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Acute Care > Cardiac > Flashcards

Cardiac Flashcards

1
Q

Describe the stages of de and repolarisation in the contraction of the heart

A

0: rapid depolarisation due to influx of Na+
1: Rapid early repolarisation, efflux K+ with inactivation of fast Na+ channels
2: Repolarisation slowed by Ca2+ influx
3. Rapid repolarisation, K+ efflux
4. Diastole with steady state resting transmembrane voltage

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2
Q

What is AF?

A

Most common arrhythmia (1-2% population)
Atrial fibrillation
Irregular baseline, ventricle contraction irregularly irregular
Increases risk of hospitalisation, stroke, cardiomyopathy

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3
Q

Treatment of AF

A

Cardioversion:
Electrical w/DC current
Chemical: amiodarone/flecanide

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4
Q

When should flecanide be avoided in AF?

A

Don’t use flecanide with underlying ischaemic heart disease or structural abnormalities

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5
Q

Do you anticoagulate AF patients?

A

Yes
Use CHA2DS2 VASc score and HAS-BLED can quantify stroke risk
WARFARIN, NOAC (DABIGATRAN, RIVAROXABAN)

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6
Q

If cardioversion for AF does not work, what do you do?

A

Rate control: Beta-blockers, VERAPAMIL, DIGITALIS
Rhythm control: SOTALOL, FLECANIDE, AMIODARONE
Catheter ablation (if ectopic foci and paroxysmal AF)

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7
Q

8 causes of pathological bradycardia

A
  • Cardiac surgery
  • Chronic degeneration of AV or SA nodes
  • Cholestatic jaundice
  • Hypothermia
  • Hypothyroidism
  • Ischaemia/infarction of SA node
  • Raised ICP
  • Drugs: amiodarone, beta-blockers, diltiazem/verapamil, lithium salts, morphine, clonidine, anticholinesterase inhibitors (donepezil, rivastigmine)
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8
Q

Treatment of pathologic/symptomatic bradycardia

A

Stop ß-blockers/other causative drugs
Treat underlying cause (levothyroxine)
Acutely Atropine (reduces vagal inhibition) IV 500micrograms, repeat every 3-5mins

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9
Q

What is a sinus pause?
Causes?
Symptoms?

A 
Sa node fails to generate impulse
Caused by:
•	Acute myocarditis
•	Digoxin toxicity
•	Fibrosis of SA node (ageing)
•	SE of antiarrythmic drug
•	MI
•	Stroke
Breathlessness, lethargy, dizziness, collapse, falls
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10
Q

Treatment of sinus pause?

A

Permanent pacemaker

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11
Q

What is sick sinus syndrome?

A

Palpitations caused by sinus bradycardia, sinus pause, paroxysmal atrial/tachy arrhythmias
Treatment: pacemaker/ rate controlling drugs

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12
Q

8 causes of AV block

A
  • Cardiomyopathy
  • Conduction system fibrosis
  • Connective tissue disease
  • Hypothyroidism
  • IHD
  • Radiotherapy
  • Sarcoidosis
  • Drug induced (beta-blockers, diltiazem, digoxin)
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13
Q

When are pacemakers indicated?

A

Pacemakers are indicated in:
• RBBB/LBBB with intermittent 3rd degree AV block
• Carotid sinus hypersensitivity
• Pauses of >3secs during the day
• Sustained VT with pauses
• Symptomatic bradycardia
• Symptomatic sinus node dysfunction/2nd degree heart block

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14
Q

How do you differentiate between tachyarrhythmias?

A

Is it regular? No
⇒ irregularly irregular AF
⇒ unconscious patient VF

Is the QRS broad?
⇒ Yes means ventricular origin
⇒ No means supraventricular origin

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15
Q

What does atrial flutter look like?

A

P-wave rate>250/min
2:1 or 3:1 P:R ratio
Characteristic saw tooth baseline

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16
Q

Treatment of supraventricular tachycardia

A

Give adenosine to block AV node. If this terminates the tachycardia-> AVRT/AVNRT
If it is independent of AV node-> focal atrial tachycardia
AVRT: atrioventricular re-entry tachycardia
AVNRT: atrial node re-entrant tachycardia

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17
Q

How do you treat a patient with a tachyarrhythmia who is haemodynamically compromised?

A

Electrical cardioversion under anaesthesia and sedation

Then IV amiodarone/beta-blocker

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18
Q

How do you manage a haemodynamically stable pt with a tachyarrhythmia?

A

Continuous ECG monitoring
Vagontonic manoeuvres (carotid massage, valsalva)
IV adenosine
Rate control with IV lidocaine

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19
Q

Treatment of supraventricular tachycardia

A 
Rate control (ß-blocker, verapamil, digoxin)
Rhythm control (amiodarone, flecanide, sotalol, DC shock)
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20
Q

Prevention of supraventricular tachycardia

A

Amiodarone
Sotalol
Quinidine
Procainamide

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21
Q

Causes of AF

A
  • Atrial septal defect
  • Cardiomyopathies
  • Diabetes mellitus
  • COPD
  • CKD
  • HTN
  • Obesity
  • CCF
  • Thyroid dysfunction
  • Valvular heart disease
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22
Q

Define 1st degree heart block

A

Conduction across AV node is delayed
Prolonged PR interval
Doesn’t need treatment

23
Q

Define 2nd degree heart block

A

Mobitz 1: PR interval progressively lenthens until QRS in dropped
Mobitz 2: Fixed number of p waves conduct (eg 3P to every 1 QRS). Conduction block at bundle of His

24
Q

Where is the conduction block with Mobitz 2 2nd degree AV block?

A

Bundle of His

25
Q

Define 3rd degree heart block

A

Complete dissociation between atria and ventricle contraction (P waves and QRS)
Atrial signal fails to reach ventricles
Can lead to sudden cardiac death

26
Q

Describe sinus arrhythmia

A

HR INcreases on INspiration

27
Q

What is left axis deviation?

4 causes

A 
(I +ve, AVF –ve)
•	Left bundle branch block (treat w/pacemaker)
•	Left ventricular hypertrophy
•	Inferior MI
•	Wolff-Parkinson White Syndrome
28
Q

Name 5 causes of right axis deviation

A
  • Lateral MI
  • Lung consolidation (COPD, PE)
  • Right ventricular hypertrophy
  • Hyperkalemia
  • WPW syndrome
29
Q

How do p-waves change in atrial enlargement?

A

Spiked in right atrial enlargement, mountains in left atrial enlargement.

30
Q

What can t wave morphology show?

A
  • Flattening/inversion = ischaemia

* Tall, peaked = hyperkalaemia

31
Q

Name 3 types of supraventricular tachycardia

A
  • Sinus tachycardia
  • Atrial flutter
  • Atrial fibrillation
32
Q

Describe ventricular tachycardia

Treatment?

A

Raised HR, absent p wave, wide QRS.

CPR if unconscious, electrical cardioversion under anaesthetic if awake. Beta-blockers/AMIODARONE.

33
Q

Define ventricular fibrillation

A

Ventricles don’t contract defined way. Absent p wave, QRS and T. Irregular waves with varying morphology and amplitude.

34
Q

Treatment of ventricular fibrillation

A

CPR (shockable)

35
Q

What is PEA?

A

Pulseless electrical activity

Non shockable because the electrical system in the heart is actually working properly

36
Q

How do you calculate oxygen content?

A

Hb x SaO2 x 0.13 (ml/L)

37
Q

What is venous return influenced by?

A
  • Cardiac output
  • Muscle pump
  • Venous valves
  • Thoracic pump
38
Q

Why should heavily pregnant ladies by positioned in left lateral position?

A

To avoid obstructing IVC

39
Q

What 7 things determine blood flow?

A 
Blood viscosity-
•	Haematocrit
•	Temperature (hypothermic)
•	RBC membrane integrity
Vessel wall-
•	Lumen (tone)
•	Driving pressure
•	Endothelial integrity
•	Length
40
Q

What is dangerous about injecting steroids (eg for muscle gain)

A

Hyperlipidaemia
Liver cancer
Pancreatitis
Poor perfusion

41
Q

Why is a cardiac MRI done?

A

Only in stable patients
Investigation for cardiac ischaemia/post infarction
Congenital heart defect visualisation

42
Q

Define ACS

A

Acute coronary syndrome

Lack of oxygen reaching heart tissue, causing myocardial ischaemia due to atheroma formation in coronary arteries

43
Q

Pathophysiology of MI

A
  • Endothelial injury (raised LDL, toxins from smoking, hypertension, hemodynamic stress)
  • Expression of adhesion molecules
  • Platelet adhesion and PDGF released
  • Insudation of lipids and LDL oxidized by macrophages
  • Adhesion and migration of monocytes into macrophages
  • Uptake of LDL’s lipid by macrophages-> foam cells
  • Smooth muscle proliferation & migration to intima
  • Cap forms over foam cells
  • Smooth muscle produces matrix and turns into myofibroblasts
  • Foam cells secrete cytokines
  • More inflammatory cells are recruited
  • Foam cells apoptose and secrete lipid
  • Inflammatory cells produce proteases and weaken cap
  • Rupture of cap = haemorrhage from plaque microvessels
  • Platelet thrombus and coagulation
  • Embolism or fibrosis or resolution
44
Q

Signs and symptoms of MI

A
  • Intense compressive chest pain-> L arm and jaw
  • Nausea and vomiting
  • Sweating and clammy
  • Dyspnoea (SOB)
  • Longer than 20 mins (ie not angina)
45
Q

How is an MI diagnosed

A
  • Increased troponin levels
  • Symptoms of ischaemia
  • ECG changes (ST elevation, T wave inversion, deep Qs)
  • Loss of myocardium on echo
  • 4th heart sound
  • Angiography showing constriction/blockage
46
Q

Describe the treatment of an MI

A
  • 1º angioplasty
  • Antiplatelet (ASPIRIN, CLOPIDOGREL)
  • Thrombolysis (rTPA)
  • Anticoagulant (HEPARIN, WARFARIN, NOAC)
  • Pain relief (opiate)
  • GTN
  • O2
  • Antiemetic (METOCLOPRAMIDE)
  • Protect myocardium (ATENOLOL, LISINOPRIL ACEi)
  • Secondary prevention (statin, lifestyle, aspirin)
47
Q

Define pericardial tamponade

A

Accumulation of fluid in the pericardial space, resulting in reduced ventricular filling and subsequent haemodynamic compromise

Medical emergency-> pulmonary oedema, shock & death.

48
Q

Name 9 causes of pericardial tamponade

A

Same as pericarditis causes
• Malignancy
• Acute MI/post transmural infarction (fibrinous exudate)
• Infection (esp viral, HIV)
• Ureamia (metabolic toxins causing inflammation, from kidney failure)
• Radiation
• Autoimmune (RA, SLE)
• Trauma (penetrating injury)
• Iatrogenic cardiac perforation (central line placement, pacemaker insertion, cardiac catheterization, sternal bone marrow biopsies, pericardiocentesis)
• Aortic dissection

49
Q

Signs and symptoms of pericardial tamponade

A
  • Tachypnoea
  • Tachycardia
  • Cold & clammy extremities
  • Elevated jugular venous pressure (on inspiration/Kussmaul)
  • Pulsus paradoxus (exaggeration of inspiration lowering BP)
  • Chest pressure
  • Decreased urine output
  • Confusion
  • Dysphoria (impending death, restless)
  • Others based on underlying cause (eg weight loss if malignancy)
50
Q

Differential diagnosis in pericardial tamponade

A
  • Cardiogenic Shock
  • Pericarditis
  • Pneumothorax
  • Pulmonary Embolism
51
Q

What would be seen on echo to diagnose pericardial tamponade

A
  • An echo-free space posterior and anterior to the left ventricle and behind the left atrium
  • Early diastolic collapse of the right ventricular free wall
  • Late diastolic compression/collapse of the right atrium
  • Swinging of the heart in the pericardial sac
  • Left ventricular pseudohypertrophy
  • Inferior vena cava plethora with minimal or no collapse with inspiration
  • A greater than 40% relative inspiratory augmentation of blood flow across the tricuspid valve or greater than 25% relative decrease in inspiratory flow across the mitral valve
52
Q

What would be seen on ECG to diagnose pericardial tamponade?

A

Sinus tachycardia, low-voltage QRS complexes which alternate, PR depression

53
Q

What would be seen on CXR to diagnose pericardial tamponade?

A

Cardiomegaly
Chest wall trauma
Pericardial calcifications

54
Q

Management of pericardial tamponade

A
  • O2
  • Fluids
  • Leg elevation
  • Emergency subxiphoid percutaneous drainage
  • Pericardiocentesis (with or without echocardiographic guidance)
  • Percutaneous balloon pericardiotomy

Acute Care (11 decks)

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