Cardiology Flashcards
1
Q
Classification system for MI in the next 10 years
A
QRISK3 Score
QRISK >10% => start on Statin (atorvastatin 20mg @ night)
2
Q
Secondary Prevention of Cardiovascular Disease
A
Aspirin
Atorvastatin
Atenalol
ACE Inhibitor
3
Q
Side Effects of Statins?
A
Myopathy (Check Creatinine Kinases)
Type II Diabetes
4
Q
Difference Between Stable and Unstable Angina
A
Stable: Relieved by Rest or GTN
Unstable: Random symptoms including while at rest
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
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
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)
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
9
Q
RCA Heart Area Supply
ECG Leads?
A
Inferior Heart Area:
- Right Atrium
- RV
- Inferior LV
- Posterior Septum
ECG Leads: II, III, aVF
10
Q
Circumflex Heart Area Supply
ECG Leads?
A
Lateral Heart Area:
- Left Atrium
- Posterior LV
ECG Leads: I, aVL, V5-6
11
Q
Left Anterior Descending (LAD) Heart Area Supply
ECG Leads?
A
Anterior Heart Area:
- Anterior LV
- Anterior Septum
ECG Leads: V1-4
12
Q
Left Coronary Artery Heart Area Supply
ECG Leads?
A
Anterolateral Heart Area
ECG Leads: I, aVL, V3-6
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
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)
15
Q
ECG Changes in STEMI
A
ST-Segment Elevation
New Left Bundle Branch Block
16
Q
ECG Changes in NSTEMI
A
ST Segment Depression
Deep T Wave Inversion
Pathological Q Waves
17
Q
Differential of Raised Troponins
A
Myocardial Ischemia
Chronic Renal Failure
Sepsis
Myocarditis
Aortic Dissection
Pulmonary Embolism
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)
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
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%
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
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)
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)
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)
25
Presentation of Acute LVF
Rapid onset Breathlessness
- Excarcebated by lying flat and improves on sitting up
- Type 1 Resp Failure
26
Acute Heart Failure Exam Findings
Increase RR
Reduced O2 sats
Tachycardia
3rd Heart Sound
Bilateral Basal Crackles
Hypotension (Cardiogenic Shock)
Right-sided as well => Elevated JVP, Peripheral Edema
27
Workup for Heart Failure Pt
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
28
What is BNP?
- Mechanism
- Causes of Elevation
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
29
What is considered a normal Ejection Fraction?
>50% as measured by Echocardiography
30
Chest XRAY findings in Heart Failure
Cardiomegaly (Cardiothoracic Ratio >.5)
Upper lobe venous diversion
Bilateral Pleural Effusions
Fluid in Interlobular Fissures
Fluid in Seotal Lines (Kerley Lines)
31
Management of Acute Heart Failure
**Pour SOD**
- **Pour** away (STOP) IV Fluids
- **S**it Up
- **O**xygen (if <95%)
- **D**iuretics (Furosemide 40mg)
+ Monitor fluid intake, urine output, U&E bloods
In severe cases:
- CPAP
- Inotropes
32
Presentation of Chronic Heart Failure
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)
33
Diagnosis of Chronic Heart Failure
Clinical Presentation
BNP Blood Test (NT-proBNP)
Echocardiogram
ECG
34
Management of Chronic Heart Failure
**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
35
Causes of Cor Pulmonale
COPD (Most Common)
PE
Interstitial Lung Disease
Cystic Fibrosis
Primary Pulmonary Hypertension
36
Presentation/Signs of Cor Pulmonale
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)
37
Primary vs. Secondary Hypertension
**Primary** (95%) developed on its own w/ no secondary cause
**Secondary Hypertension** (ROPE)
- **R**enal Disease
- **O**besity
- **P**regnancy Induced Hypertension/Pre-Eclampsia
- **E**ndocrine (Hyperaldoronism/Conn's Syndrome (2.5% of hypertension) diagnosed with Renin:aldosterone ratio blood test)
38
Complications of Hypertension
Ischemic Heart Disease
Stroke/Hermorage
Hypertensive retinopathy
Hypertensive Nephropathy
Heart Failure
39
Management of Hypertension
Potassium Ballance?
Medications:
- **A**CE Inhibitor / ARB (those w/ dry cough)
- **B**eta Blocker (Bisprolol)
- **C**alcium Channel Blocker (Amlodipine)
- Thiazi**D**e: (Indapamide)
Potassium:
- Thiazides => HYPOLKALEMIA
- Spironolactone/ACE Inhibitors => HYPERKALEMIA
40
What is S1 Heart Sound Indicative of?
Closing of AV valves (Tricuspid/Mitral) at start of **Systolic** contraction of ventricles
41
What is S2 Heart Sound Indicative of?
Closing of Semilunar Valves (Pulmonary/Aortic) once systolic contraction is complete
42
What is S3 Heart Sound Indicative of?
.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
What is S4 Heart Sound Indicative of?
Heard Directly before S1
ALWAY ABNORMAL, indivative of Stiff/Hypertrophic Ventricle causing turbulent flow
44
4 Valve areas to auscultate
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
Special Maneuvers to emphasize Murmurs?
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
**Mitral Stenosis**
- Cause
- Character
- Associations/Signs
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
**Mitral Regurgitation**
- Cause
- Character
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
**Aortic Stenosis**
- Cause
- Character
- Associations/Signs
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
**Aortic Regurgitation**
- Cause
- Character
- Associations/Signs
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
Benefits of Bioprosthetic Heart Valves vs. Mechanical?
Biosprothetic (10 year Life)
Mechanical (>20 Year life) but require lifelong warfarin
- INR Target 2.5-3.5 (Higher than normal 2-3)
51
Complications of Mechanical Heart Valve?
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
Indication/Procedure of TAVI
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
Mortality/Organisms of Concern for Infective Endocarditis
Symptoms/Signs
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
Atrial Fibrillation Associations/Presentation
Associations:
- Irregularly irregular ventricular contractions
- Tachycardia
- Heart Failure
- Risk of Stroke
Presentation
- Palpitations
-SOB
- Syncope
55
Differential for Irregularly Irregular Pulse
Atrial Fibrillation
Ventricular Ectopics (Disappear when Heart Rate is over a certain threshold. Regular heart rate during exercise suggestive)
56
Atrial Fibrilation on ECG
Absent P Waves
Narrow QRS Complex Tachycardia
Irregularly Irregular Venticular Rythem
57
Causes of Atrial Fibrillation
'SMITH'
**S**epsis
**M**itral Valve Pathology (Stenosis/Regurg)
**I**schemic Heart Disease
**T**hyrotoxicosis
**H**ypertension
58
Treatment of Atrial Fibrillation
- Rate Control
- Rhythm Control (Cardioversion/Long Term)
**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
Treatment of Paroxysimal Atrial Fibrilation
Infrequent episodes with no structural heart disease => "Pill in the Pocket"- **Flecainide** (Class 1C - Na+ Block)
Anticoagulation if **CHA2DS2-VASc** score >1
60
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?
Risk of Stroke with/without anticoagulation (5% each year w/o , 1-2% risk of stroke each year on Anticoagulation (⅔ Reduction))
**CHA2DS2-VASc**
- **C**onwgestive heart failure
- **H**ypertension
- **A**ge > 75 _(Scores 2)_
- **D**iabetes
- **S*troke or TIA previously _(Scores 2)_
- **V**ascular Disease
- **A**ge 65-74
- **S**ex (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
4 Cardiac Arrest Rhythms seen in a pulseless, unresponsive patient
Shockable
- **Ventricular Tachycardia**
- **Ventricular Fibrilation**
Non-Shockable
- **Pulseless Electrical Activity**
- **Asystole** (no significant electrical activity)
62
Tachycardia Treatment?
- Unstable
- Stable (Narrow/Broad QRS)
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
Characteristics of Atrial Flutter
Atrial Contraction at 300bpm, Ventricular 150bpm
**sawtooth apearance** on ECG w/ p-wave after p-wave
64
Treatment of Atrial Fibrillation?
Rate/Rythym control w/ Beta Blockers or cardioversion
Treat reversible underlying (Thyrotoxicosis, hypertension)
Radiofrequency Ablation of re-entrant circuit
Antigoagulation (CHA2DS2VASc Score)
65
Characteristics of Super Ventricular Tachycardia
Narrow Complex Tachycardia (QRS <.12)
66
Acute Management of Stable patients with SVT?
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
Wolf Parkinson White ECG Changes
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
Wolf Parkinson White Treatment
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
Causes of Torsades de Pointes
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
Management of Torsades de Pointes
- Acute
- Chronic
_Acute_
- Correct electrolytes
- Magnesium Infusion
- Defribilaiton (in event of Ventricular Tachycardia)
_Chronic_
- Avoid provoking medication
- Correct electrolyte distrubances
- Beta Blockers (NOT SOTALOL)
- Pacemaker
71
What are Ventricular Ectopics?
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
Cause/ECG Characteristics of 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)**
73
Cause/Types/ECG Characteristics of 2nd Degree Heart Block?
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
ECG Characteristics/Risks of 3rd-Degree Heart Block?
Referred to as **Complete Heart Block**
No observable relationship between p waves and QRS Complex
SIGNIFICANT RISK OF ASYSTOLE!!
75
Treatment for Bradycardia/AV Node Blocks
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
Indications for a Pacemaker
Symptomatic Bradycardia
Mobitz Type 2 AV Block
Third Degree Heart Block
Severe Heart Failure
Hypertrophic Obstructive Cardiomyopathy
77
What is this?
How to treat?
**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
What is this?
How to treat?
**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
What is this?
How to treat?
**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
What is this?
How to treat?
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
What is this?
How to treat?
**Atrial Fibrillation**
Rate Control w/ Beta Blocker or Diltiazem
82
What is this?
How to treat?
**Atrial Flutter**
Rate Control w/ Beta Blocker
83
What is this?
How to treat?
**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
What is this?
How to treat?
**Ventricular Tachycardia**
Unstable: Defibrillation
Stable: Amiodarone Infusion
85
What is this?
How to treat?
**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
What is this?
How to treat?
**Supraventricular Tachycardia**
Treat w/ Vagal Maneuvers (Valsalva/Carotid Sinus Massage) and Adenosine
87
Normal ECG: what needs to be normal?
(8 things)
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
Two things required to diagnose STEMI?
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
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”)
Aortic stenosis
Ischemic heart disease
HTN
Dilated cardiomyopathy
Anterior MI
Hyperkalemia
Digoxin poisoning
90
What event does the Q wave represent?
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
Signs of MI in CAD (aka IHD/CHD) on ECG?
1. pathological Q waves:
* > 40 ms (1 mm) wide
* > 2 mm deep
* > 25% of depth of QRS complex
* Seen in leads V1-3
2. left bundle branch block
* Broad QRS (>3small square/0.12sec) and
* Deep S wave in V1 and
* No Q wave in V5/V6
3. ST-segment and T wave abnormalities (for example, flattening or inversion).
92
What’s a tall tented P wave, and what is a tall tented T wave?
Tall tented P wave = p pulmonale (enlarged right atrium)
Tall tented T wave = hyperkalemia
93
What does a sawtooth p-wave mean?
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
A PR interval longer than 5 small squares is which cardiac arrhythmia?
Lengthened PR interval means the first degree heart block, the AV node is holding on to the impulse for a little too long.
95
What is the arrhythmia that causes progressively lengthening PR intervals that reset themselves after a few complexes?
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
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
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
How long should a normal P-R interval be?
0.12-0.2 seconds = 3-5 small squares
98
What’s a tall tented P wave, and what is a tall tented T wave?
Tall tented P wave = p pulmonale (enlarged right atrium)
Tall tented T wave = hyperkalemia
99
What kind of heart block increase the P-R interval
First degree, mobitz type 1 and mobitz type 2
