module 5 Flashcards

1
Q

Preload is

A

directly related to the venous return to the heart and reflects end-diastolic volume (EDV) which is the resting volume of the heart.

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2
Q

This is known as the Frank-Starling Law

A

When the diastolic filling of the heart is increased or decreased with a given volume, the displacement of the heart is also altered. In other words, when preload is increased, stroke volume is increased and vice versa.

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3
Q

What is compliance

A

‘distensibility of the ventricle … the change in ventricular volume for a given change in pressure’.

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4
Q

Contractility

A

refers to the strength and efficiency of myocardial contraction.

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5
Q

Afterload

A

represents the impedance to blood leaving the heart.

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6
Q

ejection pressure:

A

end-systolic pressure opposing the vascular resistance

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7
Q

• stroke volume:

A

the volume of blood ejected from the heart at each contraction

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8
Q

• intrinsic factors:

A

functional characteristics of heart

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9
Q

• extrinsic factors:

A

neural or hormonal control

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10
Q

Shock

A

is an acute process in which the mechanisms to maintain cardiovascular homeostasis are disrupted resulting in an imbalance between cellular oxygen supply and cellular oxygen demand. Adequate cellular perfusion depends on a functioning cardiorespiratory system as well as adequate vascular tone and intravascular volume.

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11
Q

compensatory mechanisms of shock

A

• activation of the sympathetic nervous system
• release of antidiuretic hormone (ADH)
• stimulation of the renin-aldosterone-angiotensin (RAA) system
or
• Increased HR
• Vasoconstriction – including decrease peripheral perfusion and peripheral temperature
• Decreased urine output
• Maintenance of BP

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12
Q

Congestive heart failure (CHF) is described by many authors as

A

insufficient oxygen delivery to meet the metabolic demands caused from inadequate cardiac function or circulation.

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13
Q

drugs that support cardiac function (contractility):

A

ace inhibitors
beta blockers
inotropes

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14
Q

drugs that decrease volume load (preload/congestion):

A

diuretics

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15
Q

drugs that reduce resistance to emptying (afterload):

A

vasodilators

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16
Q

Frusemide

A

is effective to decrease circulating volume and reduce preload, thereby relieving dilatation of the ventricles and pulmonary congestion.

17
Q

ACE inhibitors (angiotensin converting enzyme)

A

cause vasodilation. Used for reduction of afterload and ↓ ventricular wall stress. Captopril is a commonly used ACE inhibitor

18
Q

• Digoxin:

A

cardiac glycoside that blocks myocardial cellular sodium-potassium pump causing an increase in the uptake of calcium thereby increasing the efficiency of contraction. Digoxin also has antiarrhythmic properties and prevents sympathetic over stimulation.

19
Q

• Beta blockers:

A

block the release of the stress hormones adrenaline and noradrenaline in certain parts of the body. This results in a slowing of the heart rate and reduces the force at which blood is pumped around your body.
They can also block your kidneys from producing angiotensin II, this results in lowering your blood pressure.

Propranolol, atenolol, carvedilol are beta blockers.

20
Q

• Aldosterone antagonists:

A

preventing sodium/water reabsorption and decreasing potassium loss. Spironolactone is an aldosterone antagonist.

21
Q

ECG tracing explanation

A

The SA node impulse depolarizes the right and left atria by contiguous spread, producing the P wave.
• When the atrial impulse arrives at the atrioventricular (AV) node, it passes through the node at a much slower velocity than any other part of the heart, producing the PR interval.
• Once the electrical impulse reaches the Bundle of His, the conduction velocity becomes very fast and spreads simultaneously down the left and right bundle branches to the ventricular muscle,
through the Purkinje fibres, producing the QRS complex.
The repolarization of the ventricle produces the T wave, but the repolarization of the atria is not usually visible on the ECG tracing

22
Q

• The P wave reflects

A

atrial depolarization (contraction)

23
Q

• The QRS complex represents

A

the onset of ventricular depolarization

24
Q

• The T wave indicates

A

ventricular repolarization: occurs just before ventricles start to relax
T wave is wider than the QRS complex because relaxation occurs more slowly

25
Q

Hypokalaemia –

A

defined as serum potassium less than 3.5 mmol/L
• Decreased extracellular potassium causes myocardial hyperexcitability which may result in action
potentials to fire prematurely & disrupting the normal cardiac cycle
• Commonly caused be excessive GI losses
• ECG findings include a flattened T wave

26
Q

Hyperkalaemia –

A

defined as serum potassium greater than 5.0 mmol/L

  • Often caused by increased intake of K+ supplements (i.e. parenteral additives/ oral supplements) or transfusions of packed red blood cells
  • ECG findings include a peaked T wave with hyperkalaemia
27
Q

Sinus arrhythmia

A

• Variation in regularity in heart rate originating from the sinus node (p wave)
• Usually a benign rhythm and occurs in paediatrics often during sleep. HR will increase with inspiration
and decrease with expiration

28
Q

Superventricular tachycardia

A

Most common non-arrest arrhythmia in childhood and most common to cause cardiovascular instability in infancy.
• Generally, rates in infants are 250 to 300 beats/min; in children up to 250 beats/min; in adolescents 150-
220 beats/min.

29
Q

Ventricular tachycardia

A
  • Less common in children.
  • Potentially life threatening arrhythmia, always requiring prompt intervention.
  • Wide complex tachycardia which originates in the ventricle
  • Patients may have a pulse with minimal to severe haemodynamic effects
  • If the patient is pulseless the treatment is CPR and defibrillation.
30
Q

Pulseless electrical activity

A

Absence of palpable pulse or other signs of circulation despite the presence of a rhythm on the monitor

31
Q

Adrenaline

A

increase myocardial contractility and rate by stimulating the ß1 receptors, as well as increasing blood pressure through increasing vascular tone by stimulating the α1 receptors.1

32
Q

Adrenaline is the first line drug for:

A
pulseless ventricular tachycardia 
ventricular fibrillation
pulseless electrical activity 
bradycardia
asystole
33
Q

Adenosine

A

Used in supraventricular tachycardia to temporarily block abnormal conduction and slow the heart rate.

34
Q

Amiodarone

A

Used to treat tachyarrhythmias, such as VT, or refractory VT/VF if unresponsive to defibrillation and adrenaline.

35
Q

Atropine

A

Used in bradycardia caused by vagal stimulation.

Sedative and amnesic actions.

36
Q

Midazolam

A

Used to sedate patient prior to the administration of muscle relaxants.

37
Q

Suxamethonium

A

Fast acting neuromuscular blocking agent. Used for muscle paralysis to assist with intubation.

38
Q

Vecuronium

A

Neuromuscular blocking agent with a longer action. Used for muscle paralysis for the control of ventilation and to assist with intubation.