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Anaesthesiology > CVS > Flashcards

CVS Flashcards

1
Q

How calculate pulse pressure?

A

Systolic-diastolic

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2
Q

How many seconds is a big block on ECG

A

0,2 seconds
So 1 small block is 0.04 seconds

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3
Q

Normal size P wave?

A

≤3 small blocks wide
≤ 2,5 small blocks high

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4
Q

Normal width QRS?

A

≤ 3 small blocks wide

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5
Q

Pathology if QRS broad and preceded by P wave?

A

Conduction defect

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6
Q

Pathology if QRS broad and not preceded by P wave?

A

Ventricular rhythm origin mostly

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7
Q

Pathology if QRS narrow and not preceded by P wave?

A

Rhythm originates between sa node and ventricle (not sinus)

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8
Q

Normal size of T wave?

A

Max 2/3 height of QRs

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9
Q

Pathology if peaked t wave?

A

Hyper K

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10
Q

Where does Pr interval span and normal size?

A

Beginning of P wave to beginning QRS (segment from end of P wave)

≤5 small blocks (1 big block)

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11
Q

Prolonged Pr interval pathology?

A

First degree heart block

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12
Q

How calculate rate on EcG?

A

300÷ number of big blocks between 2 r waves or
Number of QRS on bottom rhythm strip lead 2 repeat x6

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13
Q

Which rhythms do we cardiovert? (3)

A

• AFib
• atrial flutter types 1 and 2
• other unstable supraventricular tachycardias
Ventricular tachycardia with pulse

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14
Q

Identify pathology picture 35

A

Atrial fibrillation
• no p waves!
• irregular irregular rhythm!
• absence isoelectric baseline
• variable ventricular rate
• fibrillatory waves may be present and mimic p waves!

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15
Q

Identify pathology picture 36

A

Atrial flutter: saw-tooth pattern p waves

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16
Q

Identify pathology picture 37

A

Sinus bradycardia
Normal P, QRs, t but hr ≤60

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17
Q

Treatment sinus bradycardia?

A

Atropine if emergency
Glycopyrolate if not

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18
Q

Identify pathology picture 38

A

Sinus tachycardia
Normal P, QRs, t, but hr >100

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19
Q

Identify pathology picture 39

A

Afib

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20
Q

Identify pathology picture 40

A

Atrial flutter

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21
Q

Identify pathology picture 41

A

First degree heart block
• prolonged Pr interval > 5 small blocks

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22
Q

Identify pathology picture 42

A

Second degree heart block mobitz type 1
Pr interval increases then skips QRs

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23
Q

Identify pathology picture 43

A

Second degree heart block mobitz type 2
Pr interval constant then skips QRs

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24
Q

Identify pathology picture 44

A

Third degree heart block
No correlation between P waves and QRs complexes

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25
Q

Treatment second degree mobitz type 2 and third degree heart block?

A

Refer for pacemaker prior to elective surgery
(First and second degree mobitz 1 no treatment)

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26
Q

Identify pathology picture 45

A

Nodal/junctional rhythm originating between av node and ventricle
• narrow complex QRs
• no P wave

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27
Q

Treatment nodal/junctional rhythm?

A

Pacemaker if symptomatic

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28
Q

Identify pathology picture 46

A

Premature ventricular contractions (PVC) / ventricular extra systoles
• broad QRs
• no P wave
• t opposite direction to QRs

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29
Q

Treatment premature ventricular contractions/ ventricular extra systoles?

A

Treat if > 5 / min or multi focal/polymorphic (don’t look the same), decreased CO, R on T phenomenon, or unstable patient. Not necessary to treat if just bradycardia
First line lignocaine
Second line amiodarone

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30
Q

Identify pathology picture 47

A

V tach

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31
Q

Identify pathology picture 48

A

V fib

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32
Q

Identify pathology picture 49

A

Torsades de pointes

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33
Q

Treatment torsades de pointes?

A

MgSO4

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34
Q

Identify pathology picture 50

A

Atrial flutter
Saw tooth pattern P waves

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35
Q

Identify pathology picture 51

A

Sinus tachycardia

36
Q

Identify pathology picture 52

A

Morbitz type 1 second degree heart block

37
Q

Identify pathology picture 53

A

Torsades de pointes

38
Q

Identify pathology picture 54

A

Nodal / junctional tachycardia

39
Q

Identify pathology picture 55

A

Ventricular extra systole

40
Q

Name 11 causes cardiac arrest

A

6 H ‘s and 5 t’s
Hypovolaemia
Hypoxia
Hydrogen: acidosis
Hyper or hypo K
Hypothermia
Hypoglycaemia
Toxins
Tamponade
Tension pneumothorax
Thrombosis (coronary and pulmonary)
Trauma

41
Q

The relationship between cardiac output and left ventricular end diastolic volume is known as what?

A

Starling’s law of the heart

42
Q

Name 5 factors that affect ventricular preload

A

• venous return
• blood vol
• distribution of volumes: posture, intrathoracic pressure, pericardial pressure, venous tone
• rhythm (atrial contraction)
• heart rate

43
Q

Define Laplace’s law and what it refers to

A

Afterload.
Circumferential stress = (intra ventricular pressure X ventricular radius) ÷ (2 x wall thickness)

44
Q

Formula for SVR? (Systemic vascular resistance)

A

80 x ([map- CVP] ÷ co )

45
Q

Define inotropy

A

Contractility
Intrinsic ability myocardium to pump in absence of changes to preload or after load.
Related to rate of myocardial muscle shortening
Dependent on intracellular calcium concentration during systole

46
Q

Name 5 causes of decreased myocardial contractility (inotropy)

A

•Anoxia
•Acidosis
• depletion catecholamine stores within heart
• ischaemia or infarction (loss functioning muscle mass)
• most anaesthetics and antiarrythmics are also negative inotropes

47
Q

Name 4 mechanisms of immediate physiological blood pressure control

A

Autonomic nervous system. Changes sensed by hypothalamus and brainstem centrally, baroreceptors peripherally. Decrease arterial blood pressure countered by:
• increased SNS tone
• increased adrenaline secretion
• decreased vagal activity (psns)
Resulting in systemic vasoconstriction, elevation heart rate, enhanced contractility
And vice versa

48
Q

Name 3 mechanisms of intermediate physiological blood pressure control

A

Minutes to hours
• activate RAAS (angiotensin is potent arteriolar vasoconstrictor)
• increase secretion arginine vasopressin (potent arteriolar vasoconstrictor leading to increase SVR and water retention) aka ADH
• alteration normal capillary fluid exchange (fluid moves from IV to interstitium to decrease BP and vice versa)

49
Q

Name 2 mechanisms of long term physiological blood pressure control

A

• Slower renal mechanisms
• alteration total body sodium and water balance to restore bp to normal
If hypotension, sodium and water will be retained and vice versa

50
Q

Name 5 acute target organ damageS and complications by hypertension

A

• Intracranial haemorrhage / encephalopathy
• acute coronary syndromes or acute heart failure
• aortic dissection
• nephropathy
• papilloedema

51
Q

Map must be maintained within which limits in hypertensive patients?

A

Within 20-30% of baseline

52
Q

Name 4 physiological factors that influence oxygen demand of the heart

A

• Basal requirements: fever, thyrotoxicosis, cold
• heart rate
• contractility
• wall tensions: pre load, after load
Increase in any 1 of these will increase demand

53
Q

Name 4 factors that influence oxygen supply or delivery (D02) to the heart

A

• Oxygen: fi02, haematocrit, oxygen dissociation curve , oxygen extraction, saturation , haemoglobin
• coronary artery patency: atherosclerosis, spasm, endothelial damage, vasoactive substances
• coronary perfusion pressure: aortic dp, LVEDP ( coronary blood flow = (AoDP - LVEDP) / coronary vascular resistance
• perfusion time: tachycardia
Cardiac output: hr and Sv
Haemoglobin
Diastolic pressure and time

54
Q

Name the 4 basic stages heart failure

A

A: risk factors eg smoking, diabetes, cad, ht… Any disease that cause remodelling
B: structural - systolic lv dysfunction and ejection fraction 45%
C: symptomatic eg sob, fatigue, decreased effort tolerance, oedema
D: refractory

55
Q

How can Hf be treated pre-op? (4)

A

• Preload: consider negative fluid balance to decrease preload
• contractility: optimise inotropy to improve it
• after loads: vasodilators eg nitrates to decrease it
• inodilators: levosimendan

56
Q

Which heart failure patients must have elective surgeries postponed

A

Nyha class 3 or 4 until symptoms reduced to 1 or 2.

57
Q

What type ventilation should be used for patients with heart failure and why?

A

Positive pressure ventilation
Offload L ventricle

58
Q

Management and goals valve regurgitation? (4)

A

“Full, fast and forward”
-fluid bolus preload (full)
-increased inotropy (contractility)
-increase heart rate to 80-100 (fast) (avoid bradycardia!- prolongs regurg )
-lower systemic vascular resistance (forward)

Maintain sinus rhythm
Maintain or slightly increase preload; decrease afterload

59
Q

Coronary perfusion pressure formula?

A

Arterial diastolic pressure - LV end diastolic pressure

60
Q

Management and precautions for stenotic heart lesions intra-op? (5)

A

Fixed cardiac output lesion, therefore:
-maintain preload (euvolaemia) AND afterload (AVOID SPINAL - can’t compensate for drop BP) ( very sensitive to fluid overload ! - pulmonary odema because fixed CO )
-maintain contractility
-avoid tachycardia (tachycardia reduce diastolic filling time so keep at 60- 80)
-maintain sinus rhythm (patient dependent on atrial kick/contraction for ventricular filling much more than normal patients) (otherwise decrease preload which decrease SV)
- maintain systemic vascular resistance (avoid neuraxial anaesthesia)

61
Q

How does valvular stenosis affect stroke volume?

A

• Av stenosis (mitral or tricuspid): decreased ventricular preload
• semilunar stenosis (pulmonary or aortic ): increased ventricular afterload
Therefore decreased stroke volume and pressure overload. Compensation is concentric hypertrophy.

62
Q

How does valvular regurgitation affect stroke volume?

A

•No change in preload, afterload or contractility.
• decrease effective stroke volume by regurgitant volume with every contraction

Therefore decreased stroke volume and volume overload. compensation is eccentric hypertrophy.

63
Q

Which antibiotic prophylaxis can be given to patients at risk of infective endocarditis? (3)

A

• Oral amoxicillin or
• im/iv ampicillin/cephazolin
• clindamycin if penicillin allergy

64
Q

Which drug combination can be used to blunt the sympathetic stimulation response during laryngoscopy causing a rise in blood pressure?

A

Sufentanil (opioid) and propofol

65
Q

Blood pressure formula?

A

Cardiac output (HR x SV -preload, contractility, afterload) x systemic vascular resistance

66
Q

Define cardioversion

A

Shock delivered on the r wave of a QRS complex to convert abnormal rhythm back to sinus - this synchronisation avoids shock delivery during the relative refractory period of the cardiac cycle (on the t wave) which could cause v fib

Set defibrillator mode to synchrnoized shock! Use 100 J

67
Q

Define defibrillation

A

Random administration of shock during cardiac cycle at higher energy 200 j biphasic (360 monophasic)

68
Q

Name the 3 indications for defibrillation

A

• Pulseless ventricular tachycardia
• ventricular fibrillation
• cardiac arrest due to or resulting in v fib

69
Q

Pharmacological treatment A fib? (2)

A

• Beta blockers / CCB
• digoxin/amiodarone

70
Q

Treatment V tach?

A

• Defib iF unstable
• amiodarone/lignocaine if stable

71
Q

Name 6 complications associated with administering anaesthesia to uncontrolled hypertensives

A

• End organ failure and ischaemia eg retinopathy, renal failure…
• stroke
• labile swinging blood pressures (drop at inductionvery low, very high at intubation etc. Not steady,worse outcome)
• heart failure
• pulmonary oedema
• vascular anastomosis disruption

72
Q

Maximum blood pressure to receive elective surgery?

A

SBP < 160-180
Diastolic <110

73
Q

Coronary blood flow formula?

A

Cbf= cerebral perfusion pressure ÷ coronary vascular resistance

74
Q

Minimum haemoglobin and haematocrit in ischaemic heart disease?

A

Hb > 10
Hct ≥ 13

75
Q

Basic CVS goal when administering anaesthesia to ischaemic heart disease patient?

A

Increase oxygen supply to heart: optimised coronary perfusion pressure (diastolic optimised and LVEDP low as possible with with diuretics), optimise oxygen content blood
Decrease oxygen demand to heart: by decreasing heart rate eg with opioids, regional block

76
Q

Can a patient with a history of mi receive anaesthesia?

A

Delay iF mi in previous 6 months.

77
Q

Name 7 things and states to be careful to avoid perioperatively in heart failure patients

A

• Hypotension and tachycardia
• positions that precipitate hf: trendelenburg
• auto transfusion post cs
• hypercarbia
• hypoxaemia
. Hyperinflation lungs
• fluid overload (maintain higher preload but reduce after load)

78
Q

Which induction agents should be avoided in heart failure (2)

A

• Propofol
• thiopentone
Careful with ketamine- can increase bp and hr → increase oxygen demand heart

79
Q

Which muscle relaxant should be avoided in heart failure

A

Pancuronium: cause tachycardia

80
Q

Best anaesthetic agents for heart failure?

A

Induce with etomidate
Maintain with sevo

81
Q

Induction and maintenance agent of choice in stenotic heart lesions? (3)

A

• Etomidate
• sevoflurane
• high dose total opioid anaesthesia with fentanyl /sufentanyl (monitor depth)

82
Q

which induction agents must be avoided in stenotic heart lesions? (3)

A

• Thiopentone (acute decrease SVR )
• ketamine (tachycardia)
• propofol (myocardial depression)

83
Q

What is enoxaparin?

A

Type of lmwh

84
Q

How long after administration of prophylactic dose 0,5mg /kg lmwh may neuraxial anaesthesia be performed?

A

> 12 hours
Next dose may be given > 4 hours after spinal

85
Q

How long after administration of therapeutic dose 1 mg /kg lmwh may neuraxial anaesthesia be performed?

A

> 24 hours

86
Q

List 6 drugs useful in treating arrhythmias

A

• Lignocaine
• amiodarone
Magnesium sulphate
• adenosine
• calcium gluconate
• beta blockers

Anaesthesiology (24 decks)

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