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Pete FFICM SOE/OSCE > Gen - Classifications, Definitions 12 - > Flashcards

Gen - Classifications, Definitions 12 - Flashcards

1
Q

Classifying an Aortic Dissection

A

Stanford, DeBakey and European Cardio society

Stanford - A: Ascending aorta and arch
B - descending, distal to left subclavia

DeBakey:

1 - Ascending into the arch
2 - ascending only
3 - descending only - A above diaphragm, B below

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2
Q

Risk factors for dissection

A

Hypertension
Advanced Age
Male
Smoker

Family Hx
Pregancy
Trauma
Congenital - Marfans, Ehler’s, Co-arctation, Turners.

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3
Q

Complications of a dissection

A

By organ system

CVS; aortic regurgitation, 
          MI,. Ischaemia
          Tampanade
          Hypertension 
          Hypotension - shock/tampanade
          Limb ischaemia

Neuro - ischaemic stroke
Paraplegia

Pulm - Effusions

Renal - AKI

Haem - transfusion / coag

GI - mesentEric ischaemia

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4
Q

Imaging for dissection

A

CXR - mediastinum, heart enlarged. Calfication

TTE - see intimate flap, assess for regurgitation and function

TOE - true and false lumens

CT - confirms diagnosis and plan op.

MRI - extent of flap

Aortograph - gold standard but rare

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5
Q

Manage dissection based on A and B

A

A and complicated B - CTC

A - surgical emergency, sternotomy and CPB. Reduce BP

B - beta blockers/anti hypertensives
Complicated B - left lat thoracotomy

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6
Q

Classify arrhythmia

A

By heart rate: >100 tachy < 60 Brady

Where it originates - SVT, VT

Regularity - irregularity

Also - tachy divided into broad and narrow complexes

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7
Q

Commonest arrhythmia is ICU

A

AF

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8
Q

Type of tachy and causes

A

Sinus - increased sympathetic tone, or compensating for dilation, low CO, hypoxia, anaemia, hyperthermia

Atrial tachy - channlelopathy, structural

AV tachy - nodal and non-nodal reentrants

VT - electrolytes, K and Mg, and after ischaemia. Maybe long QT

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9
Q

Causes of AF

A 
Hypovolaemia
Sepsis
Low K, low Mg
Hypoxia
Ischaemia
PE
Thyrotoxicosis
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10
Q

When to cardiovert AF

A

Hypotension <90
Oedema
Chest pain
Reduced GCS

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11
Q

Assess need for anticoag in AF

A

CHADSVASC score

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12
Q

Define atrial flutter

A

Supra-ventricular tachycardia

Presence of a re entry circuit in the RA

Atrial rate = 300

AV node blocks rapid flutter waves, therefore vent rate lower

Does not respond to vagal

Adenosine - underlying rhythm, not a cure

Tx - rate control, chemical/electrical cardio

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13
Q

AVNRT

A

Atrioventricular Nodal Re-Entrant Tachy

Type of SVT - causes palpitations in structurally normal heart

140-280/min

Two functional pathways round AV node

Slow posterior and fast anterior.

Gives rise to:
Slow-fast AVNRT 80% - P waves hidden in QRS,
Fast slow 10%
Slow slow 5%

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14
Q

Tx AVNRT

A

Vagal
Adenosine
Beta blockers or CCB
Flecanide / Amiodarone

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15
Q

AVRT

A

AV re-entrant tachy

SVT. Re-entry circuit distinct from AV node

Pre-excitation—> tachy because AV doesn’t delay.

Commonest WPW

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16
Q

WPW and ECG finding

A

Aberrant conduction via the BUNDLE OF KENT
Accessory path)

Delta wave - slurred upstroke
PR interval <120
T wave deflects opposite to QRS (QRS/T discordance)

Tall R wave, T wave inversion in pre-cordial waves, mimics RVH/LVH

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17
Q

Types of WPW

A

Type A - positive delta in precordial dominant S in V1 (left side path)

Type B - negative delta wave in V1

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18
Q

Treatment of AVRT

A

Vagal
Adenosine (may cardiovert)
CCB first line
DCCV

Antidromic AVRT may look like VT, if in doubt treat as VT

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19
Q

What if you get AF with WPW

A

the AV node is bypassed direct to ventricles

Use of adenosine/b blockers INCREASES conduction and may cause VT or VF

Treat - procainamide of DCCV

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20
Q

Causes of Long QT

A

Congenital - Romano Ward (AD) Jervell Lange Neilson (AR)

Electrolytes - low K, low Mg, low Ca

MI

SAH

Hypothermia

Drugs - Antiarrhythmics - Amio, sotolol
Abx - eryth, clarity, fluconazole
Ondansetron
TCA/SSRI

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21
Q

Classify anti-arrhythmic

A

Vaughan Williams Class

1 - Na channel blocker

2 - beta block - bisoprolol/metoprolol - SVT

3 - K block Prolong phase 3, increases AP duration, - amio, SVT/VT

4 - Ca block - reduce SA/AV - verapamil/diltiazem , SVT

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22
Q

Classify group 1 Vaughan William

A

Na blockers, reduce rate of rise of phase 0

1a - Prolong refractory - Procainamine (SVT/VT)

1b - Shortened ARP - lignocaine/phenytoin (VT)

1c - no change - Flexanide (SVT/VT)

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23
Q

Stages of action potentia

A

0 depolar (fast Na)

1) Repolar (k efflux
2) Plateura K out, Ca in
3) repolar, Ca closes

4 RMP Na/K

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24
Q

Define asthma

A

Chronic inflammatory condition of airways

Presents as breathless, wheeze and cough, with diurnal variance

FEV1/FVC < 65%
FEV1 < 70%
Increase by 12% with bronchodilator

associated with autopsy

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25
Q

Pathophys of asthma

A

Chronic airway inflammation

Smooth muscle hypertrophy

Goblet cell hyperplasia

Increased reactivity, oedema and secretions.

Leads to mucous plugging and scarring - epithelial collagen deposition

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26
Q

Moderate asthma

A

Increasing symptoms
PEFT 50-75% of best

No severe feature

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27
Q

Severe asthma

A

One of

PEFR 33-50%
RR>25
HR>110
Can’t complete sentences

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28
Q

Life threatening asthma

A 
Ix:
PEFR < 33%
SpO2 < 92%
PaO2 < 8
Normal CO2
Clinical:
Low GCS
Exhaustion
Hypotension
Cyanosis
Silent chest
arrhythmia
Low resp effort
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29
Q

Near fatal asthma

A

Raised CO2 needing MV and raised inflation pressures

30
Q

When to tube asthma

A 
Poor or deteriorating resp effort
Exhaustion
Worsening hypoxia
Drowsy
Resp Arrest
31
Q

Drugs in asthma

A

Salbutamol 2.5 to 5mg inhaled
Ipratropium 250-500mcg inhaled

Steroids - pred 40 or hydro 100

Mg - 2g iv over 20 minutes

OTHERS:
Iv salbutamol
Aminolphyline

No role fo Abx

32
Q

Vent features of asthma

A

High resistance and obstruction to flow
Gas trapping / breath stacking, dynamic hyperinflation

Barotrauma - cardiovascular depression

Low PEEP, 80% of iPEEP, do an expir hold

Prolong IR 1:2, 1:4

Controlled hypoventilation
Slow rate 10-14
Low Tv
Plat<30
Permissive hypercapnoea
Decompress
33
Q

Other drugs in asthma

A 
Ketamine
Sevo 
Aminophyline
Paralysis
VV ECMO
34
Q

Risks for near fatal asthma

A 
Previous ICU with MV
Oral steroid daily use
Increasing use of salbutamol
Poor compliance
Age>40
35
Q

Define a BPF

Define Air leak

A

Abnormal communication between the bronchial tree and the pleura

Extrusion of Air from a normally gas filled cavity

36
Q

Classify Air leaks

Classify BPF

Differ from PTx

A

Leaks - Cerfolio class - Continuous, inspired, expired, forced

BPF - central - from tracheal and bronchi, peripheral from airways

BPF - central bronchial tree to pleura, PTx - communication from rupture bleb or alveolar duct

37
Q

Causes of a BPF

Risk factors

A

Pulmonary resection (pneumonectomy > lobectomy)

Causes
Trauma, 
ARDS
Infection, pneumonia, TB
Necrotising lung disease - chemo/radio
Iatrogenic - lines
PTx
Mechanical vent

Risk

Right side procedures
Uncontrolled infection
Pre-op steroid, infection, radiation
Malignancy

38
Q

Imaging for BPF

A

CXR
CT
Bronch - methylene blue
VQ - xenon

39
Q

Physiological issues of a BPF

A 
Can’t apply PEEP
Loss of Tv
Can’t re-expand
Inappropriate cyclonic
Delated wean
40
Q

Ventilation in BPF

A

Minimise miunute volume and distension
Reduce PEEP, Tv, Insp time and RR
Permissive hypercapnoea and lower SaO2

Spontaneously vent

Try and stop mechanical vent

Consider - one lung ventilation, double ventilators, DLT, blocker

41
Q

Pathophysiology of burns - broad headings

A

Systemic inflammatory response —-> permeability —> oedema

Inhalation lung injury - ARDS/airway obstruction

Hypermetabolism - (high protein catab, low synthesis) — immunosuppressed, wound healing, infections

42
Q

Severity of burns

A

Area or depth

Area - Lund Browder, rule of 9s, palm area 1%

Depth - Supeficial - dermis only
Partial - superficial/deep dermal
Full - all layers. Painless

43
Q

Broad headings of burn management

A

ATLS. Get the extent of the burn and assess inhalation injury

A +C spine - large tube, uncut.

C - iv access, parklands

D - avoid hypothermia and analgesia

E - surgical -debride/escharotomy

44
Q

Causes of hypercalcaemia

A

Malignancy - myeloma, ectopic PTH

Endocrine - Hyperparathyroid. (Adenoma, MEN). Hyperthyroid

Granuloma - Sarcoidosis TB

Drugs - thiazide, lithium, aminophyliine, Vitamin D

Other - Rhabdo, renal failure, milk alkali

45
Q

ECG in hyper cacaemia

A

Short QTc
Long PR
Wide WRS
Wide T waves

AV block and arrest

46
Q

ECG in hypocalcaemia

A

Prolonged QTc
AV block
Torsades

47
Q

When does PTH act

A

Low Ca

Release ca from bone, increased reabsorption of DCT

Reduced PO reabsoprtion, therefore more Ca (less complexes)

Vit D converts wot 1, 25 vit D3…increased GI Ca absorption

48
Q

Calcitonin

A

Thyroid C cells

In response to high Ca

Inhibit ca absorption
Inhibit osteoclasts
Stimulate osteoblasts

Inhibit reabsoprtion in kidney, but inhibit phosphate reabs too

49
Q

Causes of hypocalcaemia

A

Primary hypoparathyroid
Vit D deficiency
Congenital deficiency - DiGeorge

Malnutrition - less intake, malabsorption, Vit D ricketyts, Osteomalacia

Misc - TLS, Rhabdo, renal failure, pancreatitis

Drugs - furosemide, calcitonin, bisphos, phenytoin

50
Q

PAWP pressures

Distances

A

RA - 3-8mmHg. 15-20cm
RV - 25/0-10. 25-30
PA - 25/ 10-20 10cm after that
PCWP - 4-12

51
Q

Measured and derived outputs

A 
Measured
CO
CVP
RAP, RVP, PAP, PCWP
SvO2
Temp

Derived (CO = (MAP-CVP)/SVR)

CI
SV
SVI
SVR
SVRI
PVR
PVRI
52
Q

Features of an oesophageal doppler

A

Stroke distance - Area under curve x CSA = SV

Mean acceleration/PV, markers of contractility
PV 90-120cms 20 year old reduces with age

Flow time corrected -time spent in systole corrected to rate 60
Low - high afterload, high, Low afterload (vasoplegia)

53
Q

Assumptions of a oesophageal Doppler

A

Angle of probe to direction of flow is constant
Ratio of flow in ascending to descending is constant
Laminar flow
CSA is a constant

70% of the CO is in the descending aorta

54
Q

Where to place Doppler

A

35-40cm

55
Q

Define cardiogenic shock

A

Evidence of tissue hypoperfusion due to primary cardiac failure, AFTER correction of pre load. Tissue demand for oxygen cannot be met .

Characterised:
SBP <90
HR>60
Oliguria
Organ congestion
CI< 2.1 litres/m2/minute
56
Q

Causes of cardiogenic shock

A 
Acute coronary syndromes
Arrhythmias
Valve - endocarditis, muscle rupture, decompensated AS
Viral myocarditis - coxsackie 
Tampanade

High output failure - thyroid, anaemia

Decompensating chronic failure- hypertensive, dilated cardiomyopathy,

57
Q

Pathophysiology of cardiogenic shock

A

Impaired LV systolic OR diastolic

Diastolic:
Increased LVEDP —> lungs congested —> hypoxaemia —-> ISCHAEMIA

Systolic: Low SV —> low CO — hypotension, reduced systemic perfusion.

Reduced coronary perfusion —> ischaemi

Reduced systemic perfusion —> vasoconstriction and fluid retain.

ALL LEADS TO MYOCARDIAL DYSFUNCTION

58
Q

Inotropic options in cardiogenic shoc

A

Adrenaline
Dobutamine

Consider vasodilator to reduce after load and therefore work
Enoximone (PDE3–> increased cAMP) reduced SVR, inotropic

GTN - venodikate

Vasopressor if BP low - norad/vasopressin (V1 - constriction, 2 water retention)

Levosimendin

IABP/VAD

59
Q

Goals of cardiogenic shock tx

A

Reduce to oxygen demand —> reduce HR and afterload

Improve deliver - perfusion (dilators/inotropes)
O2 Delivery - FiO2, ?blood

60
Q

Contra indications to IABP

A

Aortic regurgitation
Dissection
Severe PVD

LVOT
Sepsis
Can’t be anti-coagulated
Arterial tortuously

61
Q

Complications of IABP

A

Bleeding, haematoma
Pseudoanurysm
Dissect/perf

Mesenteric and renal ischaemia
Cerebral ischaemia
Helium embolus
Haemolysis
Low platelets
62
Q

Pathophysiology of BSD

A

CVS - Catecholamine storm on herniation. Constriction and tachy

Increased afterload - ischaemia

Cushings may occur - hypertension with brady

Herniation - loss of tone, dilation, hypotension.

Resp - pulmonary oedema, apnoea

Endo - pit ischaemia, DI, fluid loss, electrolytes, low temp, hypothyroid

Coagulapathy

63
Q

Vent parameters in BSD

A 
Lung recruitment
LPV 4-8, PEEP 5-10
Insp<30
Chest physio
Head up

normal pH
PaO2>10
CO2 4.5 to 6
SpO2 > 94

64
Q

Things to in BSD

A

Metabolic - methylpred - reduced EVLW, improve O2
(Also improves organ survival)

Warm to 36-37

Endocrine - insulin 4-10
Vasopressin
T3 was but isn’t
If high Na - water NG

Haem - blood/products to optimise delivery. But transfusion affects transplant
Correct coagulopathy

65
Q

Features of cranial DI

A

Urine output > 4ml/kg/hour

Na>145
Serum Osm>300

Urine <200

66
Q

Treat cranial DI

A

Treat before results back
DDAVP
Fluid admin with minimal sodium

67
Q

Causes of cirrhosis

A

Alcohol
Hep B/C
Drugs - methotrexate, methydopa

Cholestasis - primary biliary cirrhosis/sclerosis cholangisit

Autoimmune hep

Hereditary - Wilsons, Haemachromatosis

Vascular - Budd Chiari

Non alcoholic fatty liver

68
Q

Prognostication CLD

A

Child Pugh
MELD

Childs - Enceph, Ascites, Albumin, Bilirubin, INR
A - 5-6
B - 7-9
C - 10-15

MELD
Bilirubin, INR, Creatinine

SOFA
UK ELD - transplant scores

69
Q

Why do patients with Cirrhosis end up in ICU

A

Bleeding - varices or coagulopathy

Hepatic enceph, low GCS

Alcoholic Hep

AKI

Sepsis

70
Q

Portal pressure in portal hypoertension

A

> 10mmHg

71
Q

Define HRS

A

Pre renal AKI, not responsive to fluids in patients with fulminant liver failure

Criteria
Cirrhosis and ascites
Cr > 133
No change in Cr after two days dieuretic withdraw and albumin expansion
No Shock
No nephrotoxic S
No parenchymals disease
72
Q

Types of HRS

Tx

A

1 - rapidly progressive decline in kidney function, mortality 50%

2 - indolent

Pete FFICM SOE/OSCE (199 decks)

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