefore LAMA is recommended. Investigate: Chest X-Ray, ECG, full blood count, arterial blood gas
Less than – Obstructive - COPD  Arterial blood gas – PCO2 within blood Tx:
Above – Restrictive eg interstitial lung disease LAMA  LAMA + LABA (preferred) OR LAMA  LABA +ICS  Inhaled therapy, systemic corticosteroids and/or antibiotics
(in COPD – CO2 will decline – emergency)
– may not be good to give O2.  Oxygen / non-invasive ventilation? – maintain ssats aimed for Pt
Chest Imaging – X-Rays and CT scan GROUP D:
 Resp physiotherapy – help w/ breathing
X-Ray: Lungs look thinner and taller – hyper Can start w/ LAMA.
 Morphine (don’t give to young patients due to opoid dependency) – e.g 2.5mg or
extended lung – diaphragm is also flattened. If Pt has severe Sx (>20 CAT) = LAMA +
oramorph can work well.
LABA
 Tx of Cor Pulmole – dilated right ventricle and atrium
Assess severity: Diuretics
 Spirometry, breathless (MRC scale) LABA/ICS may be used = greatest
Give digoxin if sPt has AF
 Exercise capacity (6 min walk test) likelihood of preventing exacerbations.
ACEi, CCB, BBlockers are NOT recommended.
 BMA
 PaO2 / PaCO2 LAMA + LABA + ICS if Sx persist.
Management of exacerbations:
 Cor pulmonale – enlargement of right side of the heart, secondary to COPD If Pt’s health is deteriorating and Sx are worsening/ severe  hospital management is
GOLD needed.
Stage Post bronchodilator FEV1 / FVC Key points:
FEV1 (%pred*) Exacerbation:
Stage 1 - Mild >80 <0.7 Mild – treat with short acting bronchodilators only
Stage 2 - Moderate 50-79 <0.7 Moderate – SABA + a/biotics or oral corticosteroids
Stage 3 -Severe 30-49 <0.7 Severe – Pt requires hospitalisation – emergency – manage breathlessness and anxiety
Stage 4 - Very Severe <30 <0.7 Initial management:
Management:
*%prediction based on height, weight etc  Supplemental O2
Tx:
Aims of Tx:  Increase dose/frequency of bronchodilator – consider giving via nebuliser; specify
 Smoking cessation – v. helpful
Assessment(Ax) of Sx effect on daily life should also be carried out.  Sx relief – improve driving gas and prescribe compressed air it pt is hypercapnic (too much CO2)
 Inhaled therapies and/or Oral therapies
mMRC dyspnoea scale: health  Offer predisolone 30mg OD for 5-7 days
 Oxygen or non-invasive ventilation (for those
Grade Description  Prevent complications  Oral a/biotics for signs of pneumonia / bac infection.
with Pt who cannot process CO2)
0 Not troubled except on strenuous exercise  Slow down the  Penicillin, doxycycline macrolide and/or follow local guide – review when culture
 Other Tx:
1 SOB when hurrying or walking slightly uphill progression results are available
Pulmonary rehab (6 weeks – exercises),
2 Slower walk compared to others due to dyspnoea (No cure to COPD)  NIV: for hypercapnic and Pt not responding to medical Tx.
vaccination (influenza and pneumococcal),
3 Stops for breath after about 100m or after a few mins on the level lung surgery
4 Too breathless to leave house / SOB when dressing/ undressing  Management of complications ASTHMA:
Most common respiratory disease
CAT (COPD Assessment Inhaled therapies: Chronic inflammatory disease of bronchial airways characterised by:
Test): Wheezing, chest tightness, dyspnoea and cough
Breathlessness and exercise Ventolin (Salbutamol) or Atrovent (Ipatropium)
Questionnaire that helps limitation (1st line)
measure the impact Pathophysiology:
Exacerbation or persistent LABA – E.G Serevent
COPD has on Pt’s  Intermittent airway obstruction caused by:
breathlessness Seretide (LABA and ICS) – being phased out due to price and
wellbeing and daily life. Chronic inflammation
high steroid content
Hyper-responsiveness of airways
Persistent exacerbations or LABA/LAMA/ICS
Combined Ax: Increased mucus production due to inflammatory response
breathlessness
  Inadequate control  Fixed airway remodels  underlying lung damage 3. If uncontrolled – add in LABA as combination inhaler
SLEEP – A CLINICAL PERSPECTIVE
Aetiology: 4. Stop LABA - Increase ICS dose to medium A physiological must.
 Genetics – ask FHx Sleep deprivation – increased risk of Alzheimer’s and cancer
 Immunology – allergy – ask if Pt has eczema or hayfever? IgE mediated 5. Try leukotriene receptor antagonist or LAMA / or theophylline Sleep reduces HR and BP – sleep deprivation can lead to vascular diseases.
inflammation)
Ask Pt if there are any triggers? 6. Higher dose of ICS Stages of sleep:
 Environment – increased exposure to allergen/ pollution? Stage EEG NOTES
7. Add oral steroids with Tx NON REM Stage 1 Theta waves Light sleep
Diagnosis NON REM Stage 2 Sleep spindles and K-complexes Deeper sleep
Sx are diurnal – day to day peak flow variability. Reversible w/ bronchodilators Asthma Action Plan:
NON REM Stage 3 Delta Deep sleep – parasomnias
Sx are variable and is usually worse at night Written by doctor/ asthma nurse – personalised to Pt’s needs.
REM Beta Dreams – Loss of muscle tone
Educated the patient on self-management.  improve health outcomes
What are the Sx?:
Obstructive Sleep Apnoea:
 Cough, wheezing, dyspnoea, chest tightness, sputum production, reduction in Review – assessment of control:
Cessation or reduction of airflow during sleep which prevents airway flow into and out of
exercise tolerance. Have you had any Sx that disturbed your sleep?
lungs.
 Usually associated w/ triggers (eg. pollen, cold air, dust) How many times have you used your blue inhaler?
Prevalence increases with age. Usually more common in men.
Has your Sx limited your ability to perform normal daily activities?
Definitions:
On examination, patient might seem normal. Apnoea – cessation of breathing for at least 10 seconds + decrease in O2 sats by 4% or
 Listen out for: wheezing. – may be high or low pitch. Review peak flow diaries, inhaler techniques and check spirometry.
over.
 Look out for: chest deformity – is it hyperinflated? Hypopnea – more than 50% reduction in tidal volume for at least 10 seconds and decrease
 Silent chest – life threatening If asthma is not controlled – go up a step in the Tx approach above^.
in O2 sats.
If stable – aim to reduce ICS to min dose that maintains control.
Investigations: Ax of Sleepiness:
ACUTE asthma management:
Epwroth Scale:
PEAK FLOW: Moderate: 50-75% PEF pred
How likely to dose off in the situations listed in the scale? 0-3 (3 – high chance)
Peak flow recording. In asthma, >3 days per week or above 20% variability. No features of severe asthma but increased Sx.
Severe: PEF 33-50% pred
PEF (max) – PEF (min) x 100 Risk factors:
Variability: RR>25
PEF average  Male gender
HR >100 – tachycardiac
 Elevated BMI – collar size greater than 43cm
Inability to complete sentences
 Smoker
SPIROMETRY:  Alcohol
FEV1/FVC = may be normal but if its less than 0.7, this suggest an obstructive airway Life threatening:
Unable to do PEF but if they do its less than 33%  Sedatives or strong analgesics
condition
Also, look at reversibility – does it get better with a bronchodilator? Hypoxic – sat is less than 92% and paO2 is less than 8kPa
Cyanosis – blueish extremities due to low oxygen levels Normal individuals: -ve pharyngeal pressure on inspiration  increased contractility of
Asthma = more than 12% improvement and more than 200ml improvement in FEV1
Silent chest muscles in this are counteracts problem. However, in people with sleep apnoea  -ve
More than 400ml is suggestive of asthma
Confusion pressure leads to airway collapse.
Management:
BRONCHIAL HYPER-RESPONSIVENESS:  Record PEF
Often obvious from patient’s Hx.  Maintain O2 sats to 92%
Require formal measurements.  ABG – if CO2 is normal or high  Pt is close to arrest – EMERGENCY.
Other investigations;  B2 agonist – given in nebules.
 Blood test – inflammatory markers (eosinophils, lymphocytes and mast cells)  Corticosteroids (PO pred 40mg or iv hydrocort 200mg)
 Hallmark of asthma is eosinophilia (high eosinophil count during an asthma attack)  Magnesium sulphate if unresponsive to above Tx
 Can examine sputum but not a routine form of investigation.  IV aminophylline – poor response to everything else.
RESPIRATORY TRACT INFECTIONS:
Investigation of allergy: ICU referral:
Skin prick testing – small amount of allergy inoculated under the skin  causes a local  Hypercapnia
 Resp infections = common GP presentations.
inflammatory response. Wheal and flare  Low pH
 6th leading cause of death in UK and USA; 5-10% of Pt w/ pneumonia require ITU
 Worsening hypoxia
admissions
MANAGEMENT:  Exhaustion
CHRONIC asthma management:  Drowsiness Upper Respiratory Tract Infections
Minimise Sx and avoid future instances of exacerbations.  Low PEF despite Tx  E.g common cold, tonsillitis, laryngitis, sinusitis
No limit to physical activity and minimal steroid use.
 70% are viral
Discharge when:
 Tx is to manage Sx
Non – pharmacological:  Bronchodilator dosage is reduced
 Bac infections settle within days
 Avoid triggers  After 24 hrs – nebuliser therapy has been stopped and happy to use inhaler – does
 A/biotics should only be given if:
 Smoking cessation Pt have good technique?
Severe, persistent or if Pt is immunosuppressed
 Breathing technique training  If PEF is above 75% pred
 And diurnal variability of PEF is less than 25% Centor Criteria:
Pharmacological:
Gives indication of the likelihood of a sore throat being due to bac infections.
1. Pt should be on a SABA – used as reliever salbutamol /terbutalline Review PT after discharge and tell them to see GP within 2 days.] A score of >3 = consider a/biotics
What’s the reason for the exacerbations?
2. If asthma is not control  add in a low dose steroid (ICS) Check inhaler technique and how they self -manage? What’s the criteria?
 Tonsillar exudate – white spots on throat
  Tender anterior cervical lymphadenopathy – swollen lymph nodes Aspiration Pneumonia:  Bacteria: Staphylococcus aureus, pseudomonas aeruginosa and Burkholderia
 Fever over 38 degrees Celsius Results from inhalation of oropharyngeal contents into lower airways causing lung injury cepacia.
 Absence of cough and therefore resulting in bacterial infection. (bac may be aerobic or anaerobic – may come  Chloride and sodium levels are constantly elevated in CF.
from normal oral flora) Most common mutation in CF is at position 508  phenylalanine is deleted resulting in an
Pneumonia incorrect fold.
Lower resp tract infection – usually caused by bacteria. Common in Pt w/ altered mental status  impaired gag reflex or swallow reflux
CF Classes and defects
British Thoracic Society definition of pneumonia: St. George’s Guideline Class of
Mutation Defect Effect of mutation
Community acquired pneumonia: 1st Line If severe Alternative if allergic mutation
Outside hospital or healthcare facilities. HAP Doxycyline PO Benzylpenicillin IV Levofloxacin IV/PO 1 Lack of CFTR synthesis No CFTR chloride channels
 Cough w/ SOB/ chest pain, purulent sputum + Gentamicin IV CFTR destroyed – does not reach cell
2 Defective protein synthesis
 One systemic Sx – fever, sweats, shiver or pain Aspiration Doxycyline PO + Benzylpenicillin IV Levofloxacin IV + surface
 New focal chest signs on examination Pneumonia Metronidazaole PO + Metronidazole IV Metronidazaole IV CFTR reaches cells surface but channel
3 Defective channel regulation
In Hospital: is open properly
 Sx and signs consistent w/ acute lower resp infection Exacerbations of Lung Disease: CFTR function is poor and conduction
4 Defective chloride conduction
 CXR shadows w/o explanations Pt with lung disease such as cystic fibrosis and COPD are susceptible to infections. of CL is defective
Organisms 5 Reduced CFTR protein Decreased CFTR production
CAP (community acquired pneumonia) severity assessment:  Pseudomonal aeruginosa Increased turnover of CFTR at CFTR is unstable but functional –
6
 Non- tuberculous mycobacteria cell surface removed and destroyed
CURB 65  Murkholderia cepia
C Confusion  Aspergillus Tx:
U Urea >7mmol/L 1 point for A/biotic treatment – follow local guidelines, take into account Pt previous cultures Ivacaftor (Kalydeco) – CFTR potentiator:
R Resp Rate >30 breaths/min each criterion  Makes the CFTR channel open for longer
B Blood pressure <90mmHg systolic or <60mmHg diastolic Complications of Pneumonia:  Binds to defective protein at cell surface and opens the Cl channel – allows Cl to
65 Age is >65  Para pneumonic effusion – accumulation of fluid flow through therefore regulating water content on cell surface.
 Empyema – pus in pleural cavity  Decrease t1/2 of channels.
Why do we assess the severity?  Lung abscess
0-1: low risk; 30-day mortality less than 3%  Acute resp distress syndrome Lumacaftor – CFTR corrector:
2: moderate risk – requires hosp admission 30-day mortality 9%  Sepsis  Corrects deltaF508 protein
3-5: high risk; ICU admission; 30-day mortality 15-40%  Resp Failure  Helps CFTR channel form the correct shape –

Tx: KEY POINTS: Potentiator is commonly used in combination with corrector

 Supportive care: Not everyone w/ resp tract infection requires antibiotics howvere it may be fatal to not
o Fluids give a/biotics to some.  important to check severity New Tx:
o Oxygen Triple therapy with tezacafor, ivacaftor and a new compound  nebulised liposome gene
o Chest physio When choosing a/biotics consider: therapy  expensive – not in NHS scheme
o If Pt is really unwell – require resp support  Pt specific factors
 Antibiotics – but which one though? Lol  Likely organisms Types of gene therapy:
Has to be effective against the causative agent and safe for Pt. Also should be in a  Route of administrations  Virus vector
formulation that can deliver the drug to the site of infection.  Liposome
Organisms in CAP:
 Haemophilus influenza Atypical Bac
 Staphylococcus aureus  Mycoplasma pneumonia
Viral:  Legionella pneumonia
Influenza virus. RSV, adenovirus  Chlamydophila pneumoniae
CYSTIC FIBROSIS (CF)
St. George’s Guideline  Autosomal recessive disorder that affect epithelial cells of the respiratory GI and LUNG CANCER:
CAP 1st Line Alternative if allergic reproductive tracts and leads to abnormal exocrine gland secretions. CANCER:
CURB 0 – 1 Doxycyline PO Amoxicillin PO  INHERITED from both parents: An individual inherits a defective CF gene (one from Malignant cell growth, abnormal/uncontrolled cell division and growth, metastatic spread.
CURB 2 - 5 Benzylpenicillin IV + Levofloxacin IV/PO each parent).  Lung cancer is the most common cancer with the greatest percentage of deaths
Doxycyline PO/ Clarithromycin IV  Particularly damaging to the lungs, leading to COPD in childhood and early resulting from the condition. (24%)
adulthood.
CLINICAL SCENARIOS: Environmental factors:
Hospital Acquired Pneumonia (HAP): Pathophysiology: Smoking, UV, Alcohol, some bacteria such as helicobacter
Acquired ~48hrs of hospital admission. CF is a gene defect that affects the movement of salt and water in and out of cells. Some cancers have a strong genetic component such as HER2 in breast cancer.
 Dysfunction of CF transmembrane conductance regulator protein (CFTCR).
Caused by:  CFTCR – largely expressed in epithelial cells of airways, the GI tract (including  Cancers can spread locally, haematologically and through the lymphatic system.
 Whatever causes CAP pancreas and biliary system, the sweat glands, and the genitourinary system.
 Or Gram –ve bacilli e.g E.coli  CFTCR – functions as Cl channel but has other regulatory functions. – Alterations in Effects of cancer:
 Pseudomonas aeruginosa chloride transportations excessive Na+ absorption abnormally thick secretions  Loss/ alteration of organ/tissue function
 MRSA in glandular tissues.  Local site-specific Sx
 This largely affects the bronchioles, pancreatic ducts often progressing to  Effects can be indirect
Ventilation associated pneumonia: destruction of these organs.
Occurs more than 48 hrs after endotracheal intubation (tube insertions through mouth or Cilia also becomes affected and therefore cannot move the dehydrated mucus along. Factors affecting cancer prognosis:
nose).  Pt w/ CF are prone to infections. This is due to failure to clear inhaled bacteria.  Tissue
 Type of cancer
  Histology  Syncope after meal
 Cancer stage/spread  Constipation
 PAF – Pt may look fine compared to people experiencing fainting
Tx: Surgery, chemo, radiotherapy, biological/endocrine Tx.
REFLEX SYNCOPE ORTHOSTATIC SYNCOPE CARDIOGENIC SYNCOPE
LUNG CANCER: Vasovagal syncope: Volume depletions Brady arrhythmia
 Common in those over 60 y/o Prolonged standing *, Sinus bradycardia
 Most common form of cancer amongst males. emotional stress, blood Medication S/E Sinus pauses
 3rd most common in females draw and severe pain Beta blockers AV block
 20% - survive 1 year. (abdominal) Antidepressants
Antipsychotics Tachyarrhythmia
Aetiology: Smoking is the most common cause followed by passive smoking. Can also be Situational: Ventricular tachycardia
caused by radiation, petroleum products and oils. Coughing, urinating, Autonomic failure seen in:
sneezing, post exercise and Diabetes Mechanical:
Sx: defecation Alcoholism Aortic stenosis
 Persistent/ chronic cough Metastatic lung disease Sx: Parkinson’s Cardiomyopathy
 Pt might cough up blood (haemoptysis)  Bone metastasis: pain and Carotid sinus
 Weight loss/ loss of appetite/ anorexia hypercalcaemia, facture hypersensitivity
 SOB and chest pain  Neurological: headache, weakness, *____
 Hoarse voice confusion
 General fatigue – lassitude (lack of  Adrenal failure Differentiate w/ seizure:
energy)  Lymph nodes – enlarged? If it lasts for longer than 5 min – unlikely to be syncope.
 Recurrent infections
 Malaise – general feeling of discomfort If LOC <5 min but presented w/ 
 Tonic – clonic Sx
Lung cancer is known to metastasise into the bran = neurological Sx.  Bladder/bowel incontinence
 Post-event confusion lasting for more than a few mins (individuals that experience
Manifestations: Prognosis and Tx: syncope usually recover quickly)
 Finger clubbing Non-small cell: If individual experiences LOC w/ Sx above – may be a seizure
 Rashes  Surgery If no Sx above present  syncope
 Radiotherpay
Investigations:  Chemo Investigation:
 CXR Table Tilt test:
 CT/Scan Small cell  GOLD standard test for neuro-cardiogenic syncope
 Blood test and LFT Responsive to chemo  Test baro-receptor function and check vasovagal response.
 Tissue biopsy  Can be a diagnostic method if Sx are produced

Treatment:
Fludrocortisone: widely used
 Not to be used long-term
 Store in the fridge
 Initial dose 50mcg and build up
 Check Pt for signs of hypokalaemia
 S/E: oedema and fluid retention

SYNCOPE: Midodrine: Alpha 2 agonist

Sudden loss of consciousness due to transient global cerebral hypo perfusion; sudden drop  Most effective drug
of bp = brain turns off.  ‘pill in the pocket’
Can occur in individuals who are very young or very old or as a S/E of medication.  Avoid dosage after 6pm
4 components of syncope:  Avoid in older males with urological problems and it may cause difficulty with urine
 Abrupt, transient LOC flow.
 Loss of postural tone  individual may fall to the ground or slump whilst sitting
 Short duration Newer drugs are being developed for Neurogenic Orthostatic Hypotension.
 Spontaneous recovery Neurogenic OH  deficit of norepinephrine

*presyncope = prodrome such as heachache, dizziness and visual disturbances but does not Droxipoda: significant improvement in dizziness
result in syncope *  Significant reduction in falls
Pure autonomic failure:  Check supine and standing BP
 Known as idiopathic orthostatic hypotension.  Monitor standing HR
 Happens in 55-75 y/o
 More common in men
 Concealed for years due to compensatory mechanism
Sx:
 Generalised weakness and dizziness
 Gait disturbance
*Simple faint:
N+V and Excessive sweating