Inpatient management Flashcards

1
Q

Why is fluid balance critical in inpatient management?

A

Fluid overload → increases interstitial fluid, impairing oxygen & nutrient diffusion, harming renal & lung function

Fluid deficit → reduces perfusion, promotes catabolism, insulin resistance & cellular stress

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2
Q

How can fluid balance be monitored?

A

Clinical signs of hydration & perfusion
- mucous membranes
- pulse rate & quality
- blood pressure
- peripheral oedema
- chest auscultation & lung ultrasound for pulmonary oedema

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3
Q

What are solutions for fluid imbalances?

A

Adjust fluid therapy rates, use diuretics if needed

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4
Q

What is oncotic pressure?

A

Pressure exerted by proteins (mainly albumin) in blood to keep fluid inside blood vessels

Also called Colloid Osmotic Pressure (COP)

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5
Q

What happens when albumin is low (hypoalbuminaemia)?

A

Less oncotic pressure → fluid leaks out of blood vessels into tissues (causing oedema)

At same time, this can lead to low blood volume (hypovolemia), worsening perfusion

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6
Q

What are the clinical signs of hypoalbuminaemia?

A

Because fluid leaks out of blood vessels, patients may show:
- Peripheral oedema
- Pulmonary oedema on auscultation/ultrasound
- Flat caudal vena cava → Suggests low blood volume (hypovolemia)
- Low blood pressure (hypotension)
- Poor pulses

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7
Q

How is low oncotic pressure/hypoalbuminaemia managed?

A

Increase protein intake (feeding tube may be needed)

Plasma transfusion for oncotic support

Avoid synthetic colloids (risk of acute kidney injury)

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8
Q

What are the most common electrolyte disturbances in critical illness?

A

Hypokalemia (low potassium) due to reduced intake → Weakness, low head carriage, plantigrade stance

Sodium (losses or redistribution secondary to hyperglycaemia) → mentation disturbances, cerebral dehydration/swelling

Chloride (hand in hand with sodium or losses from GI → vomiting, symptoms associated with underlying disease

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9
Q

How are electrolyte disturbances monitored?

A

Electrolytes via blood/gas machine or biochem

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10
Q

How are electrolyte disturbances treated?

A

Supplementation with fluids

Where electrolytes are high - specific treatment approaches

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11
Q

What are the causes, respiratory responses, and clinical signs of acidosis?

A

Occurs when there is excess acid in body, classified into metabolic & respiratory acidosis

Metabolic – increased acid e.g. lactate, uraemia, ketones
Associated with increased RR & reduced PCO2

Respiratory – retained CO2 e.g. brainstem injury or respiratory paralysis (botulism/tetanus)
Associated with reduced RR & increased PCO2

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12
Q

What causes alkalosis, and how does it affect respiration?

A

Metabolic Alkalosis: Loss of acid (e.g., severe vomiting, pyloric foreign body). Causes reduced RR, increased PCO₂ & hypochloraemia

Respiratory Alkalosis: CO₂ loss from hyperventilation due to pain, stress, or fear

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13
Q

How are acid/base imbalances diagnosed?

A

pH measurement (blood gas machine)

PCO₂ levels (blood gas machine)

Respiratory rate (RR)

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14
Q

How are acid/base imbalances treated?

A

Hartmann’s (alkalinising) for acidosis

Saline (acidifying) for alkalosis

Treat underlying cause (e.g. pain)

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15
Q

Why is mentation monitoring important?

A

Indicates brain oxygenation, perfusion status & intracranial disease

Uses Modified Glasgow Coma Scale for standardisation

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16
Q

What are key cardiac abnormalities in critical patients?

A

Bradycardia → Check potassium levels

Arrhythmias (e.g., V-Tach) → Common in systemic disease

Poor contractility → Seen in sepsis, DCM, late-stage HCM

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17
Q

How are cardiac issues monitored and treated?

A

ECG monitoring (intermittent or continuous)

POCUS (ultrasound) to assess contractility

Lidocaine for V-Tach, Pimobendan for poor contractility

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18
Q

What do different blood pressure patterns indicate?

A

Low systolic + diastolic BP (low total BP)→ Hypovolemia

Low diastolic BP (wide gap) → inappropriate vasodilation: Distributive shock (e.g. sepsis, SIRS)

Low systolic BP (small gap) → Poor cardiac contraction

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19
Q

What are systolic and diastolic pressure an indirect measure for?

A

Systolic pressure – indirect measurement of cardiac contraction force

Diastolic pressure – indirect measure of vascular tone

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20
Q

How do you treat blood pressure issues?

A

Treatment based on underlying cause

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21
Q

What are some possible causes of hypothermia?

A

Reduced energy conservation
- e.g. anaesthesia, wet, exposure

Reduced energy production
- e.g. starvation, metabolic exhaustion, hypoxia

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22
Q

What are some possible causes of hyperthermia?

A

Increased energy conservation
- e.g. BOAS, hot day, exercise

Increased energy production
- e.g. inflammation/infection –> pyrexia

23
Q

Why should hypothermia be corrected slowly?

A

Rapid warming can cause metabolic mismatch, harming heart & brain

24
Q

How can oxygen & ventilation be monitored?

A

Basic:
- MM colour, resp rate & effort, pulse oximetry, lung ultrasound

Advanced:
- Blood gas analysis (PaO₂, FiO₂/PaO₂ ratio)

25
Q

How are oxygenation & ventilation issues treated?

A

Oxygen therapy

26
Q

What are causes of anaemia in critical patients?

A

Reduced production (chronic disease)

Destruction/haemolysis (immune-mediated or sepsis)

27
Q

How can RBC/haemoglobin be monitored?

A

Mucous membranes
Resp rate
Heart rate
Haematology/PCV
Blood smear
Saline agglutination test

28
Q

How can anaemia be treated?

A

Oxygen therapy

Transfusion if needed
- pRBCs or whole blood

29
Q

How does disruption of the endothelial glycocalyx contribute to coagulation disorders?

A

Endothelial glycocalyx is protective layer of blood vessel endothelium

Disruption (due to disease, trauma, or colloid administration) exposes endothelium, triggering coagulation cascade

In severe cases, this can lead to Disseminated Intravascular Coagulation (DIC), causing widespread clotting & bleeding

30
Q

How can coagulation disorders be monitored?

A

Mucous membranes - Petechiae

Bleeding from IV canula sites

Increased RR/RE (e.g. pulmonary thromboembolism (PTE))

Primary coagulation tests (platelet counts & BMBT)

Secondary haemostasis tests (coagulation factors (PT, APTT))

Fibrinolysis tests (D-dimers & FDPs)

Global coagulation test (thromboelastography (TEG))

31
Q

How can coagulation disorders be treated?

A

Fresh frozen plasma transfusion for coagulation factors

Platelet transfusion

Other supportive care
- e.g. oxygen therapy for PTE

32
Q

What are common kidney issues in critical patients?

A

Acute kidney injury (low urine output)

Reduced renal function

Hyperkalemia (life-threatening, must be treated ASAP)

33
Q

How can renal function be monitored?

A

Fluid balance & urine output
- acute increase/decrease in urine output

Urinalysis (USG, cytology)

Biochemistry (urea, creatinine, phosphate, potassium)

34
Q

How can issues of renal function be treated?

A

Hyperkalaemia treatment is priority

Managing fluid balance through ins/outs

Avoid fluid overload

Diuretics (e.g. furosemide) to encourage urine output if overload is developing

35
Q

What are the risks of GI dysfunction in critical patients?

A

Ileus (gut stasis) → Can cause bacterial translocation & sepsis

Malnutrition → Increases catabolism & weakens recovery

36
Q

How can GI motility & nutrition be monitored?

A

Signs of vomiting/diarrhoea
BCS
Weight
MCS

37
Q

How can GI motility & nutrition issues be treated?

A

Food (GI diet, tube feed if indicated)

Reduce other medications if possible (e.g. opiates)

Anti-emetics/anti-nausea meds (e.g. maropitant, ondansetron)

Prokinetic agents if obstruction ruled out (e.g. metoclopramide)

38
Q

What are possible causes of hypoglycaemia in critical care?

A

Increased usage/storage
- increased metabolic rate, septicaemia!, insulinoma, xylitol

Increased loss
- renal losses

Lack of intake
- nutritional or malabsorption

39
Q

What are possible causes of hyperglycaemia in critical care?

A

Reduced usage
- diabetes mellitus!/DKA, insulin resistance

Increased mobilisation
- Stress, TBI!

40
Q

How can glucose be monitored?

A

Blood glucose checks

Signs of weakness, reduced mentation, wobbly (look drunk)

41
Q

How can hypoglycaemia be treated?

A

Food & glucose supplementation

Treat underlying cause

42
Q

How can hyperglycaemia be treated?

A

Treat underlying cause

43
Q

How can critical illness weaken immune function?

A

Increased risk of secondary infections, even in non-infectious diseases

Wounds source of infection

44
Q

How can immune function be monitored?

A

GI signs indicating GI disruption

WBC counts (esp. left shift neutrophilia)

Hypoglycaemia

Temperature

Surgical sites/canula sites

Urinalysis (e.g. UTI)

Wound checks & dressing changes
- wound dressing is barrier to infection

45
Q

How can decreased immune function be treated?

A

Find source & control it

Sample - culture & sensitivity

Antibiotics if needed

Clean & debride traumatic wounds

Appropriate dressing to stage of healing

46
Q

Why does critical illness affect drug dosage?

A

Critical illness affects organ function (liver & kidney) & as a result, metabolic pathways & speed of metabolism/clearance

47
Q

How can drug dosage & metabolism be monitored?

A

Liver function tests (urea, bile acids)

Liver damage tests (ALT, ALP, GGT, GLDH)

Renal function (urea, creatinine, phosphate, potassium)

Be aware of individual drug side effects & signs to look for

48
Q

How can drug dosage in critical patients be managed?

A

Tempering of drug dosages based on effect, regular monitoring of their need, e.g.:
- Pain scores for analgesic drugs
- BP for vasopressors
- Signs of nausea for anti-emetics

Aim for lowest effective dose

49
Q

Why is it important to control pain in critical patients?

A

Important welfare consideration

Uncontrolled pain can result in worse outcomes & delayed wound healing

50
Q

How can pain be monitored?

A

Pain scores (e.g. Glasgow composite measure pain scale)

Repeat exams regularly

51
Q

How can pain be treated?

A

Opiates
- Full Mu (e.g. methadone, morphine, fentanyl)

NSAIDS
- take care if concerns re BP & renal blood supply/function

Local anaesthetics
- local blocks or systemic administration (e.g. lidocaine CRI)

NMDA receptor antagonists
- Ketamine CRI or amantadine

Others
- e.g. a2 agonists, gabapentin

52
Q

Why are nurses essential to caring for critical patient?

A

They are hands on with patient

Will notice changes before you

Can perform many procedures (often better than you)

53
Q

How do you maximise nursing as a vet?

A

Listen to them

Involve them in decision making & case discussions, ask for their opinion, empower them

If things go wrong – debrief with them, learn from mistakes made (esp. your own) & be humble

Remember you are team

54
Q

Why is TLC important?

A

Human interaction improves patient recovery