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
Pathophys of asthma
Chronic airway inflammation Smooth muscle hypertrophy Goblet cell hyperplasia Increased reactivity, oedema and secretions. Leads to mucous plugging and scarring - epithelial collagen deposition
26
Moderate asthma
Increasing symptoms PEFT 50-75% of best No severe feature
27
Severe asthma
One of PEFR 33-50% RR>25 HR>110 Can’t complete sentences
28
Life threatening asthma
``` Ix: PEFR < 33% SpO2 < 92% PaO2 < 8 Normal CO2 ``` ``` Clinical: Low GCS Exhaustion Hypotension Cyanosis Silent chest arrhythmia Low resp effort ```
29
Near fatal asthma
Raised CO2 needing MV and raised inflation pressures
30
When to tube asthma
``` Poor or deteriorating resp effort Exhaustion Worsening hypoxia Drowsy Resp Arrest ```
31
Drugs in asthma
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
Vent features of asthma
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
Other drugs in asthma
``` Ketamine Sevo Aminophyline Paralysis VV ECMO ```
34
Risks for near fatal asthma
``` Previous ICU with MV Oral steroid daily use Increasing use of salbutamol Poor compliance Age>40 ```
35
# Define a BPF Define Air leak
Abnormal communication between the bronchial tree and the pleura Extrusion of Air from a normally gas filled cavity
36
Classify Air leaks Classify BPF Differ from PTx
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
Causes of a BPF Risk factors
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
Imaging for BPF
CXR CT Bronch - methylene blue VQ - xenon
39
Physiological issues of a BPF
``` Can’t apply PEEP Loss of Tv Can’t re-expand Inappropriate cyclonic Delated wean ```
40
Ventilation in BPF
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
Pathophysiology of burns - broad headings
Systemic inflammatory response —-> permeability —> oedema Inhalation lung injury - ARDS/airway obstruction Hypermetabolism - (high protein catab, low synthesis) — immunosuppressed, wound healing, infections
42
Severity of burns
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
Broad headings of burn management
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
Causes of hypercalcaemia
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
ECG in hyper cacaemia
Short QTc Long PR Wide WRS Wide T waves AV block and arrest
46
ECG in hypocalcaemia
Prolonged QTc AV block Torsades
47
When does PTH act
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
Calcitonin
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
Causes of hypocalcaemia
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
PAWP pressures Distances
RA - 3-8mmHg. 15-20cm RV - 25/0-10. 25-30 PA - 25/ 10-20 10cm after that PCWP - 4-12
51
Measured and derived outputs
``` Measured CO CVP RAP, RVP, PAP, PCWP SvO2 Temp ``` Derived (CO = (MAP-CVP)/SVR) ``` CI SV SVI SVR SVRI PVR PVRI ```
52
Features of an oesophageal doppler
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
Assumptions of a oesophageal Doppler
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
Where to place Doppler
35-40cm
55
Define cardiogenic shock
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
Causes of cardiogenic shock
``` 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
Pathophysiology of cardiogenic shock
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
Inotropic options in cardiogenic shoc
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
Goals of cardiogenic shock tx
Reduce to oxygen demand —> reduce HR and afterload Improve deliver - perfusion (dilators/inotropes) O2 Delivery - FiO2, ?blood
60
Contra indications to IABP
Aortic regurgitation Dissection Severe PVD LVOT Sepsis Can’t be anti-coagulated Arterial tortuously
61
Complications of IABP
Bleeding, haematoma Pseudoanurysm Dissect/perf ``` Mesenteric and renal ischaemia Cerebral ischaemia Helium embolus Haemolysis Low platelets ```
62
Pathophysiology of BSD
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
Vent parameters in BSD
``` 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
Things to in BSD
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
Features of cranial DI
Urine output > 4ml/kg/hour Na>145 Serum Osm>300 Urine <200
66
Treat cranial DI
Treat before results back DDAVP Fluid admin with minimal sodium
67
Causes of cirrhosis
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
Prognostication CLD
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
Why do patients with Cirrhosis end up in ICU
Bleeding - varices or coagulopathy Hepatic enceph, low GCS Alcoholic Hep AKI Sepsis
70
Portal pressure in portal hypoertension
>10mmHg
71
Define HRS
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
Types of HRS Tx
1 - rapidly progressive decline in kidney function, mortality 50% 2 - indolent