CVS Flashcards

1
Q

SA node -

A

the dominant pacemaker with an intrinsic rate of 60-100 bpm

(NORMAL HEART RATE) - the fastest depolarising tissue

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2
Q

ECG paper:

A
- Horizontally:
• One small box = 0.04s/40ms
• One large box = 0.20s 
- Vertically:
• One large box = 0.5mV
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3
Q

Cardiac output (L/min) =

A

Stroke volume (L) x Heart rate (BPM)

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4
Q

HEART SOUNDS:

A
  • S1 - mitral and tricuspid valve closure
  • S2 - aortic and pulmonary valve closure
  • S3 - in early diastole during rapid ventricular filling, normal in children and pregnant women, associated with mitral regurgitation and heart failure
  • S4 - ‘Gallop’, in late diastole, produced by blood being forced into a stiff hypertrophic ventricle - associated with left ventricular hypertrophy
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5
Q

ANGINA:

A

Aspirin:
Betablockers - 1st line antianginal: Reduce force of contraction of heart E.g. Bisoprolol and atenolol
Glyceryl Trinitrate (GTN) spray - 1st line antianginal:
- Nitrate that is a venodilator
Ca2+ channel antagonists/blocker: verapamil
- Primary arterodilators
- Dilates systemic arteries = BP drop

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6
Q

ACUTE CORONARY SYNDROME:

includes

A

STEMI, unstable angine, NSTEMI

- Pain relief:
• GTN spray
• IV opioid
- Anti-emetic 
- Oxygen
- Antiplatelets: 
    - aspirin
    - 2Y12 inhibitors (oral): Inhibit ADP-dependant activation of IIb/IIIa glycoproteins thereby preventing amplification response of platelet aggregation : - E.g. Clopidogrel, Prasugrel & Ticagrelor
   -  Glycoprotein IIb/IIIa antagonists (IV): E.g. Abciximab, Tirofiban and Eptifbatide
- Beta blockers (IV & oral):
 • E.g. Atenolol (IV then oral) or Metoprolol (IV then oral)
- Statins (oral):
• HMG-CoA reductase inhibitors
• E.g. Simvastatin, Pravastatin and Atorvastin 
- ACE inhibitors (oral):
• E.g. Ramipril and Lisonopril
• Monitor renal function 
- Coronary revascularisation:
• PCI
• CABG - high risk mortality in high risk groups e.g. recent MI
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7
Q
  • ACUTE MYOCARDIAL INFARCTION:

Tx:

A

Pre-hospital:
• Aspirin 300mg chewable
• GTN (sublingual)
• Morphine
Hospital:
• IV morphine
• Oxygen if their sats are below 95% or are breathless
• Beta-blocker - Atenolol
• P2Y12 inhibitor - Clopidogrel
Coronary revascularisation:
• PCI:
- Presented to all patients who present with an acute STEMI who can be transferred to a primary PCI centre WITHIN 120 MINUTES of first medical contact
- If not possible then give patient fibrinolysis and then transfer to PCI centre after infusion
• CABG
- Fibrinolysis - enhance the breakdown of occlusive thromboses by the activation of plasminogen to form plasmin

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8
Q

Cardiac failure:
def
Tx:

A

The inability of the heart to deliver blood and thus O2 at a rate that is commensurate with the requirement of metabolising tissue of the body

  • Diuretics:
    • Promote sodium and thus water loss thereby reducing ventricular filling pressure (preload) decreasing systemic and pulmonary congestion
    • symptomatic relief
    • Loop diuretic - furosemide
    • Thiazide diuretic - bendroflumethiazide (inhibit sodium reabsorption in the distal convoluted tubule)
    • Aldosterone antagonist (thereby inhibiting ADH release resulting in water loss) - spirolactone & epelerone - note with these beware of renal impairment and hyperkalaemia
    -ACE inhibitors:
    • Ramipril, enalipril, captopril
    • Side effects: cough (since inhibit ACE and thus the breakdown of substance P and bradykinin which results in cough)
    • If cough is a problem then can give angiotensin receptor blockers (not as effective as ACE-inhibitors) e.g. canderstan or valsartan
    -Beta-blockers:
    • Bisoprolol, nebivolol, carvedilol
    • Start at low dose and titrate upwards
    • DO NOT GIVE TO ASTHMATICS
    -Digoxin
    -Inotropes
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9
Q
  • Biventricular failure:
A
  • Shortness of breath due to right ventricular failure

* Leg oedema due to left ventricular failure

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10
Q

• VALVULAR HEART DISEASES:
- MITRAL VALVE DISEASE
- Mitral stenosis
Tx:

A

Its a mechanical problem and medical therapy does not prevent progression

  • Beta-blockers e.g. Atenolol and digoxin which control heart rate and thus prolong diastole for improved diastolic filling
  • Diuretics for fluid overload e.g. Furosemide
  • Percutaneous mitral balloon valvotomy:
  • Mitral valve replacement
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11
Q
  • MITRAL REGURGITATION:
    Def
    Tx:
A

Backflow of blood from the left ventricle to the left atrium during systole

  • Medications:
    • Vasodilators such as ACE-inhibitors e.g. Ramipril or Hydralazine (smooth muscle relaxer)
    • Heart rate control for atrial fibrillation with Beta blockers (Atenolol), Calcium channel blockers and digoxin
    • Anticoagulation in atrial fibrillation and flutter
    • Diuretics for fluid overload e.g. Furosemide
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12
Q
  • AORTIC REGURGITATION:
    Main causes
    RF
    Tx:
A
  • Main causes:
    • Congenital bicuspid aortic valve (BAV) - chronic
    • Rheumatic fever - chronic
    • Infective endocarditis - acute
    • Risk factors:
  • SLE
  • Marfan’s and Ehlers-Danlos syndrome - connective tissue disorders
  • Aortic dilatation
  • Infective endocarditis or aortic dissection
  • Vasodilators such as ACE-inhibitors such as Ramipril will improve stroke volume and reduce regurgitation but only if patient is symptomatic or has hypertension
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13
Q
  • INFECTIVE ENDOCARDITIS:

Tx:

A
  • Staphylococcus aureus (IVDU, diabetes and surgery) - most common cause
  • Pseudomonas aeruginosa
  • Streptococcus viridans (dental problems) - GRAM POSITIVE, alpha haemolytic and optochin resistant (Strep. mutans, strep, sanguis, strep. milleri & strep. oralis)
  • Antibiotic treatment (which one is decided on organism ascertained from cultures) for 4-6 weeks
  • If not staphylococcus then use penicillin ideally Benzylpenicillin & Gentamycin (doesn’t work on own since cannot get through bacterial cell wall)
  • If staphylococcus then use Vancomycin & Rifampicin (if MRSA)
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14
Q

• Hypertrophic cardiomyopathy (HCM):

Def + Tx:

A
  • Ventricular hypertrophy/thickening of the muscle
  • Amiodarone - anti-arrythmatic medication, if at high risk of arrhythmia then can place an implantable cardiac defibrillator
  • Calcium channel blocker e.g. Verampil
  • Beta-blocker e.g. Atenolol
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15
Q

Arrythmogenic right ventricular cardiomyopathy:

A

Progressive genetic cardiomyopathy characterised by progressive fatty and fibrous replacement of ventricular myocardium

Beta-blockers e.g. Atenolol for patients with non-life-threatening arrhythmias
• Amiodarone for symptomatic arrhythmias
• Occasionally cardiac transplant indicated i.e. in cardiac failure or devastating arrhythmia

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16
Q
BICUSPID AORTIC VALVE (BAV):
ATRIAL SEPTAL DEFECTS (ASD):
VENTRICULAR SEPTAL DEFECTS (VSD):
-explained
\+/- Tx:
A
  • 2 instead of three cusps– early stenosis
    -Shunt is left-to-right
    Thus NOT blue i.e. acyanotic
    -20% of all congenital heart defects
    • Higher pressure in left ventricle than right ventricle =left-to-right shunt = acyanotic. If moderately sized lesion; furosemide, ACE inhibitor e.g. ramipril and digoxin may suffice
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17
Q

PATENT DUCTUS ARTERIOSUS:

A

persistent communication between the proximal left pulmonary artery and the descending aorta (after birth)
Eisenmenger’s syndrome with differential cyanosis that is clubbed and blue toes BUT pink and not clubber fingers
-Indometacin (prostaglandin inhibitor) can be given to stimulate duct closure

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18
Q
  • COARCTATION OF THE AORTA:

- TETRALOGY OF FALLOT:

A

A narrowing of the aorta at, or just distal to, the insertion of the ductus arteriosus (distal to the origin of the left subclavian artery)

Most common form of CYANOTIC congenital heart disease: - A large, maligned Ventricular Septal Defect (VSD (right to left): surgical treatment during first two years of life due to the progressive cardiac debility and cerebral thrombosis risk

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19
Q

Heart abnormalities

A
- COARCTATION OF THE AORTA:
PATENT DUCTUS ARTERIOSUS:
 BICUSPID AORTIC VALVE (BAV):
ATRIAL SEPTAL DEFECTS (ASD):
VENTRICULAR SEPTAL DEFECTS (VSD):
TETRALOGY OF FALLOT:
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20
Q

DEXTROCARDIA:

A

• Heart points to the right side of chest instead of to the left

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21
Q

ACUTE PERICARDITIS:
def
Tx:

A

• Acute inflammation of the pericardium; with or without effusion

  • Restrict PA
  • NSAID e.g Ibuprofen for two weeks or Aspirin for two weeks
  • Colchicine for 3 weeks however is limited by nausea and diarrhoea but does reduce recurrence
    • Recurrent or relapsing pericarditis:
  • About 20% develop idiopathic relapsing pericarditis (within 6 weeks during weaning off NSAIDs OR intermittently)
  • first line is oral NSAIDs e.g. Ibuprofen
  • Colchicine more effective than Aspirin alone
  • In resistant cases, oral corticosteroids e.g. Prednisolone may be effective, and in some patients, pericardiectomy (removal of part/most of the pericardium) may be appropriate
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22
Q

HYPERTENSION:
Normal
Stages
Treatment GOAL is 140/90mmHg

this is the commonest cause of … and a makor risk of …

Tx:

A

140/90mmHg=normotensive

Stage 1 hypertension:
- More than or equal to 140/90mmHg clinic BP
- Daytime average Ambulatory blood pressure monitoring (ABPM - 24hr BP monitor) or Home blood pressure monitoring (HBPM); greater than or equal to 135/85mmHg
Stage 2 hypertension:
- More than or equal to 160/100mmHg clinic BP
- Daytime average ABPM or HBPM greater than or equal to 150/95mmHg
Severe hypertension:
- Clinic systolic BP greater than or equal to 180mmHg and/or
diastolic BP greater than or equal to 110mmHg
- Start immediate anti-hypertensive drug treatment!

140/90mmHg

cardiac failure … atherosclerosis and cerebral haemorrhage

ACD pathway:
A - ACE-inhibitor e.g. Ramipril or Enalapril, or Angiotensin receptor blocker (ARB) (use if ACEi is contraindicated e.g. due to cough) e.g. Candesartan or Losartan
C - Calcium channel blocker (CCB) e.g. Nifedipine or Amlodipine
D - Diuretics e.g. Bendroflumethiazide (thiazide, distal tube - less potent) or Furosemide (loop diuretic, loop of henle - more potent)
NOTE: Beta-blocker e.g. Bisoprolol or Metoprolol (B1 selective) are NOT the FIRST LINE TREATMENT FOR HYPERTENSION but consider in young people especially if they are intolerant of ACEi/ARB
Less than 55 yrs old:
- Ramipril/Candesartan - + Nifedipine
- + Bendroflumethiazide - + Furosemide
Older than 55 yrs/black/African-Caribbean origin:
- Ramipril/Candesartan + Nifedipine
- + Bendroflumethiazide
- + Furosemide

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23
Q

Arrhythmias may cause:

A
  • Sudden death
  • Syncope
  • Heart failure
  • Chest pain
  • Dizziness
  • Palpitations
  • No symptoms at all

Tachycardia: 100bpm
Brady <60bpm

24
Q

Conduction pathways of the heart - SINUS RHYTHM (NORMAL):

A
  • SAN → Action potential → Muscle cells of atria → Depolarisation of the AVN → Slow → Interventricular septum → Bundle of His → Right and left bundle branches → Free walls of both ventricles → Purkinje cells → Ventricular myocardial cells
25
Q

ATRIAL FIBRILLATION:
def
tx:
Dx of stroke:

A

(A chaotic irregular atrial rhythm at 300-600bpm; the AV node responds intermittently, hence an irregular ventricular rate)

Cardioversion:
- Conversion to sinus rhythm achieved electrically by DC shock e.g. defibrillator - NOTE: give low molecular weight heparin e.g. Enoxaparin or Dalteparin to minimise the risk of thromboembolism associated with cardioversion
- If this fails then achieved medically by IV infusion or anti- arrhythmic drug such as flecainide or amiodarone
Ventricular rate control: Achieved by drugs that block AV node:
• Calcium channel blocker e.g. Verapamil
• Beta-blocker e.g. Bisoprolol
• Digoxin
• Anti-arrhythmic e.g. Amiodarone

  • Long term & stable patient management: either
    • Rate control:
  • AV nodal slowing agents plus oral anticoagulation
  • Beta-blocker e.g. Bisoprolol
  • Calcium channel blocker e.g. Verapamil or Diltiazem
  • If above fails then try Digoxin and then consider Amiodarone
    • Rhythm control:
  • Advocated for younger, symptomatic and physically active patients
  • Cardioversion to sinus rhythm and use Beta-blockers e.g. Bisoprolol to suppress arrhythmia
  • Can use pharmacological cardioversion e.g. Flecainide if no structural heart defect or use IV Amiodarone instead if there is structural heart disease
  • Appropriate anti-coagulation e.g. Warfarin due to thromboembolism risk with cardioversion

CHA2DS2VAS2 score

26
Q

ATRIAL FLUTTER:
def
Tx:

A

• Atrial flutter is usually an ORGANISED atrial rhythm with an atrial rate
typically between 250-350bpm

  • Electrical cardioversion but anticoagulate before e.g low molecular weight heparin e.g. Enoxaparin or Dalteparin if acute i.e. atrial flutter started less than 48 hours ago
  • Catheter ablation -creating a conduction block to try an restore rhythm and block offending re-entrant wave
  • IV Amiodarone to restore sinus rhythm and use a beta-blocker e.g. Bisoprolol to suppress further arrhythmias
27
Q

HEART BLOCK
ATRIOVENTRICULAR BLOCK: • There are three forms
• First-degree AV block:
• Second-degree AV block:

A

1st - PR interval to greater than 0.22 seconds
Causes:
• Hypokalaemia
• Myocarditis
• Inferior MI
• Atrioventricular node (AVN) blocking drugs e.g. beta blockers (Bisoprolol), calcium channel blockers (Verapamil) and Digoxin

2nd:-  Mobitz 1+11 block
Atrioventricular node (AVN) blocking drugs e.g. beta blockers (Bisoprolol), calcium channel blockers (Verapamil) and Digoxin - Inferior MI

Mobitz II block:
• PR interval is constant and QRS interval is dropped
• Failure of conduction through the His-Purkinje system
• Causes:
- Anterior MI
- Mitral valve surgery
- SLE and Lyme disease - Rheumatic fever
Recent-onset, narrow-complex AV block that has transient causes may
responses to IV atropine
- One option is permanent pacemaker

28
Q

Right bundle branch block (RBBB): On ECG:

A
  • Looks like maRRow
  • maRRow - Right bundle branch block - MarroW:
    • M-QRS looks like an M in lead V1
    • W-QRS looks like W in V5 & V6
    • Causes wide physiological splitting of the SECOND HEART SOUND
29
Q
  • Left bundle branch block (LBBB): On ECG:
A
  • Looks like wiLLiam
  • wiLLiam - Left bundle branch block
  • WilliaM:
    • W-QRSlookslikeaWinleadsV1&V2 • M - QRS looks like an M in leads V4-V6
    • Causes reverse splitting of the SECOND HEART SOUND
30
Q

Sinus tachycardia Tx:

A

Defined as heart rate greater than 100bpm

Treated by treating causes
• If necessary then beta-blockers can be used e.g. Bisoprolol

31
Q

SUPRAVENTRICULAR TACHYCARDIA (SVT): NOTE: TACHYARRHYTHMIA & TACHYCARDIA can be used INTERCHANGEABLY

• ATRIOVENTRICULAR JUNCTIONAL TACHYCARDIAS:

ATRIOVENTRICULAR NODAL RE-ENTRANT TACHYCARDIA (AVNRT):

ATRIOVENTRICULAR RE-ENTRANT TACHYCARDIA (AVRT):

Treatment FOR BOTH:

A

Arise from the atria or atrioventricular junction

  • Patients presenting with haemodynamic instability (hypotension & pulmonary oedema) require emergency cardioversion
  • If stable then vagal manoeuvres:
    • Breath-holding
    • Carotid massage
    • Valsalva manoeuvre - abrupt voluntary increase in intra-abdominal and intrathoracic pressure by straining - several seconds after the release of the strain, the resulting intense vagal effect may terminate the AVNRT or AVRT
  • If manoeuvres unsuccessful then IV adenosine - causes complete heart block for a fraction of a second and is highly effective at terminating AVNRT and AVRT
  • Surgery:
    • Catheter ablation of the accessory pathway in AVRT • Modification of the slow pathway in AVNRT
32
Q

VENTRICULAR TACHYARRHYTHMIAS: Umbrella term encompassing:

Name, Def, Tx:

A
  • Ventricular ectopics: • Premature ventricular contraction: Give beta-blockers e.g. Bisoprolol if symptomatic
  • Ventricular tachycardia: more than 100bpm with at least 3 irregular heart beats in a row: Give beta-blockers e.g. Bisoprolol if symptomatic
  • Sustained ventricular tachycardia:
    Ventricular tachycardia for longer than 30 seconds.
  • Haemodynamically unstable (e.g. hypotensive or pulmonary oedema):
    • Emergency electrical cardioversion - Stable:
    • IV beta-blocker e.g. Esmolol
    • IV Amiodarone
  • Prevented by the use of beta-blockers and implantable cardiac defibrillator
  • Ventricular fibrillation: very rapid and irregular ventricular activation with NO MECHANICAL EFFECT i.e NO CARDIAC OUTPUT: cardiac arrest so electrical defibrillation
33
Q

LONG QT syndrome (def)

Tx:

A

ventricular repolarisation - QT interval is greatly prolonged
- Treat underlying cause
- If acquired long QT then give IV isoprenaline (contraindicated for congenital
long QT)

34
Q

An aneurysm

FALSE vs TRUE

Aortic aneurysms classified as …

A

a dilation of the artery to TWICE the normal diameter

T=involves all layers of arterial wall
F=blood collects in the outer adventiitia

abdominal (AAA) or thoracic (TAA)

35
Q

TAA

Tx:

A

surgery if ruptured or symptomatic
monitoring
BP control - bisoprolol

36
Q

Aortic dissection:

Tx:

A

(begins with a tear in the intima (inner wall).
Blood then penetrates the diseased medial layer and flows between the
layers of the aorta, forcing the layers apart resulting in dissection)

50%+ are hypertensive - require urgent antihypertensive medication to reduce blood pressure to less than 120mmHg - give IV beta- blockers e.g. IV metoprolol or vasodilators e.g. IV GTN

  • Adequate analgesia e.g. morphine
  • Surgery to replace aortic arch
  • Endovascular intervention with stents
  • Patients require long term follow-up with CT or MRI
37
Q

PERIPHERAL VASCULAR DISEASE (PVD):

A

(partial blockage of leg or peripheral vessels by an atherosclerotic plaque and or resulting thrombus resulting in insufficient perfusion of the lower limb resulting in LOWER LIMB ISCHAEMIA)
(commonly aorta-iliac and infra-inguinal arteries)

38
Q

Thrombotic disease (more common nowadays):

Symptoms:
RF modification:
Tx:

A

The 6 P’s:

  • Pain
  • Pallor
  • Perishing cold
  • Pulseless
  • Paralysis
  • Paraesthesia - abnormal tingling or prickling - ‘pins & needles’
  • The more P’s present the more sudden and the more complete your ischaemia

• Antiplatelet agent such as P2Y12 inhibitor e.g. Clopidogrel to prevent
progression and minimise risk

SURGICAL EMERGENCY requiring REVASCULARISATION WITHIN 4-6 HOURS TO SAVE THE LIMB

39
Q

Shock is the..

A

term used to describe acute circulatory failure with inadequate or inappropriately distributed tissue perfusion (meaning there is inadequate substrate (glucose & oxygen) for aerobic cellular respiration), resulting in generalised hypoxia and/or an inability of the cells to utilise oxygen

40
Q

Recognising shock:

Effects of shock:

How to measure shock

A
  • Skin is pale, cold, sweaty and vasoconstricted
  • Pulse is weak and rapid
  • Pulse pressure reduced - mean arterial pressure (MAP) may be maintained - NOTE; ARTERIAL BP is NOT A GOOD INDICATOR OF SHOCK since it will be maintained until a very large amount of blood loss
  • Reduced urine output
  • Confusion, weakness, collapse and coma
  • Prolonged hypotension which can lead to life threatening organ failure after recovery from the acute event
  • This may be linked to the inflammatory response but we don’t fully understand how this works BUT inflammatory, coagulation and microvascular processes ALL appear to interact
  • Check capillary refill time (CRT):
    • NOT GOOD if it takes more than 3 seconds to turn pink after 5 seconds
    of compression = EARLIEST & MOST ACCURATE SIGN OF SHOCK
41
Q

Haemorrhagic Shock Classification

A
(Tennis Score):
Class I:
• 15% blood loss
• Pulse below 100 bpm 
• BP normal
• Pulse pressure normal
• Resp rate; 14-20
• Urine output greater than 30ml/hr 
• Slightly anxious
Class II:
• 15-30% blood loss
• Pulse greater than 100 bpm (tachycardia - earliest sign)
• BP normal due to autonomic response (increased sympathetic activity) 
• Pulse pressure decreased
• Resp rate; 20-30
• Urine output: 20-30ml/hr
• Mental status: mildly anxious
- Class III:
• 30-40% blood loss
• Pulse above 120 bpm
• BP decreased
• Pulse pressure decreased 
• Resp rate; 30-40
• Urine output: 5-15ml/hr
• Mental status: confused
42
Q

Clinical presentation of different types of shock:

A
- Hypovolaemic shock:
• Inadequate tissue perfusion:
- Skin: cold, pale, clammy, slate-grey,
- Brain: drowsiness and confusion
• Increased sympathetic tone
• Tachycardia - narrow pulse pressure and weak pulse 
• Sweating
• BP may be maintained initially but later hypotension
• Bradycardia
- Cardiogenic shock:
• Signs of myocardial failure
• Raised jugular venous pressure (JVP) 
• Gallop rhythm
• Basal crackles and pulmonary oedema
- Septic shock:
• Pyrexia (fever) and rigors (feels cold)
• Nausea and vomiting
• Vasodilation with warm peripheries 
• Bounding pulse
- Anaphylactic shock:
• Signs of profound vasodilation 
• Warm peripheries
• Low BP
• Tachycardia
• Bronchospasm
• Pulmonary oedema
43
Q

Organ systems at risk of SHOCK:

A
  • Kidneys - Acute tubular necrosis
  • Lung - Acute Respiratory Distress Syndrome (ARDs)
  • Heart - Myocardial ischaemia and infarction
  • Brain - confusion, irritability and coma
44
Q

Factors controlling BP and thus targets for BP control therapy:

A

Since; Cardiac output x Peripheral resistance = BP - can target peripheral resistance to alter BP

45
Q

ANGIOTENSIN CONVERTING ENZYME (ACE) INHIBITORS:

A

Indicated for; hypertension, heart failure and diabetic nephropathy

• ACE inhibitor end in ‘pril’
• Also REDUCE circulating levels of ALDOSTERONE
• Examples:
- RAMIPRIL
- ENALAPRIL
- PERINDOPRIL
- LISINOPRIL
- TRANDOLAPRIL
teratogenic
46
Q

ANGIOTENSIN II RECEPTOR BLOCKERS (ARB):

A
• Indicated for; hypertension, diabetic neuropathy and heart failure (when ACE inhibitor is contraindicated) also contraindicated in pregnancy too.
• ARB’s end in ‘sartan’
• Angiotensin receptor blocker acts on AT-1 receptor (angiotensin receptor)
• Examples:
- CANDESARTAN 
- LOSARTAN
- VALSARTAN
- IRBESARTAN
- TELMISARTAN
47
Q

CALCIUM CHANNEL BLOCKERS (CCB):

Types

A

Indicated for; hypertension, ischaemic heart disease (IHD) i.e. angina and arrhythmia (tachycardia)
A lot but not all end in ‘pine’ - these are vasodilators Diltiazem & Verapamil have effects on electrical conductivity Examples:
- AMLODIPINE
- DILTIAZEM
- VERAPAMIL
- NIFEDIPINE
- FELODIPINE
- LACIDIPINE
L-type calcium channel blockers (block ion channels and NOT RECEPTORS):
• Dihydropyridines: nifedipine, amlodipine, felodipine, lacidipine:
- Preferentially affect vascular smooth muscle
- Peripheral arterial vasodilators
• Phenylalkylamines: verapamil:
- Main effect is on heart
- Reduce HR (negatively chronotropic) and force of contraction of the heart (negatively inotropic)
• Benzothiozepines: diltiazem:
- Intermediate heart/peripheral vascular effects

48
Q

BETA-ADRENOCEPTOR BLOCKERS (BETA-BLOCKERS):

A
Lower down list in terms of use
Indicated for; ischaemic heart disease (IHD) - angina, heart failure, arrhythmia and hypertension A lot end in ‘olol’
Examples:
- BISOPROLOL
- CARVEDILOL
- PROPRANOLOL
- METOPROLOL
- ATENOLOL (antagonist at beta-1 adrenoceptor) 
- NADOLOL
49
Q

BETA-ADRENOCEPTOR BLOCKERS (BETA-BLOCKERS):

B1, B2

A

B-1 = HEART
B-2 = LUNGS (causes airway smooth muscle to relax)
Selectivity is relative rather than absolute i.e. it is dose-related, if dose is high enough then ALL will be non-selective
Thus be careful and use blockers smartly e.g. use SELECTIVE B-1 (but note selectivity is linked to dose so best to avoid in asthma) in asthma since if non-selective used then will block B-2 resulting in airway constriction and thus the worsening of asthma

50
Q

DIURETICS:

A

• Indicated for; hypertension and heart failure • Classes & Examples:
-Thiazides (cause Na+ and thus water loss in urine) and related drugs - act on DISTAL TUBE - LESS POTENT, tend to end in ‘thiazide’:
• BENDROFLUMETHIAZIDE
• HYDROCHLOROTHIAZIDE
• CHLOROTHALIDONE

-Loop diuretics (act on LOOP OF HENLE - MORE POTENT):
• FUROSEMIDE - blocks NA/K/2Cl (NKCC2) transporter
• BUMETANIDE

-Potassium-sparing diuretics:
SPIRONOLACTONE
EPLERENONE
NB: these two have the potential to antagonise aldosterone (anti-aldosterone)

  • Aldosterone antagonists
51
Q

OTHER ANTIHYPERTENSIVES:

A
• Alpha-1 adrenoceptor blockers:
- DOXAZOSIN
• Centrally acting (i.e. on brain) anti-hypertensives: 
- MOXONIDINE
- METHYLDOPA - CAN BE USED IN PREGNANCY 
• Direct renin inhibitor:
- ALISKIREN
52
Q

CHRONIC HEART FAILURE:

A
  • Symptomatic treatment of congestion:
    • Diuretics usually loop diuretics e.g. Furosemide
  • Disease influencing therapy - neurohumoral blockade:
    • Inhibition of renin-angiotensin-aldosterone system e.g. ACE-inhibitors and ARB’s
    • Inhibition of the sympathetic nervous system e.g. beta-blockers such as BISOPROLOL which are effective at blocking reflex sympathetic responses which stress the failing heart
  • First line treatment:
    • ACE inhibitors e.g. Ramipril and beta-blocker e.g. Bisoprolol • Low dose and slow uptitration
  • Second line:
    • Aldosterone antagonists
    • If ACE-inhibitor intolerant then give ARB’s (not as good as ACE-i) e.g. Candesartan
    • If ACE-I and ARB intolerant then give Hydralazine/nitrate combination (peripheral vasodilators)
  • Consider digoxin or ivabradine (rate-limiting drug)
53
Q

CARDIAC NATRIURETIC PEPTIDES:

  • Two types:
  • Main effects
  • Examples
A
  • Atrial natriuretic peptide (ANP) - atria
  • B-(brain) natriuretic peptide (BNP) - ventricles (found in brain and heart)

• Increased renal excretion of sodium (natriuresis) and water (diuresis)
• Relax vascular smooth muscle (except efferent arteriole of renal glomeruli to preserve filtration pressure in kidney whilst still removing Na+ and thus H2O thus no renal damage)
• Increased vascular permeability
• Inhibits the release or actions of:
- Aldosterone, angiotensin II, endothelin (most potent vasoconstrictor) and ADH
• Counter-regulatory system to the renin-angiotensin system
- Thus in heart failure there is raised natriuretic peptides in serum blood - its
the bodies response to heart failure

Cardiac natriuretic peptides are metabolised by Neutral Endopeptidase (NEP or neprilysin)
NEP inhibition increases levels of natriuretic peptides
Sacubitril - is a neprilysin inhibitor
Valsartan - is a ARB
Entresto - is a combination of sacubitril and valsartan - VERY EFFECTIVE IN HEART FAILURE
NITRATES:
- Arterial and venous dilators
- Reduce preload and afterload
- Lower BP
- Indicated for; ischaemic heart disease (angina) and heart failure - Examples:
• ISOSORBIDE MONONITRATE - long-acting
• GTN (GLYCERYL TRINITRATE) SPRAY - sublingual spray, potent vasodilator, commonly give headache
• GTN infusion

54
Q

Coronary artery disease:

CHRONIC STABLE ANGINA TREATMENT: -

A

Antiplatelet therapy:
• ASPIRIN
• CLOPIDOGREL (P2Y12 inhibitor) - use if aspirin intolerant
- Lipid-lowering therapy:
• Statins e.g. SIMVASTATIN, ATORVASTATIN, ROSUVASTATIN &
PRAVASTATIN
- Short acting nitrate:
• GTN spray for acute attack - DILATES veins to reduce the preload of the heart
- First line treatment:
• Beta blocker e.g. BISOPROLOL
• Calcium channel blocker e.g. AMLODIPINE
- If intolerant then SWITCH i.e. if using beta-blocker then switch to calcium channel blocker
- If not controlled then COMBINE
- If intolerant and uncontrolled then consider monotherapy or combination
with:
• Long acting nitrates:
- Ivabradine - Nicorandil - Ranolazine

55
Q

Coronary artery disease:

ACUTE CORONARY SYNDROMES (NSTEMI & STEMI) TREATMENT:

A

Pain relief:
• GTN spray
• Opiates - DIAMORPHINE (also helps calm patient) Dual antiplatelet therapy:
• Aspirin plus P2Y12 inhibitor (oral) e.g. TICAGRELOR, PRASUGREL or CLOPIDOGREL
Antithrombin therapy:
• Heparin e.g. FONDAPARINUX (injection)
Consider a glycoprotein IIb/IIIa inhibitor (IV) e.g. TIROFIBAN, EPTIFBATIDE or ABCIXIMAB
Background angina therapy:
• Beta blocker e.g. BISOPROLOL:
- Beta blockers help to relieve pain from angina by:
• Reducing O2 demand by slowing heart rate and reducing myocardial contractility
• Improve O2 distribution by slowing heart rate • Long acting nitrate e.g. IVABRADINE
• Calcium channel blocker e.g. AMLODIPINE - Lipid lowering therapy:
• Statins e.g. SIMVASTATIN
- Therapy for LVSD/heart failure as required:
• ACE-I e.g. RAMIPRIL
• Beta blocker
• Aldosterone antagonist

56
Q

ANTIARRHYTHMIC DRUGS:

classification

A
  • Vaughan Williams Classification:
    • Classes 1 & 3 = Rhythm control
    • Classes 2 & 4 = Rate control
    • Class 1:
  • Sodium channel blocker e.g. FLECAINIDE
    • Class 2:
  • Beta-adrenoceptor blockers (Beta-blockers):
    –Non-selective e.g. PROPRANOLOL, NADOLOL & CARVEDILOL
    –Selective (B-1) e.g. BISOPROLOL and METOPROLOL
    –NOTE: PROPRANOLOL is the most useful beta blocker to help control the arrhythmias which occur immediately following a MI since it also BLOCKS SODIUM CHANNELS
    • Class 3:
  • Prolong the action potential:
    • AMIODARONE
    • SOTALOL
    • BOTH can result in QT PROLONGATION which can be FATAL
    • Class 4:
  • Calcium channel blockers:
    • VERAPAMIL (more effective than amlodipine since it DOES NOT effect the calcium channel at rest)
    • DILTIAZEM
    • AMLODIPINE
  • Sympathetic drive e.g. adrenaline worsens arrhythmia
  • DIGOXIN: Inhibits the Na/K pump - found everywhere in body
    • Main effect on heart:
  • Bradycardia (due to increased vagal (parasympathetic) tone)
  • Increased ectopic activity - can trigger extra heartbeats i.e. minor arrhythmias
  • Increased force of contraction (DIRECT POSITIVE INOTROPIC EFFECT on heart muscle) by increased intracellular Ca2+ - Slowing of AV conduction