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Clinical Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Classification system for MI in the next 10 years

A

QRISK3 Score

QRISK >10% => start on Statin (atorvastatin 20mg @ night)

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2
Q

Secondary Prevention of Cardiovascular Disease

A

Aspirin

Atorvastatin

Atenalol

ACE Inhibitor

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3
Q

Side Effects of Statins?

A

Myopathy (Check Creatinine Kinases)

Type II Diabetes

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4
Q

Difference Between Stable and Unstable Angina

A

Stable: Relieved by Rest or GTN

Unstable: Random symptoms including while at rest

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5
Q

Investigations for Angina?

A

CT Coronary Angiography (Gold Standard)

Physical Exam (Heart Sounds, heart Failure)

ECG

FBC

U&Es (Prior to starting ACE)

LFTs (Prior to Statins)

Lipid Profile

Thyroid Function Tests

HbA1C/Fasting Glucose

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6
Q

Management of Angina

  • Immediate
  • Long term
  • Secondary prevention?
A

Immediate: GTN Spray as required. GTN when symptoms start, again after 5 minutes. If still pain then call ambulance

Long Term:

  • Beta Blocker (Bisoprolol 5mg)
  • Calcium Channel Blocker (Amlodipine 5mg)

Secondary Prevention

  • Aspirin (75mg )
  • Atorvastatin (80mg)
  • ACE Inhibitor
    • Beta Blocker already on
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7
Q

Procedural/Surgical Interventions for Stable Angina

A

Percutaneous Coronary Intervention (PCI) with coronary Angioplasty

  • Brachial/Femoral Artery
  • Ballon Dilation followed by Stent

Coronary Artery Bypass Graft

  • Midline Sternotomy Scar
  • Graft vein from pts. Leg (Great Saphenous Vein- Inner Calf)
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8
Q

Acute Coronary Syndrome Pathophysiology

A

Thrombus blocking coronary artery. Composed mostly of platelets hence whey anit-platelet medication (Aspirin, Clopidogrel, Ticagrelor) are effective

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9
Q

RCA Heart Area Supply

ECG Leads?

A

Inferior Heart Area:

  • Right Atrium
  • RV
  • Inferior LV
  • Posterior Septum

ECG Leads: II, III, aVF

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10
Q

Circumflex Heart Area Supply

ECG Leads?

A

Lateral Heart Area:

  • Left Atrium
  • Posterior LV

ECG Leads: I, aVL, V5-6

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11
Q

Left Anterior Descending (LAD) Heart Area Supply

ECG Leads?

A

Anterior Heart Area:

  • Anterior LV
  • Anterior Septum

ECG Leads: V1-4

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12
Q

Left Coronary Artery Heart Area Supply

ECG Leads?

A

Anterolateral Heart Area

ECG Leads: I, aVL, V3-6

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13
Q

Differentiating Types of Acute Coronary Syndrome?

A

Pt Presents with Chest Pain Perform ECG:

  • ST elevation OR new bundle branch block => STEMI

NO ST Elevation then perform Troponin Blood Test (Baseline + 6/12 hours after symptom onset)

  • Troponin RAISED or ECG Changes ( ST Depression, T-Wave Inversion or Pathological Q Waves) => NSTEMI
  • Troponin NORMAL and ECG NORMAL => Unstable Angina or MSK Chest Pain
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14
Q

Symptoms of Acute Coronary Syndrome

A

Central Constricting Chest Pain along w/:

  • Nausea
  • Sweating
  • Feeling of impending doom
  • SOB
  • Palpitations
  • Pain radiating to jaw/arms

Symptoms must persist >20 minutes at rest, otherwise consider stable angina

Diabetics often do not experience chest pain (Silent MI)

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15
Q

ECG Changes in STEMI

A

ST-Segment Elevation

New Left Bundle Branch Block

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16
Q

ECG Changes in NSTEMI

A

ST Segment Depression

Deep T Wave Inversion

Pathological Q Waves

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17
Q

Differential of Raised Troponins

A

Myocardial Ischemia

Chronic Renal Failure

Sepsis

Myocarditis

Aortic Dissection

Pulmonary Embolism

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18
Q

Investigations for Acute Coronary Syndrome

A

CT Coronary Angiography (Gold Standard)

Physical Exam (Heart Sounds, heart Failure)

ECG

FBC

U&Es (Prior to starting ACE)

LFTs (Prior to Statins)

Lipid Profile

Thyroid Function Tests

HbA1C/Fasting Glucose

Chest XRAY (Pumonary Edema/Other causes of chest pain)

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19
Q

Acute STEMI Treatment

A

Primary PCI (Within 2 hours of presentation)

Thrombolysis (If PCI not available within 2 hours):

  • Streptokinase

-Alteplase

+/- Apririn/Ticagrelor Loading

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20
Q

Acute NSTEMI Treatment

A

Beta Blockers

Asprin (300mg)

Ticagrelor (180mg)

Morphine

Anticoagulant: LMWH (Enoxaparin for 2-8 days)

Nitrates (GTN) to relieve coronary spasm

O2 only if sats <95%

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21
Q

What is the risk assesment score following an NSTEMI

A

GRACE Score

  • > 5% Medium Risk
  • > 10% High risk

Medium/High Risk go for PCI within 4 days of admission

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22
Q

Complications of MI

A

Death

Rupture of Heart Septum/Papillary Muscles

Edema (heart failure)

Arrythmia and Aeurism

Dressler’s Syndrome (Localized immune response 2-3 weeks post MI presenting with pleuritic chest pain, fever, pericardial rub on auscultation)

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23
Q

What is Dressler’s Syndrome?

  • Presentation
  • Diagnosis
  • Management
A

Post-Myocardial Infarction Syndrome

Presentation: Localized immune response 2-3 weeks post MI presenting with pleuritic chest pain, fever, pericardial rub on auscultation

Diagnosis:

  • ECG (Global ST elevation and T Wave Investion)
  • Echocardiogram (Pericardial Effusion)
  • Inflammatory Markes (CRP/ESR)

Management

  • NSAIDs (Ibuprophin/Aspirin)
  • Steroids/Pericardiocentesis (Severe cases)
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24
Q

Causes of Acute Heart Failure vs. Chronic

A

Acute Heart Failure:

  • Iatrogenic (Aggressive IV Fluids in Elderly)
  • Sepsis
  • MI
  • Arrhythmia

Chronic Heart Failure:

  • Ischemic Heart Disease
  • Valvular Heart Disease (Aortic Stenosis)
  • Hypertension
  • Arythmia (Afib)
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25
Q

Presentation of Acute LVF

A

Rapid onset Breathlessness

  • Excarcebated by lying flat and improves on sitting up
  • Type 1 Resp Failure
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26
Q

Acute Heart Failure Exam Findings

A

Increase RR

Reduced O2 sats

Tachycardia

3rd Heart Sound

Bilateral Basal Crackles

Hypotension (Cardiogenic Shock)

Right-sided as well => Elevated JVP, Peripheral Edema

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27
Q

Workup for Heart Failure Pt

A

History/Exam

ECG (Ischemia/Arrythmia)

ABG

Chest XRAY (Cardiomegaly (Cardiothoracic Ratio >.5) Upper lobe venous diversion, Kerley Lines)

Bloods (Infection, Kidney Function, BNP, Troponin)

ECG

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28
Q

What is BNP?

  • Mechanism
  • Causes of Elevation
A

Hormone released by ventricle when heart is overloaded

Relaxes smooth muscles of blood vessels reduces SVR. Also acts as a diuretic at kidneys to reduces circulating volume

Sensitive for heart failure but not Specific. Also Elevated due to:

  • Tachycardia
  • Sepsis
  • PE
  • Renal Impairment
  • COPD
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29
Q

What is considered a normal Ejection Fraction?

A

> 50% as measured by Echocardiography

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30
Q

Chest XRAY findings in Heart Failure

A

Cardiomegaly (Cardiothoracic Ratio >.5)

Upper lobe venous diversion

Bilateral Pleural Effusions

Fluid in Interlobular Fissures

Fluid in Seotal Lines (Kerley Lines)

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31
Q

Management of Acute Heart Failure

A

Pour SOD

  • Pour away (STOP) IV Fluids
  • Sit Up
  • Oxygen (if <95%)
  • Diuretics (Furosemide 40mg)

+ Monitor fluid intake, urine output, U&E bloods

In severe cases:

  • CPAP
  • Inotropes
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32
Q

Presentation of Chronic Heart Failure

A

Breathlessness (worsened by exertion)

Cough (Forthy Sputum)

Orthopnea (SOB when laying down, ask about pillows at night)

Paroxysmal Nocturnal Dyspnea (Severe attack of SOB and cough at night)

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33
Q

Diagnosis of Chronic Heart Failure

A

Clinical Presentation

BNP Blood Test (NT-proBNP)

Echocardiogram

ECG

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34
Q

Management of Chronic Heart Failure

A

ABAL

  • ACE Inhibitor (Ramipril) or ARB (Candesartan)
  • Beta Blocker (Bisoprolol)
  • Aldosterone Antagonist (When reduced ejection fraction and A/B not controlling. Spironolactone/Eplenerone)
  • Loop Diuretics (Furosemide- Symptomatic Improvement)

U&E’s should be closely monitored whilst on diuretics, ACE Inhibitors and Aldosterone Antagonists due to electrolyte disturbances

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35
Q

Causes of Cor Pulmonale

A

COPD (Most Common)

PE

Interstitial Lung Disease

Cystic Fibrosis

Primary Pulmonary Hypertension

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36
Q

Presentation/Signs of Cor Pulmonale

A

Presentation:

  • Asymptomatic
  • SOB
  • Breathlessness on Exertion
  • Syncope

Signs

  • Hypoxia
  • Cyanosis
  • Raised JVP
  • Peripheral Edema
  • 3rd Heart Sound
  • Murmurs (pan systolic tricuspid regurg)
  • Hepatomegaly (Back pressure through hepatic vein)
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37
Q

Primary vs. Secondary Hypertension

A

Primary (95%) developed on its own w/ no secondary cause

Secondary Hypertension (ROPE)

  • Renal Disease
  • Obesity
  • Pregnancy Induced Hypertension/Pre-Eclampsia
  • Endocrine (Hyperaldoronism/Conn’s Syndrome (2.5% of hypertension) diagnosed with Renin:aldosterone ratio blood test)
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38
Q

Complications of Hypertension

A

Ischemic Heart Disease

Stroke/Hermorage

Hypertensive retinopathy

Hypertensive Nephropathy

Heart Failure

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39
Q

Management of Hypertension

Potassium Ballance?

A

Medications:

  • ACE Inhibitor / ARB (those w/ dry cough)
  • Beta Blocker (Bisprolol)
  • Calcium Channel Blocker (Amlodipine)
  • ThiaziDe: (Indapamide)

Potassium:

  • Thiazides => HYPOLKALEMIA
  • Spironolactone/ACE Inhibitors => HYPERKALEMIA
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40
Q

What is S1 Heart Sound Indicative of?

A

Closing of AV valves (Tricuspid/Mitral) at start of Systolic contraction of ventricles

41
Q

What is S2 Heart Sound Indicative of?

A

Closing of Semilunar Valves (Pulmonary/Aortic) once systolic contraction is complete

42
Q

What is S3 Heart Sound Indicative of?

A

.1 seconds after 2nd heart sound

Due to rapid ventricular filling causing chordae tendinae to pull tight (Normal in 15-40 yos, Older indicative of HF)

43
Q

What is S4 Heart Sound Indicative of?

A

Heard Directly before S1

ALWAY ABNORMAL, indivative of Stiff/Hypertrophic Ventricle causing turbulent flow

44
Q

4 Valve areas to auscultate

A

Pulmonary- 2nd Intercostal (LEFT Sternal Border)

Aortic- 2nd Intercostal (RIGHT Sternal Border)

Tricuspid- 5th Intercostal (LEFT Sternal Border)

Mitral- 5th Intercostal (Apex (mid-clavicular))

Erb’s Point (Heart Sounds (S1/S2))- 3rd Intercosta

45
Q

Special Maneuvers to emphasize Murmurs?

A

Pt on left side (Mitral Stenosis) - Listen at 5th intercostal Apex

Pt sat up leaning forward and holding expiration (Aortic Regurgitation) - Listen at 2nd intercostal LEFT

46
Q

Mitral Stenosis

  • Cause
  • Character
  • Associations/Signs
A

Caused by:

  • Rheumatoid Heart Disease
  • Infective Endocarditis

Character:

  • Mid-diastolic, low pitched ‘rumblin’ murmur
  • Loud S1 (Thick Valves snapping shut)
  • Louder with Pt on left side - Listen at 5th intercostal Apex

Associations:

  • Malar Flush
  • Atrial Fibrillation
47
Q

Mitral Regurgitation

  • Cause
  • Character
A

Caused by:

  • Age => weakening
  • Ischemic Heart Disease
  • Rheumatoid Heart Disease/Infective Endocarditis
  • Connective tissue (Ehlers Danlos/Marfan)

Character:

  • Pan-Systolic high-pitched ‘whistling’ murmur
  • Radiating to left axilla
48
Q

Aortic Stenosis

  • Cause
  • Character
  • Associations/Signs
A

Caused by:

  • Idiopathic age-related calcification
  • Bicuspid Valve Presidposes
  • Rheumatic Heart Disease

Character:

  • Ejection-systolic high-pitched murmur
  • Crescendo/Decrescnedo
  • Radiates to Carotids

Associations/Signs:

  • Slow rising pulse
  • Narrow Pulse pressure
  • Exertional Syncope
49
Q

Aortic Regurgitation

  • Cause
  • Character
  • Associations/Signs
A

Caused by:

  • Idiopathic age-related weakness
  • Connective tissue (Ehlers Danlos/Marfan)

Character:

  • Early diastolic soft murmur
  • Louder with Pt sat up leaning forward and holding expiration- Listen at 2nd intercostal Right

Associations/Signs:

  • Corrigan’s Pulse (Collapsing Pulse)- rapidly disappearing pulse at carotids
  • Heart Failure
50
Q

Benefits of Bioprosthetic Heart Valves vs. Mechanical?

A

Biosprothetic (10 year Life)

Mechanical (>20 Year life) but require lifelong warfarin

  • INR Target 2.5-3.5 (Higher than normal 2-3)
51
Q

Complications of Mechanical Heart Valve?

A

Thrombus fomation (lifelong warfarin. INR Target 2.5-3.5 (Higher than normal 2-3)

Infective Endocarditis (2.5% of pts)

Hemolysis=> Anemia (Blood churned up by valve)

Click (S1 Mechanical Mitral, S2 Mechanical Aortic)

52
Q

Indication/Procedure of TAVI

A

Treatment of SEVERE aortic stenosis

  • Local/general Anaestetic
  • Catheter into FEMORAL ARTERY
  • Wire via XRAY guidance to aortic valve
  • Ballow stretches the stenosed valve replaced with a bioprosthetic one

Long term efficacy still unknown. In younger, fitter patients opened surgery still first line

53
Q

Mortality/Organisms of Concern for Infective Endocarditis

Symptoms/Signs

A

2.5% of pts with surgical valve replacement of which 15% die

Gram Positive Cocci:

  • Staphylococcus
  • Streptococcus
  • Enterococcus

Symptoms:

  • Fever
  • Chest Pain/Palpitations
  • Fatigue

Signs

  • Roth Spots
  • Bilateral Crackles
  • Splinter hemorages/Janeway Lesions
54
Q

Atrial Fibrillation Associations/Presentation

A

Associations:

  • Irregularly irregular ventricular contractions
  • Tachycardia
  • Heart Failure
  • Risk of Stroke

Presentation

  • Palpitations

-SOB

  • Syncope
55
Q

Differential for Irregularly Irregular Pulse

A

Atrial Fibrillation

Ventricular Ectopics (Disappear when Heart Rate is over a certain threshold. Regular heart rate during exercise suggestive)

56
Q

Atrial Fibrilation on ECG

A

Absent P Waves

Narrow QRS Complex Tachycardia

Irregularly Irregular Venticular Rythem

57
Q

Causes of Atrial Fibrillation

A

‘SMITH’

Sepsis

Mitral Valve Pathology (Stenosis/Regurg)

Ischemic Heart Disease

Thyrotoxicosis

Hypertension

58
Q

Treatment of Atrial Fibrillation

  • Rate Control
  • Rhythm Control (Cardioversion/Long Term)
A

Rate Control (1st Line to get HR <100bpm to allow sufficient time for ventricular refilling)

  • Beta Blocker (1st Line- Atenolol)
  • Calcium Channel Blocker (Diltiazem (not in HF))
  • Digoxin (only in sedentary people, risk of toxicity/necessitates monitoring)

Rhythm Control (Offered to pts with reversible cause of AF, New onset AF, AF with HF, Symptomatic despite rate control

  • Immediate cardioversion if AF present <48 hours and are hemodynamically unstable).
  • Delayed cardioversion (AF present for >48 Hours and Stable + Anticoagulation for 3 weeks)
  • Pharmicologic Cardioversion: Flecanide (Class 1C - Na+ Block) / Amiodarone (Class III - K+/Na+ Block)
  • Electrical Conversion (Shock back into Sinus Rythym)
  • Long term Rhythm Control (Beta Blockers (1st Line), Amiodarone (Heart Failure/LV Dysfunction)
59
Q

Treatment of Paroxysimal Atrial Fibrilation

A

Infrequent episodes with no structural heart disease => “Pill in the Pocket”- Flecainide (Class 1C - Na+ Block)

Anticoagulation if CHA2DS2-VASc score >1

60
Q

What is the classification tool for determining whether a patient with atrial fibrillation should be started on anticoagulation?

  • Risk of Stroke with/without anticoagulation
  • What are factors that increase risk of stroke?
  • What is the treatment?
A

Risk of Stroke with/without anticoagulation (5% each year w/o , 1-2% risk of stroke each year on Anticoagulation (⅔ Reduction))

CHA2DS2-VASc

  • Conwgestive heart failure
  • Hypertension
  • Age > 75 (Scores 2)
  • Diabetes
  • **S*troke or TIA previously (Scores 2)
  • Vascular Disease
  • Age 65-74
  • Sex (Female)

Treatment:

  • Warfarin (Target INR for AF Therapy is 2-3). Reversible w/ Vitamin K and affected by Leafy greens, Cranberry Juice, Alcohol
  • DOACS (Apixaban, Dabigatran, Rivaroxaban) No monitoring, no interactions, less bleed risk (irreversible tho)
61
Q

4 Cardiac Arrest Rhythms seen in a pulseless, unresponsive patient

A

Shockable

  • Ventricular Tachycardia
  • Ventricular Fibrilation

Non-Shockable

  • Pulseless Electrical Activity
  • Asystole (no significant electrical activity)
62
Q

Tachycardia Treatment?

  • Unstable
  • Stable (Narrow/Broad QRS)
A

Unstable (Up to 3 synchronized shocks, consider Amiodarone Infusion)

Stable

NARROW Complex (QRS <.12s)

  • Atrial Fibrilation: rate control w/ Beta Blocker or Diltiazem
  • Atrial Flutter: rate control w/ Beta Blocker
  • Supraventricular Tachycardia: Treat w/ Vagal Maneuver and Adenosine

BROAD Complex (QRS >.12s)

  • Ventricular Tachycardia: Amiodarone Infusion
63
Q

Characteristics of Atrial Flutter

A

Atrial Contraction at 300bpm, Ventricular 150bpm

sawtooth apearance on ECG w/ p-wave after p-wave

64
Q

Treatment of Atrial Fibrillation?

A

Rate/Rythym control w/ Beta Blockers or cardioversion

Treat reversible underlying (Thyrotoxicosis, hypertension)

Radiofrequency Ablation of re-entrant circuit

Antigoagulation (CHA2DS2VASc Score)

65
Q

Characteristics of Super Ventricular Tachycardia

A

Narrow Complex Tachycardia (QRS <.12)

66
Q

Acute Management of Stable patients with SVT?

A

Continuous ECG Monitoring, then stepwise:

  • Valsalava Maneuver (Blow hard against plastic syringe)
  • Carotid Sinus Massage (Massage carotid on one side gently)
  • Adenosine (or Verapamil)- slows conduction through AV Node
  • Direct Current Cardioversion
67
Q

Wolf Parkinson White ECG Changes

A

Extra conduction pathway through the Bundle of Kent leads to:

  • Short PR interval (<.12s)
  • Wide QRS complex (>.12s)
  • Delta wave (Slurred upstroke of QRS)
68
Q

Wolf Parkinson White Treatment

A

Radiofrequency Ablation of the secondary pathway (Bundle of Kent)

Note: Afib/Aflut and WPW risk of Polymorphic Wide Complex tachycardia. Most antiarythmics (Beta blockers, CC Blockers, Adeniosine) increase risk thus are contraindicated in pts. w/ WPW that develop atrial arrhythmia

69
Q

Causes of Torsades de Pointes

A

Prolonged QT interval is a finding characteristic of prolonged repolarization of the muscles in the heart. Can lead to Torsades which either spontaneously dissipates or progresses to Ventricular Tachycardia

Causes of Prolonged QT:

  • Long QT Syndrome
  • Medications (Antipyshcotics, Citalopram, Flecanide, Sotalol, Amiodarone, Macrolides)
  • Electrolyte Disturbances (Hypokalemia, Hypomagnesemia, Hypocalcemia)
70
Q

Management of Torsades de Pointes

  • Acute
  • Chronic
A

Acute

  • Correct electrolytes
  • Magnesium Infusion
  • Defribilaiton (in event of Ventricular Tachycardia)

Chronic

  • Avoid provoking medication
  • Correct electrolyte distrubances
  • Beta Blockers (NOT SOTALOL)
  • Pacemaker
71
Q

What are Ventricular Ectopics?

A

Premature ventricular beats caused by random electrical discharges outside atria (Common at all ages by more common in pts with heart conditions)

Diagnoses on ECH as individual random BROAD QRS complexes on normal background ECG

Bigeminy (Happens after every sinus beat)

72
Q

Cause/ECG Characteristics of 1st Degree Heart Block?

A

Delayed conduction through the AV node. Despite this every atrial impulse leads to a ventricular contraction (Every p wave=> QRS)

Presents as a PR>.2s (5 small or 1 big square)

73
Q

Cause/Types/ECG Characteristics of 2nd Degree Heart Block?

A

2nd degree heart block occurs when some atrial impulses don’t make it through AV node => instances where there are p waves without QRS

Wenckebach’s Phenomenon (Mobitz Type I)

  • Atrial Impulses become gradually weaker until it doe snot pass through AV. After failing, becomes strong again and cycle repeats
  • On ECG: Increasing PR interval until absent QRS complex after p wave

Mobitz Type 2

  • Intermitted failure of AV Conduction
  • On ECG: Missing QRS complexes, usually in set ratio (3 p waves to each QRS = 3:1)
  • RISK OF ASYSTOLE!!
74
Q

ECG Characteristics/Risks of 3rd-Degree Heart Block?

A

Referred to as Complete Heart Block

No observable relationship between p waves and QRS Complex

SIGNIFICANT RISK OF ASYSTOLE!!

75
Q

Treatment for Bradycardia/AV Node Blocks

A

Stable: observe

Unstable/Risk of Asystole (Mobitz Type 2, 3-rd Degree or previous Asystole)

  • First line: Atropine (6 doses 500mcg IV up to 3mg)
  • Then: Inotopes (Noradrenaline) and Transcutaneous cardiac pacing (deriliator)
76
Q

Indications for a Pacemaker

A

Symptomatic Bradycardia

Mobitz Type 2 AV Block

Third Degree Heart Block

Severe Heart Failure

Hypertrophic Obstructive Cardiomyopathy

77
Q

What is this?

How to treat?

A

1st Degree Heart Block

Delayed conduction through the AV node. Despite this every atrial impulse leads to a ventricular contraction (Every p wave=> QRS)

Presents as a PR >.2s (5 small or 1 big square)

Treatment if unstable:

  • First line: Atropine (6 doses 500mcg IV up to 3mg)
  • Then: Inotopes (Noradrenaline) and Transcutaneous cardiac pacing (deriliator)
78
Q

What is this?

How to treat?

A

Wenckebach’s Phenomenon (Mobitz Type I)

  • Atrial Impulses become gradually weaker until it doe snot pass through AV. After failing, becomes strong again and cycle repeats
  • On ECG: Increasing PR interval until absent QRS complex after p wave

Treatment if unstable:

  • First line: Atropine (6 doses 500mcg IV up to 3mg)
  • Then: Inotopes (Noradrenaline) and Transcutaneous cardiac pacing (deriliator)
79
Q

What is this?

How to treat?

A

Mobitz Type 2

  • Intermitted failure of AV Conduction
  • On ECG: Missing QRS complexes, usually in set ratio (3 p waves to each QRS = 3:1)
  • RISK OF ASYSTOLE!!

Treatment:

  • First line: Atropine (6 doses 500mcg IV up to 3mg)
  • Then: Inotopes (Noradrenaline) and Transcutaneous cardiac pacing (deriliator)
80
Q

What is this?

How to treat?

A

Referred to as Complete Heart Block

No observable relationship between p waves and QRS Complex

SIGNIFICANT RISK OF ASYSTOLE!!

Treatment:

  • First line: Atropine (6 doses 500mcg IV up to 3mg)
  • Then: Inotopes (Noradrenaline) and Transcutaneous cardiac pacing (deriliator)
81
Q

What is this?

How to treat?

A

Atrial Fibrillation

Rate Control w/ Beta Blocker or Diltiazem

82
Q

What is this?

How to treat?

A

Atrial Flutter

Rate Control w/ Beta Blocker

83
Q

What is this?

How to treat?

A

Wolff-Parkinson-White Syndrome

Extra conduction pathway through the Bundle of Kent leads to:

  • Short PR interval (<.12s)
  • Wide QRS complex (>.12s)
  • Delta wave (Slurred upstroke of QRS)

Treat with Radiofrequency Ablation

84
Q

What is this?

How to treat?

A

Ventricular Tachycardia

Unstable: Defibrillation

Stable: Amiodarone Infusion

85
Q

What is this?

How to treat?

A

Ventricular Fibrillation

Ventricular fibrillation (v-fib) is a common cause of out-of-hospital cardiac arrest. In this case, the heart quivers ineffectively and no blood is pumped out of the heart. On the monitor, v-fib will look like a frenetically disorganized wavy line. Ventricular fibrillation may be fine or coarse; coarse ventricular fibrillation is more likely to convert after defibrillation than fine v-fib.

86
Q

What is this?

How to treat?

A

Supraventricular Tachycardia

Treat w/ Vagal Maneuvers (Valsalva/Carotid Sinus Massage) and Adenosine

87
Q

Normal ECG: what needs to be normal?

(8 things)

A
  1. Rate: 60-100bpm (300/no of large squares R-R)
  2. Rhythm: regular sinus rhythm, p waves starting 120-200ms before a QRS complex (see only 2 waves? Must be QRS and T, can’t have a lone P)
  3. Axis: QRS has positive deflection in leads 1 and 2 means normal axis
  4. QRS: less than 120ms
  5. Q: deeper in leads 3 and aVR is normal
  6. ST interval: should be isoelectric (flat/in line with) the baseline
  7. T: higher in chest leads, lower in limb leads, down turned in aVR and V1
  8. QT interval: varies depending on HR
88
Q

Two things required to diagnose STEMI?

A

ST elevation >/=1mm in leads 2 and 3

New left bundle branch block
(WiLLiaM: W in V1+V2, M in V3+V4, wide QRS, no Q waves in 1, V5 and V6)

Changes in ECG:
Initially = normal ecg in 20% of cases
Within hours = Tall tented T waves, new LBBB and ST elevation
Within days = T wave inversion and pathological Q waves

89
Q

Causes of Left bundle branch block?

(“Where the left bundle Is blocked in the interventricular septum so the depolarisation starts in the right and moves to left, normal heart has left to right depolarisation”)

A

Aortic stenosis

Ischemic heart disease

HTN

Dilated cardiomyopathy

Anterior MI

Hyperkalemia

Digoxin poisoning

90
Q

What event does the Q wave represent?

A

The normal left to right depolarisation of the interventricular septum

Hence we lose the Q waves in Lateral leads V5/V6 in left bundle branch block

Not normally seen in V1-3

91
Q

Signs of MI in CAD (aka IHD/CHD) on ECG?

A
  1. pathological Q waves:
  • > 40 ms (1 mm) wide
  • > 2 mm deep
  • > 25% of depth of QRS complex
  • Seen in leads V1-3
  1. left bundle branch block
  • Broad QRS (>3small square/0.12sec) and
  • Deep S wave in V1 and
  • No Q wave in V5/V6
  1. ST-segment and T wave abnormalities (for example, flattening or inversion).
92
Q

What’s a tall tented P wave, and what is a tall tented T wave?

A

Tall tented P wave = p pulmonale (enlarged right atrium)

Tall tented T wave = hyperkalemia

93
Q

What does a sawtooth p-wave mean?

A

Atrial flutter

MOA: The SAN is firing at a beat of 300 per minute, the AVN wants to control the ventricular rhythm so only lets every other, or second, or third impulse through.

This means that atrial flutter gives predictable rates of 75, 100 or 150 bpm.

94
Q

A PR interval longer than 5 small squares is which cardiac arrhythmia?

A

Lengthened PR interval means the first degree heart block, the AV node is holding on to the impulse for a little too long.

95
Q

What is the arrhythmia that causes progressively lengthening PR intervals that reset themselves after a few complexes?

A

This is second degree heart block mobitz type 1 also known as wenckebach.

The PR interval lengthens progressively before it drops a P wave entirely and then resets.

96
Q

What is the arrhythmia that causes a normal PR interval but then occasional dropped QRS complexes? I.e. the p waves continue at the same rate but the QRS doesn’t follow it

A

This is second degree heart block Mobitz type 2.

This is the one which requires a long ECG strip taken, in order to catch these dropped QRS complexes.

97
Q

How long should a normal P-R interval be?

A

0.12-0.2 seconds = 3-5 small squares

98
Q

What’s a tall tented P wave, and what is a tall tented T wave?

A

Tall tented P wave = p pulmonale (enlarged right atrium)

Tall tented T wave = hyperkalemia

99
Q

What kind of heart block increase the P-R interval

A

First degree, mobitz type 1 and mobitz type 2

Clinical Medicine (8 decks)

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