Quick n dirty Patho Flashcards
Pneumothorax definition
gas within the pleural space
PTX hx
dyspnea, pleuritic chest pin, spontaneous, trauma, iatrogenic
PTX Physical
tachypnea, tachycardia, decreased AE, hypoxemia, high PIP + pPlats, subcutaneous air, hyperresonance, (obstructive findings: JVP, hypotension, tracheal deviation)
PTX imaging
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
PTX Tx
chest tube, or leave if not significant
Massive HTX definition
1500ml release, or 200ml over 2-4 hours =
Massive HTX tx
emergency thoracotomy
HTX defintion
blood within the pleural space is termed hemothorax. often from aortic rupture, Myocardial rupture, injuries to hilarity structures, lung parenchyma, or intercostal vessels
HTX imaging
CXR - whiteout
POCUS - anechoic fluid ++spine sign
HTX tx
chest tube 4/5th intercostal
Pulmonary Embolism definition
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
PE hx risk/clinical
risk: hypercoag, vessel injury, venous stasis.
clinical: dyspnea, CP, cough, dvt, shock, sudden death (hemoptysis associated with PE infarction )
PE imaging
CT or VQ scan
PE Tx
- UFH
- very conservative volume optimization
- norepi, dobutatmine +/- e[I
- embolectomy
- tPa (for hemodynamically unstable patients)
Massive Hemoptysis definition
life threatening hemoptysis when hemoptysis results in life-threatening event including significant airway obstruction, significant abnormal gas exchange, or hemodynamic instability
massive hemoptysis hx
bronchiectasis, cystic fibrosis, TB, myectomas, lung cancer
massive hemoptysis imaging
bronchoscope, CXR, CT-A
massive hemoptysis tx
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
CAP definition
CAP is defined as an acute infection of the pulmonary parenchyma in a patient who has acquired the infection in the community
Dx of CAP
CAP generally required the demonstration of an infiltrate on chest radiography in a patient with clinical compatible syndrome
PNA hx
fever, cough, pleurite chest pain, sputum production, tachypnea
PNA imaging
infiltrates on plain film is considered the gold standard for dx pneumonia when clinical and microbiologic features are supportive
PNA TX
empiric treatment directed at the most likely pathogens to start
RV spiral of death
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
causes of severe RV afterload
PE, Severe PH
RV failure imaging
parasternal long n short, CT
RV failure potential tx
potentially diuresis, norepinephrine + dob, +e/- epi
-not more fluids
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
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
3 common causes of ARDS
sepsis, PNA, trauma
ARDS treatments
VILI, use of sedatives, potentially paralytics, hemodynamic mgmt, nutritional support, glucose control, DVT, prophylaxis, and GI bleeding, conservative fluids
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
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
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
asthma imaging
CXR = hyperinflated, flattened hemi-diaphragms
Asthma Treatment
- inhaled IV steroids (decreases IgE)
- ventolin (B2 agonist)
- atrovent (anti-muscarinic)
- NIPPV
- High flow for MV (consider ZEEP )
Asthmatic Dynamic hyperinflation ( I can condense this more…)
- expiration usually occurs as passive movement
- resistance to airflow (bronchospasm) results in decreased expiratory flow
- decreased expiratory flow results in longer time required to expire the full Vt
- if expiration is interrupted before its natural end by the next inspiration, some unexpired residual gas remains in the chest
- this gas exerts a pressure onto the respiratory circuit
- as a result the alveolar pressure at the end of expiration is higher than zero (zero being atmospheric)
- this process of incomplete emptying is called dynamic hyperinflation, and the positive pressure alveolar pressure is called intrinsic PEEP or auto-PEEP
AECOPD defintion
AECOPD has 2 of the following
1) worsening dyspnea
2) increased sputum production
3) increased purulence
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
COPD imaging
CXR - very dark, hyperinflated, flattened hemi-diaphgrams, potentially increased pulmonary vasculature (PH) +/- blebs
COPD tx
ventolin atrovent steriods abx NIPPV MV
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
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»_space; than expiratory volumes significantly
Treatment of DHI in COPD
- change vent settings (decrease RR, decrease I-TIME, prolong expiratory time)
- Reduce demand (reduce anxiety, pn, fever)
- reduce flow resistance
(suction, use large ETT, bronchodilator) - counterbalance expiration flow limitations
(external PEEP)
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
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
Central cord syndrome
MUDE Motor loss Upper extreme > lower loss Distal worse than prox -extension injuries
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
spinothalamic
pn/temp
crosses over 1-2 vertebrae above
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
upper motor neuron
CNS/spinal cord
lower motor neuron
PNS
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
summary effects of PEEP on RV
1) decrease venous return
2) decreased hypoxia pulmonary vasoconstriction
3) increased pulmonary vasculature resistance due to vascular compression
Increased PIPs with normal pLats
Resistance Issue.
worsening asthma, obstruction of ETT, excessive airway secretions, clogged HME, small ETT, high flow rate
Increased PIP with elevated pPlats
PTX, ARDS, PNA, Pulmonary edema, atelectasis, pleural effusion, bronchial intubation.
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
5 effects of PEEP on pulmonary system
- increased FRC
- Decreased in intrapulmonary shunt
- Reduction of alveolar opening and closing (preventing atelectacto-trauma VILI)
- increased in intrathoracic pressure (decrease venous return, decrease in LV transmural pressure -> afterload)
- Distention of normally aerated alveoli
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
Glucose targets in sepsis
4.5-6 mmol/L as per NICE-SUGAR trial
Sepsis Physical
- bend the neck (meningitis)
- listen to all lung zones (PNA)
- listen for murmurs (endocarditis)
- palpate RUQ (billiary)
- palpate flanks (nephritis)
- Palpate belly (perforation/ileus)
- examine the skin (necrotizing fasciitis)
reasons to treat seizures prophylactically, maybe.
- hx of seizures/current seizures
- temporal lobe pathology
- depressed skull #
- penetrating trauma to cranial vault
CCP goals of care for TBI
- cerebral blow flow
- venous outflow
- brain parenchyma
when to consider ETT with SCI
- use of spinal access muscles (shrug shoulders/tracheal tugging)
- no bicep curls
Sepsis approach
- source control
- Abx
- Optimize VO2/DO2
- Adjuncts ( steroids, Vitamin C)
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)
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
equation of EF
SV/EDV X 100
Oxygen Consumption equation
CO= CaO2-CvO2
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
End organ perfusion markers
aloc, lactate, urine output cap refill, look at their trends, scvo2
Atherosclerosis pathophysiology
- LDL can deposit in the tunica intimacy, and then become oxidized.
- Oxidized LDLs activate the endothelial cells to attract WBCs
- Monocytes enter the tunica intimacy and become macrophages, and macrophages take up these oxidized LDLs and then become foam cells.
- Foam cells eventually die, spilling out their lipid content, which grows the plaque and increases its pressure.
- The plaque then can rupture and cause coagulation, causing thrombus, impeding blood flow.
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
Rescue PCI
after failed lysis, st resolution <50%, ongoing ischemic changes, shock
Facilitated PCI
Use thrombolysis to “facilitate” a smoother PCI
Elevated troponin without ECG changes
type 2 MI, supply and demand.
increased demand from systemic critical illness
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
Heart Failure triple therapy
- ACE-I
- Beta Blockers
- Spironolactone
Acute decompensated Heart failure Forrester classification
- Dry + Warm (adequately perfused, hemodynamically compensated)
- Dry + Cold (Hypoperfused and hypovolemic)
- Wet + warm (congestion but well-perfused)
- Wet + Cold (congested and hypotensive)
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
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)
Dilated cardiomypathies causes
- Genetic
- Infection
- Systemic Immune-Mediated Disease
- Toxic and overload
- drugs
- Endocrine/metabolic
- Peripartium
Dialated cardiompathy treatments
adress underlining cause, treat heart failure, prevent arrthymia, prevent thromboembolic events, heart transplant
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
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.
Treatment for Aortic Stenosis
Preload: increased
Afterload: normal
HR: Decreased
Contractility: Increased
