Quick n dirty Patho Flashcards
1
Q
Pneumothorax definition
A
gas within the pleural space
2
Q
PTX hx
A
dyspnea, pleuritic chest pin, spontaneous, trauma, iatrogenic
3
Q
PTX Physical
A
tachypnea, tachycardia, decreased AE, hypoxemia, high PIP + pPlats, subcutaneous air, hyperresonance, (obstructive findings: JVP, hypotension, tracheal deviation)
4
Q
PTX imaging
A
CXR –> white visceral pleural line on chest radiograph, wont see bronchovascular markings beyond the white line
POCUS –> No lung sliding, lung point, lung pulse M-mode barcode
easier found on Ct than CXR, also can turn the cxr opposite contrast
5
Q
PTX Tx
A
chest tube, or leave if not significant
6
Q
Massive HTX definition
A
1500ml release, or 200ml over 2-4 hours =
7
Q
Massive HTX tx
A
emergency thoracotomy
8
Q
HTX defintion
A
blood within the pleural space is termed hemothorax. often from aortic rupture, Myocardial rupture, injuries to hilarity structures, lung parenchyma, or intercostal vessels
9
Q
HTX imaging
A
CXR - whiteout
POCUS - anechoic fluid ++spine sign
10
Q
HTX tx
A
chest tube 4/5th intercostal
11
Q
Pulmonary Embolism definition
A
PE is a form of venous thromboembolism that obstructs the pulmonary artery or one of its branches by material that originated elsewhere in the body
12
Q
PE hx risk/clinical
A
risk: hypercoag, vessel injury, venous stasis.
clinical: dyspnea, CP, cough, dvt, shock, sudden death (hemoptysis associated with PE infarction )
13
Q
PE imaging
A
CT or VQ scan
14
Q
PE Tx
A
- UFH
- very conservative volume optimization
- norepi, dobutatmine +/- e[I
- embolectomy
- tPa (for hemodynamically unstable patients)
15
Q
Massive Hemoptysis definition
A
life threatening hemoptysis when hemoptysis results in life-threatening event including significant airway obstruction, significant abnormal gas exchange, or hemodynamic instability
16
Q
massive hemoptysis hx
A
bronchiectasis, cystic fibrosis, TB, myectomas, lung cancer
17
Q
massive hemoptysis imaging
A
bronchoscope, CXR, CT-A
18
Q
massive hemoptysis tx
A
large bore ETT, normal vent settings usually.
- bad lung down
- bronchial alveolar lavage
- single lung ventilation potentially
- double lumen ventilation
- bronchial blockade
- reverse coagulation
- Inhaled TXA
19
Q
CAP definition
A
CAP is defined as an acute infection of the pulmonary parenchyma in a patient who has acquired the infection in the community
20
Q
Dx of CAP
A
CAP generally required the demonstration of an infiltrate on chest radiography in a patient with clinical compatible syndrome
21
Q
PNA hx
A
fever, cough, pleurite chest pain, sputum production, tachypnea
22
Q
PNA imaging
A
infiltrates on plain film is considered the gold standard for dx pneumonia when clinical and microbiologic features are supportive
23
Q
PNA TX
A
empiric treatment directed at the most likely pathogens to start
24
Q
RV spiral of death
A
RV dilation, TV insufficiency, RV wall tension, Neurohormonal activation, myocardial inflammation, RV O2 demand, RV ischemia, decreased contractility, decreased LV preload, decreased systemic BP, decreased RV coronary perfusion, decreased RV O2 delivery —> cardiogenic/obstructive shock –> death
25
causes of severe RV afterload
PE, Severe PH
26
RV failure imaging
parasternal long n short, CT
27
RV failure potential tx
potentially diuresis, norepinephrine + dob, +e/- epi
| -not more fluids
28
Acute respiratory distress syndrome definition
Berlin's criteria:
1 week resp symptoms, with bilateral lung infiltrates that are non-cariogenic in origin. then modified into PF ratios for severity
29
ARDS pathophysiology, big boy.
Healthy lungs regulate the movement of fluids to maintain a small amount of interstitial fluid and dry alveoli.
In ARDS, this regulation is interrupted by lung injury, causing excessive fluid in both the interstium and alveoli.
Consequences include: **impaired gas exchange **decreased compliance ** increased pulmonary arterial pressure
++deeper++
ARDS is a consquence of an alveolar injury producing diffuse damage. This injury causes release of IL-1,IL6,IL8, and TNF damaging alveolar and capillary epithelium. Damage to the capillary endothelium allows proteins to escape from the vascular space. The oncotic gradient that favours resorption of fluids lost and fluid poors into the interstium, overwhelming the lymphatic system.
Consequences include: **impaired gas exchange **decreased compliance ** increased pulmonary arterial pressure
30
3 common causes of ARDS
sepsis, PNA, trauma
31
ARDS treatments
VILI, use of sedatives, potentially paralytics, hemodynamic mgmt, nutritional support, glucose control, DVT, prophylaxis, and GI bleeding, conservative fluids
32
Asthma definition
A common chronic disorder of the airways that is complex and characterized by variable and recurring symptoms, airway obstruction, bronchial hyper responsiveness and an underlying inflammation
33
Asthma pathophysiology
Reversible airway inflammation in the setting of acute IgE mediated inflammation and constriction. Basophils, mast cells and eosinophils degranulate to release histamine and increased mucus production and decrease lumen of bronchiole. Complicated by smooth muscle constriction
34
critical Asthma Hx
- previous icu admins
- ≥2 non-icu hospitalization in the past year
- ≥3 ED visits in the past month for asthma exacerbation
- chronic us of oral corticosteroids
- medication non-compliance
- using ≥2 SABA pressurized MDI month
- poverty with no access to health care
35
asthma imaging
CXR = hyperinflated, flattened hemi-diaphragms
36
Asthma Treatment
- inhaled IV steroids (decreases IgE)
- ventolin (B2 agonist)
- atrovent (anti-muscarinic)
- NIPPV
- High flow for MV (consider ZEEP )
37
Asthmatic Dynamic hyperinflation ( I can condense this more...)
1. expiration usually occurs as passive movement
2. resistance to airflow (bronchospasm) results in decreased expiratory flow
3. decreased expiratory flow results in longer time required to expire the full Vt
4. if expiration is interrupted before its natural end by the next inspiration, some unexpired residual gas remains in the chest
5. this gas exerts a pressure onto the respiratory circuit
6. as a result the alveolar pressure at the end of expiration is higher than zero (zero being atmospheric)
7. this process of incomplete emptying is called dynamic hyperinflation, and the positive pressure alveolar pressure is called intrinsic PEEP or auto-PEEP
38
AECOPD defintion
AECOPD has 2 of the following
1) worsening dyspnea
2) increased sputum production
3) increased purulence
39
COPD patho
1) Bronchioles in COPD lose elastic fibers and are destroyed and become collapsible.
2) additionally, destruction of the alveoli and lose surface area
3) there's an obstruction because air cannot get out of the lung. The alveoli are all destroyed and large sacs of air, and can't get back into the obstructed, collapsed bronchioles
40
COPD imaging
CXR - very dark, hyperinflated, flattened hemi-diaphgrams, potentially increased pulmonary vasculature (PH) +/- blebs
41
COPD tx
```
ventolin
atrovent
steriods
abx
NIPPV
MV
```
42
AutoPEEP in COPD
- alveoli remain inflated at end-expiration due to obstruction, so alveolar pressure is greater than atmospheric pressure
- In the absence of inspiratory effort, intrapleural pressure approximates alveolar pressure.
- AutoPEEP increasing WOB to overcome the positive pressure in the alveoli during inspiration, the diaphragm must generate enough negative pressure to exceed the auto-PEEP and transmit negative pressure to the central airways, generating airflow
43
Recognizing DHI
1) High autoPEEP (check ur fucking vent)
2) Failure of expiratory flow to return to zero before next breath (waveforms)
3) Trigger dyssynronchy
4) Inspriration volumes >> than expiratory volumes significantly
44
Treatment of DHI in COPD
1. change vent settings (decrease RR, decrease I-TIME, prolong expiratory time)
2. Reduce demand (reduce anxiety, pn, fever)
3. reduce flow resistance
(suction, use large ETT, bronchodilator)
4. counterbalance expiration flow limitations
(external PEEP)
45
Caurda Equina Syndrome
* *decreased bowel
* *decreased bladder
* *decreased sexual function
Injury distal to L2 spinal cord, caused by compression/trauma or lumbar disc. Damage to multiple nerves of the caudal equina
Treatment: surgical decompression within 48 hours
46
Brown Sequard Syndrome
Ipsilateral loss of:
1) upper motor neuron weakness
2) ipsilateral hemiparesis
3) loss of proprioception
Contralateral loss of:
1) pain 2) temperature
47
Central cord syndrome
```
MUDE
Motor loss
Upper extreme > lower loss
Distal worse than prox
-extension injuries
```
48
Dorsal column
All sensory (spine to cortex)
- proprioception
- deep touch
- tactile sensation
- vibration
- fine sensory
goes to ascending up dorsal tract, decussation at medulla then hits thalamus then goes to cortex
49
spinothalamic
pn/temp
| crosses over 1-2 vertebrae above
50
Somatic reflexes
automatic, reflex arc is felt from the afferent spinal nerve then at the level of the vertebra it relays information to the intraneuron area which correlates to a motor efferent response
51
upper motor neuron
CNS/spinal cord
52
lower motor neuron
PNS
53
How does PEEP effect the Left heart
1) Decrease preload (decreased venous return)
2) Decreases LV afterload.
(By decreasing LV unloading. Decrease LV afterload due to baroreceptor response from increased intraaortic pressure)
3) Decreased SV due to intreventricular dependence
4) decreased MVO2
5) increased pressure gradient from thorax to periphery
6) increased hydrostatic displacement of alveolar edema
54
summary effects of PEEP on RV
1) decrease venous return
2) decreased hypoxia pulmonary vasoconstriction
3) increased pulmonary vasculature resistance due to vascular compression
55
Increased PIPs with normal pLats
Resistance Issue.
worsening asthma, obstruction of ETT, excessive airway secretions, clogged HME, small ETT, high flow rate
56
Increased PIP with elevated pPlats
PTX, ARDS, PNA, Pulmonary edema, atelectasis, pleural effusion, bronchial intubation.
57
asthma vent settings for:
1) mode
2) fio2 target
3) PIP target
4) pPlat
5) PEEP
6) VT
7) vCalc 80-100L/min
8) RR
9) I:E ratio
10) expiratory time
```
Mode AC-V
FiO2 Adjust to SaO2 of >92%
PIP Adjust to level above peak airway pressures. Caution at PIP >50 cmH20
pPlat <30cmH20
PEEP ZEEP if paralyzed and sedated. Some patients require small amounts of PEEP to match intrinsic PEEP. However, intrinsic PEEP les than COPD
VT 4-8ml/kg
vCalc 80-100L/min
RR 6-10 BPM
IE 1:4, 1:5
Expiratory Time 4-5 seconds
```
58
5 effects of PEEP on pulmonary system
1. increased FRC
2. Decreased in intrapulmonary shunt
3. Reduction of alveolar opening and closing (preventing atelectacto-trauma VILI)
4. increased in intrathoracic pressure (decrease venous return, decrease in LV transmural pressure -> afterload)
5. Distention of normally aerated alveoli
59
Sepsis induced caridomyopathy
In sepsis induced cardiomyopathy, the myocardium is functionally and structurally injured by inflammatory cytokines and mitochondrial dysfunction.
Its characterized by: decreased EF, LV dilation and a recovery time of 7-10 days
60
Glucose targets in sepsis
4.5-6 mmol/L as per NICE-SUGAR trial
61
Sepsis Physical
1. bend the neck (meningitis)
2. listen to all lung zones (PNA)
3. listen for murmurs (endocarditis)
4. palpate RUQ (billiary)
5. palpate flanks (nephritis)
6. Palpate belly (perforation/ileus)
7. examine the skin (necrotizing fasciitis)
62
reasons to treat seizures prophylactically, maybe.
1. hx of seizures/current seizures
2. temporal lobe pathology
3. depressed skull #
4. penetrating trauma to cranial vault
63
CCP goals of care for TBI
1. cerebral blow flow
2. venous outflow
3. brain parenchyma
64
when to consider ETT with SCI
1. use of spinal access muscles (shrug shoulders/tracheal tugging)
2. no bicep curls
65
Sepsis approach
1. source control
2. Abx
3. Optimize VO2/DO2
4. Adjuncts ( steroids, Vitamin C)
66
how does PPV increase LV preload
preload can be increased because of pushing of fluid from west zone 3 to return to the heart (depend on fluid status)
67
How does PPV decrease LV afterload
by increasing intrathoracic pressure, creating a bigger gradient from the thorax to periphery.
also, decrease in LV afterload due to baroreceptor response to increase intrathoracic pressure on the aorta
68
equation of EF
SV/EDV X 100
69
Oxygen Consumption equation
CO= CaO2-CvO2
70
LaPlace's Law
• Wall tension (T) = Transmural Pressure (P) x Radius ( r ) / 2xWall thickness (h)
Wall tension relates to work that the heart has to do
71
End organ perfusion markers
aloc, lactate, urine output cap refill, look at their trends, scvo2
72
Atherosclerosis pathophysiology
1. LDL can deposit in the tunica intimacy, and then become oxidized.
2. Oxidized LDLs activate the endothelial cells to attract WBCs
3. Monocytes enter the tunica intimacy and become macrophages, and macrophages take up these oxidized LDLs and then become foam cells.
4. Foam cells eventually die, spilling out their lipid content, which grows the plaque and increases its pressure.
5. The plaque then can rupture and cause coagulation, causing thrombus, impeding blood flow.
73
STEMI medical mgmt
- PCI/lysis
- Anticoagulation (UHF, LMWH)
- Dual antiplatelet (ASA, P2Y12 [Ticagrelor/plavix])
- Beta Blockers
- ACE-Inhibtors/ARBs
- Statins
- Potassium >4 /Mag levels >1
74
Rescue PCI
after failed lysis, st resolution <50%, ongoing ischemic changes, shock
75
Facilitated PCI
Use thrombolysis to "facilitate" a smoother PCI
76
Elevated troponin without ECG changes
type 2 MI, supply and demand.
| increased demand from systemic critical illness
77
MI complications
```
DARTHVADER
D-eath
A-rrthymia
R-upture
T-amponade
H-eart Failure
V-alve disorder
A-neurysm
D-dressler Syndrome
E-mbolism
R-egurgitation/reoccurance
```
78
Heart Failure triple therapy
1. ACE-I
2. Beta Blockers
3. Spironolactone
79
Acute decompensated Heart failure Forrester classification
1. Dry + Warm (adequately perfused, hemodynamically compensated)
2. Dry + Cold (Hypoperfused and hypovolemic)
3. Wet + warm (congestion but well-perfused)
4. Wet + Cold (congested and hypotensive)
80
pressures of the heart
Think of it as change: 5, 10, 25, 100
or
```
RA= 2-8
RV= 15-30/2-8
PA= 15-30/4-12
LA=2-10/
LV=100-140/3-12
```
81
STEMI mimiks
ELEVATION.
```
E-electrolytes (hyperK)
L-left bundle branch
E - (BER)
V - Ventricular hypertrophy
A- Arrhythmia/aneurysm (VT/brugada/LV-An)
T-takotsubo, TBI
I-Infarct MI, Injury(contusion)
O- Osborn wave (hypothermia)
N- Non-athersclerotic vasospasm (prenzmental)
```
82
Dilated cardiomypathies causes
- Genetic
- Infection
- Systemic Immune-Mediated Disease
- Toxic and overload
- drugs
- Endocrine/metabolic
- Peripartium
83
Dialated cardiompathy treatments
adress underlining cause, treat heart failure, prevent arrthymia, prevent thromboembolic events, heart transplant
84
HCM causes and characteristics
**Distinct from ventricular hypertrophy as HCM is disproportionally effects the SEPTUM**
familial, symptoms related to diastolic dysfunction and LV outflow obstruction
85
Whats HCM with SAM
HCM with Systolic Anterior Motion. Where the mitral valve becomes sucked back into the LVOT during systole, physically obstructing flow. Sounds awful.
86
Treatment for Aortic Stenosis
Preload: increased
Afterload: normal
HR: Decreased
Contractility: Increased
87
Treatment of Aortic Regurgitation
Preload: normal
afterload: decrease
HR: high normal
Contractility: increase
88
Tx of Mitral stenosis
Preload: normal
Afterload: normal
HR: Decrease
Contractility: normal
89
Tx of mitral regurg
preload- decrease
afterload- decrease
HR- high normal
Contractility - Increase
90
Rheumatic heart disease
1. Group-A Strep (GAS) pharyngitis leads to both an innate and adaptative immune response
2. The immune response gets activated leading to the development of cross-reactive antibodies and cross-reactive T-cells which effect the joints, heart, skin and brain.
3. Scaring, stretching of the left-sided heart are typically effected. Causing either stenosis or regurgitation
91
Autonomic factors affecting HR
- autonomic innervation
- hormones
- fitness level
- age
92
Factors affecting Stroke volume
-heart size
-fitness level
-gender
-contractility
-duration of contraction
-preload
(EDV)
-afterload (resistance)
93
ACA perfuses
frontal lobe
94
MCA perfuses
blood flow to the frontal, partial, temporal lobe
95
PCA perfuses
supplies blood flow occipital lobe
96
ACA stroke syndrome
Will give you contralateral leg weakness only
97
MCA stroke syndrome
right: arm, face, contralateral + neglect
left: arm, face, contralateral and speech
98
internal capsule
everything from the motor and sensory - face, arm, and leg weakness contralateral
99
post arrest targets
| MAP, CO2, PaO2, Hb and temp
```
MAP 80
PaO2 80-100
PcO2 35-40
Hb- 90
temp 34-36
```
100
SCI map goals
85mmHg
101
Ischemic Stroke lysed n non-lysed
pre-post lysis - SBP 180
| non-lysed - 220
102
AAA targets and treated with
SBP 100-120 mmHg, HR 55-60. Labetalol and nitroprusside
103
SAH, Epidual, intercapsle, ischemic cva with hemorrhagic transformation
SBP 140
104
Undifferentiated TBI
80-90
105
Coagulation goals for neurotrauma
- INR < 1.5
- Platlets > 100 (platlets)
- PTT <40 (FFP)
- Fibrinogen > 1 (Cyroprecipitate)
- Hb >90g/L
- warfarin = octaplex is supra-therapeutic.
- Heparin reversal = protamine
-Inquire about TXA within 3 hours for cerebral contusion/subdural hematoma
106
Causes of increased right sided afterload
1. Left-sided heart failure (increasing pulmonary vasculature pressures)
2. End stage COPD
3. PE
4. Obstructive sleep apnea
107
HFpEF
Diastolic Failure, hard ventricle, normal EF
108
HFrEF
Systolic failure
109
Rheumatic Heart Disease patho
1. Group A Strep (GAS) pharyngitis leads to both an innate and adaptive immune response.
2. The immune response gets activated leading to the development of cross-reactive antibodies and cross-reactive T cells which effects the joints, heart, skin and brain.
3. Scaring, stretching of the left-side heart are typically effected. causing either stenosis or regurgitation.
110
Cardiac Tamponde
-Hemodynamically unstable
-Narrow Pulse pressure
-RV collapse
-Pulsus Paradoxus, >10mmHg and during inspiration - relating to physiologic interdependence
-becks triad
-low voltage ECG
Pocus) 1 pericardial 2. RV collapse 3. dilated IVC
111
Pericarditis treatment
Mostly symptom mgmt, NSAIDS
112
Infectious endocarditis casuses
IVDU, Dental infection, artificial valve and any implanted devices.
113
Post Arrest Care and post arrest targets
1. Identify cause
2. Neurocritical care
3. Shock MGMT
4. Ischemia/reperfusion
114
Discuss IABP and how it works
The IABP consists of a balloon catheter, which is typically inserted percutaneously into the femoral artery and advanced into the descending thoracic aorta, and a pump that controls inflation/deflation.
**The balloon is inflated as diastole beings, augmenting aortic pressure and thus coronary perfusion during the diastolic period. During systole the balloon is deflated and help augment the pull of fluid from the ventricle, decreasing afterload.
115
Hypovolemia causes
Diarrhea, dehydration, diuresis, hemorrhage
116
Three top tips for pharmacology
1) if your liver or kidneys are fucked, your drug handling will be also
2) Its better to give too little and have to give additional than other way around
3) whenever you give a drug, you give its effect and side effect
117
Ketamine, go.
NMDA antagonism, dissociated anesthesia.
- Induction 1-2mg/kg
- augments opiates
- sedation/induction
- cardio-stable but still has those negative effects
- unstable patient 1mg/kg
- delirium, augment with midaz
- bronchodilation
- hypersalvation
- not appropriate for ACS
118
Mysthesia Gravis definition
MG is an acquired autoimmune disorder of the neuromuscular junction characterized by weakness of skeletal muscles, proximal weakness.
119
when do you intubate a MG patient
-< 20ml/kg
120
Myasthenia Gravis Patho
immunoglobulin autoantibodies play a pathogenically important role by attaching ACh receptors and reducing the number of Ach receptors over time, therefore unable to depolarize muscles
121
Guillain-Barre Syndrome
Acute demyelinating disease.
-Exposure to make antibodies (GI, UTI, PNA) to fight off pathogen, but antibodies cross react with myelin and destroy myelin in the major peripheral nerves because of that nerves weather away and you get weak and decreases saltatory conduction. Starts peripherally at first, then centrally.
Miller Fisher = GBS with Cranial nerve involvement
122
GBS tx
IV IG, plasma exchange
123
MG tx
IV IG, Plasma Exchange + steroids
124
Pulsus paradoxus patho
i. During normal spontaneous breathing, inspiration causes blood to fill the RA from the vena cava and causes increased RV filling with a slight bulge or ventricular septum into the LV
ii. This causes a small decrease in LV ejection with systole (increased afterload/decreased LVEDV). In normal breathing, SBP can normal fall on spiration by 10mmHg
iii. Pulsus Paradoxus is an exaggeration of this normal BP variation with breathing. It is defined as a fall in SBP by more than 10mmHg during spontaneous inspiration.
In mechanically ventilated patients, a reversal of this pressure variation occurs, PPV displaces the LV wall inward during systole to assist in LV emptying. This causes a slight rise in SBP during mechanical inspiration.
125
HCM ECG
1. large dagger-like “septal Q waves” in the lateral — and sometimes inferior — leads
2. LVH due to the abnormally hypertrophied interventricular septum
126
cardiac axis deviated to left and causes
too much LV muscle 💪 or bad right sided infarct💔
- lead 1 is more positive and aVF is negative
127
extreme right cardiac deviation
think metabolic or tox, like TCA.
-negative in both
128
Alteplase name and IV regimen
t-PA. Bolus + infusion (usually for CVA - must be given within 4.5 hours, but aim for within 3 hours)
129
Tenecteplace name and IV regimen
TNK. 1x Bolus, weight based max 50mg
130
Preferred P2Y12 and dose
Ticagrelor 180mg
131
Plavix dose for STEMI
300mg
132
Infectious endocarditis causes
IVDU, dental infections, artificial valve replacement and anything impacted
133
infective endocarditis tx
prolonged ABX, typically won't replace valve unless refractory HF or size of vegation meets criteria
134
aortic aneurysm complications
-rupture, aortic regurgitation, tracheal or esophageal compression, pulmonary artery outflow obstruction, septic embolism
```
a-aortic insufficiency
o-occlusion of coronary arteries
r-rupture
t-tamponade
i.=ischemia of viscera
c=cva
```
135
Aortic dissection BP targets
100-120mmHg, HR 55-60 - think labetalol
136
DVT prophylaxis contraindications
Post brain bleed, HIT (heparin induced thrombocytopenia) and recent neurosurgery
137
Severe acute hypertension tx
PO = clonidine
IV = hydralzine/labetalol
carefully ~25% below presenting BP within 24 hours
SBP >180,DBP >120
138
Pacing position 1
chamber being paced
139
Transvenous box has
sensitivity, voltage, and rate
140
Pacing position 2
chamber being sensed
141
Pacing position 3
response to sensing
142
VVI =
Ventricular pacing and seeing (temporary)
143
DDD =
Pacing and sensing the atria and ventricular (most common)
| -Permanent DDD
144
Ductus Arteriosus
By pass pulmonary circulation (connects pulmonary artery and aorta)
145
Ductus Venous
In the liver circulation, between the umbilical vein and IVC
146
Patent Foramen Ovale
Shunt from the atrium right to left, prostaglandin releases causes it to close.
Smaller shunt opening that is essentially a valve, because during fetal circulation, blood travels to the right to left in the Atrium, and then after delivery, when breathing starts, PFO essentially closes because pressure in the LA keeps the valve shut essentially
147
Eisenmenger Syndrome
□ ASD/VSD increases PA pressure with left to right shut
□ Overtime, PVR increases resulting in bidirection flow
Pulmonary Vascular Resistance increases, shunt reverse Right - to - Left --> Eisenmenger syndrome.
148
Post arrest Care steps
1. Identify cause and history
2. Neurocritical care
3. Shock MGMT
4. Ischemia/reperfusion
149
NAGMA causes and tx
Hyperchlorermia, RTA, GI losses = treated with HCO3-
150
Metabolic alkalosis subcategory and tx
1. Volume (Cl) responsive
- tx with NaCl.
- Chloride will bind with H+ and Na+ with Hco3- and drop pH
2. non-volume response = malignant causes usually, long term non CCP tx
151
Normal hemodynamics: SvO2,CO, SV, SVR, CVP, PAWP
SvO2 70%
CO 4-8L/m
SV 60-100mL/beat
SVR 800-1200
CVP 2-6mmHg
PAWP 6-12mmHg
152
Hard signs of neck injuries
- expanding hematoma
- severe active bleeding
- shock not responding to fluid
- decrease or absent radial pulse
- vascular bruits/thrills
- cerebral ischemia
- airway obstruction
153
Soft sign of neck injuries
- hemoptysis, hematemesis
- oropharyngeal blood
- dyspnea
- dysphonia, dysphagia
- subcutaneous or mediastinal air
- chest tube air leak
- nonexpanding hematoma
- focal neurologic deficits
154
zones of the neck
```
Zone 1
○ Clavicle to cricoid cartilage
Zone 2
○ Cricoid cartilage of angle of mandible
Zone 3
- Angle of the mandible to base of the skull
```
155
Hemostasis 5 stages
1. vasoconstriction
2. primary hemostasis - platelet plug
3. secondary hemostasis - coagulation
4. fibrinolysis - dissolves the clots, restores function
5. regeneration - repair
156
Ectopic pregnancy definition and most common clinical presentation
An ectopic pregnancy is an extrauterine pregnancy. Almost all pregnancies occur in the Fallopian tube.
the most common clinical presentation of ectopic pregnancy is first-trimester vaginal bleeding and/or abdominal pain
157
Ruptured ectopic pregnancy definition and presentation
If there is a rupture of and hemorrhage from the structure in which the pregnancy is implanted, usually the Fallopian tube, patients can become hemodynamically unstable.
Sudden onset of severe and persistent abdominal pain, syncope and hemodyanic instability. Clinical dx made primarily on finding of echogenic fluid in the pelvic cul-de-sac during POCUS
158
Ruptured AAA tx
Dissection SBP <120-100mmHg with HR 55-60
Actually rupture is a surgical emergency, end-vascular or open repair of the rupture. High mortality.
159
AAA rupture presentation
Dead.
Ruptured AAA is uniformly fatal, with death occurring within hours. Hemodyncamilly unstable patients with known AAA who present with classic symptoms (hypotension/backpn/pulsatile mass) should be taken directly to the OR for immediate control of hemorrhage and repaid of the aneurysm.
160
Mesenteric Ischemia definition
Ischemia affecting the small intestine is generally referred to as mesenteric ischemia.
161
Mesenteric ischemia patho
Occlusive arterial obstruction is due to acute embolism or thrombosis and most commonly affects the superior mesenteric artery
Venous thrombosis is due obstruction of the intestinal outflow tract, including the superior and inferior mesenteric veins and splenic and portal veins.
Non-occlusive mesenteric ischemia is a result of low-flow state and is most commonly due to vasoconstriction from low-cardiac output or the use of vasopressors
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Bowel obstruction definition
bowel obstruction occurs when the normal flow of intraluminal contents is interrupted. either functional obstruction or mechanical
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Bowel obstruction patho
Mechanical obstruction is caused by either intrinsic luminal obstruction or extrinsic compression of the small bowel - hernias, malignancies, and infective/inflammatory disorders
- Obstruction leads to progressive dilation of
- The bowel will become edematous, normal absorptive function is lost and fluid is sequestered into the bowel lumen. Then ischemic necrosis of the bowel is most commonly caused by twisting of the bowel
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pancreatitis definition
Acute pancreatitis is an inflammatory condition of the pancreases by enzyme-mediated auto digestion
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Pancreatitis patho
The bile duct from the gallbladder and liver connects to the pancreatic duct, which connects to the duodenum. Normally, the pancreas releases exocrine digestive enzymes into the intestine. In acute pancreatitis the inflammation damages and destroys the pancreatic cells and digestive enzymes are released in the pancreas itself and not into the duct, damaging tissue and vasculature. ++ lipase in the blood
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pancreatitis etiologies - GETSMASHED
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Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom
Hypercalcemia/lipidemia
ERCP
Drugs
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SAH 6 complications
1. rebreeding
2. seizures
3. hydrocephalus
4. arrhythmia
5. Na+ disorders (CSW, SIADH, DI)
6. Vasospasm
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Cerebral salt wasting patho
CSW is characterized by hyponatremia and ECF depletion due to inappropriate sodium wasting in the urine. occurs due to hypothalamus and
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SIADH defintion
the SIADH is a disorder of impaired water excretion caused by the inability to suppress the secretion of ADH
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SIADH patho
often involves the hypothalamus. ADH secretion results in a concentrated urine and therefore a reduced urine volume. This leads to water retention, which increased TBW, which lowers plasma concentration by dilution.
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SIADH Tx
HTS 3% 50-100ml/Hr
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UGIB definition, patho and causes
UGIB - any bleeding proximal to ligament of Treitz. BUN:Cr ratio >30 suggests UGIB.
presents with hematemesis (vomiting blood or coffee-ground like emesis and/or melon)
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UGIB Treatment
ABCs etc, type and screen, avoid intubation as possible to allow for resuscitation first.
- transfuse 1:1:1, reverse coagulopathies
- give PPI
- give octreotide (25mcg bolus then 25-50mcg/hr)
- balloon tamponade
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LGIB
Bleeding distal to ligament of Treitz
| -acute lower GI bleeding refers to blood
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LGIB causes
diverticular disease, vascular extasia, mesenteric ischemia, mocker's diverticulum
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CSW tx
HTS 3% 50-100cc and fludrocortisone 0.1-0.3mg/daily
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DI definition
Diabetes inspidus is characterized by decreased release of ADH resulting in variable degree of polyuria
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Diabetes Inspidius patho
occurs with damage to hypothalamus and decreased ADH production, results in increased sodium and polyuria
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DI Tx
replace ADH with DDAVP 2mcg q 12 hours or vasopressin 0.03units/min
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acute kidney injury definition
AKI is an abrupt and usually reversible decline in GFR. This results in an elevation of serum blood urea nitrogen (BUN), creatinine, and other metabolic waste products thet are normally excreted by the kidney
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patho of AKI, pre/intra/post renal injury
Pre-renal: decreased perfusion of normal kidney, hypovolemia, poor cardiac output, renal artery and small vessel disease.
Intra-renal: Glomerular injury - glomerulonephritis (nephrotic syndrome), tubular - acute tubular necrosis, interstitial disease and vasculitis.
Post-renal injury: obstruction to urinary outflow, ureter - renal stone, urethras and bladder outlet - prostate enlargement
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AKI RF
Meds - NSAIDS, ACE-I, ARBs,
Drugs - cocaine, etoh,
Contrasts - iodinated contrast
systemic disease - gout, HTN, CAD, sepsis, hepatic disease, malignancy
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AKI mgmt summary
1) ID patients who need to go for urgent RRT
a) hypervolemia with pulmonary edema
b) severe hyperkalemia
c) life-threatening ureic syndrome
d) toxic exposure
2) volume assessment and mgmt
3) manage electrolytes and balances
4) manage acid-base disturbances
5) hemodialysis indications
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Hemodialysis indication
- refractory hyperK
- refractory hypo/hypernatremia
- hypervolemia with pulmonary edema
- uremia with pericarditis/seziures
- refractory acidosis (<7.1)
- dialyzable toxins - lithium, asa, methanol, ethylene glycol,
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kidney damage is identified by
presence of albuminuria
186
decreased kidney function is ID by
eGFR < 60mL/min
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general difference between HHS from DKA
they are differentiated by absence of ketoacidosis and degree of hyperglycaemia.
188
DKA pathophysiology
1. The damaged pancreas results in a decrease production of insulin, this creates an increase in gluconeogenesis, and decrease in glycolysis, resulting in hyperglycaemia creating polyuria, polydipsia and glucosuria.
2. Theres also an increase in lipolysis, which creates free fatty acids that go to the liver and undergo ketogenesis, which produces more ketones resulting in hyperketonemia. Ketones are acidic, resulting in pH drop.
189
DKA definition
is characterized by the triad of hyperglycaemia, anion gap metabolic acidosis and ketonemia.
190
DKA aetiologies (5 I's)
1. infection
2. intoxication
3. infarction
4. inappropriate withdrawal from insulin
5. intercurrent illness
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HHS Definition
Progressive hyperglycaemia and hyperosmolarity in patients with poorly controlled T2DM and limited access to water and commonly a precipitating illness
192
HHS pathophysiology
Progressive hyperglycaemia and hyperosmolarility in patients with poorly controlled T2DM
Three main factors:
1. insulin resistance
2. inflammatory state with pro inflammatory cytokines resulting in increased hepatic glugoneogesis and glycogenolysis
3. osmotic diuresis and renal excretion of glucose
Because of hyperglycaemia, water is pulled into the intravascular compartment. Kidneys aren't able to reabsorb this much glucose, so a lot of glucose is lost in the urine where water continues to follow (polyuria).
- Creating a loss of intravascular volume and high concentration of osmotically-active solutes (hyperosmolarity)
- T2DM insulin that's present inhibits keto genesis pathway
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tPA MOA
Tissue plasminogen activator converts plasminogen to plasmin which breaks down cross-linked fibrin to several fibrin degradation products
194
Phases of hemostasis
1. vasoconstriction
2. primary hemostasis - platelet aggergation
3. secondary hemostasis - coagulation cascade
4. fibrinolysis
5. regeneration
195
Activated Partial thromboplastin time (aPTT)
is used to assess deficiencies or inhibitors of the intrinsic pathway factors and common pathway factors
196
Anti-Xa assay are used to measure
the anticoagulation activity of an anticoagulant that inhibits clotting factor Xa such as heparin, LMWH, and fondaparinux
197
INR international normalized ratio
INR= PT/mean normal PT
198
Prothrombin Time
the PT is used to assess deficiencies or inhibitors of the extrinsic pathways
199
D-dimer
are breakdown products generated by the action of plasmin on cross-linked fibrin
200
APAP overdose pathophysiology
• Pathophysiology:
○ Tylenol is metabolized 97% by glucuronidation, sulfation and 3% by CYP450.
○ The CYP450 converts Tylenol into NAPQI, which is broken down by glutathione into non-toxic metabolites.
○ During Tylenol OD, Glutathione levels get depleting leaving high levels of NAPQI.
○ NAPQI are hepatotoxic resulting in liver damage
The nomogram is used to direct decision on time and APAP levels for NAC treatment.
201
Tylenol metabolism
```
○ Glucuronidation
○ Sulfation
○ CYP450 + Glutathione
○ Unchanged
§ NAPQI created cellular toxicity
§ NAPQI builds up and results in hepatic necrosis
NAPQI is the cause for APAP toxicity
```
202
principle of therapy for Tylenol
```
○ NAC (N-acetylcysteine)
§ Enhances sulfation
§ Glutathione precursor
§ Glutathione substrate
Free radial scavenger and antioxidant
```
203
Hypernatremia fluid replacement equation
Desired water replacement in first day in ml = 3ml/kg bodyweight x 10 (then divide by 24 to get hourly rate; and add the additional water losses)
204
how do you manipulate Flow (vCalc)
product of Vt and iTime
205
How do you adjust PIP
I-Time, and decrease flow (Vt) and decrease resistance
206
liver cirrhosis patho
An increase in intrahepatic vascular resistance due to architectural distension and deficiency of NO
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Varices patho
Varices develop from the esophagus and stomach dilation of preexciting vessels and active angiogenesis. They increase in size with the severity of portal HTN and can rupture with bleeding when the pressure exceeds a maximal portion
208
Portal HTN
results from combination of increased intrahepatic resistance and splanchic arterial vasodilation.
209
varices medical mgmt
vasopressin, octerotide, blood, Blakemore
210
Surviving sepsis campaign advocates for one hour bundle that focuses on protocolized care that includes the following:
- obtain lactate levels
- get cultures
- source control
- start broad spectrum empiric antibiotics
- give 30cc/kg fluid bolus for hypotension or lactate >4
- start vasopressors if MAP remains <65 during or after fluid bolus
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Sepsis definition
○ Life-threatening organ dysfunction caused by a dysregulated host responsive to infection
Organ dysfunction defined as an increase of two or more points in the SOFA score
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Septic shock
- Fullfill the criteria for sepsis
| - despite adequate fluid-resuscitation requires vasopressors to maintain a MAP >65 and a lactate > 2
213
Simple heart failure definition
inability of the heart to meet the metabolic demands of the body at normal ventricular filling pressures, implies impaired function
214
Simple definition of cardiomyopathy
Refers to a group of disease of the heart muscle. Implies altered structure.
215
Urine Alkalinization
Ion trapping
| Acids are ionized in alkaline environment
