Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 3 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Describe the principles of thromboembolism prevention in Atrial Fibrillation

A

Risk of stroke and systemic embolism should be assessed using the CHA2DS2-VASc Score

Men with a score of 1 or more and women with a score of 2 or more are more likely to benefit from oral anticoagulation

OACs prevent the majority of ischaemic strokes in AF and can prolong in life, a net clinical benefit is almost universal

Vitamin K Antagonists (e.g Warfarin) - Only treatment to be used in patients with mitral stenosis or mechanical valve prosthesis

DOACs (e.g. Dabigatran, Apixaban, Rivaroxaban) - Predictable onset and offset without need for regular monitoring

Non-pharmacological approaches include transcatheter occlusion of the left atrial appendage, where it is endothelialised by the cardiac tissue (it has been shown to be non-inferior to VKAs for stroke prevention in non-valvular AF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the microbiology of organisms associated with infective endocarditis

A
  • In descending order of frequency
  • Staph. Aureus
    • Associated with IVDU
  • Staph Epidermis
    • Device/Line Related IE or Early PVE
  • Strep Viridans (oral Streptococci)
    • NVE
  • Strep Gallolyticus (non-oral Streptococci)
  • Enterococci

The above account for more than 85% of all cases of IE

Most commonly S. Aureus (26.6%)

The remainder below account for a small minority

  • HACEK (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella Corrodens, Kingella)
  • Candida Species
  • Other/Polymicrobial
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the non-pharmacological management of hypertension

A

Exercise

Weight Loss

Reduction in Na Intake

Reduction in Alcohol Intake

Smoking Cessation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the pathophysiology and treatment of Transposition of the Great Arteries

A

Pulmonary Artery and Aorta are switched

LV –> Pulmonary A.

RV –> Aorta

Treated by prostaglandins to keep the ductus arteriosus patent followed by an arterial switch operation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the pathophysiology of heart failure

A

Dysfunction of the ventricles begins with myocardial damage which may be due to infection or ischaemia

This results in a perceived reduction in the circulating volume and pressure

Compensatory mechanisms are initiated to correct this, including increase in sympathetic tone, RAS activation, adrenaline and natriuretic peptide release

Angiotensin II is produced, which increased sodium and water retention which initially helps to increase the blood volume and pressure to maintain cardiac output

However, in the long term these mechanisms perpetuate the disease

Increased HR = Increased Oxygen Demand

Increased Total Peripheral Resistance = Increased Workload - Contributes to Underperfusion and Ischaemia of the heart

Increased Stretching of Ventricular Wall = Reduced Contractility - Leads to fluid transudation into interstitial tissue causing peripheral and pulmonary oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the diagnosis of infective endocarditis and its diagnostic criteria

A

3 Sets of Blood Cultures

Echocardiography (TTE as first line)

Elevated WCC/CRP

ECG

Haematuria or Pyuria on Urinalysis

-

Modified Duke Criteria states a diagnosis of IE is definite in the presence of 2 major criteria, 1 major and 3 minor criteria or 5 minor criteria

Major Criteria: Blood Cultures +ve for IE and Evidence of Endocardial Involvement

Minor Criteria: Predisposition, Fever, Vascular Phenomena, Immunological Phenomena, Microbiological Evidence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the pathophysiology and treatment of Coarctation of the Aorta

A

‘a narrowing in the aorta, most commonly at the site of insertion of the ductus arteriosus, just distal to the left subclavian artery’

Acyanotic defect with a left to right shunt

Typically presents at Day 3, when ductus arteriosus closes

Upper body hypertension and lower body hypotension

May require surgical balloon opening and stenting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the pathophysiology of acute coronary syndromes

A

ACS is a spectrum of disease from Unstable Angina on one end to STEMI at the other, with NSTEMI in the middle

The typically arise on a background of atherosclerosis and coronary artery disease

When a plaque in the coronary arteries ruptures and disrupts blood flow, heart muscle supplied by that vessel will become ischaemic and soon will infarct and necrose

These are typically Type 1 MIs

Type 2 MIs are due to an increased oxygen demand or decreased oxygen supply (e.g. due to heart failure, sepsis etc.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe complications of an acute myocardial infarction

A

Arrhythmias (AF, VT, VF)

Heart Failure

Cardiogenic Shock

Myocardial Rupture

Psychological Effects (Anxiety and Depression)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe and diagnose this ECG

A

Regular, Sinus Rhythm

150bpm

P Waves followed by QRS Complex (1:1)

Narrow QRS

= Sinus Tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the management of common valvular heart disorders

A

Symptomatic medical management of heart failure symptoms, AF, oedema etc with Beta Blockers, ACE Inhibitors, Digoxin, Diuretics, Nitrates

Surgical valve replacement is an option for some, with either a tissue or mechanical valve (the latter requires life-long anticoagulation but generally lasts longer)

Procedural options include TAVI (transcatheter aortic valve implantation), MitraClip (transcatheter mitral valve repair) or valvuloplasty (widening of a stenotic aortic valve using a balloon catheter)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

State which lead in a standard 12 lead ECG represents each position in the heart (i.e. Anterior, Lateral, Inferior, Septal)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe and diagnose this ECG

A

Regular Rhythym

Rate - 83bpm

ST elevation in V1-4

Reciprocal ST depression in III

Hyperacute peaked T waves in V2-4

= (Anterior) STEMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the clinical features of infective endocarditis

A

May be acute or sub-acute onset

Fever

Breathlessness

Night Sweats

Fatigue

Anorexia

Dyspnea

Weight Loss

New Heart Murmur

Symptoms of Heart Failure

Embolic Phenomena (Stroke, Pleuritic Chest Pain, Abdominal Pain, Back Pain)

Splinter Haemorrhages

Janeway Lesions

Petechial Rash

Osler’s Nodes

Roth Spots (Retina)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the pathophysiology and treatment of Tetralogy of Fallot

A

Ventricular Septal Defect + Overriding Aorta + RV Outflow Obstruction (Pulmonary Stenosis) + RV Hypertrophy

Cyanotic defect with right to left shunt

Curative open heart surgery to repair various defects

Management of acute ‘tet spells’ with beta-blockers and oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Discuss strategies for prevention and treatment of peripheral vascular disease

A

Smoking Cessation

Control of Hypertension

Statins (should be prescribed to all patients with symptomatic coronary artery disease, regardless of cholesterol levels)

Improve Glycaemic Control

Weight Management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the basic physics underlying an ECG

A

ECG records the electrical activity of the heart from the skin

This is usually done by a 12-Lead ECG, where a lead is an electrical vector

Unipolar Leads measure the potential variation at a single point (Limb Leads aVR, aVL and aVF and Chest Leads V1-V6)

Bipolar Leads measure the potential difference between two points (Leads I, II and III)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

State causes/precipitants of Atrial Fibrillation

A

Coronary Artery Disease, Structural Heart Disease, Heart Failure, Valvular Disease, Hypertension

Thyroid Dysfunction, COPD, Diabetes, Obesity, Electrolyte Disturbance, Pulmonary Emboli

Infection, Smoking, Caffeine, Alcohol Excess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the common bradyarrhythmias

A
  • Sinus Bradycardia
    • Rate <60bpm
    • Regular, Narrow QRS
    • P Waves Present
    • P:QRS - 1:1
  • Junctional Bradycardia
    • Rate <60bpm
    • Regular, Narrow QRS
    • No P Waves
  • Second Degree AV Block
    • Slowest Rate (<60bpm)
    • Irregular, Narrow QRS
    • P:QRS is not 1:1
  • Complete AV Block
    • Rate <60bpm
    • Regular, Broad QRS
    • No Relation Between P and QRS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the pathophysiology and treatment of an Atrial Septal Defect

A

Acyanotic defect with a left to right shunt

Most common defect is a Secundum ASD (basically a patent foramen ovale) followed by a Primum ASD (basically a partial AVSD)

Can result in arrhythmias, heart failure, wheeze, split-second heart sound and an ejection systolic murmur

Percutaneous catheterisation is most often used for secundum defects with surgical closure reserved for more complex defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

State a systematic approach to interpreting an ECG

A
  1. Consider clinical context
  2. Check date, time and patient details
  3. Assess technical quality (artefaxct, paper speed (normal is 25mm/s) and gain (normal is 10mV/mm)
  4. Identify P wave, QRS complex and T wave
  5. Measure HR
  6. Check intervals
  7. Look at P/QRS/T morphology

N.B - Do not rely on automatic interpretation and look at old ECGs if possible

22
Q

Describe the non-pharmacological management of Atrial Fibrillation

A
  • Acute Rhythm Control
    • Synchronised Direct Current Cardioversion
      • 3 weeks of anticoagulation prior to DCCV followed by 4 further weeks of anticoagulation
    • Transcatheter Therapy
      • Isolation of pulmonary veins by Radio Frequency Ablation or Cryoballoon
    • Surgical Therapy
      • Maze procedure (channelled impulse propagation)
  • Rate Control
    • Transcatheter Therapy
      • Ablation of AV node/His bundle, resulting in iatrogenic 3rd-degree heart block
      • Controls ventricular rate in AF, however, renders patient Pt pacemaker dependent for life
23
Q

Describe and diagnose this ECG

A

Regular, Sinus Rhythm

Rate = 56bpm

P:QRS is 1:1

Sinus Bradycardia

24
Q

Describe the pharmacological management of hypertension

A
  • ACE Inhibitor
    • e.g. Lisonipril
  • Angiotensin II Receptro Blocker
    • e.g. Candesartan
  • Ca Channel Blocker
    • e.g. Amlodipine
  • Thiazid-Like Diuretics
    • e.g. Bendroflumothiazide
  • Beta-Blocker
    • e.g. Atenolol
25
Q

Describe the complications of hypertension

A

Stroke, MI, Heart Failure, Renal Failure

HTN doubles cardiovascular disease risk for every 20mmHg increase in systolic pressure

26
Q

Describe the investigation and treatment of acute limb ischaemia

A

Investigations: MRI, CT Angiography or Invasive Arteriogram

Management: Angioplasty, Bypass Surgery, Thrombolysis or Embolectomy

27
Q

Describe and diagnose this ECG

A

Irregular Rhythym

Narrow QRS

No discernible P waves

= Atrial Fibrillation

28
Q

Describe the pharmacological management of Atrial Fibrillation

A

Strategies include Rate versus Rhythm control

NICE recommends rate control as the first line strategy in most patients

  • Rate Control
    • Class IV: Calcium Channel Blockers (e.g. Verapamil or Diltiazem)
    • Class II: Beta Blockers (e.g. Carvedilol or Bisoprolol)
    • Class V: Other (e.g. Digoxin)
  • Rhythm Control
    • Class I: Na Channel Blockers (e.g. Flecainide)
    • Class III: K Channel Blockers (e.g. Amiodarone)
29
Q

Describe the main imaging techniques used in cardiology and their indications

A
  • ECG
    • Representation of electrical activity of the heart, showing abnormalities of rhythm, conduction or repolarisation
    • Used in myocardial infarction, AF
  • CXR
    • Can give information on the cardiac silhouette, pulmonary vasculature and great vessels
    • Can be used to detect pulmonary oedema and pleural effusions
  • Echocardiography
    • Transthoracic or Transoesophageal
    • Gives information on blood flow through the heart (function), valves and chambers (structure)
    • Can be used in conjunction with doppler
    • Indications include valve assessment, pericardial assessment and assessment of inducable ischaemia
  • Nuclear Perfusion Imaging
    • Used to assess ischaemia and ejection fraction
  • Cardiac CT
    • Used to assess coronary artery or great vessel anatomy
    • Requires low heart rate and radiation dose
  • Angiography
    • Both diagnostic and therapeutic
    • Used to assess ischaemia, valves, ventricular pressure or in Primary PCI
    • Risks include CVA, MI or death
  • Cardiac MRI
    • Indications include assessment of structure and function, great vessel assessment and tissue characterisation (e.g. infiltrative cardiomyopathies or previous infarction)
30
Q

Describe the management options for acute myocardial infarction

A

Oxygen and ECG

Aspirin 300mg PO

Morphine 5-10mg IV

Metoclopramide 10mg IV (Anti-Emetic)

Ticagrelor 180mg PO

Heparin 5000U IV

Activate Primary PCI Team and Arrange Immediate Transfer to GJNH

If not suitable for PPCI, thrombolysis should be given with Tenecteplase (and Clopidogrel in place of Ticagrelor)

31
Q

Describe investigations used in the diagnosis of Atrial Fibrillation

A

ECG: Irregularly Irregular Rhythm, No Discernible P Waves, Absence of Isoelectric Baseline, Fibrillatory Waves

TFTs, Echocardiogram, LFTs, U&Es, CRP, Blood Cultures

32
Q

Describe the clinical manifestations and natural history of peripheral vascular disease

A

PVD is associated with atherosclerosis and arterial narrowing in the periphery, resulting in reduced blood and oxygen supply to muscles and other tissues

Intermittent Claudication is a muscle pain (ache, cramp or fatigue) on mild exertion, usually in the calf, that is relieved by rest

Chronic Limb Ischaemia (i.e. Stable Angina) may present with dry skin, diminished or absent pulse, ulceration or peripheral discolouration

Acute Limb Ischaemia is an acute thrombotic occlusion of a pre-existing stenotic arterial segment or by an embolus

33
Q

Describe options for non-pharmacological management of heart failure

A

Lifestyle Modification

Implantable Cardioverter Defibrillator

Cardiac Resynchronisation Therapy

CABG

Ventricular Assist Device

Transplant

34
Q

Describe the mechanism of action of drugs used to manage heart failure

A
  • ACE Inhibitors or Angiotensin II Receptor Blocks
    • e.g. Enalapril or Valsartan
    • Reduce activity of AngII to reduce afterload and fluid retention to slow progression of LV dysfunction
  • Beta Blockers
    • e.g. Carvedilol
    • Reduces afterload and HR to reduce work on the heart
  • Mineralocorticoid Receptor Antagonist
    • e.g. Spironolactone
    • Inhibits sodium resorption to reduce retention of sodium and water
  • Ivabradine
    • Acts on the ‘funny channel’ to reduce HR
  • Digoxin
    • Increases force of contraction while reducing rate of conduction through the AV node
35
Q

Describe the pathogenesis of and pathological changes seen in mitral regurgitation

A

May be due to endocarditis, rheumatic valve disease, Marfan’s syndrome, cardiomyopathy or Ehlers-Danlos syndrome

Causes pressure overload in both the LA and LV, causing LA and LV dilation

Can lead to pulmonary hypertension, secondary right heart dilation and atrial fibrillation

Symptoms include SOB, palpitations, RH failure symptoms

Signs include a pan-systolic murmur, heave, displaced apex

36
Q

Describe the pathogenesis of and pathological changes seen in aortic stenosis

A

Stenosis arises from thickening and calcification of the valve leaflets

Stenosis results in a pressure overload in the LV leading to LV hypertrophy

May arise congenitally, or due to rheumatic valve disease

Symptoms include SOB, (pre)syncope, chest pain and reduced exercise capacity

Signs include an ejection systolic murmur and slow rising pulse

37
Q

Describe the pathogenesis of and pathological changes seen in aortic regurgitation

A

Can arise due to a variety of reasons, including degeneration, rheumatic valve disease, aortic root dilation, Marfan’s. SLE or endocarditis

Backflow of blood into the LV causes a volume overload and LV dilation

Symptoms include SOB and reduced exercise tolerance

Signs include a diastolic crescendo murmur

38
Q

Describe the causes of hypertension

A

Primary HTN is by definition idiopathic (risk factors include age, gender, ethnicity, diet, physical activity, obesity, alcohol excess and stress)

Secondary HTN accounts for 5-10% of cases and causes include hyperaldosteronism, thyroid disorders, phaeochromocytoma, renal artery stenosis, NSAIDs and cocaine use

39
Q

Describe and diagnose this ECG

A

Regular Rhythym

No Relation Between P and QRS

HR <60bpm

Complete Heart Block

40
Q

Describe features of a normal ECG

A

Sinus Rhythym (each P wave is followed by a QRS complex)

Normal HR

PR interval <1 large square (<200ms)

QR interval <3 small squares (<120ms)

QT interval <11 small squares (<440ms)

Positive QRS complex in leads I and II

P wave upright in inferior leads

ST segment flat

T wave has same polarity as QRS complex

41
Q

Describe and diagnose this ECG

A

Irregular Rhythm

Saw Tooth Pattern

No discernible P waves

= Atrial Flutter

42
Q

Describe the radiological signs of heart failure

A

Pleural Effusions

Cardiomegaly

Kerley B Lines (horizontal lines of the periphery of the lower posterior lung fields)

Upper Lobe Pulmonary Venous Congestion

Interstitial Oedema

43
Q

Describe features of critical ischaemia in the imminently non-viable limb

A

‘limb pain that occurs at rest, or impending limb loss that is caused by severe compromise of blood flow to the affected extremity’

Clinically presents with 6 Ps:

Pain

Pallor

Paraesthesia

Paralysis

Pulseless

Perishing Cold

44
Q

Describe long term management following an acute myocardial infarction

A

Monitor in Coronary Care Unit

Secondary prevention pharmacotherapy (ACEi, Beta Blockers, Statins, Nitrates, Aspirin

Echocardiogram for assessment of LV function

Cardiac Rehabilitation

45
Q

Describe the diagnosis of an acute myocardial infarction

A

Clinical history consistent with ACS

ECG changes (ST elevation/depression in 2 contiguous leads)

Raised troponin

HEART score >5

46
Q

Describe the narrow complex tachyarrhythmias

A
  • Sinus Tachycardia
    • Rate >100bpm
    • Regular, Narrow QRS
    • P Waves Present
    • P:QRS is 1:1
  • Atrial Fibrillation
    • Variable Rate (Fast)
    • Irregular, Narrow QRS
    • No P Waves
  • Atrial Flutter
    • Rate approx. 300bpm
    • Regular, Narrow QRS
    • May Get Variable AV Block
    • Sawtooth Atrial Activity
  • Supraventricular Tachycardia
    • Rate >150bpm
    • Regular, Narrow QRS
    • P:QRS is 1:1
    • P Waves May be Present
47
Q

Describe the clinical presentation of heart failure

A

Symptoms: Dyspnea, Orthopnoea, PND, Fatigue, Exercise Intolerance, Cough, Ankle Swelling

Signs: Peripheral Oedema, Elevated JVP, 3rd Heart Sound, Displaced Apex (Cardiomegaly), Lung Crackles (Pulmonary Oedema), Pleural Effusion

48
Q

Describe the investigations used in the diagnosis of hypertension

A

Office BP Measurement

24 Hour Ambulatory BP Monitoring (BP taken every 20-30mins throughout the day)

Home BP Monitoring (2 readings, twice a day, taken over 4-7 days)

Other tests include U&Es, Glucose, Lipid Profile, TFTs, LFTs, Urinalysis, ECG, Echo, Renal Ultrasound, Renin, Aldosterone

Assess CV risk, presence of secondary HTN or end organ damage

49
Q

Describe the clinical presentation of coronary artery disease

A

Chest, Back or Jaw Pain (typically crushing)

Sweatiness, Clamminess

SOB

Tachycardia

Distress

Crackles

Elevated JVP

Shock

Arrhythmia

50
Q

Describe the pathogenesis of and pathological changes seen in mitral stenosis

A

Almost always caused by rheumatic valve disease

Obstruction of the mitral valve leads to pressure overload in the left atrium and pulmonary circulation which can result in atrial/pulmonary hypertension, AF and secondary right heart failure

Symptoms include SOB, palpitations, chest pain, syncope, RH failure symptoms and haemoptysis

Signs include a loud S1 and an opening snap close to S2

51
Q

Describe the management of infective endocarditis

A

Empirical antibiotics should be given as soon as blood cultures are obtained

NVE: Amoxicillin + Flucloxacillin + Gentamicin

PVE: Vancomycin + Gentamicin + Rifampicin

IV treatment give for at least 4-6 weeks

40-50% of patients undergo cardiac surgery due to valve dysfunction leading to heart failure, uncontrolled infection or to prevent embolism

52
Q

Describe the pathophysiology of Tricuspid Atresia and its surgical management

A

Malformation of the tricuspid valve, resulting in an inability of blood flow from the right atrium to the right ventricle

Therefore, it requires both an atrial and ventricular septal defect so blood can pass from the right atrium to the pulmonary arteries

Managed surgically by the Fontan or TCPC procedure

In Fontan circulation, the single ventricle supports systemic circulation while systemic venous return is directed to pulmonary arteries (bypassing the ventricular mass)

The ASD is closed and the pulmonary aa. grafted to the RA, bypassing the RV

Phase 3 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions