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Main Conditions > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is the Sequence of the layers of the Heart

6 layers and one cavity

A

Fibrous Pericardium -> Parietal Serous Pericardium -> Pericardial Cavity -> Visceral Serous Pericardium (Epicardium) -> Myocardium -> Endocardium.

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2
Q

What is Atherosclerosis and what can it lead to?

affects medium and larger arteries

A
  • Combination of fatty deposits in artery wall and stiffening of the artery walls.
  • Chronic Inflammation + activation of the immune system in artery wall -> Lipid deposition -> atheromatous plaques
  • Plaques -> Stiffening artery walls -> HTN
  • Plaques -> stenosis -> reduced blood flow (angina)
  • Plaques -> Plaque Rupture -> thrombus formation -> blockage -> ischaemia

RF
- old age
- FH
- Male
- Raised Cholesterol
- Smoking
- Alcohol
- Poor diet
- Poor sleep
- Obesity
- Stress

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3
Q

Primary Prevention of CVD vs Secondary Prevention

A
  • Primary Prevention: for Pts that have never had a diagnosis of CVD
  • Secondary Prevention: Post-diagnosis of angina, MI, TIA, Stroke, Peripheral Arterial Disease

Excercisw 150 min per week moderate/75 min vigourous intensity p/week
Strength training 2x a wk

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4
Q

QRISK3 Score

Medication for Primary Prevention is based on QRISK 3 score

A
  • QRISK3 score predicts mortaility of a patient within the next 10 years from Stroke or MI
  • Results >10%: Prescribe atorvastatin 20mg every night.

For EVERY T1DM or CKD patient:
- Atorvastatin 20mg offered as primary prevention.

  • Chronic kidney disease (eGFR less than 60 ml/min/1.73 m2)
  • Type 1 diabetes for more than 10 years or are over 40 years
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5
Q

Statins Mechanism of action & Side effects

Atorvastatin, Simvastatin etc

A
  • Reduce cholesterol production in liver by inhibitng HMG CoA reductase
  • Check Lipids every 3m (aim for 40% reduction in Cholesterol)
  • Check LFT within first 3m + 12m as they can increase ALT & AST

Statins are taken at night as liver produces cholesterol at night.

Side Effects
* Myopathy (muscle weakness & pain)
* Rhabdomyolysis (muscle damage - important to check Cretinine Kinase in pt’s with muscle pain)
* T2DM

Contraindications
- Macroclide Abx’s - When taking clarithromycin or erythromycin - STOP Statins
- Pregnancy

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6
Q

What are some alternatives to statins - if they’re not tolerated well.

A

Ezetimibe
* Inhibiting the absorption of cholesterol in the intestine.
* Also used as combination with a statin when statins alone are inadequate.

PCSK9 inhibitors (evolocumab and alirocumab)
* Monoclonal antibodies that lower cholesterol.
* They are highly specialist treatments, given as a subcutaneous injection every 2-4 weeks.

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7
Q

Secondary prevention of CVD - What are the 4 A’s

Secondary prevention after developing cardiovascular disease depends on the specific condition

A

A – Antiplatelet medications (e.g., aspirin, clopidogrel and ticagrelor)
A – Atorvastatin 80mg
A – Atenolol (or an alternative beta blocker – commonly bisoprolol) titrated to the maximum tolerated dose
A – ACE inhibitor (commonly ramipril) titrated to the maximum tolerated dose

in MI - Dual Platelet is offered

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8
Q

What is Familial Hypercholeterolaemia?

A
  • Autosomal Dominant
  • high levels of LDL -> Early CVD
  • mutations in the gene which encodes LDL-Receptor Protein.
  • cholesterol >7.5mmol and/or
  • CVD event in first degree relative U60
  • Tendon xanthomata (hard nodules in the tendons containing cholesterol, often on the back of the hand and Achilles)
  • Xanthelasma - see other card.

Clinical diagnosis: Simon Broome criteria

Management
* Specialist Referral
* Genetic testing
* High dose statins

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9
Q

What is Xanthelasma?

  • Tendon xanthomata (hard nodules in the tendons containing cholesterol, often on the back of the hand and Achilles)
A
  • Yellowish Papules + plaques caused by lipid deposits commonly seen on eyelid.

Management
* Surgical excision
* topical tricholoroacetic acid
* laser therapy
* electrodesiccation.

not necessary to have lipid abnormality

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10
Q

What is Stable Angina and its investigations

A
  • Atheresclerotic build up in arteries causing chest pain during exertion due to lack of sufficient blood supply
  • Constricting chest pain - with no radiation

unstable when symptoms present at rest. -> ACS

Investigations
* Cardiac Exam, BP, BMI
* ECG for other modalities
* FBC (anaemia)
* LFTs (monitor before starting statin)
* Lipid Profile
* TFT (?thyroid disease)
* Cardiac Stress testing
* CT coronary angiography
* gold standard Invasive coronary angiography

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11
Q

What are the management options for Stable Angina

RAMPS

A
  • R Refer to Cardio
  • A Advice regarding diagnosis
  • M Medical Management
  • P Procedural/Surgical interventions
  • S Secondary Prevention

Immediate Management: GTN Spray (Use 3 times spaced out every 5 mins -> Call ambulance. Side Fx GTN: Headaches, diziness.

Longterm Management: Beta Blocker (bisoprolol), CCB (verapamil), amlodipine given if b-blocker prescribed w/CCB

Surgical: PCI or CABG (using saphenous vein, radial artery or interanal thoracic artery)

Secondary prevention:
A – Antiplatelet medications (e.g., aspirin, clopidogrel and ticagrelor)
A – Atorvastatin 80mg
A – Atenolol (or an alternative beta blocker – commonly bisoprolol) titrated to the maximum tolerated dose
A – ACE inhibitor (commonly ramipril) titrated to the maximum tolerated dose

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12
Q

ACS Presentation

STEMI - NSTEMI - Unstable angina

What is Silent MI

A
  • Central tightening chest pain
  • Radiation to Left and Jaw and/or Arms
  • N&V
  • Sweating & Clamminess
  • feeling of impeding doom
  • Dyspnoea
  • Palpitations
  • Maybe Slightly Tachycardic

Symptoms should continue at rest for more than 15 minutes.

Silent MI when pt doesn’t feel symptoms of chest pain in ACS - Elderly, Diabetic, Females susceptible.

Cardiogenic shock is a poor prognostic factor in ACS

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13
Q

Investigations to determine ACS

A
  • ECG: If MI or not to determine location of MI.
  • Troponin: Cardiac Marker

Other investigations
* Baseline Bloods: FBC, U&E, LFT, Lipids and Glucose
* CXR: look for pulmonary oedema, rule other modalities out
* ECHO: Assess damage to heart, specifically LV function

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14
Q

ECG changes for ACS

basics for STEMI and NSTEMI

A

STEMI:
* ST- Segment Elevation
* New LBBB

NSTEMI:
* ST Segment depression
* T Wave inversion

Unstable Angina:
* Normal ECG
* May have some ST depression or T wave inversion (rare)

Pathological Q Waves - deep infarct (transmural) appear >6h after onset.

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15
Q

4

What are the coronary territories on a ECG

Location of MI, ECG change & which artery is affected.

A

Anterior MI: ECG V1-4 - LAD artery
Anterolateral MI: ECG I, aVL, V3-6 Left Coronary Artery
Inferior MI: ECG II, III, aVF Right Coronary artery
Lateral MI: ECG I, aVL, V5-6 Left Circumflex

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16
Q

NOT COMPLETED

Management of NSTEMI

MONA is standard in all ACS

A
  • Morphine, Oxyen (If <94%), Nitrates (caution if hypotensive), Aspirn (300mg)
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17
Q

Management of STEMI

MONA is standard in all ACS

STEMI: ST elevation by >2.5 small squares in M <40y in V2-3. > 2small squares in >40y. In F 1.5 small squares

A
  • Morphine, Oxyen (If <94%), Nitrates (caution if hypotensive), Aspirn (300mg)
  • PCI (within 120m) - Praugrel given, Radial Acess, Unfractioned Heparin + bailout glycoprotein IIb/IIIa inhibitor (tirofiban)
  • Fibrinolysis (>2h+<12h) - give antithrombin - post procedure give ticagrelor. ECG 60-90m later, if not resloed then PCI

Consider Fibrinolysis if PCI being delayed

if >12h and still exhibiting symptoms = PCI

  • in PCI drug eluting stents given over bare metal stents as chnce of restenosis lowered.
  • patients undergoing PCI with femoral access: bivalirudin with bailout GP
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18
Q

Secondary Prevention post-MI

A

Secondary prevention:
A – Antiplatelet medications (e.g., aspirin, clopidogrel and ticagrelor)
A – Atorvastatin 80mg
A – Atenolol (or an alternative beta blocker – commonly bisoprolol) titrated to the maximum tolerated dose
A – ACE inhibitor (commonly ramipril) titrated to the maximum tolerated dose

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19
Q

Types of Myocardial Infarction

4 types

Used more for exams and not clinical practise

A
  • Type 1: Traditional MI due to an acute coronary event
  • Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)
  • Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
  • Type 4: MI associated with procedures such as PCI, coronary stenting and CABG

You could remember these with the “ACDC” mnemonic:

Type 1: A – ACS-type MI
Type 2: C – Can’t cope MI
Type 3: D – Dead by MI
Type 4: C – Caused by us MI

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20
Q

What are the complications of Myocardial Infarction

10 major complications

A
  1. Cardiac Arrest - Pts develop V.Fib -> cardiac arrest. Most common cause of death post MI
  2. Cardiogenic Shock - ventricular myocardium is damaged in the infarction the ejection fraction of the heart may decrease -> Cardiogenic shock
  3. Chronic HF - ventricular myocardium may become dysfunctional resulting in chronic heart failure
  4. Tachyarrythmias - V. Fib most common, Ventricular Tachycardia also common
  5. Bradyarrythmias - AV Block common following Inferior MI
  6. Pericarditis - in first 48h, pain on lying, pericardial rub
  7. LV Aneurysm - due to damage, persistent ST elevation and left ventricular failure, increased risk of stroke
  8. LV Free wall rupture - leads to cardiac tamponade, Urgent pericardiocentesis and thoracotomy
  9. Ventricular Septal Defect - Acute HF with pansystolic murmur
  10. Acute Mitral Regurgitation - due to ischaemia or rupture of the papillary muscle. hypotension + pulmonary oedema, Systolic murmur
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21
Q

What is Dressler’s Syndrome?

A
  • Tends to occur around 2-6 weeks following a MI.
  • autoimmune reaction against antigenic proteins as myocardium recovers
  1. Fever
  2. Pleuritic pain
  3. pericardial effusion
  4. raised ESR.
  • It is treated with NSAIDs.
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22
Q

What is Brugada Syndrome

including ECG changes

A
  • inherited cardiovascular disease with may present with sudden cardiac death
  • Autosomal Dominant
  • common in asians
  • mutation in the SCN5A

ECG Changes

  • convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave
  • partial right bundle branch block

Choice of investigation

  • flecainide or ajmaline

Management

  • implantable cardioverter-defibrillator
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23
Q

Side effects + Contraindications of beta blockers.

atenolol propranolol

A

Side effects
* bronchospasm
* cold peripheries
* fatigue
* sleep disturbances, including nightmares
* erectile dysfunction

Contraindications
* uncontrolled heart failure
* asthma
* sick sinus syndrome
* concurrent verapamil use: may precipitate severe bradycardia

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24
Q

Side effects of Nitrates

expand on nitrate tolerance

A

Side-effects
* hypotension
* tachycardia
* headaches
* flushing

Mechanism of Action
* Release of NO -> activate guanylate cyclase -> Converting GTP to cGMP -> low intracellular Ca2+
* Dilated Coronary arteries and reduced venous return, less pressure on less ventricle -> less myocardial O2 demand

  • Many patients who take nitrates develop tolerance and experience reduced efficacy
  • If you develop tolerance then you should reduce times b/ween dose from 12h to 8h.
  • Pt’s taking isosorbide mononitrate -modified release will not experience this.
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25
Q

What are the main DVLA rules with regards to CVD

A
  • Angioplasty (elective) - 1 week off driving
  • CABG - 4 weeks off driving
  • acute coronary syndrome- 4 weeks off driving (1 wk if successfully treated by angioplasty)
  • angina - driving must cease if symptoms occur at rest/at the wheel
  • pacemaker insertion - 1 week off driving
  • implantable cardioverter-defibrillator (ICD) 6m (permanent) 1m (temp)
  • successful catheter ablation for an arrhythmia- 2 days off driving
  • aortic aneurysm of 6cm or more - notify DVLA. Licensing will be permitted subject to annual review.
    an aortic diameter of 6.5 cm or more disqualifies patients from driving
  • heart transplant: do not drive for 6 weeks, no need to notify DVLA
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26
Q

Mechanism and Interactions of Clopidogrel

antiplatelet agent - thienipyridines

other similar drugs:-
- Prasugrel
- ticagrelor
- ticlopidine

A
  • Antagonist of P2Y12 adenosine diphosphate (ADP) receptor - inhibiting activation of platelets

Interactions
- PPIs - make Clopidogrel less effective
- omeprazole concerning
- lanzoprazole fine for now!

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27
Q

When should you consider Clopidogrel over Ticagrelor

A
  • Ticagrelor considered mainstay however if there is a high risk of bleeding then opt for Clopidogrel
  • In bleeding risk give Clopidogrel over Praugrel.
28
Q

Primary Hypertension

Essentia Hypertension

The vast majority (around 90-95%) have primary, or essential, hypertension. This is where there is no single disease causing the rise in blood pressure but rather a series of complex physiological changes which occur as we get older.

A
  • a clinic reading persistently above >= 140/90 mmHg, or:
  • a 24 hour blood pressure average reading >= 135/85 mmHg

Diagnosis

  • 24h ABPM
  • 2nd line: home readings

Important with newly diagnosed hypertension

  • fundoscopy: to check for hypertensive retinopathy
  • urine dipstick: to check for renal disease, either as a cause or consequence of hypertension
  • ECG: to check for left ventricular hypertrophy or ischaemic heart disease
  • HbA1c: exisiting diabetes or not as it’s a RF

Symptoms in significatnly raised BP > 200/120 mmHg.
* headaches
* visual disturbance
* seizures

29
Q

Secondary Hypertension

A
  • Most common cause of 2ndry HTN: primary hyperaldosteronism (incl. Conns)

Renal causes: glomerulonephritis, pyelonephritis, adult polycystic kidney disease, renal artery stenosis

Endocrin causes: phaeochromocytoma, Cushing’s syndrome, Liddle’s syndrome, congenital adrenal hyperplasia (11-beta hydroxylase deficiency), acromegaly

Drug causes: steroids, monoamine oxidase inhibitors, the combined oral contraceptive pill, NSAIDs, leflunomide

Others; Pregnancy, Coarction of Aorta

30
Q

Management of Hypertension

Stage 1 treat if <80y

stage 1 HTN 135/85
Stage 2 HTN 150/95
Severe TN 180/? or 120/?

A

Lifestyle: a low salt diet is recommended, aiming for less than 6g/day, ideally 3g/day.

Step 1
Patient <55y or with Diabetes

  • ACE inhib (-pril)
  • ARB (2nd line)

Patient >55y or Black/African

  • CCB - Amlodipine

Step 2
If on ACEinhib + CCB or Thiazide like diuretic (indapamide)
If on CCB + ACEinhib or Thiazide like diuretic (indapamide) (ARB in black)

Step 3
Ace inhib/ARB + CCB + Diuretic (ramipril/losartan + amlodipine + indapamide)

Step 4
Perform relevant chekcs (Postural drop etc)
if potassium < 4.5 mmol/l add low-dose spironolactone
if potassium > 4.5 mmol/l add an alpha- or beta-blocker

Black Diabetic man: ARB as ACEinhib not tolerated

31
Q

Atrial Flutter

a form of supraventricular tachycardia characterised by a succession of rapid atrial depolarisation waves.

A

ECG: ‘sawtooth’ appearance

  • as the underlying atrial rate is often around 300/min the ventricular or heart rate is dependent on the degree of AV block. For example if there is 2:1 block the ventricular rate will be 150/min

Management
* is similar to that of atrial fibrillation although medication may be less effective
* atrial flutter is more sensitive to cardioversion however so lower energy levels may be used

32
Q

Atrial Fibrillation

A

Types

  • First detected
  • Recurrent: more than 2 epis of AF
  • Paroxysmal: Spontaneously terminate + last less than 7 days
  • Persistent: last more than 7 days
  • Permanent AF there is continuous atrial fibrillation which cannot be cardioverted

Signs

  • Palpitations
  • Dyspnoea
  • Chest pain
  • Irregulary Irregular pulse

Ix

  • ECG: Irregularly Irregular rhythm + absent P waves

Management
* >48h Rate Control: rate-limiting calcium channel blocker (diltiazem) - others incl digoxin and/or B blockers (contraindicated in asthma)
* <48h Rhythm Control: Cardioversion or amiodarone in heart disease, flecainide (if no structural heart disease)
* Stroke Prevention: ChadsVasc - apixaban (warfarin second line)

MISc

  • signs of haemodynamic instability (e.g. hypotension, heart failure) they should be electrically cardioverted
  • Electrical cardioversion is synchronised to the R wave
  • 48h+ and want to rhythm control then 3 weeks of anticoag therapy before.

ORBIT to assess risk of bleed

Rhythm control first in: coexistent heart failure, first onset AF or where there is an obvious reversible cause.

Important to perform rhythm control in first 48h as patient can get stroke with cardio version. if over 48h then consider patients who have been on long term anticoags prior

33
Q

CHA2DS2 VASC score in AF

transthoracic echocardiogram has been done to exclude valvular heart disease, which in combination with AF is an absolute indication for anticoagulation.

A

Congestive Heart Failure : 1pt
Hypertension: 1pt
Age (1 or 2): 1pt for 65-74y 2pt for 75y>
Diabetes: 1pt
Stroke (previously): TIA or VTE etc: 2pt
Vascular Disease: 1pt
Sex: Female = 1pt

ORBIT TO SEE RISK OF BLEED

Results

0: No treatment

1:
Males: Consider anticoagulation
Females: No treatment (this is because their score of 1 is only reached due to their gender)

2: or more Offer anticoagulation

34
Q

Heart Block

In atrioventricular (AV) block, or heart block, there is impaired electrical conduction between the atria and ventricles. There are three types: with one group having 2 subtypes

A

First Degree Heart Block

  • PR interval > 0.2 seconds
  • Asymptomatic

Second Degree Heart Block Mobitz 1

  • Prolonging PR until beat drops

Second Degree Heart Block Mobitz 2

  • Constant PR then beat drops

Third Degree Heart Block (complete)

  • there is no association between the P waves and QRS complexes

Features of Complete HB

  • syncope
  • heart failure
  • regular bradycardia (30-50 bpm)
  • wide pulse pressure
  • JVP: cannon waves in neck
  • variable intensity of S1
35
Q

Supraventricular Tachycardia

Supraventricular tachycardia is caused by the electrical signal re-entering the atria from the ventricles. so ventricles contract again in short succession when signal goes back up to AVN. This causes a self-perpetuating electrical loop without an endpoint, resulting in narrow complex tachycardia.

A
  • Episodes are characterised by the sudden onset of a narrow complex tachycardia on ECG
  • Differentiated from AF due to normal rhythm but like AF no p waves seen

Acute management

  • Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe
  • carotid sinus massage
  • intravenous adenosine
    rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg
    contraindicated in asthmatics - verapamil is a preferable option
  • electrical cardioversion in shock

Prevention

  • beta-blockers
  • radio-frequency ablation

Paroxysmal SVT: where SVT reoccurs and remits in same patient over time.

36
Q

Left Bundle Branch Block

A
  • ECG: in LBBB there is a ‘W’ in V1 and a ‘M’ in V6
  • New LBBB is always pathological.

Causes

  • myocardial infarction
  • hypertension
  • aortic stenosis
  • cardiomyopathy
  • rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
37
Q

Right Bundle Branch Block

A
  • ECG: in RBBB there is a ‘M’ in V1 and a ‘W’ in V6

Causes

  • normal variant - more common with increasing age
  • right ventricular hypertrophy
  • chronically increased right ventricular pressure - e.g. cor pulmonale
  • pulmonary embolism
  • myocardial infarction
  • atrial septal defect (ostium secundum)
  • cardiomyopathy or myocarditis
38
Q

Pericarditis

inflammation of the pericardial sac. Acute: 4-6wk

A

Causes
* viral infections (Coxsackie)
* tuberculosis
* uraemia
* post-myocardial infarction: fibrinous pericarditis or autoimmune pericarditis (Dressler’s syndrome)
* connective tissue disease: systemic lupus erythematosus, rheumatoid arthritis
* hypothyroidism
* malignancy: lung cancer, breast cancer
* trauma

Features

  • Pleuritic chest pain. Is often relieved by sitting forwards
  • non-productive cough, dyspnoea and flu-like symptoms
  • pericardial rub on auscultation

Ix

  • widespread, Saddled Shaped ST elevation
  • PR Depression
  • Transthoracic ECHO#
  • Raised Trop in 30% of cases

Management

  • Usually Self limiting
  • Avoid Strenous excercise
  • NSAID + Colcichine for viral pericarditis

Constricitve Pericarditis

  • Usally result of TB infection
  • Kussmaul’s sign is positive
  • JVP shows prominent x and y descent
  • RHF
  • CXR: pericardial calcification
39
Q

Cardiac Tamponade

Cardiac tamponade is characterized by the accumulation of pericardial fluid under pressure.

A

Beck’s Triad

  1. hypotension
  2. raised JVP
  3. muffled heart sounds

Other Signs

  • dyspnoea
  • tachycardia
  • an absent Y descent on the JVP - this is due to the limited right ventricular filling
  • pulsus paradoxus - an abnormally large drop in BP during inspiration
  • ECG: electrical alternans

Management
* urgent pericardiocentesis

40
Q

Myocarditis

particularly considered in younger patients who present with chest pain

inflammation of the myocardium

A

Causes
* viral: coxsackie B, HIV
* bacteria: diphtheria, clostridia
* spirochaetes: Lyme disease
* protozoa: Chagas’ disease, toxoplasmosis

Presentation

  • usually young patient with an acute history
  • chest pain
  • dyspnoea
  • arrhythmias

Ix

  • ↑ inflammatory markers in 99%
  • ↑ cardiac enzymes
  • ↑ BNP
  • ST elevation

Management

  • treatment of underlying cause e.g. antibiotics if bacterial cause
  • supportive treatment e.g. of heart failure or arrhythmias

Complications
* heart failure
* arrhythmia, possibly leading to sudden death
* dilated cardiomyopathy: usually a late complication

41
Q

Infective

Endocarditis

Staph Aureus - Gram +ve most common

the mitral valve is most commonly affected - in IVDU it is TRICUSPID

A
  • Staph Aureus - Gram +ve most common in IVDU
  • Strep Viridans - most common in dental issues

Poor prognostic factors
* Staphylococcus aureus infection
* prosthetic valve (especially ‘early’, acquired during surgery)

Signs

  • New or “changing” heart murmur
  • Splinter haemorrhages (thin red-brown lines along the fingernails)
  • Petechiae (small non-blanching red/brown spots) on the trunk, limbs, oral mucosa or conjunctiva
  • Janeway lesions (painless red flat macules on the palms of the hands and soles of the feet)
  • Osler’s nodes (tender red/purple nodules on the pads of the fingers and toes)
  • Roth spots (haemorrhages on the retina seen during fundoscopy)
  • Splenomegaly (in longstanding disease)
  • Finger clubbing (in longstanding disease)

Management

  • Blind: Amoxicillin + gentamicin
  • Native valve endocarditis caused by staphylococci: flucloxacillin (vancomycin)

Indications for surgery
* severe valvular incompetence
* aortic abscess (often indicated by a lengthening PR interval)
* infections resistant to antibiotics/fungal infections
* cardiac failure refractory to standard medical treatment
* recurrent emboli after antibiotic therapy

Prophylaxis

  • none for dental procedures
  • any episodes of infection in people at risk of infective endocarditis should be investigated and treated promptly to reduce the risk of endocarditis developing
42
Q

Duke Criteria Infective Endocarditis

A

The Modified Duke criteria are a set of clinical guidelines used for diagnosing infective endocarditis, focusing on major and minor criteria related to clinical, laboratory, and imaging findings.

Infective endocarditis diagnosed if
* pathological criteria positive, or
* 2 major criteria, or
* 1 major and 3 minor criteria, or
* 5 minor criteria

43
Q

Ventricular Tachycardia

Ventricular ectopics refers to abnormal heartbeats originating in the ventricles rather than the usual electrical pathways, often detected on an electrocardiogram (ECG) and potentially associated with various cardiac conditions.

A
  • Ventricular tachycardia (VT) is broad-complex tachycardia originating from a ventricular ectopic focus.

Types of V. Tachycardia

  1. monomorphic VT: caused by myocardial infarction
  2. polymorphic VT: A subtype of polymorphic VT is torsades de pointes which is precipitated by prolongation of the QT interval. Treat w, MgSulfate

Management

  • Adverse signs (systolic BP < 90 mmHg, chest pain, heart failure: immediate cardioversion
  • amiodarone: ideally administered through a central line
  • Verapamil should NOT be used in VT
44
Q

Prolonged QT Syndrome

Long QT syndrome (LQTS) is an inherited condition associated with delayed repolarization of the ventricles.

A
  • may lead to ventricular tachycardia/torsade de pointes and can therefore cause collapse/sudden death
  • slow delayed rectifier potassium channel
  • normal corrected QT interval is less than 430 ms

Management

  • avoid drugs which prolong the QT interval
  • beta-blockers
  • implantable cardioverter defibrillators in high risk cases

Drugs that cause prolonged QT
* amiodarone, sotalol, class 1a antiarrhythmic drugs
* tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)
* methadone
* chloroquine
* terfenadine**
* erythromycin
* haloperidol
* ondanestron

45
Q

Wolf Parkinson White Syndrome

Supraventricular Tachycardia

A

Wolff-Parkinson White (WPW) syndrome is caused by a congenital accessory conducting pathway between the atria and ventricles leading to atrioventricular re-entry tachycardia (AVRT). As the accessory pathway does not slow conduction AF can degenerate rapidly to VF.

definitive treatment: radiofrequency ablation of the accessory pathway

46
Q

Aortic Stenosis

L.V to Aorta blood struggles to get through

A

Symptomatic Disease:

  • Chest pain
  • Dyspnea
  • Syncope/presyncope
  • Ejection systolic murmur, classically to carotids

Severe Aortic Stenosis:

  • Slow-rising pulse
  • Thrill
  • LV hypertrophy/failure

Causes:

  • Degenerative calcification >65y
  • Bicuspid aortic valve <65y
  • William’s syndrome
  • Post-rheumatic disease
  • Subvalvular: HOCM

Management:

  • Asymptomatic: Observe
  • Symptomatic: Valve replacement
  • Consider surgery if asymptomatic, gradient >40 mmHg with LV dysfunction
  • Options: Surgical AVR, TAVR, Balloon valvuloplasty

* soft/absent S2 + S4

The murmur associated with aortic stenosis is best heard in the aortic area, which is typically the second right intercostal space at the sternal border.

47
Q

Mitral Regurgitation

AKA Mitral insufficiency b/ween LA and LV

RF

  • women
  • Lower body mass
  • Age
  • Renal dysfunction
  • Prior myocardial infarction
  • Prior mitral stenosis or valve prolapse
  • Collagen disorders e.g. Marfan’s Syndrome and Ehlers-Danlos syndrome
A

Causes

  • Papillary Muscle damage post MI
  • Mitral Valve Proplapse
  • Infective endocarditis
  • rheumatic fever

Presentation

  • Asymptomatic in many
  • LV Failure
  • Pulmonary HTN
  • fatigue, shortness of breath and oedema.
  • pansystolic murmur heard best at apex radiating to axilla

Ix

  • ECHO
  • broad P waves

Management

  • acute cases involves nitrates, diuretics, positive inotropes and an intra-aortic balloon pump to increase cardiac output
48
Q

Mitral Stenosis

A

Causes

  • Rheumatic Fever
  • Others: carcinoid and endocardial fibroelastosis

Features

  • dyspnoea
    ↑ left atrial pressure → pulmonary venous hypertension
  • haemoptysis
  • Mid late diastolic Murmur
  • Opening snap + loud s1
  • Malar Flush
  • AF
  • low volume pulse

Ix

  • ECHO
  • CXR: left atrial enlargement may be seen

Management

  • Asymptomatic: monitor on ECHO
  • Symptomatic: percutaneous mitral balloon valvotomy OR valve replacement
49
Q

Aortic Regurgitation

caused either by disease of the aortic valve or by distortion or dilation of the aortic root and ascending aorta.

A

Features

  • early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre
  • collapsing pulse
  • wide pulse pressure
  • Quincke’s sign (nailbed pulsation)
  • De Musset’s sign (head bobbing)

Management

  • surgery: aortic valve indications include:
  • symptomatic patients with severe AR
  • asymptomatic patients with severe AR who have LV systolic dysfunction
50
Q

Aortic Aneurysm

RF: Smoking HTN Syphilis Ehlers Danlos & Marfans

Result of the failure of elastic proteins within the extracellular matrix. Aneurysms typically represent dilation of all layers of the arterial wall. Most aneurysms are caused by degenerative disease.

A
  • Diameters of 3cm and greater, are considered aneurysmal
  • Screening for an abdominal aortic aneurysm consists of a single abdominal ultrasound for males aged 65.
  • USS every 12m for 3-4.4cm or vascular surgery referral if more than 5.5cm (2wk) if 3-5.4cm (12wk)
  • treat with elective endovascular repair

Features normal aneurysm

  • asymptomatic mostly

Feautres Ruptured AAA

  • severe, central abdominal pain radiating to the back
  • pulsatile, expansile mass in the abdomen
  • patients may be shocked (hypotension, tachycardic) or may have collapsed

Management Ruptured AAA

  • immediate vascular review with a view to emergency surgical repair.

CT ANGIOGRAM FOR DIAGNOSIS

51
Q

Aortic Dissection

Aortic dissection is a rare but serious cause of chest pain.

tear in the tunica intima of the wall of the aorta

RFs
* hypertension: the most important risk factor
* trauma
* bicuspid aortic valve
* collagens: Marfan’s syndrome, Ehlers-Danlos syndrome
* Turner’s and Noonan’s syndrome
* pregnancy
* syphilis

A
  • Tearing chest pain radiating to back
  • pulse deficit
  • aortic regurgitation
  • hypertension

Types

  • type A - ascending aorta, 2/3 of cases
  • type B - descending aorta, distal to left subclavian origin, 1/3 of cases
  • Type A chest pain Type B Back pain

Ix

  • CXR widened mediastinum
  • CT Angiography: a false lumen is a key finding in diagnosing aortic dissection
  • Transoesophageal echocardiography (TOE) for CT contraindication

Management

  • Type A: surgery
  • Type B: conservative, IV Labetalol to reduce BP
52
Q

Arterial & Venous Ulcers

Buerger’s disease?

Other causes of Ulcers:

  • Marjolin’s ulcer: SCC
  • Neuropathic ulcers
  • Pyoderma gangrenosum
A

Venous Ulcers

  • due to venous hypertension, secondary to chronic venous insufficiency
  • other causes calf pump dysfunction or neuromuscular disorders
  • Oedema
  • brown pigmentation
  • eczema
  • Above ankles
  • Painless
  • Management: 4 layer compression banding after exclusion of arterial disease or surgery

Arterial Ulcers

  • Toes and heels mostly
  • deep, punched-out’ appearance
  • Painful
  • no pulse and cold
  • low ABPI

Deep venous insufficiency is related to previous DVT and superficial venous insufficiency is associated with varicose veins

53
Q

Intermittent Claudication

three main types of Peripheral arterial disease

  1. intermittent claudication
  2. critical limb ischaemia
  3. acute limb-threatening ischaemia
A

RF: Smoking

Symptoms

  • Pain/aching/burning on walking
  • Relief at rest

Ix

  • ABPI: 0.6-0.9 (normal =1)
  • duplex ultrasound is the first line investigation

Management:

  • Statin + clopidogrel
  • Exercise training
54
Q

Critical Limb Ischaemia

A

Features should include 1 or more of:

  • rest pain in foot for more than 2 weeks
  • ulceration
  • gangrene

Ix

  • An ankle-brachial pressure index (ABPI) of < 0.5 is suggestive of critical limb ischaemia.

Management:

  • Statin + clopidogrel
  • Exercise training
  • endovascular revascularization: Short segement lesions <10cm
  • Surgical revascularization: long segment lesions (> 10 cm),
  • Amputation in unresolveable cases
55
Q

Acute limb-threatening ischaemia

one or more of the 6 Ps

A
  1. pale
  2. pulseless
  3. painful
  4. paralysed
  5. paraesthetic
  6. ‘perishing with cold’

Ix
* handheld arterial Doppler examination.
* Doppler signals are present, an ankle-brachial pressure index (ABI) should also be obtained.

Initial management

  • IV opioid
  • LMWH

Definitive management:
* intra-arterial thrombolysis
* surgical embolectomy
* angioplasty
* bypass surgery
* amputation: for patients with irreversible ischaemia

Thrombus Vs Embolus

An attempt is generally made to determine whether the ischaemia is due to a thrombus (due to rupture of atherosclerotic plaque) and embolus (e.g. secondary to atrial fibrillation):

56
Q

Heart Failure

managemnt acute vs chronic

Furosemide is only symptomatic relief drug

A

Acute Management

  • IV Furosemide
  • Oxygen: for sats
  • Nitrates: (not if hypotensive)
  • Resp Failure: CPAP
  • inotropic agents if cardiogenic shock (hypotensive)
  • Stop betablockers if Bradycardic

Chronic

  • First line: ACEi + B Blocker
  • 2nd line: Spironolactone +/or SGLT-2 inhibitors (dapagliflozin)
  • 3rd line: ivabradine (LVEF <35%)
    sacubitril-valsartan (LVEF <35% - struggle with ACEi or ARB)
    cardiac resynchronisation therapy
    digoxin (not known to reduce mortality)

Others

  • annual influenza vaccine
  • one-off pneumococcal vaccine (repeat x5y in asplenia, splenic dysfunction or chronic kidney disease)

monitor potassium when giving spironolactone as combo with ACEi they can cause Hyperkalemia

57
Q

Dilated Cardiomyopathy

Classic causes include
alcohol
Coxsackie B virus
wet beri beri
doxorubicin

A
  • most common form of cardiomyopathy, accounting for 90% of cases.
  • classic findings of heart failure
  • systolic murmur: stretching of the valves may result in mitral and tricuspid regurgitation
  • S3
  • ‘balloon’ appearance of the heart on the chest x-ray
  • dilated heart leading to predominately systolic dysfunction
58
Q

Restrictive Cardiomyopathy

Classic causes include
* amyloidosis
* post-radiotherapy
* Loeffler’s endocarditis

A

In contrast to dilated cardiomyopathy, where the heart chambers become enlarged and weakened, restrictive cardiomyopathy involves the stiffening of the heart muscle, limiting its ability to fill with blood properly, thus compromising its ability to pump effectively.

59
Q

Genetic

Hypertrophic Cardiomyopathy

Hypertrophic Obstructive Cardiomyopathy

A
  • Leading cause of sudden cardiac death in young athletes
  • Usually due to a mutation in the gene encoding β-myosin heavy chain protein

Management
* Amiodarone
* Beta-blockers or verapamil for symptoms
* Cardioverter defibrillator
* Dual chamber pacemaker
* Endocarditis prophylaxis*

60
Q

Arrhythmogenic right ventricular Dysplasia cardiomyopathy

A
  • Right ventricular myocardium is replaced by fatty and fibrofatty tissue
  • Around 50% of patients have a mutation of one of the several genes which encode components of desmosome
  • ECG abnormalities in V1-3, typically T wave inversion. An epsilon wave is found in about 50% of those with ARV - this is best described as a terminal notch in the QRS complex
61
Q

Shock

Haemorragic, Septic, Neurogenic, Anaphylactic, Cardiogenic

A

Haemorragic

  • Parameter Class I <750ml Class II 750-1500ml Class III 1500-2000ml Class IV >2000ml

Septic

  • infection that triggers a particular Systemic Inflammatory Response Syndrome (SIRS). This is characterised by body temperature outside 36 oC - 38 o C, HR >90 beats/min, respiratory rate >20/min, WBC count >12,000/mm3 or < 4,000/mm3.
  • excessive inflammation, coagulation and fibrinolytic suppression.

Neurogenic

  • This occurs most often following a spinal cord transection
  • decreased sympathetic tone or increased parasympathetic tone

Anaphylactic

  • defined as a severe, life-threatening, generalised or systemic hypersensitivity reaction.

Cardiogenic

  • main cause is ischaemic heart disease
62
Q

Phlbetis

Thrombophlebitis

inflammation associated with thrombosis of one of the superficial veins, usually the long saphenous vein of the leg.

A
  • Usually non infective but can get secondary infection making it septic
  • ultrasound scan to exclude concurrent DVT.
  • Patients with superficial thrombophlebitis should have anti-embolism stockings and can be considered for treatment with prophylactic doses of LMWH for up to 30 days or fondaparinux for 45 days.
  • If LMWH is contraindicated, 8-12 days of oral NSAIDS should be offered.
63
Q

Advanced Life Support

stepwise

atropine is no longer recommended for routine use in asystole or pulseless electrical activity (PEA)

A
  • Defibrillation: a single shock for VF/pulseless VT followed by 2 minutes of CPR.
  • In monitored patient: 3 quick successive (stacked) shocks’, rather than 1 shock followed by CPR
  • during a VF/VT cardiac arrest, adrenaline 1 mg is given once chest compressions have restarted after the third shock
    repeat IV adrenaline 1mg every 3-5 minutes whilst ALS continues
  • Amiodarone 300 mg should be given to patients who are in VF/pulseless VT after 3 shocks have been administered.
  • a further dose of amiodarone 150 mg should be given to patients who are in VF/pulseless VT after 5 shocks
  • lidocaine used as alternative

Non shockable rhythm

  • adrenaline 1 mg as soon as possible for non-shockable rhythms

thrombolytic drugs
should be considered if a pulmonary embolus is suspected
if given, CPR should be continued for an extended period of 60-90 minutes

64
Q

Causes of reversible Cardiac Arrest

A

H

  • Hypoxia
  • Hypovolaemia
  • Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
  • Hypothermia

T
* Thrombosis (coronary or pulmonary)
* Tension pneumothorax
* Tamponade - cardiac
* Toxins

65
Q

Bradycardia - Peri-arrest rhythm

A
  • atropine, up to a maximum of 3mg
  • transcutaneous pacing
  • isoprenaline/adrenaline infusion titrated to response
66
Q

Tachycardia Peri arrest rhythm

A

synchronised DC shocks should be given. Up to 3 shocks can be given;

  • amaiadrone
  • followed by 24 hour infusion

Narrow Complex Tachycardia

  • vagal manoeuvres followed by IV adenosine

Main Conditions (15 decks)

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