CPR and critical patient monitoring Flashcards

1
Q

A Swan–Ganz catheter is used to measure which parameter?
a. Central venous pressure
b. Pulmonary artery occlusion pressure
c. Direct arterial blood pressure
d. Pleth Variability Index

A

B

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2
Q

A “shark-fin” appearance to a capnography would indicate which abnormality?
a. Endoesophageal intubation
b. Spontaneous breathing during mechanical ventilation
c. Airway or breathing circuit obstruction
d. Impending cardiac arrest

A

C

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3
Q

A right-shifted oxyhemoglobin dissociation curve could be the result of which phenomenon?
a. Acidemia
b. Hypothermia
c. CO poisoning
d. Hypocapnia

A

A

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4
Q

Absence of lung sounds in a lung field can be an indicator of which pathology?
a. Pneumothorax
b. Pericardial effusion
c. Tracheal collapse
d. Pulmonary edema

A

A

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5
Q

The most accurate monitor for veterinary patients is:
a. one that is utilized at the appropriate time
b. a trained and experienced veterinary technician
c. one that is connected to the patient at all times
d. pulmonary artery catheter monitoring

A

B

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6
Q

When interpreting an arterial blood pressure wave, which of the following findings may indicate vasoconstriction in the patient?
a. The dicrotic notch is low and approaches the diastolic pressure
b. An overdampened waveform is present
c. The dicrotic notch is high and approaches the systolic pressure
d. An underdampened wave form is present

A

C

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7
Q

In a patient suffering from head trauma and increased intracranial pressure, which of the following can directly contribute to worsening intracranial pressure?
a. Hypothermia
b. Hypercapnia
c. Tachycardia
d. Increased PVI

A

B

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8
Q

Cardiac output is the product of:
a. heart rate and stroke volume
b. stroke volume and intrathoracic pressure
c. oxygen carrying capacity and heart rate
d. cardiac preload and vasodilation

A

A

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9
Q

Under normal circumstances, a patient that has an EtCO2 of 40^mmHg is expected to have a PaCO2 of approximately:
a. 25–28^mmHg
b. 35–40^mmHg
c. 42–47^mmHg
d. 48–53^mmHg

A

C

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10
Q

Hypocapnia can commonly be caused by:
a. decreased cardiac output
b. hypoventilation
c. hyperthermia
d. respiratory acidosis

A

A

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11
Q

Irreversible ischaemic injury occurs within about ____ of CPA.

A

4 minutes

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12
Q

What is the goal of CPR?

A

To restore the flow of RBC through circulation

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13
Q

What are the goals of chest compressions?

A
  • replace the functions of the ventricles
  • provide blood flow to the lungs for gas exchange
  • deliver oxygen to the tissues for energy production
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14
Q

Ideal chest compressions only achieve approximately ____ of normal cardiac output.
a. 10%
b. 25%
c. 30%
d. 100%

A

C

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15
Q

What is the cardiac pump theory?

A

Chest compressions performed directly over the ventricles increasing intraventricular pressure. There is closing of the mitral & tricuspid valves and opening of the aortic and pulmonic valves during compressions and thus backflow of blood is prevented. Elastic recoil of the chest between compressions creates negative pressure within the heart allowing the ventricles tio fill with blood before the next compression. This method of compressions provides maximum stroke volume,

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16
Q

What is the thoracic pump theory?

A

Chest compressions are performed at the widest portion of the chest and compress the aorta to raise the overall intrathoracic pressure and push blood from the aorta into systemic circulation. Upon recoil, negative pressure allows blood to flow into the cranial and caudal vena cava and into the heart and pulmonary vessels. It is passive blood flow and the valves of the heart do not close.

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17
Q

What is the best positioning and technique for CPR in round, med-lrg breed dogs?

A

Lateral, thoracic pump

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18
Q

What is the best positioning and technique for CPR in keel, med-lrg breed dogs?

A

Lateral, cardiac pump

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19
Q

What is the best positioning and technique for CPR in flat breed dogs?

A

Dorsal, cardiac pump

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20
Q

What is the best positioning and technique for CPR in cats and small breed dogs?

A

Lateral, cardiac pump

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21
Q

The goals of ventilation in CPR are to provide ventilation and oxygenation. What does this mean?

A

Ventilation: CO2 excretion that has been created as a by product of metabolism in the tissues

Oxygenation: transport O2 into arterial blood to be delivered to the tissues and to be used for metabolism

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22
Q

Hypoventilation in CPR can lead to

A

increased CO2 leading to peripheral vasodilation and pooling of blood in the peripheral system

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23
Q

Hypoventilation in CPR can lead to

A

increased CO2 leading to peripheral vasodilation and pooling of blood in the peripheral system. This decreases blood flow to the heart, brain and lungs and may result in increased ICP

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24
Q

Hyperventilation in CPR can lead to

A

reduced CO2 leading to peripheral vasoconstriction increasing the resistance the blood flow, compromising cerebral perfusion. Hyperventilation decreases the ventilatory drive and therefore decreases the likelihood of the patient taking spontaneous breaths in ROSC

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25
Q

In initiating ALS the following steps are taken: obtaining IV access administering reversals and attaching monitoring. In which order are these performed according to the RECOVER guidelines?

A
  1. Attach monitoring (ETCO2, ECG)
  2. Obtain IV access
  3. Administer reversals
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26
Q

ETCO2 is determined by

A

Minute ventilation and the amount of blood returning from the tissues to the lungs

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27
Q

Poor blood flow results in _______ and is associated with poor chest compressions.

A

low ETCO2

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28
Q

What is the earlier indicator of ROSC?

A

A steep increase in ETCO2 (>30mmHg) due to a steep increase in CO

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29
Q

ETCO2 steeply increases whilst you perform chest compressions, should you stop chest compressions?

A

No. Check for pulse or evidence of perfusing rhythm before stopping

30
Q

What are the likely causes of ETCO2 to be 0 in CPR and what does this mean for the patient?

A
  • oesophageal intubation
  • poor chest compressions
  • ETT cuff inappropriately inflated
    If not corrected the patient is not being ventilated and will likely have severe tissue ischaemia.
31
Q

A ETCO2 above ____ is associated with better outcomes in CPR.

A

15mmHg

32
Q

NIBP and SpO2 monitoring are not useful in CPR as they rely on a pulsatile blood flow, true or false?

A

True

33
Q

IV fluids are only useful in CPR if there is evidence of hypovolaemia and thus in any other case should be avoided during CPR, true or false?

A

True

34
Q

Should corticosteroids be used in CPR? why/why not?

A

No. Weak evidence they work and may cause an increase in glucose which has deterimental effects in CPA patients, including:
- perpetuating brain ischaemia
- causing GI ulceration
- reducing prostaglandin production leading to poor renal perfusion and ischaemia

Yes. Anaphylaxis and hypoadrenocorticism

35
Q

When is OCCPR immediately indicated?

A
  • Pleural space disease
  • Pericardial disease
  • Patients in surgery
  • Giant breeds with round chests
  • Unsuccesful closed-chest CPR >10min
36
Q

There is no shown benefit in performing OCCPR in patients <20kg, true or false?

A

True

37
Q

What is coronary perfusion pressure (CoPP)?

A

surrogate for overall myocardial perfusion and is the difference between aortic diastolic pressure and right arterial pressure. Is in summary the net pressure generating flow to the myocardium. Normal 15mmHg

38
Q

What are vasopressors used for in CPR?

A

Vasopressors increase peripheral vascular resistance redirecting blood flow from peripheries to core organs. This raises aortic DP. The aim is to increase CPP and CoPP

39
Q

What are the three choices of vasopressor therapy in CPR?

A
  1. LD epinephrine 0.01mg/kg
  2. HD epinephrine 0.1mg/kg
  3. vasopressin 0.8u/kg
40
Q

Stimulation of the vagus nerve can lead to

A

Severe bradycardia and CPA due to decreased BP and perfusion

41
Q

High vagal tone can result from

A
  • severe GI disturbances
  • Opthalmic surgery
  • Opiates
  • Laryngeal manipulation
  • Disease of the respiratory tract i.e. coughing
42
Q

How is vagally mediated bradycardia treated?

A

Parasympatholytics

43
Q

What are the main consequences of prolonged CPA?

A
  • myocardial ischaemia
  • reperfusion injury on ROSC
  • acid-base disturbances
44
Q

What are some pharmocological options for prolonged CPA?

A
  • HD epinephrine (once off)
  • Bicarb (maximises epinephrine and vasopressin pH <7)
  • CaGlu for increased K (stabilise RMP, improve contractility and vascular tone)
45
Q

What is the goal of defibrillation?

A

depolarise as many ineffective myocardial cells and drive them into their refractory period and stop ineffecctive activity.
“resync electrical activity”

46
Q

What shock energy is used in biphasic electrical defib? How often can it be performed?

A

2-4J/kg. Start low and increase each shock by 50% to a max. of 10J/kg. Can shock every cycle.

47
Q

After successful defibrillation there is no blood flow therefore BLS should be restarted immediately, true or false?

A

True

48
Q

What are the main therapeutic goals of post cardiac arrest care?

A
  • prevent rearrest
  • optimise oxygenation and ventilation as well as tissue perfusion
  • Treat the underlying cause of arrest
49
Q

What are the post cardiac arrest treatment goals?

A
  • SpO2 94-98%
  • PaO2 80-100mmHg
  • SvO2 >70%
  • Lactate <2.5
  • MAP >80mmHg
  • Correction of hypovolaemia
  • Correction of arrhythmias
  • CO2 26-36mmHg (cats), 32-43mmHg (dogs)
50
Q

What is the systemic response to ischaemia and reperfusion following CPR?

A

Global ischaemic event leads to whole body reperfusion injury and is a severe sepsis like syndrome. There is activation of inflammation, coagulation and endothelium.

51
Q

How is ischaemia and reperfusion injury addressed following CPR?

A
  • early haemodynamic optimisation
  • glycaemic control
  • corticosteriods if vasopressor-dependent shock occurs after CPA.
52
Q

What is the pathophysiology of post cardiac arrest brain injury?

A

Until about 4min of CPA, ATP is still available and utilised but after that ATP is depleted which causes membrane potentials to be lost and large amounts of Na, Ca, Cl enter cells causing them to swell and disrupt cellular mebranes. This causes mitochondrial damage and ROS are produced that cause oxidative damage to neuronal cells leading to apoptosis and necrosis of these cells.

53
Q

How do we avoid post cardiac arrest brain injury?

A
  • controlled reperfusion
  • mild hypocalcaemia
  • avoid hyperoxaemia
  • Permissive/therapeutic hypothermia
54
Q

What is the concept of mild therapeutic hypothermia. How long is it performed for? How do we rewarm?

A

Reduce mitochondrial injury and dysfunction, reduce Ca influx and neuronal excitotoxicity, decrease cerebral metabolism, reduce ROS production and suppress seizure activity
- Temp 32-34 for 24-48h
- rewarm 0.25-0.5/hour

55
Q

What are the purpose of catecholamines?

A

Treat low arterial blood pressure and improve myocardial activity as well as cardiac output

56
Q

A monitored variable is only useful when…

A

changes in that variable are linked to an intervention or therapy that affects outcome

57
Q

Patients adapt respirations to

A

minimise their work of breathing

58
Q

Why is a normal cardiovascular system necessary

A

Carry oxygenated blood from the lungs to the body

59
Q

Inadequate global perfusion is considered an indicator of

A

Circulatory shock

60
Q

Normal heart rates

A

Cats 140-200bpm
Small Dogs 70-120bpm
Large dogs 60-120bpm

61
Q

Normal respiratory rate

A

8-20

62
Q

What can bradycardia result in?

A

Low cardiac output, poor perfusion, electrolyte imbalances, neurologic disease, donsuctioor imminent cardiac arrest

63
Q

Kirby’s rule of 20

A

Fluid balance
oncotic pull
albumin
Heart rate/rhythm/contractility
Perfusion & blood pressure
glucose
acid-base and electrolytes
Nutrition
Pain control
Coagulation
RBC & Hb
GI motility & mucosal integrity
Mentation
Oxygenation & ventilation
Renal function
Nursing care and mobilisation
wound care & bandage change
TLC
Drug doses and metbaolism
Immune function/AB/wbc

64
Q

If refractory VF in CPR

A

Amiodarone 2.5-5mg/kg IV/IO
lidocaine 2mg/kg IV/IO

65
Q

Goal of ROSC

A

To sustain spontaneous circulation, maintain perfusion to the vital organs, attenuate further injury & rearrest

66
Q

Early goal directed therapy

A

Used to achieve physiologic end-points
- haemodynamic optimisation (oxygen, fluid therapy, vasopressors, inotropes, RBC’s)
- reduce O2 requirements (sedation, mechanical ventilation, neuromuscular blockade, temp control)
- glycaemic control

67
Q

Post cardiac arrest (PCA) brain injury

A

Result of global reperfusion injury rather than ischaemia. Protease activation, ROS production, oxidative injury leading to cerebral oedema, neuronal death.

68
Q

An ECG tracing in CPA is evidence of

A

myocardial membrane potential still exists

69
Q

Controlled reoxygenation

A

oxygen is a substrate for ROS production and although aim of ROSC is the rapidly improve oxygenation after global ischaemia hyperoxaemia may cause oxidative brain injury and increase neuronal degeneration.

70
Q

Long term and immobile ICU patients are at risk of

A

Decubital ulcer formation
Ileus
Pneumonia
Atelectasis
Malnutrition
Neuromuscular disorders
Protein wasting
Depression