Flashcards in CVS Deck (133):
Causes of Hypertension
Renal - PKD, RVD, PAN, GN
Endo - Conns, Cushings, Pheo, Acro, Hyperthyroidism
Drugs - Cocaine, OCP, NSAIDS
Toxaemia of pregnancy
Overload of fluid
Signs of end-organ damage in HTN
Cardiac - IHD, LVF - CCF, AR/MR
Aorta - aneurysm/ dissection
Neuro - CVA (ishaemic/haemorrhagic); encephalopathy ( malignant HTN - headaches, seizure, coma)
Eyes - HTN retinopathy
Renal - Proteinuria, CRF
Classification of hypertensive retinopathy
Keith - Wagener classification
1) Tortous A and silver wiring
2) AV nipping
3) flame haemorrhages and cotton wool spots
Investigations for hypertension
1) 24h ABPM
2) Bloods - FBC, UE, Glucose, Fasting lipids, eGFR
3) 12-lead ECG
4) Urine - haematuria; alb:Cr
5) Calculate 10 year CV risk
Management for hypertension
- educate; stop smoking; reduce alcohol; reduce salt; reduce caffiene; increase exercise
- treat if >140/90 and end organ damage/ CV risk >20% or if >160/100
- 1st line --> <55/DM - ACEi; >55/black - CaCB/ thiazide
- 2nd line --> ACEi +CCB
- 3rd line --> +thiazide
- 4th line ---> + spironolactone / a/b blocker
Target BP for hypertensive
<130/80 if DM
<150/90 if >80
Name and give SE of ACEi
- And name of ARB
Lisinopril , Ramipril
ARB - Canaesartan
SE: renal impairment; persistent dry cough; angioedema; rash; hypotension; pancreatitis; hyperkalaemia; GI effects.
Name and give SE of dihydrop
SE--> abdominal pain; nausea;
palpitations, flushing, oedema; headache;
dizziness; sleep disturbances; fatigue
Name and give SE of Thiazide
SE--> postural hypotension; hypokalaemia;
hypomagnesaemia; hyponatraemia; hypercalcaemia; metabolic alkalosis; hyperuricaemia; impotence; hyperglycaemia.
a) malignant hypertension
b) malignant hypertension + encephalopathy
1) reduce BP over a few days to avoid stroke
2) Atenolol / Long-acting CaCB
1) sodium nitroprusside infusion- monitor BP intra- A
2) Reduce BP to <110 over 4 hours
NYHA Heart Failure Classification
Class I- No limitation of physical activity
Class II- Slight limitation of physical activity (symptomatically mild heart failure)
Class III - Marked limitation of physical activity (symptomatically moderate heart failure)
Class IV- Symptoms at rest
(symptomatically severe heart failure)
Which murmur has increased intensity on inspiration and why
Right - Inspiration ↑ venous blood return to the right
side of the heart.
Grading of murmurs
Grade 1: Very faint.
Grade 2: Soft.
Grade 3: Heard easily.
Grade 4: Loud, with a palpable thrill
Grade 5:Very loud, with thrill. May be heard when stethoscope is partly off the chest.
Grade 6:Very loud, with thrill. May be heard with stethoscope entirely off the chest
Causes of Mitral Stenosis
- Rheumatic fever or
- Old Age and calcification
Effects of Mitral Stenosis
High LA pressure
Pulmonary venous hypertension
Pulmonary arterial hypertension
Right ventricular hypertrophy
Right heart failure
Signs of MS
- Atrial Fibrillation
- Malar flush
- Tapping apex beat due to palpable 1st heart sound
- Loud S1
- Opening snap
-Rumbling MDM best heard with BELL at APEX lying on LEFT
- Signs of RHF -
↑ JVP, Oedema, Ascites
Signs of Pulmonary Oedema on CXR
B lines (Kerley
Diversion to upper lobes
ECG changes in MS
o Atrial Fibrillation
o Bifid P wave if SR (Left atrial delay)
o RVH - right axis deviation and tall R waves in
leads V1 and V2
Causes of Mitral Regurgitation
o Prolapsing mitral valve
o Rheumatic mitral regurgitation (the cusps are
shrunken and fibrotic)
o Papillary muscle rupture post MI
o Cardiomyopathy of any sort
o Connective tissue disorders
Signs of MR
- Pulse in sinus rhythm
-Displaced, volume loaded apex beat
- Auscultation - Panstyolic murmur radiating to the axilla
Signs of MR on CXR and ECG
CXR - cardiomegaly
ECG - Bifid p wave and LVH
Causes of Aortic Stenosis
Bicuspid Aortic Valve (under 65)
Age related Calcification (over 65)
Symptoms of AS
Exercise-induced syncope, angina and dyspnoea develop
Signs of AS
– Character = slow rising
– Volume = low volume with narrow pulse pressure
oForceful apex beat
o Ejection systolic murmur radiating to carotids
Findings on CXR and ECG in AS
o Relatively small heart with a prominent, dilated,
ascending aorta. → ‘post-stenotic dilatation’
o left ventricular 'strain' pattern (depressed ST
segments and T wave inversion in leads orientated towards the left ventricle)
Causes of Aortic Regurgitation
oRheumatic fever (commonest)
o Bicuspid valve
o Infective Endocarditis
Pathology of AR
Reflux of blood from aorta to LV in diastole.
For cardiac output to be maintained, total
volume to be pumped into aorta must ↑, therefore LV size must increase.
Signs of AR
– Collapsing pulse(wide pulse pressure)
Quincke's sign - capillary pulsation in the nail
De Musset's sign - head nodding with each
Pistol shot femorals - a sharp bang heard on
auscultation over the femoral arteries in time with
– Displaced apex beat
o High-pitched early diastolic murmur best heard at the left sternal edge in the fourth ICS with the patient leaning forward and their breath held in expiration
ECG changes in AR
How to calculate a regular and irregular rate on ECG
300 divided by the number of big squares
between the R-R interval.
Count the total number of QRS complexes in a
10 second rhythm strip (50 large squares) and
multiply by 6.
ECG changes in Atrial flutter and why
Sawtooth” P waves - usually most prominent in lead II.
The atria depolarize in an organized circular movement due to re-entry. The atria contract at around 300 bpm, which results in a fast sequence of p-waves in a sawtooth pattern.
For most AVN 300 bpm is too fast to conduct the signal to the ventricles.
2:1 conduction = rate of 150 3:1 conduction = rate of 100 4:1 conduction = rate of 75
What is the normal PR interval
0.12 - 0.2 milliseconds (3-5 small squares)
What is 1st degree Heart Block
P-R interval prolonged by constant amount (> 5 small squares).
What are the types of second degree Heart block
•Mobitz I (Wenckebach)
o Progressive lengthening of P-R until one QRS is dropped
• Mobitz II
o Intermittent failure of AV node to conduct atrial
depolarisations to the ventricles
o May be fixed i.e. 2:1 / 3:1 P-R interval
Describe 3rd degree Heart Block and the causes
• No relationship between P waves and QRS complexes
• Rate usually 30-50bpm
• Stoke-Adams attacks
o Fibrosis of AVN/ Bundle of His
o Drugs e.g. Digoxin toxicity, Diltiazem
Describe the criteria is used to measure LVH on an ECG
Sokolow-Lyon Voltage criteria
o S wave in V1 + R wave in V5 or V6 =>35mm
or 3.5 large ECG squares
o If severe T wave inversion may also be seen in
How would you assess RVH on on ECG
wave >5mm in Right ventricular leads + RAD
How is the QRS affected in BBB
Widened in BBB
WiLLiaM and MaRRoW
o LBBB: WinV1andaMinV6
Causes of ST elevation
Pericarditis: Concave and widespread over many leads
Causes of ST depression
> 1mm in 2 consecutive limb leads or
> 2mm in 2 consecutive chest leads
+ Level or Downsloping
Features of MI on ECG
Acute infarct: ST elevation
Recent infarct: T wave inversion & Pathological Q
waves (> 1/4 height QRS)
• Old infarct: Q waves remain
• Also new onset LBBB
Location of MI and correlating Blood vessels
> V1-V2: Septal and V3-V4: Anterior
> V5-V6: Lateral and I, aVL: High Lateral
> V2-6 - L mainstem
> II, III, aVF: Inferior
ECG changes in PE
S1, Q3, T3
Large S wave in lead I
Q wave inversion in lead III
T wave inversion in lead III
o Tachycardia (the most common finding on ECG!)
ECG changes in Hyperkalaemia
Low flat P waves
Broad bizarre QRS
Slurring into the ST segment
Tell tented T waves
Causes of Heart Failure
Ischaemic heart disease (70%)
Non-Ischaemic Dilated Cardiomyopathy (25%)
Valve disease; CHD; AF; HB; Anaemia; Pericardial disease; Pul HTN; PE; Alcohol
Pathophysiology of Heart failure
Reduced CO - compensation
o Starling effect dilates heart to enhance contractility
oRAS and ANP/BNP release
- ↓ CO - decompensation
o Progressive dilatation --> impaired contractility + functional valve regurgitation
o Hypertrophy --> Relative myocardial iscaemia
o RAAS activation --> Na+ and fluid retention --> ↑ Venous P --> oedema
o Sympathetic excess --> increase afterload --> ↓ CO
Severe HF - ↓ CO even at rest despite ↑ venous pressure and sinus
Causes of LHF
1. Ischaemic Heart Disease
2. Non Ischaemic Dilated Cardiomyopathy
4. Mitral / Aortic Valve Disease
o MS - LA HTN and signs LHF
Symptoms of LHF
o Fatigue (common)
o Exertional dyspnoea
o Orthopnoea / PND
Signs of LHF
o Displaced Apex Beat --> Cardiomegaly
o Gallop Rhythm and tachycardia on Auscultation - S3
o Features of MR - Dilatation of the mitral annulus
o Pulmonary oedema
o Dependent Pitting Oedema
o Cold peripheries
Causes of RHF
Chronic Lung Disease (Cor pulmonale)
PE or Pulmonary Hypertension
Tricuspid / Pulmonary Valve Disease
Symptoms of RHF
Anorexia / Nausea
Signs of RHF
↑ JVP ± V waves of tricuspid regurgitation
Cardiomegaly - Dilatation of the RV +- TR
Tender and smooth
Dependent Pitting Oedema
Management of HF
• Low level exercise
• Low salt diet
• Stop smoking
1) ACEi/ARB + β-Blockers + Furosemide
2nd line - Spironolactone; GTN
3rd line - Digoxin
- Cardioresynchronisation therapy ± implaented cardioverter defribillator
- LV Assist Device and Artificial Heart
- Cardiac transplant
Pathophysiology of atherosclerosis and in ACS
• Triggered by injury
• Lipoproteins oxidised - taken up by macrophages =
• Release of cytokines → accumulation fat and smooth
• Plaque formation
- Rupture of a coronary artery plaque
- Platelet aggregation and adhesion
- Localised thrombus, vasoconstriction
- Myocardial ischaemia
Risk factors for ACS
• Non - modifiable
o Male gender
o Family History
o Ethnic origin
Initial management of ACS
Airway, Breathing, Circulation IV access
Morphine (2.5-10mg IV, plus antiemetic)
Nitrates (GTN spray 2 puffs sublingually)
Investigations for ACS
- Bloods - FBC, LFT, UE, Glucose, Lipids, CK, Troponin I
- Portable CXR
Presentation of STEMI
o Chest pain - not relieved by GTN
o N&V, sweating
o May be painless +/- atypical (diabetics)
o May present as acute pulmonary oedema,
SOB, syncope, cardiogenic shock etc.
ECG findings in STEMI
o ST elevation
o New LBBB
o +/- T wave inversion
o +/- Pathological Q waves
Management of STEMI
PCI (Percutaneous Coronary Intervention)
Indications for Thrombolysis and PCI in STEMI
o < 12 hours onset pain + any 1 of the following:
o ST elevation >1mm in 2+ consecutive limb leads
o ST elevation >2mm in 2+ consecutive chest leads
o Posterior infarct o New onset LBBB
If can undergo <90 min from onset
- Same as thrombolysis and if doesn't fulfil criteria or thrombolysis CI
Contraindications for Thrombolysis
Haemorrhagic stroke or Ischaemic stroke < 6 months CNS neoplasia
Recent trauma or surgery
GI bleed < 1 month
Advanced Liver Disease Infective Endocarditis
Complications of thrombolysis
• Intracranial haemorrhage
• Reperfusion arrhythmias
• Systemic embolisation of thrombus
• Allergic reaction (especially if Streptokinase)
Complications of STEMI
S - Sudden death
P - Pump failure / Pericarditis
R - Rupture papillary muscles or septum E - Embolism
A - Aneurysm / Arrhythmias
D - Dressler’s syndrome
Drugs to discharge with pt after STEMI and risk prevention
• ACE inhibitor
• Address modifiable risk factors
• 1 month off work
• Need to inform DVLA – no driving for 4 weeks.
Presentation of NSTEMI and unstable angina
• Rest angina / Increasing angina
• New-onset severe angina
ECG changes for NSTEMI and unstable angina
• T wave inversion
• ST depression
How to differentiate between NSTEMI and unstable angina
Check Troponin I 12 hours after onset of pain to
distinguish between NSTEMI and UA. NSTEMI will have a positive Troponin I and Unstable Angina will have a negative troponin.
Management of NSTEMI/UA
o Nitrates (GTN infusion)
o ACE inhibitors
o Calcium channel antagonists
3. Antiplatelet o Aspirin
Consider PCI if:
↑ Troponin I
Recurrent angina / ischaemic ECG changes despite optimal medical therapy
Features of heart failure
Poor LV function
PCI < 6 months / previous CABG
Pathophysiology of LV failure
The heart is unable to maintain sufficient cardiac output to meet the demands of the body.
• Compensatory mechanisms are not yet operative in acute LVF.
• The cardiac output is reduced. Failure of the ventricles to eject blood results in increased intracardiac pressures and pulmonary capillary pressure.
Presentation of LV failure
• Presents as acute pulmonary oedema:
o Acute breathlessness
o Cough & frothy pink sputum
o Orthopnoea, paroxysmal nocturnal dyspnoea
o Collapse, arrest, cardiogenic shock
o Distressed, pale and sweaty
o Fine crepitations bilaterally
o Gallop rhythm: S-3
Causes of LVF
o Myocardial ischaemia
o Aortic stenosis or aortic incompetence o Mitral incompetence
Management of LVF
• Airway, Breathing, Circulation
• Sit upright
• 100 % O2 via non rebreather mask
• IV access and monitor ECG
• Morphine 2.5-5mg IV (with antiemetic)
• If SBP >100mmHg – Nitrate (GTN) IV infusion
• Furosemide 40-80mg IV
Investigations for LVF
• ECG: Arrhythmia, tachycardia, MI, LVH
• Bloods: FBC, U&E, CK, Troponin I
Mechanisms of tachycardias
1. Accelerated automaticity
o An area of myocardial cells depolarises faster
than the SA node
2. Triggered activity
o Myocardial damage
o Propagating action potential
keeps meeting excitable myocardium.
o There must be 2 pathways around an area of conduction block.
Precipitating factors for VT
Precipitating factors for SVT
Precipitating factors for AF
• Mitral valve disease
• Lung disease
• Post op
• Pericardial disease
Types of SVT (narrow)
o Sinus tachycardia
o Atrial flutter (some)
o Atrial tachycardia
o Junctional tachycardia
o AV node re-entry
o Accessory patheay e.g. WPW
o Atrial fibrillation (AF)
o Atrial flutter (some)
o Multifocal atrial tachycardia
Management of regular SVT
• ABC+O2+IV access
• Vagal Manoeuvres
• Adenosine 6mg rapid IV bolus; +12 +12 - monitor ECG continuously
• SEEK HELP
• DC cardioversion if haemodynamically unstable
Management of AF
Control rate with b-blockers or digoxin IV
If onset <48h consider amiodarone 300mg IV 20-60 min; then 900mg over 24g
Types of broad complex tachycardias
- Including Torsades de pointes
o SVT with BBB
Differences between SVT and VT
o Is slowed or terminated by vagal manoeuvres /
o Atrial and ventricular coupling
o QRS >160ms
o Independent atrial activity o Fusion / Capture beats
Management of VT
ABC (if pulseless = arrest protocol)
No adverse signs
o Amiodarone / Lidocaine
o K+/Mg2+ if needed
o Sedation and DC cardioversion
Adverse signs (↓ BP, HF, ↓ GCS; Chest pain, ↑HR)
DC cardioversion Amiodarone / Lidocaine
Causative organisms of infective endocarditis
Pathophysiology of IE
Endothelial damage/ damaged valve
platelet and fibrin deposited
Adherence and colonisation of bacteria
Fibrin aggregates protect the bacteria vegetation from host defence mechanisms
Consequences of IE
o Disruption of the valve cusps, commonly
leading to mitral or aortic regurgitation.
o Vegetations embolise.
o Deposition of immune complexes.
Clinical presentation of IE
• HEART MURMUR + FEVER
1. Systemic infection
o Weight loss
2. Valvular / Cardiac damage
o Changing Murmur- AR/MR
o Heart failure
o Conduction Abnormalities
o Renal (haematuria)
4. Immune Vasculitis
o Roth spots (Retinal infarcts with surrounding haemorrhage)
o Oslers nodes
o Janeway lesions
o Splinter haemorrhages
DUKES CRITERIA FOR IE
BE FIVE PM
Blood culture +ve
o Typical organism in 2 separate cultures. OR
o Persistently positive cultures (3 sets, at different times, from different places, at peak temperature).
Endocardium involvement - o Positive echocardiogram (Vegetation, abscess, prosthetic valve damage).
o New valvular regurgitation.
2 Major OR 1 Major, 3 Minor OR 5 Minor
Management of IE
Involve microbiologist and cardiologist
Benzylpenicillin and Gentamycin 4 weeks IV
Investigations for IE
Bloods: FBC (anaemia), U&E, LFT, CRP ↑, Blood Cultures x 3
Risk factors for IE
o Structural congenital heart disease
o Acquired valve disease
o Prosthetic valves
o Previous endocarditis
Presentation of acute pericarditis
o Chest pain
2. Worse on inspiration
3. Central chest pain
4. Radiating to left shoulder
5. Eased sitting forward
o Pericardial friction rub
o Serial ECG changes
o Tachycardia and Tachypnoemia
o +/- Dyspnoea, Fever
If Constrictive pericarditis:
- signs RHF
↑JVP, severe ascites, hepatomegaly, Kussmaul’s sign (JVP ↑ with inspiration)
- Hypotension, Pulsus Paradoxus (↓ in palpable pulse and ↓ in systolic BP on inspiration)
- Loud high-pitched S3 (pericardial knock)
Pathophysiology of pericarditis
• Pericardium is acutely inflamed.
• Infiltration of polymorphonuclear (PMN) leukocytes
and pericardial vascularisation.
o May develop constrictive pericarditis
Exudates & adhesions encase the heart within a non expansile pericardium.
o May develop a pericardial effusion
Serous or haemorrhagic.
May lead to cardiac tamponade.
Causes of Pericarditis
Viral - Coxsackie; EBV; HIV
Bacterial - pneumonia, TB, staph
- ABx for at least 4 weeks and drainage of pericardial fluid
Direct pulmonary extension
Penetrating injury to chest wall (trauma or surgery)
Subdiaphragmatic suppurative lesion
Drugs - penicillinm, isoniazid
Other - RA/SLE; Lung tumour, uraemia
Investigations of pericarditis
• Bloods: FBC, U&E, LFT, CRP, CK, Troponin I
• Further investigations:
o Virology screen
o Blood cultures
o Antistreptolysin titre
o Rheumatoid factor
o Antinuclear antibodies (ANA)
o Anti-DNA antibodies
o Tuberculin testing
o Sputum for acid-fast bacilli
• Echocardiography (ECHO)
o If pericardial effusion or tamponade is suspected.
o If there is a pericardial effusion, you may see
right ventricle compression as this is compromised first.
• CT / MRI
ECG changes in Pericarditis
o Stage 1: Saddle shaped ST elevation (Diffuse
concave upward ST elevation, except aVR and V1 (usually
o Stage 2: Occurs several days later. ST
segment returns to baseline, followed by T
o Stage 3: T wave inversion.
o Stage 4: ECG returns to the pre-pericarditis
baseline weeks to months after onset.
Treatment of pericarditis
If a cause is found, this should be treated!
Bed rest and oral NSAIDs
o High-dose aspirin, indometacin or ibuprofen.
o But NOT post-MI: NSAID associated with
o Corticosteroids have been used when the
disease does not subside rapidly.
o Pericardial window
What is a pericardial effusion
Abnormal accumulation of fluid in the pericardial cavity.
What is Cardiac Tamponade
Pericardial effusion causing haemodynamically significant cardiac compression.
Pericardial pressure increases inhibiting venous return to the heart.
This results in reduced cardiac output, hypotension and shock.
Aetiology of Pericardial effusion/ cardiac tamponade
o Iatrogenic (cardiac surgery / catheterisation / anticoagulation)
o Aortic dissection
o Spontaneous bleed (uraemia / thrombocytopenia) o Cardiac rupture post-MI
o Idiopathic pericarditis
o Infection (including TB)
Presentation of Pericardial effusion/ cardiac tamponade
o Cardiac arrest
Slowly developing tamponade
o Cough, hiccups, dysphagia
Signs of Pericardial effusion/ cardiac tamponade
• Beck’s triad: o ↑JVP
o Muffled heart sounds
• Kussmaul’s sign (JVP ↑ with inspiration)
• Pulsus paradoxus (↓ in palpable pulse and ↓ in systolic BP on
Management of Pericardial effusion/ cardiac tamponade
• Get senior help
• ABC, IV Access and fluids, ECG, Bloods
• USS guided Pericardiocentesis
o Needle inserted at level of Xiphisternum, aim for tip of left scapula, aspirating continuously.
o Send the pericardial fluid for microbiology and
• A drain may be left in temporarily to allow sufficient
release of fluid
Example of β - Blockers and Action
Bisoprolol; Atenolol; Propanolol.
Action: Negatively inotrophic & chronotrophic.
SE of β - Blockers
GI disturbances; bradycardia; fatigue; cold peripheries; heart failure; hypotension; dizziness; sexual dysfunction; peripheral vasoconstriction; bronchospasm.
CI of β - Blockers
Asthma; marked bradycardia; heart block; uncontrolled heart failure; PVD; Prinzmetal's angina; hypotension; cardiogenic shock.
Example of Non-dihydropyridines calcium channel blocker and action
Verapamil & Diltiazem
Negatively inotrophic / chronotrophic but DO NOT
USE IN HEART FAILURE
Example of Dihydropyridines calcium channel blocker and action
Amlodipine, Felodipine, Nifedipine
Dilates peripheral arteries, ↓ after-load, dilates coronary vessels, act on vessels > myocardium
SE of calcium channel blocker
o Verapamil & Diltiazem: constipation; N&V;
flushing, headache, dizziness; fatigue.
o Dihydropyridines: abdominal pain; nausea;
palpitations, flushing, oedema; headache;
dizziness; sleep disturbances; fatigue.
CI of calcium channel blocker
o Verapamil & Diltiazem: HF, 2nd or 3rd degree
heart block, cardiogenic shock.
o Dihydropyridines: Unstable angina, significant
Example of nitrates and SE
Examples: Isosorbide Mononitrate (PO); GTN infusion (IV); GTN spray (S/L).
Side effects: postural hypotension; tachycardia; throbbing headache; dizziness.
CI of nitrates
persensitivity to nitrates; hypotensive conditions; hypovolaemia; hypertrophic obstructive cardiomyopathy; AS; MS; cardiac tamponade; constrictive pericarditis; marked anaemia.
Action of ACEi
Inhibits conversion of angiotensin 1 into angiotensin 2, therefore inhibiting angiotensin 2 having its effects:
o Increasing sympathetic activity.
o Fluid retention by kidney – via Increase in
aldosterone and direct action.
o Arteriolar vasoconstriction.
o Stimulating ADH secretion causing increased
ACE inhibitors also cause:
o Reversal of left ventricular hypertrophy
CI of ACEi
hypersensitivity to ACEi (angioedema); renal artery stenosis; pregnancy; aortic stenosis; toxicity.
Example of loop diuretic and action
Action: Blocks Na+/K+/Cl- co-transporter in the apical
membrane of the thick ascending limb of loop of Henle.
SE of Loop diuretics
Hypokalaemia; metabolic alkalosis; sodium & magnesium depletion; hypovolaemia & hypotension; deafness; nausea; allergies.
Action of Thiazides
Inhibits Na+ reabsorption at the beginning of
the distal convoluted tubule. Blocks Na+/Cl- symporter
that is associated with the luminal membrane.
CI of thiazides
Refractory hypokalaemia; hyponatraemia; hypercalcaemia; symptomatic hyperuricaemia; Addison's disease.
Example and actino of K+ sparing diuretics
Act on collecting tubules.
Spironolactone is an aldosterone antagonist.
Amiloride directly inhibiting sodium channels
SE of K+ sparing diuretics
GI disturbances; impotence;
gynaecomastia; menstrual irregularities; lethargy; headache; confusion; hyperkalaemia; hyponatraemia; hepatotoxicity.
Example and action of statins
Lowers cholesterol levels in blood by:
o Blocking liver enzyme hydroxy-methylglutaryl- coenzyme A reductase (HMG-CoA reductase), thereby inhibiting liver synthesis of cholesterol.
o This leads to upregulation of expression of LDL receptors on liver cells causing ↑ absorption of LDL from the circulation.
SE of statins
myositis; rhabdomyolysis; headache; altered LFTs; paraesthesia; GI effects.
CI of statins
active liver disease; pregnancy; breast-feeding.
Action of aspirin
Suppresses production of prostaglandins and thromboxane by irreversibly inactivating the cyclooxygenase (COX) enzyme.
• Irreversibly blocks the formation of thromboxane A2 in platelets, inhibiting platelet aggregation.
Action of Clopidogrel
Inhibits ADP-induced aggregation through an active metabolite.
LMWH v UFH
o Binds to Antithrombin III (ATIII).
o ATIII is an endogenous inhibitor of coagulation.
o Increases ATIII ability to inhibit factors IXa, Xa,
XIa, XIIa (serine proteases) and thrombin (unfractionated).
o UHF fully reversible with Protamine.
- Need daily plateleys
o Inhibits factor Xa but not thrombin.
o LMWH not fully reversible with Protamine.
SE and CI of herparin
SE - haemorrhage; UFH (Heparin induced thrombocytopenia)
CI - uncontrolled bleeding / risk of bleeding e.g. peptic ulcer, recent cerebral
Action of warfarin
Inhibits vitamin K dependent clotting factors
(II, VII, IX, X, protein C & S). Does this through inhibiting the reductase enzyme responsible for the regeneration of the active form of vitamin K.
SE and CI of warfarin
SE - Haemorrhage
CI - peptic ulcer; severe
hypertension; bacterial endocarditis; pregnancy.
What to do in Warfarin Overdose and in major bleed
INR <6: Decrease / omit Warfarin
INR 6-8: Stop Warfarin. Restart
INR >8: If no bleeding stop
Warfarin & give 0.5- 2.5mg vitamin K if risk of bleeding.
Major bleed: Stop Warfarin. Give prothrombin complex concentrate (Beriplex) contains factors II, VII, IX, X or FFP. Give 5mg vitamin K. Get HELP!
Causes of bradycardia
Drugs - Amiodarone, b-b, CaCB, Digoxin
Vagal hypertonia (athletes)
Infection (myocarditis; rheumatic; IE)
Sick sinus syndrome
O - Low T3/4; K; Temp
Neuro - ↑ ICP