Gen - Classifications, Definitions 12 - Flashcards
Classifying an Aortic Dissection
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
Risk factors for dissection
Hypertension
Advanced Age
Male
Smoker
Family Hx
Pregancy
Trauma
Congenital - Marfans, Ehler’s, Co-arctation, Turners.
Complications of a dissection
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
Imaging for dissection
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
Manage dissection based on A and B
A and complicated B - CTC
A - surgical emergency, sternotomy and CPB. Reduce BP
B - beta blockers/anti hypertensives
Complicated B - left lat thoracotomy
Classify arrhythmia
By heart rate: >100 tachy < 60 Brady
Where it originates - SVT, VT
Regularity - irregularity
Also - tachy divided into broad and narrow complexes
Commonest arrhythmia is ICU
AF
Type of tachy and causes
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
Causes of AF
Hypovolaemia Sepsis Low K, low Mg Hypoxia Ischaemia PE Thyrotoxicosis
When to cardiovert AF
Hypotension <90
Oedema
Chest pain
Reduced GCS
Assess need for anticoag in AF
CHADSVASC score
Define atrial flutter
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
AVNRT
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%
Tx AVNRT
Vagal
Adenosine
Beta blockers or CCB
Flecanide / Amiodarone
AVRT
AV re-entrant tachy
SVT. Re-entry circuit distinct from AV node
Pre-excitation—> tachy because AV doesn’t delay.
Commonest WPW
WPW and ECG finding
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
Types of WPW
Type A - positive delta in precordial dominant S in V1 (left side path)
Type B - negative delta wave in V1
Treatment of AVRT
Vagal
Adenosine (may cardiovert)
CCB first line
DCCV
Antidromic AVRT may look like VT, if in doubt treat as VT
What if you get AF with WPW
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
Causes of Long QT
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
Classify anti-arrhythmic
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
Classify group 1 Vaughan William
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)
Stages of action potentia
0 depolar (fast Na)
1) Repolar (k efflux
2) Plateura K out, Ca in
3) repolar, Ca closes
4 RMP Na/K
Define asthma
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
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
Moderate asthma
Increasing symptoms
PEFT 50-75% of best
No severe feature
Severe asthma
One of
PEFR 33-50%
RR>25
HR>110
Can’t complete sentences
Life threatening asthma
Ix: PEFR < 33% SpO2 < 92% PaO2 < 8 Normal CO2
Clinical: Low GCS Exhaustion Hypotension Cyanosis Silent chest arrhythmia Low resp effort
Near fatal asthma
Raised CO2 needing MV and raised inflation pressures
When to tube asthma
Poor or deteriorating resp effort Exhaustion Worsening hypoxia Drowsy Resp Arrest
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
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
Other drugs in asthma
Ketamine Sevo Aminophyline Paralysis VV ECMO
Risks for near fatal asthma
Previous ICU with MV Oral steroid daily use Increasing use of salbutamol Poor compliance Age>40
Define a BPF
Define Air leak
Abnormal communication between the bronchial tree and the pleura
Extrusion of Air from a normally gas filled cavity
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
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
Imaging for BPF
CXR
CT
Bronch - methylene blue
VQ - xenon
Physiological issues of a BPF
Can’t apply PEEP Loss of Tv Can’t re-expand Inappropriate cyclonic Delated wean
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
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
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
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
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
ECG in hyper cacaemia
Short QTc
Long PR
Wide WRS
Wide T waves
AV block and arrest
ECG in hypocalcaemia
Prolonged QTc
AV block
Torsades
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
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
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
PAWP pressures
Distances
RA - 3-8mmHg. 15-20cm
RV - 25/0-10. 25-30
PA - 25/ 10-20 10cm after that
PCWP - 4-12
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
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)
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
Where to place Doppler
35-40cm
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
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,
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
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
Goals of cardiogenic shock tx
Reduce to oxygen demand —> reduce HR and afterload
Improve deliver - perfusion (dilators/inotropes)
O2 Delivery - FiO2, ?blood
Contra indications to IABP
Aortic regurgitation
Dissection
Severe PVD
LVOT
Sepsis
Can’t be anti-coagulated
Arterial tortuously
Complications of IABP
Bleeding, haematoma
Pseudoanurysm
Dissect/perf
Mesenteric and renal ischaemia Cerebral ischaemia Helium embolus Haemolysis Low platelets
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
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
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
Features of cranial DI
Urine output > 4ml/kg/hour
Na>145
Serum Osm>300
Urine <200
Treat cranial DI
Treat before results back
DDAVP
Fluid admin with minimal sodium
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
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
Why do patients with Cirrhosis end up in ICU
Bleeding - varices or coagulopathy
Hepatic enceph, low GCS
Alcoholic Hep
AKI
Sepsis
Portal pressure in portal hypoertension
> 10mmHg
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
Types of HRS
Tx
1 - rapidly progressive decline in kidney function, mortality 50%
2 - indolent
