CVS Flashcards
How calculate pulse pressure?
Systolic-diastolic
How many seconds is a big block on ECG
0,2 seconds
So 1 small block is 0.04 seconds
Normal size P wave?
≤3 small blocks wide
≤ 2,5 small blocks high
Normal width QRS?
≤ 3 small blocks wide
Pathology if QRS broad and preceded by P wave?
Conduction defect
Pathology if QRS broad and not preceded by P wave?
Ventricular rhythm origin mostly
Pathology if QRS narrow and not preceded by P wave?
Rhythm originates between sa node and ventricle (not sinus)
Normal size of T wave?
Max 2/3 height of QRs
Pathology if peaked t wave?
Hyper K
Where does Pr interval span and normal size?
Beginning of P wave to beginning QRS (segment from end of P wave)
≤5 small blocks (1 big block)
Prolonged Pr interval pathology?
First degree heart block
How calculate rate on EcG?
300÷ number of big blocks between 2 r waves or
Number of QRS on bottom rhythm strip lead 2 repeat x6
Which rhythms do we cardiovert? (3)
• AFib
• atrial flutter types 1 and 2
• other unstable supraventricular tachycardias
Ventricular tachycardia with pulse
Identify pathology picture 35
Atrial fibrillation
• no p waves!
• irregular irregular rhythm!
• absence isoelectric baseline
• variable ventricular rate
• fibrillatory waves may be present and mimic p waves!
Identify pathology picture 36
Atrial flutter: saw-tooth pattern p waves
Identify pathology picture 37
Sinus bradycardia
Normal P, QRs, t but hr ≤60
Treatment sinus bradycardia?
Atropine if emergency
Glycopyrolate if not
Identify pathology picture 38
Sinus tachycardia
Normal P, QRs, t, but hr >100
Identify pathology picture 39
Afib
Identify pathology picture 40
Atrial flutter
Identify pathology picture 41
First degree heart block
• prolonged Pr interval > 5 small blocks
Identify pathology picture 42
Second degree heart block mobitz type 1
Pr interval increases then skips QRs
Identify pathology picture 43
Second degree heart block mobitz type 2
Pr interval constant then skips QRs
Identify pathology picture 44
Third degree heart block
No correlation between P waves and QRs complexes
Treatment second degree mobitz type 2 and third degree heart block?
Refer for pacemaker prior to elective surgery
(First and second degree mobitz 1 no treatment)
Identify pathology picture 45
Nodal/junctional rhythm originating between av node and ventricle
• narrow complex QRs
• no P wave
Treatment nodal/junctional rhythm?
Pacemaker if symptomatic
Identify pathology picture 46
Premature ventricular contractions (PVC) / ventricular extra systoles
• broad QRs
• no P wave
• t opposite direction to QRs
Treatment premature ventricular contractions/ ventricular extra systoles?
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
Identify pathology picture 47
V tach
Identify pathology picture 48
V fib
Identify pathology picture 49
Torsades de pointes
Treatment torsades de pointes?
MgSO4
Identify pathology picture 50
Atrial flutter
Saw tooth pattern P waves
Identify pathology picture 51
Sinus tachycardia
Identify pathology picture 52
Morbitz type 1 second degree heart block
Identify pathology picture 53
Torsades de pointes
Identify pathology picture 54
Nodal / junctional tachycardia
Identify pathology picture 55
Ventricular extra systole
Name 11 causes cardiac arrest
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
The relationship between cardiac output and left ventricular end diastolic volume is known as what?
Starling’s law of the heart
Name 5 factors that affect ventricular preload
• venous return
• blood vol
• distribution of volumes: posture, intrathoracic pressure, pericardial pressure, venous tone
• rhythm (atrial contraction)
• heart rate
Define Laplace’s law and what it refers to
Afterload.
Circumferential stress = (intra ventricular pressure X ventricular radius) ÷ (2 x wall thickness)
Formula for SVR? (Systemic vascular resistance)
80 x ([map- CVP] ÷ co )
Define inotropy
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
Name 5 causes of decreased myocardial contractility (inotropy)
•Anoxia
•Acidosis
• depletion catecholamine stores within heart
• ischaemia or infarction (loss functioning muscle mass)
• most anaesthetics and antiarrythmics are also negative inotropes
Name 4 mechanisms of immediate physiological blood pressure control
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
Name 3 mechanisms of intermediate physiological blood pressure control
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)
Name 2 mechanisms of long term physiological blood pressure control
• 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
Name 5 acute target organ damageS and complications by hypertension
• Intracranial haemorrhage / encephalopathy
• acute coronary syndromes or acute heart failure
• aortic dissection
• nephropathy
• papilloedema
Map must be maintained within which limits in hypertensive patients?
Within 20-30% of baseline
Name 4 physiological factors that influence oxygen demand of the heart
• Basal requirements: fever, thyrotoxicosis, cold
• heart rate
• contractility
• wall tensions: pre load, after load
Increase in any 1 of these will increase demand
Name 4 factors that influence oxygen supply or delivery (D02) to the heart
• 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
Name the 4 basic stages heart failure
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
How can Hf be treated pre-op? (4)
• Preload: consider negative fluid balance to decrease preload
• contractility: optimise inotropy to improve it
• after loads: vasodilators eg nitrates to decrease it
• inodilators: levosimendan
Which heart failure patients must have elective surgeries postponed
Nyha class 3 or 4 until symptoms reduced to 1 or 2.
What type ventilation should be used for patients with heart failure and why?
Positive pressure ventilation
Offload L ventricle
Management and goals valve regurgitation? (4)
“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
Coronary perfusion pressure formula?
Arterial diastolic pressure - LV end diastolic pressure
Management and precautions for stenotic heart lesions intra-op? (5)
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)
How does valvular stenosis affect stroke volume?
• 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.
How does valvular regurgitation affect stroke volume?
•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.
Which antibiotic prophylaxis can be given to patients at risk of infective endocarditis? (3)
• Oral amoxicillin or
• im/iv ampicillin/cephazolin
• clindamycin if penicillin allergy
Which drug combination can be used to blunt the sympathetic stimulation response during laryngoscopy causing a rise in blood pressure?
Sufentanil (opioid) and propofol
Blood pressure formula?
Cardiac output (HR x SV -preload, contractility, afterload) x systemic vascular resistance
Define cardioversion
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
Define defibrillation
Random administration of shock during cardiac cycle at higher energy 200 j biphasic (360 monophasic)
Name the 3 indications for defibrillation
• Pulseless ventricular tachycardia
• ventricular fibrillation
• cardiac arrest due to or resulting in v fib
Pharmacological treatment A fib? (2)
• Beta blockers / CCB
• digoxin/amiodarone
Treatment V tach?
• Defib iF unstable
• amiodarone/lignocaine if stable
Name 6 complications associated with administering anaesthesia to uncontrolled hypertensives
• 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
Maximum blood pressure to receive elective surgery?
SBP < 160-180
Diastolic <110
Coronary blood flow formula?
Cbf= cerebral perfusion pressure ÷ coronary vascular resistance
Minimum haemoglobin and haematocrit in ischaemic heart disease?
Hb > 10
Hct ≥ 13
Basic CVS goal when administering anaesthesia to ischaemic heart disease patient?
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
Can a patient with a history of mi receive anaesthesia?
Delay iF mi in previous 6 months.
Name 7 things and states to be careful to avoid perioperatively in heart failure patients
• 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)
Which induction agents should be avoided in heart failure (2)
• Propofol
• thiopentone
Careful with ketamine- can increase bp and hr → increase oxygen demand heart
Which muscle relaxant should be avoided in heart failure
Pancuronium: cause tachycardia
Best anaesthetic agents for heart failure?
Induce with etomidate
Maintain with sevo
Induction and maintenance agent of choice in stenotic heart lesions? (3)
• Etomidate
• sevoflurane
• high dose total opioid anaesthesia with fentanyl /sufentanyl (monitor depth)
which induction agents must be avoided in stenotic heart lesions? (3)
• Thiopentone (acute decrease SVR )
• ketamine (tachycardia)
• propofol (myocardial depression)
What is enoxaparin?
Type of lmwh
How long after administration of prophylactic dose 0,5mg /kg lmwh may neuraxial anaesthesia be performed?
> 12 hours
Next dose may be given > 4 hours after spinal
How long after administration of therapeutic dose 1 mg /kg lmwh may neuraxial anaesthesia be performed?
> 24 hours
List 6 drugs useful in treating arrhythmias
• Lignocaine
• amiodarone
Magnesium sulphate
• adenosine
• calcium gluconate
• beta blockers
