Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardio > Shock, Anaphylaxis & Sepsis > Flashcards

Shock, Anaphylaxis & Sepsis Flashcards

1
Q

What are the etiologies of cardiogenic shock?

A

Myocardium: Cardiomyopathy, AMI (Can ppt shock if >40% myocardium is involved), Heart failure, Myocarditis

Circuitry: Arrhythmias

Mechanical: Valvular pathology (severe prolapse / regurg / stenosis); Septal Defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the clinical presentation of cardiogenic shock?

A
  • Laboured breathing with audible coarse crackles or wheezing
  • Tachycardia
  • Delayed Capillary Refill Time
  • HypoTN
  • Diaphoresis
  • Poor peripheral pulses

RHF: ↑ JVP
LHF: Pulmonary oedema

Valvular HF: may present w/ new onset cardiac murmurs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is cardiogenic shock managed?

A

Acute resuscitation

  • Airway: ETT w/ Mechanical Ventilation
  • Breathing: High Flow O2, maintaining SpO2 >90%
  • Circulation: Judicious use of N/S (excessive use will worsen pul edema)

Diagnostics: identify underlying cause

  • Cardiac Markers: Trop I
  • ECG: for MI and Arrhythmia
  • 2DEcho: to identify valvular lesions; TRO Tamponade

Identify +/- reverse underlying aetiology

  • Non-Arrhythmic / Obstructive causes: Dobutamine (Alt: Dopamine / NE)
  • Arrhythmia: Synchronised Cardioversion (50J for narrow QRS, 100J for wide). Always support circulation w/ fluids +/- dobutamine
  • Alternative treatment: IABP (Counter-pulsation reduces left ventricular afterload and improves coronary artery blood flow)
  • Treat underlying cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the causes of obstructive shock?

A

↓ Diastolic filling

  • Cardiac tamponade
  • Constrictive pericarditis
  • Restrictive cardiomyopathy

↓ Venous return

  • Tension pneumothorax
  • Intrathoracic tumor

↑ Ventricular afterload

  • Massive pulmonary embolism (PE)
  • Aortic dissection
  • Aortic stenosis
  • Large systemic emboli
  • Severe pulmonary hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does is the clinical presentation of someone with cardiac tamponade?

A

Beck’s Triad – Hypotension, Muffled heart sounds, Elevated JVP

Other findings – Sinus Tachycardia, Pulses Paradoxus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the ecg findings of someone with cardiac tamponade?

A
  • Sinus tachycardia
  • Low voltage QRS complexes: An ECG finding defined by a QRS amplitude < 5 mm in all limb leads or < 10 mm in all chest leads due to attenuation of the electrical signal.
  • Electrical alternans: consecutive QRS complexes that alternate in height due to the swinging motion of the heart when surrounded by large amounts of pericardial fluid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the management of cardiac tamponade?

A

Pericardiocentesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the causes of cardiac tamponade?

A

acute causes

  • aortic rupture –> stamford a dissection
  • myocardial infarction: weakened muscle rupture
  • stabbing punctures blood vessels
  • blunt trauma ruptures lots of small vessels

chronic causes

  • cancers (from lung or breast)
  • uremic pericarditis (irritates serous pericardium)
  • hypothyroidism
  • chronic inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does angioedema present?

A
  • Poorly circumscribed swellings of the subcutaneous tissue that tends to be non-pruritic, maybe instead be painful / numb / burning.
  • Lasts ~3 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is anaphylaxis?

A

A systemic allergic reaction involving ≥2 systems (not necessarily vascular)

Mucocutaneous: Generalized urticaria /flushing, swollen lips /tongue

Respi System:

  • Respi Compromise (dyspnoea, wheeze, stridor)
  • May first p/w “lump in throat” due to laryngeal edema

GIT: Crampy abdominal pain, Vomiting, Diarrhoea

Cardiovascular: Hypotension, tachycardia (i.e. Anaphylactic Shock)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is urticaria managed?

A

Antihistamines +/- PO Prednisolone (if severe)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is angioedema managed?

A

Antihistamines & PO Prednisolone +/- IM Adrenaline (if impending anaphylaxis / Airway angioedema)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is anaphylaxis managed?

A

N/S Bolus & Antihistamines (Both H1 and H2 antagonists) & IV Hydrocortisone & IM Adrenaline

Antihistamine:

  • Gen1 H1 Blocker: Promethazine, Chlorpheniramine, Diphenhydramine
  • Alt: H2 Blocker Cimetidine / Ranitidine if persisting S&S, unresponsive to H1

IV Corticosteroid – IV Hydrocortisone (IV Bolus 100mg Q6H)

  • Purpose is to stabilise mast cells and prevent biphasic phenomenon!
  • Latter refers to the recurrence of anaphylaxis S&S 12-72 hours post-event

IM Adrenaline:

  • For Anaphylaxis = 0.5ml of 1:1,000 = 0.5mg
  • For cardiac arrest = 10ml of 1:10,000 = 1mg

Alternative to adrenaline – glucagon (if pt has IHD, Severe HTN, Pregnancy, non-responders)

Requires monitoring
- In resuscitation area
Supplemental high flow O2 +/- Salbutamol
- Electrocardiogram (ECG), pulse oximetry, and viral signs q5 minutes
- Be prepared for intubation / cricothyroidotomy
- Circulatory support w/ N/S or Hartmann’s & above medications
- Observe for at least 24hrs in case of biphasic phenomenon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the definition of sepsis?

A

Life threatening organ dysfunction (confirmed by a SOFA score ≥2) caused by a dysregulated host response to infection

  • hypotension: systolic bp < 100mmHg
  • altered mental status
  • tachypnea: RR> 22/min
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the definition of septic shock?

A

A subset of sepsis in which there is profound circulatory, cellular and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone, defined as sepsis with BOTH

  • Persistent Hypotension requiring vasopressors to maintain MAP >65mmHg
  • And Serum lactate >2 mmol/L despite adequate volume resuscitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How should septic shock be managed within the 1st golden hour?

A

A: Intubate if GCS < 8 or if there reasons to suspect the patient is unable to protect his airway (eg: excessive vomiting)

B: Supplemental oxygen via nasal cannula / partial / non-rebreather mask and aim for SpO2 of 94-98%

C: 2 large bore IV cannulas in the antecubital fossa and provide a fluid challenge of 500ml of normal saline over 30 min to assess for responsiveness

  • Responsive / partially responsive – continue fluid resus of at least 30ml/kg
  • Monitor adequacy of fluid resus by inserting IDC & aim for urine o/p 0.5ml/kg/hr
  • If unresponsive to fluid challenge – consider provision of vasopressor NE
  • Aim for a MAP of ≥65mmHg

Investigations

  • measure lactate, remeasure if initial lactate is >2mmol/L
  • ABG
  • obtain blood culture prior to administration of abx: 2 sets of blood culture

Antimicrobial therapy
- administer broad spectrum abx within 1 hour of presentation

I will like to perform vitals monitoring and GCS charting in a HDU / ICU setting

I will like to further monitor the patient’s

  • Lactate
  • Urine O/P
  • MAP +/- Central Venous Pressure
  • SpO2 / SCVO2
17
Q

What are the targets to achieve within 6h of initial resuscitation for septic shock?

A

CVP 8-12

MAP ≥65mmHg

Urine 0.5ml/kg/hr

ScvO2 70% — or SpO2 94-9

18
Q

What is the fluid therapy that can be given in patients with septic shock?

A

Crystalloids

  • Either N/S or Hartmann’s is acceptable
  • However, if large volume is to be given, N/S can lead to hyperchloremia 🡪 NAGMA. Hence consider Hartmann’s if large volume!
  • Do NOT give hydroxyethyl starches

Albumin

30ml/kg crystalloids minimum within first 3h

Continue as long as there is haemodynamic improvement (BPS)

19
Q

What are the vasopressors that should be given in patient with septic shock?

A

Vasopressors – if initial 30ml/kg resus is insufficient

  • Target MAP 65 [1B]
  • Noradrenaline first line [1B]
  • Adrenaline or vasopressin 2nd line [2B]
  • Dopamine is an alternative [2C] – often given in the wards. Should be started at >5-10mcg/kg, anything lower = vasodilatory effect
  • Do NOT give low dose dopamine [1A]
  • Dobutamine if myocardial dysfunction[1C]
20
Q

Other than fluid therapy, vasopressors, how else would you manage a patient with septic shock

A

Antimicrobial therapy

  • IV Abx / Antifungal / Antiviral within 1 hour [Evidence 1B]
  • 1 or more broad spectrum abx [1B] for 7-10 days typically [2C]
  • Reassess daily for escalation
  • Procalcitonin (if no evidence of infection)

Source control

  • Anatomical diagnosis
  • Intervene within 12 hours [1C] – eg; drainage of abscess

Supportive therapy

  • Transfuse if Hb < 7, target 7-9
  • Aim for higher Hb if IHD, ACS, Haemorrhage
  • No role for EPO
  • Venous / arterial blood glucose <10mmol/L w/ insulin
  • No bicarbonate is indicated for haemodynamics or lactic acidosis
  • No FFP even if abnormal labs
  • Platelets if < 10,000 (or 20K if risk of bleeding)

DVT prophylaxis

  • LMWH [1B]
  • Pneumatic Compression Devices [2C]

Stress Ulcer Prophylaxis

  • H2RA / PPI only if there is RF for stress ulcers [1B] – PPI is preferred
  • H2RA or PPI can be used (low evidence)
  • No need to use if no RF

Nutrition

  • Start oral / enteral feeding within 48 hours [2C]
  • Avid parenteral nutrition if patient is able to be enterally fed (moderate evidence)
21
Q

How does one diagnose a central line infection?

A

When performing blood cultures on patient with suspected line infection – take 1 set of blood c/s from each lumen (central or peripheral) + 1 set from a peripheral vein

If patient has an infected central line (i.e. CVP BSI), CVP will turn positive >120min earlier the peripheral cultures – i.e. a differential time to positivity of >120 mins

This helps us localise the SITE of infection 🡪 if CVP BSI, there will be ↑ bacterial load at CVP 🡪 culture will grow faster = become +ve faster

22
Q

What is the definition of neurogenic shock?

A

Caused by a sudden loss of SNS tone to regions distal to the level of injury 🡪 VasoD + prevents reflex tachycardia to the hypotension

SNS supply is from T1-L2/3; Neurogenic Shock occurs at T5 and above (above the level of thoracic splanchnic nerves)

23
Q

How to manage neurogenic shock?

A

Exclude other reasons for shock (e.g., other injuries)

N/S Bolus to support the circulation

Inotropic support: Dopamine

24
Q

How do patients with neurogenic shock present with?

A

Classic presentation: hypotension, bradycardia, vasodilation

25
Q

compare and contrast spinal and neurogenic shock in terms of

  • definition
  • BP
  • pulse
  • bulbocarvenous reflex
  • motor
  • time
  • mechanism
A

spinal shock

  • definition: immediate temporary loss of total power, sensation and reflexes below the level of injury
  • hypotension
  • bradycardia
  • bulbocavernous reflex absent
  • flaccid paralysis
  • mechanism: peripheral neurons become temporarily unresponsive to brain stimuli

neurogenic shock

  • definition: sudden loss of sympathetic nervous system reflexes
  • hypotension
  • bradycardia
  • bulbocavernous reflex variable
  • motor variable
  • mechanism: disruption of autonomic pathways –> loss of sympathetic tone and vasodilation
26
Q

What are the blood cultures that needs to be taken to investigate possible sepsis?

A
  • Do not delay antibiotics for more than 45 min [1C]
  • Aerobic + Anaerobic x 2 sets [1C]
  • 1 x Vein, 1 x Vascular device [1C]

Cardio (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions