Dr Bernadoni Right Heart Failure

PULMONARY HTN +  RV SPIRAL OF DEATH-

Definition is mean pulmonary artery pressure >20mmHg (on R heart cath). This can be estimated based on PA pressure >35 on echo

• In patients with acute PE or with chronic pHTN and an acute VQ mismatch (eg pneumonia)

• This is translated as an increased afterload on the RV, which does not tolerate this well. Pt becomes hypotensive, shocky.

• Of note the LV will appear underfilled and hypokinetic on XR- this does not represent hypovolemia and the heart will not respond well to fluid administration.

• RV vs LV perfusion- LV gets perfused only during diastole, whereas under normal circumstances the RV gets perfusion throughout the cardiac cycle. When pHTN is present (and right heart pressures are subsequently high) the transmural pressure across the RV only allows perfusion during diastole, causing ischemia and reduced contractility. It can also leads to relative or bradycardia through hypoperfusion of the SA/AV node

This group of events is known as the RV spiral of death.

HOW TO AVOID IT-

Fluids-

These pts are rarely volume responsive in a good way. Fluid administration pushes them further into above spiral

(In the setting of PE or chronic RHF/pHTN) when patients have evidence of R heart failure on echo (dilated RV, Mcconell’s sign, low TAPSE) they will not respond well to further fluid administration.

If their RV looks small/empty too, may consider a very small fluid bolus and evaluate for effect.

Most patients will benefit from diuresis, even when they are hypotensive and have LV underfilling (diuresis improves RV function and allows the pt to better fill their LV and increase their CO

PRESSORS

Instead, aggressively support MAP with pressors-

Aim is to raised MAP without raising pulmonary blood pressure

• Norepinephrine is go to- increases contractility, gives peripheral vasoconstriction and at low doses should increased pulmonary vascular constriction much
• Vaso is next line- gives peripheral vasoconstriction but actually reduces pulmonary pressures- this is exactly what is wanted
• Can consider dobutamine as third line- start at 5mcg/kg/min

AIRWAY MANAGEMENT (+INHALED MEDS)

• Intubation should be avoided if at all possible.
• Consider use of nitric oxide prior to intubation (via BIPAP/HFNC)- see below
• Paralysis causes hypoxia and hypercarbia- leading to hypoxic vasoconstriction and worsened pulm HTN and RV afterload
• PPV increases RV afterload and reduces output

SO:

• Have push dose pressors ready and strongly consider placing an arterial line prior to intubation
• Have atropine at bedside
• Use etomidate for sedative (ketamine may increase pulmonary vascular resistance)
• Do not use straight RSI- continue ventilation (bagging or BIPAP)
• Can break from ARDS net protocols and consider high FiO2 without raising PEEP as much as normal. Keep plateau AND PEAK pressures low

If pt remains hypotensive/hypoxic use inhaled nitric oxide- start at 40ppm

Or consider inhaled epoprostenol

In the absence of the above nebulize 5mg of nitroglycerin

SYSTEMIC VASODILATORS

Many chronic pHTN pts have continuous vasodilator pumps running

If pt has pump failure/otherwise their systemic meds are stopped restart them at the same dose immediately. They can be given peripherally if necessary

MASSIVE PE

SBP <90 for 15mins (submassive PE is with RV strain based on trop, BNP, echo etc)

• Thrombolysis if bleeding risk is acceptable (this is a case by case decision taking into account a large number of factors). Note that is unclear how much thrombolysis actually causes bleeding in acute PE (studies show similar rates of bleeding with heparin alone cf heparin and tpa)
• In patients with a pulse typical is 100mg IV tPA over 2h. Can give 10mg as a push and the other 90 as an infusion over the 2 hours
• In cardiac arrest 50mg IV push
• Note above doses have minimal evidence base.
• Run heparin concurrently

INTERVENTIONAL THERAPY + ECMO

Catheter directed therapy recommended in patients with high bleeding risk, tPA contraindicated. This should initially be percutaneous embolectomy, can use catheter directed thrombolysis (tPA) if unsuccessful.

ECMO- Extra-corporeal membrane oxygenation

In PE ECMO is run Venousà Arterial (VA ECMO).

This allows circulation to bypass the heart and lungs, bypassing the failing right heart and the elevated pulmonary pressures. Helpful with the R heart failure of PE (or the reduced CO in STEMI, myocarditis, low+slow poisoning etc)

In patients with pure lung pathology (ARDS, asthma, pulmonary contusion) it can be run Venous-Venous (VàV), which bypasses the lungs but still requires good cardiac function

Consider ECMO if non ECMO mortality is >50%, even more so if >80% (and has ECMO responsive pathology)

Reserve for pts likely to have benefit (reversable cause of current illness, no major life limiting comorbidities or advanced age) and less likely to have harm (pts require heavy anticoagulation so those with high bleeding risk are likely to be harmed)

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Josh Senn- GU abx

• Don’t treat asymptomatic bacteria (>10⁵ CFU) without symptoms unless pregnant or a guy pending a urological procedure

• Use nitro 100 bid (if CrCl >30) or cephalexin qid for 5 days for uncomplicated UTI in a male or female

• Chlamydia- use 1g azithromycin PO one time. Use doxy 100mg BID for 7 days if PID. Second line levofloxacin, erythromycin, ofloxacin.

• Gonorrhea- Ceftriaxone 250mg IM x1 (+azithro or doxy). Alternatives are cefixime or gentamicin + azithro

• Trichomoniasis- metronidazole 500mg PO BID x7 days has higher cure rate than 2g one time. Topical gel does not have good cure rate. Alternative is tinidazole

• BV- 500mg BID x 7 days, can use vaginal gel BID x 7 days. Alternatives are clinda or tinidazole

• Benzathine penicillin 2M units for primary or early latent. More complex with neurosyphilis

Avery- phimosis and paraphimosis

Conditions presenting in uncircumcised or partially circumcised males.

Phimosis-

Inability to retract the foreskin

This is not an emergency. It is present physiologically at birth but most males can retract by age 5-7.

Becomes pathological when a constricting band forms between glans and foreskin.

Do not retract forcefully- treat with topical steroids and gentle daily traction, admit to urology if there is urinary obstruction

Paraphimosis-

Inability to protract the foreskin

Can cause necrosis within hours to days

Tx is manual reduction-

• Pretreat with ice/mannitol/sugar
• Dorsal penile nerve block
• Hold foreskin between index and middle finger of both hands, use both thumbs to push the glans whilst pulling the foreskin
• If this fails can consider protraction using forceps, multiple need punctures to foreskin to allow improvement edema, or aspirate glans
• As a last resort, to be performed if the above techniques fail AND urology is not available, incise a dorsal slit using scalpel, protract foreskin and then suture the inflicted wound

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Dan- Testicular torsion-

Usually caused by an abnormal fixation of the testicle within the tunica vaginalis (when present this is usually bilateral)- most commonly the bell-clapper deformity

Bimodal distribution- perinatal and at puberty. Can occur at any age but is less common over 40.

HPI/Exam

• Unilateral testicular/flank/lower abdominal pain. This is not usually positional. May be atypical or colicky pain
• In children commonly presents only as vomiting or abdominal pain
• Testicle is usually firm, elevated and in transverse lie
• Unilateral loss of cremasteric lie may increase suspicion but is not specific and is not always present/easy to identify

Differential-

• Appendiceal torsion- isolated torsion of the testicular appendix- presents with more focal pain on the posterior portion of the testicle- ‘blue dot sign’ may be seen
• Epididymitis/epididymo-orchitis- inflammation, most commonly infectious of the epididymis and/or testicle. Most commonly cause by STI in those <35, UTI in those >35 (though this is not a hard/fast rule). Look for isolated tenderness over the epididymis, symptoms of infection, prehn’s sign

Mx-

• If the diagnosis is clear contact urology immediately
• In the meantime provide supportive care
• If urologist is delayed or not available can attempt manual detorsion- manually rotate the affected testicle externally- ‘open the book’. Most testicles torse internally (internal rotational) and so the opposite motion is used to detorse. However, not all testicles torse internally, so this could worsen the patient’s condition. When effective, 540 degrees of external rotation is usually required

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Austin- Hernias-

Abnormal exit of tissue or an organ through the wall of a cavity within which it normally resides

Most common-

• Inguinal hernia- presents as groin mass. Direct inguinal hernias pass through the transversalis fascia in the Hesselbach triangle (triangle formed by inguinal ligament, rectus abdominis and the inferior epigastric vessels). Indirect inguinal hernias pass through the internal and external inguinal rings
• Ventral hernias- bowel passes through a defect in the anterior abdominal wall- can be umbilical, epigastric, incisional
• Femoral- bowel protrudes through the femoral canal. These are much more prone to strangulation and incarceration, and require urgent f/u, even if not currently incarcerated/obstructed/strangulated
•     Protrusion of the stomach through the diaphragm and into the thorax- often presents as ‘heartburn’/epigastric discomfort

Hernias should be soft, non-tender and reducible.

• Incarceration is the inability to reduce the hernia back into the cavity within which it should reside. This term is used when blood flow to the herniated section of bowel is maintained. Symptomatic hernias should be reduced in the ed to avoid strangulation.

• Strangulation is when blood flow to the hernia is impaired- this causes ischemia, necrosis, perforation, sepsis. These should NOT be reduced as this makes the ischemic portion of bowel difficult to find and moves potentially necrotic tissue back into the abdomen, causing infection. Strangulation should be suspected in a pt with significant pain, tenderness, any skin change or findings of ischemia on ct/elevated lactic acid.

Reduction-

• Grasp and elongate the hernia neck with one hand whilst applying steady pressure to the proximal portion of the hernia at the neck of the fascial defect. Pushing on the most distal portion of the hernia simply causes the hernia to bulge more proximally, preventing reduction through the fascial defect

Complications of reduction-

• Risk of reducing strangulated bowel
• Reduction en masse- this is reduction of the majority of the hernia, often with improvement in symptoms. However small portions of bowel can remain incarcerated and remain at risk for strangulation. Watch hernia patients post reduction to ensure complete resolution of symptoms- consider ct/ultrasound/surgical review if any ongoing symptoms

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Dr McGee Renal Emergencies-

Indications for emergent hemodialysis-

A- Acidosis- dialyze for pH <7.1

E- Significant electrolyte abnormality- especially hyperkalemia

I- Intoxications

O- Overload/oxygenation

U- Symptomatic uremia

Consider rhabdomyolysis as a cause for renal failure, especially in pts unable to provide good history. Tip offs are hepatitic pattern LFTs and dipstick hematuria without blood on micro.

Hyperkalemia-

Weakness, symptoms of causative pathology, AMS.

EKG changes with peaked T waves, prolonged QRS à sine wave

EKG changes do not always progress smoothly through the above stages- pts can go from NSR with narrow qrs to asystole very quickly.

Mx-

• Stabilize the membrane- with calcium. Gluconate if stable, chloride if unstable or if pt has central access
• Move the potassium back into the cells- Insulin and glucose, fluids, albuterol, bicarb if acidotic
• Typically 10 units of insulin in 1 amp of d50 is use, but this depends on the pt. if they are normoglycemic consider 2 amps of d50. If they are very hyperglycemic may consider not giving glucose. REGARDLESS, IT IS IMPERATIVE THAT BLOOD GLUCOSE IS CHECKED REGULARLY TO MONITOR FOR HYPOGLYCEMIA
• Give fluids- LR does contain potassium but the amount is negligible and not clinically significant. LR is a better choice than normal saline as the NAGMA caused by NS will increase potassium more than the minimal potassium contained in LR
• If acidotic- can bolus bicarbonate and then use 2-3 amps of bicarbonate in d5w for fluid resuscitation/maintenance
• If the patient is volume overloaded use furosemide. If normovolemic give fluids and furosemide. Can discuss diuretic use with renal if pt is hypovolemic/dry.
• Dialysis if all else fails

Drug intoxications-

Many drugs can be dialyzed out of the blood stream-

• LEMS mnemonic
• Lithium
• Ethylene glycol
• Methanol
• Salicylates
• (and others- these are the most commonly encountered clinically)

Discuss with poison control

Uremia-

End organ damage-

• Pericarditis or uveitis
• Uremic encephalopathy
• Bleeding- uremia causes platelet dysfunction

Hemodialysis access-

• Short term dialysis access- shiley/trialysis catheter- a necessary skill for EM
• Medium term- Tunneled dialysis catheters
• AV fistulas- most commonly brachiocephalic
• Peritoneal dialysis catheters

Complications of AV fistulas-

• Acute bleeding- direct pressure with a finger may stop bleeding. TXA soaked gauze may help. Avoid tourniquet placement if possible. Figure of 8 sutures can be placed if necessary, though above options should be exhausted prior. Note that heparin is given during hemodialysis- if bleeding is hard to control can give protamine, though risk of allergic reaction is common. DDAVP can improve platelet function in pts with azotemia.

• Call vascular for any fistula or graft issues

• Infected HD catheters can cause sepsis. Look at the site. Metastatic infection from the catheter is also common and can cause septic arthritis, osteomyelitis etc

• PD patients should always have clear peritoneal fluid. Abdominal pain/fever in a PD pt can be a sign of peritonitis. Dx for PD related peritonitis is different than SBP when assessed with fluid microscopy. >100 PMNs or >50% PMNs is suggestive of infection

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SANE lecture

Sexual Assault Nurse Examiner

Purpose is to evaluate and treat victims of sexual assault, collect evidence and document injuries

See male and female victims of sexual assault age 12 or older

Injury terminology-

Contusions- These are bruises. Either term is acceptable. Do not attempt to date bruises, though it can be stated that bruises are in different stages of healing

Abrasions- Scrapes/grazes/road rashes are abrasions. Vaginally, these are most common at 5 and 7 o clock.

Petechiae- burst capillaries, appearance like paint splatter. Can be the result of direct pressure or of strangulation

Incised wounds are not lacerations and should not be documented as such. Incised wounds are inflicted by sharp objects such as a knife or a piece of glass. When these are described as lacerations it may cast doubt on the mechanism of injury/use of weapons. Simple puncture wounds should be described as such – ‘puncture wound’.

Pattern injuries are bruises/contusions whose shape is suggestive of a specific mechanism (eg a bat, a bite mark). Describe these injuries as pattern injuries and document the patient reported mechanism of injury. Photographs and forensic experts will determine mechanism

GSWs- Describe as GSW or penetrating injury. Do not document entry/exit wounds- photographs and expert review will determine this

Royalty- CCU Follow Up
CASE-
37yo M, GSW to chest
Awake, stable.
RUQ fluid, no pericardial effusion.
Bullet fragment in pelvis on xray, cxr unremarkable.

Ex-lap w extensive intra-abd injury
Trans diaphragmatic pericardial window performed

POD2 pt develops chest pain
EKG with anterior q waves. Upright T wave in V1.

LEARNING POINT – Assess precordial T wave balance when you see an upright T wave in V1. Typically T waves should be more upright in V6 than in V1. If they are more upright in V6 consider ischemia in the right clinical setting.
(exceptions include LVH, LBBB, others)
BACK TO THE CASE
Pt’s troponin returned elevated and went for cath- 90% LAD, LCx with total occlusion, RCA with 90%

Pt was diagnosed with T2 NSTEMI due to low flow state in the setting of chronic obstructive CAD without acute plaque rupture

TAKE HOME-
Beware upright T waves in V1- suggestive of underlying or acute ischemia
In this setting assess precordial t wave balance
Always follow serial EKGs when concerned for ischemia

Additional discussion-
Look for signs of prior MI, may act to increase suspicion/pre-test probability for acute MI

Type 1 MI- ischemia secondary to plaque rupture
Type 2 MI- ischemia secondary to reduced blood supply (often in the setting of chronic CAD

Weeman- MICU f/u

CASE
38yo F G6 P4 presents at 20W+1D. dyspneic, pleuritic chest pain.
PMH with protein S deficiency, prior TIA during a previous pregnancy
Uses enoxaparin, methadone. Hx of drug use and alcoholism
On exam pt is in resp distress, 92% on 14L NRB. B/L reduced breath sounds
No obvious DVT
Workup w bilateral CXR infiltrate- ARDS pattern, TTE with EF 69%.

– Pt was admitted to MICU, 45L, 100% on HFNC. On abx and steroids

– Gradually worsened, became uncooperative but was eventually intubated around 1 week into stay.

– All infectious cultures and covid swab were negative, abx were stopped

– Eventually weaned vent and extubated to 4.5L NC. Sent to floor, began to deteriorate but refused ICU. Overnight BIPAP on the floor, then to HFNC and moved to ICU

– On return to ICU was started on 40mg methylprednisolone 40mg q8 and improved, transferred to floor and now on 2L

Dr Hart Neonatal ED Presentations
INTRODUCTION
Normal neonates undergo significant stress + change-
Drop in pulmonary pressures causes increased pulmonary circulation
PDA closes

Most common ER attendances are jaundice, difficulty breathing, fussiness, feeding problems, stooling issues and irritability/lethargy

Fussiness
****Differential- IT CRIES****
– I- infection
– T- Trauma.tourniquets
– C- Cardiac disease
– R- Reflux/rectal fissure, reaction (to meds)
– I- intussusception
– E- Eyes (corneal abrasion, foreign body, glaucoma)
– S- strangulation, surgical process (hernia, torsion, volvulus)
**Do a FULL exam**- take special note of HEENT, HR/monitor, GU, extremities for tourniquet, fracture, septic joint
Hair tourniquet- Usually extremities. Also penis/clitoris. Can usually unwind w forceps. If required can incise through hair, skin.
Corneal abrasions- Look for conjunctival injection. Flurorescein stain

Jaundice-
Newborn jaundice is usually catabolism of hb  unconjugated
First thing is to send fractionated bili to assess
Unconjugated causes- Physiologic, breast milk jaundice, Hemolysis- ABO incompatiblity
Conj-

Jaundice in first 24 hours of life is ALWAYS pathologic

1- Send fractionated Bili
2- Compare this to the normogram to assess home vs inpatient, phototherapy vs exchange transfusion
3- other labs, eg type and screen if requires exchange transfusion

Conjunctivits-
12-24hours of life- Chemical
2-5 days- Gonorrhea
5-14 days- Chlamydia
Gonorrhea is typically more severe and more purulent
Send pus for drain/culture- for either chlamydia/gonorrhea admit for parenteral abx (topical treatment used only for prophylaxis against gonorrhea)

Feeding/stooling problems
Feeding-
Newborns feed on demand, may be small, frequent intake, not concerning unless gaps >4 hours or so
By 1 month usually take 2=4 hours every 2-4 hours
Spitting up often secondary to overfeeding

Stooling-
Rule of 7s- >7 times per day abnormal, 100.4) <4 weeks, or <60 days if they look unwell- full sepsis workup for SBI- CBC, CMP UA, CRP, Procal, LP, urine and blood culture. CXR if resp sx.
Above may change with new literature on use of procal. See protocols in peds ED
Most common pathogens at this age are GBS, E Coli, Listeria (also consider HSV, and if any suspicion at all test and treat early)
Ampicillin and cefotaxime / amp and gent as broad abx coverage (switch ampicillin for vancomycin if high concern for meningitis)
Sepsis mimics- pertussis, CHD, Inborn error of metabolism
Always look for omphalitis- assess the umbilical stump for cellulitis, swelling, drainage, crepitus. This can progress from mild appearance to fatal very quickly (hours) given proximity to central vasculature and peritoneum. Usually cause by staph

Seizure like activity-
Differential- Seizures, infantile spasms, hypoglycemia, benign myoclonus, uncoordinated sucking movements, disconjugate eye movements
Check glucose, check temperature, cbc, rfp, magnesium

Seizure aetiology-
– Perinatal asphyxia/hypoxia/cerebral ischemia
– Infection
– Hypoglycemia
– Hyponatremia How are they making formula (too much water hyponatremic seizures)
– Trauma (SDH)
Seizure neonate mx-
1st Line- Lorazepam 0.1mg/kg
2nd Line- Phenobarbital 20mg/kg (Or levetiracetam 60mg/kg)
If seizures aren’t controlled with above and electrolytes/glucose are normal give pyridoxine (as well as other third line seizure meds)

Congenital heart Disease
Will present with shock, cyanosis, heart failure- poor perfusion, difficulty feeding, respiratory distress, hypoxia, hypotension
Crashing neonate is statistically more likely CHD than sepsis
Get four extremity blood pressures
Note absence of response to O2 suggests cardiovascular abnormality, presence of response suggests pulm
Cyanotic –
– Truncus arteriosus
– TGA
– Tricuspid atresia
– ToF
– TAPVR
– HLHS
Non cyanotic-
– ASD
– VSD
– AV canal
– Coarctation
Have a VERY low threshold for starting prostaglandins in crashing/hypotensive neonate but watch out for respiratory depression.
Once on this pathway target SaO2 of 75-80%
If prostaglandins aren’t working, consider adding inotropes in discussion w pediatric center. Consider dx of persistent pulmonary hypertension. Prostaglandins don’t work- pt’s require hyperventilation, nitric oxide, ECMO

Dr O’Brien- introduction to ED Echocardiography
4 main views used in the ED-
– Parasternal long axis (often PSLAX)- for effusion, EPSS, LVOT diameter, visual assessment of LVEF
– Parasternal short axis (often PSAX)- for AV/MV assessment. For right heart strain, regional wall motion abnormality
– Apical four chamber (often A4C)- For TAPSE, other right heart strain measures, for MV/TV assessment.
– Sub-xiphoid- For pericardial effusion, assessing IVC,
Note that required probe positioning and orientation is variable and depends on the patient, the selected machine settings. Note that all probe positioning should be relative to the heart, not the patient, and so should be learned through repeated exams.
Vast array of skill levels/uses for echo- below is most basic most advanced-
– Most basic is assessing for the presence/absence of pericardial effusion and cardiac activity- easiest in the sub-xiphoid view or the parasternal long axis. In the PSLAX assess the position of the effusion relative to the descending aorta. Anterior to the DA is pericardial effusion, posterior is pleural effusion.

– Then looking at valves (eg mitral regurgitation in a febrile IVDA – might suggest infectious endocarditis)- often via the apical apical 4 chamber

– IVC for respiratory variation in diameter- >2.1cm with <50% collapse with a sniff inhalation (in spontaneously breathing patient) suggests CVP 10 or greater, and poor fluid responsiveness. Find the IVC from the sub-xiphoid position. (note and think about/look for the many possible confounders- tricuspid valve pathology for example)

– Assess LV for systolic function. EPSS (end point septal separation) is the simplest way to do so. Follow the tip of the anterior leaflet of the mitral valve throughout the cardiac cycle on M mode. <6mm separation from the septal wall at the most anterior point suggests normal LVEF. Do this from the parasternal long axis

– Assess for HFpEF by comparing E + A waves just LV side of mitral valve on doppler mode (can do from parasternal short axis

– Assess for RV failure with views of RV for TAPSE, McConnel’s sign. Find the most rightward point of the tricuspid valve (farthest from the septum) and assess range of motion throughout the cardiac cycle on M mode. Distance moved is the TAPSE (<16mm suggests RV systolic dysfunction). Also look for RV-LV diameter >1:1 and apex of RV ‘trampolining’ on the barely moving RV free wall (McConnel’s sign). Directly calculating RV systolic pressure is more complicated.

1- Dhruv Case Presentation-

57yo M Presented with AMS- Tachycardic, hypertensive, and very febrile
Exam- LE and ocular clonus, GCS 10. PERRL size 5
Hx of BPD, Dementia, MDD
On trazodone, fluoxetine- Serotonin drugs
On memantine, olanzapine- neuroleptic
Compensated metabolic acidosis, renal failure and prolonged qtc
Normal CK

Tubed with roc + propofol then started high dose midazolam drip
Presumed dx of serotonin syndrome and started cyproheptadine
Eventually diagnosed with NMS and managed with ECT

Teaching points-
Malignant catatonia- Fever, rigidity, autonomic instability in setting of a previously diagnosed catatonic state

NMS- Dopamine deficiency presents with rigidity, AMS, autonomic instability, elevated CK, low iron, usually within a few days of medication change (note haloperidol, metoclopramide, prochlorperazine, or stopping PD drugs)

Tx for both of above is-
ABCs, stop offending agent, benzos, calls to ICU for further mx

Serotonin syndrome-

• Hyperthermia, HTN, tachycardia, clonus, GI sx
• caused by SSRIs, SNRIs, TCAs, trazodone, fentanyl, ecstasy, MDMA
• tx with cyproheptadine (first gen antihistamine with 5HT activity) and ICU

General-
Consider non infectious causes of seizure, especially withT greater than 104
A- Acidosis, alcohol, ammonia
E- Environmental, electrolytes
I-Infection, ingestion, insulin
O- OD, oxygen
U- Uraemia
T-Trauma, thyroid, thiamine
I-See above
P-Psychosis
S-Stroke, seizure, SOL, syncope

2- Jessica EMS lecture
EMS Models-
Anglo-American model- Brings pt to the healthcare, reduces pre-hospital interventions in the interest of rapid access to well facilitated care
This is more common where EM is a well developed specialty

Franco-German model- Brings healthcare to patient, attempts to reduce use of hospital, and facilitates direct admission to the ward for inpatient care where necessary
This is common in continental Europe

Minimal evidence of benefit from one vs the other

Pre-hospital physicians
In trauma may be some benefit of having pre-hospital physician, though this could be confounded by the higher likelihood of helicopter transport and rapid transport to OR in systems that have pre-hospital physicians
In STEMI physicians may delay transport and worsen outcomes
Physicians usually aren’t required on ambulances, though they may somewhat reduce need for hospital care
Pre-hospital physicians may improve outcomes of OOH arrest

General learning points-
Stroke, STEMI, trauma- pt needs to get to definitive care- MT, PCI, OR.
Highest benefit from rapid transport for definitive care

3- Harrison R9 follow up
21yo M with burns to face following an explosion, given 500 IM ketamine and 10 IM midazolam on scene
A- intact
B- sats 97% on 2L NC
C- normal HR and BP
D- GCS 10 (after meds)

Singed nasal hair
Partial thickness burns to face and hands
No signs of blast injury

CXR clear and FAST negative, COHb 3.6

Trauma, plastics consulted and pt admitted to the ICU

Learning points-
1- Blast injury-
Primary- Blast/pressure wave- affects air filled structures (ears, lungs, GI)
Secondary- Things blast throws at you- shrapnel etc
Tertiary- Blast throws you somewhere
Quarternary- other associated injury (burns, CO, cyanide etc)

2- Blast lung-
Pulmonary barotrauma
CXR- look for butterfly pattern
look for HTX, PTX
PPV may increase alveolar rupture and raise risk of air emobilism
If using MV look for lung protective strategies

3- Inhalation-
Can cause airway swelling or lower respiratory tract injury
Upper airway-
Assess upper airway, consider fibre optic view
Consider intubation for bad oropharyngeal swelling, respiratory distress, soot in the supra-glottic region.
BUT intubation and MV could cause ARDS so it’s a judgement call
If you do intubate use a 7.5 or greater if possible to help with bronchoscopy

4- Dispo-
Normal VS, normal CXR and normal exam without sx can go home
Blast lung goes to the ICU

McKinney Nephrolithiasis Lecture-
See handout for cases
https://drive.google.com/file/d/1yvrwa3Ge6q8WaCgjvug3PLZIn5T6JUJl/view
Most stones are calcium stones- these are radiopaque, recurring and more common in men. First stone is most commonly in 3rd/4th decade of life.
Uric acid stones form as large staghorn calculi, always in the presence of urease forming bacteria. They then form an infectious seed, often resulting in recurrent UTI. Radiolucent.
Cysteine stones in homocystinaemia- rare, radiolucent.
Most stones <5mm will pass spontaneously (but can take 7-30 days)

Differentials + early/POC Ix-
Classic misdiagnosis is AAA. First time kidney stone in middle aged or older patient is less common. Think Aortic emergency
Consider renal and aortic US as screening (but not definitive imaging) and consider CT w contrast / CTA especially in these patients
Females- torsion, PID, TOA
Females child bearing age- pregnancy, ectopic
BMP and lipase (consider pancreatitis), urinalysis (INFECTION, hematuria)

Imaging- Decision is complex
American Urological Society recommends CT if first time, US if recurrent

SGEM consensus statement-
http://thesgem.com/2019/12/sgem-xtra-come-together-right-now-over-renal-colic/
Younger Patients (~35 years old): Even without a history of stones, CT may be avoided as long as pain is controlled (perfect consensus).
Middle-Aged Patients (~55 years old): We recommend CT if there is no history of kidney stones.
Older Patients (~75 years old): We recommend CT regardless of history.
Pregnant and Pediatric Patients: With a typical presentation they should undergo ultrasonography and do not require initial CT if symptoms are relieved.
Radiation Dose: We recommend reduced-radiation-dose CT whenever CT is used for suspected renal colic.

ED Tx-
Simple stones-
Analgesia (NSAIDS best + fastest if patient isn’t pregnant)
Alpha blockers- usually Tamsulosin (these are pregnancy category C, calcium channel blockers such as nifedipine are used instead, though efficacy is questionable)
Fluids don’t expediate passage

ABSOLUTE INDICATIONS FOR ADMISSION-
Intractable pain/vomiting
Urosepsis requires urgent decompression surgery
AKI
Hypercalcemic crisis
Single or transplanted kidney with obstruction

RELATIVE INDICATIONS FOR ADMISSION-
Infection without sepsis or obstruction (may DC if good follow up)
Significant comorbidities
Stone >5mm and located above the pelvic brim
Urinary extravasation

Dr Shaw Cardiovascular Summary-
Pericarditis-
– Widespread ST elevation. CANNOT have ST depression ecept in aVR. Usually concave upwards. Look for PR depression (and PR elevation in aVR), downsloping TP segments. Tx with NSAIDs
Brugada-
-With syncope- cardiac monitoring, admit cards, AICD
– Type 1- wide QRS w RBBB, TWI, coved STE 2mm in V1-3
– Type 2 – saddle back
-Type 3- Either shape with less than 2mm of elevation
-risk of vfib with any type. discuss with cards, always admit if symptomatic

WPW-
-Short PR, delta wave, broad QRS
-Aberrant conduction through an accessory pathway which doesnt have the AVN’s refractory period
– Causes AV re-entry tachycardia.
-When conduction is down AVN and up accessory, this looks like a regular SVT (AKA AV nodal re-entry tachycardia) and can be treated as such
-When conduction is down accessory and up AV node it causes wide complex tachycardia. Looks like VT and could be treated as such but it can be easy to mistake for WPW with AFib so consider electricity or procainamide depending on stability
-Afib with WPW is irregular, with qrs morphology variation from beat to beat and areas of the ekg will have rates approaching 250. This should always be shocked or get procainamide (or ibutilide)
– Monitor, admit for EP, possible ablation

Torsades –
-Polymorphic VT with proven long QTc when in sinus
-Give magnesium
– Shock
– Overdrive pace (pacing at 120bpm) if refractory
Hyperkalaemia
– Causes peaked Ts, broad QRS
– treat with calcium, insulin/glucose, fluids if they can take it, furosemide if they cant. Bicarbonate if they are acidotic. Albuterol may shift intracellularly too. Dialysis may be required with anuria/renal failure. Don’t use kaexelate
– can look like VT but VT usually has rate >120 and hyperkalaemia can have very broad QRS (broader than VT)
– This is important to distinguish because hyperkalaemia is dangerous because the added potassium has similar effect to a sodium channel blocker. Giving amiodarone worsens this
Pericardial effusion / cardiac tamponade-
– Hypotension, muffled heart sounds and JVD
– EKG low voltage, electrical alternans (alternating high/low voltage)
-Alternans should lead you to POCUS assessment for effusion and tamponade

Digoxin-
-EKG- digitalis- Salvador Dali / moustache sign with characteristic st depression. This is normal for patients on digoin, not a sign of toxicity
-In OD cause atrial tachycardia with block, bidirectional VT, bradycardias
– Digibind for K >5.5, life threatening arrythmia, Dig level >10
– Calcium for hyperkalemia is controversial, dosing of digibind is complicated- talk to your tox centre

EKG territories-
-Inferior II, III, aVF- RCA/LCx
-Lateral- V5, V6, I, aVL- Distal LAD + branches (OM etc)
-Septal- V1, V2 – LAD
-Anterior- V2-6- LAD (+/- II, III if LAD wraps around the apex ‘wrap-around’/type III anatomy)
– For reciprocical changes think PAILS-
­Posterior – Anterior – Inferior – Lateral – Septal.
For reciprocal changes take the area of interest, and then go to the next one in the list. For example anterior MI will have reciprocal change in inferior leads

MI medical treatment-
Give thrombolytics if its going to be greater than two hours from first medical contact to PCI center
Treat MI with aspirin (aspirin and thrombolysis are only meds with proen mortality benefit), also nitro if its not R sided (inferior/posterior). Consider thrombolytics, heparin, other anti platelet drugs depending on local policy/case specifics

SVT (AVNRT)-
-With hypotension —> synchronised DC cardioversion
-Stable- Adenosine (6mg —>12mg—>12mg) or Diltiazem
VT-
-Stable- chemical cardioversion with amio, lido or procainamide
– Unstable- Synchronised DC cardioversion

Heart blocks-
-1st degree- prolonged but constant PR- No tx
-2nd degree- Type 1 (wenchebach)- Prolonging PR before a dropped QRS- No tx
– Type 2- Constant PR with intermittent dropped QRS- Tx bradycardia
– 3rd degree- Complete AV block with AV dissociation- Treat bradycardia
-Treat bradycardia (symptomatic) with atropine, epi, pacing,
Transvenous pacing-
-R IJV is preferrable, L SCV if not (but SCV is often used for PPM so dont mess it up)
– Will look like LBBB on an EKG, on monitor will look like STEMI

PPM complications-
– Most common cause of failure is ovr sensing
-Magnet turns off all sensing on a PPM causing PPM to take over entirely
– Magnet causes AICD to trun off
Cardiac arrest-
-Hs- Hypoxia, Hypovolaemia, H+, Hypothermia, Hyperkalaemia
-Ts- toxin, tamponade, thrombus, tension
Dissection-
– control BP nicardipine (to 100-120 systolic)
– Control HR with esmolol (to 50-60bpm)
– Type A (involving ascending aorta) are surgical

Oral Boards:
Have a system/flow/approach, use the grid layout if that helps
Remember to go through AMPLEFRIENDS
Make sure to let the patient know what you’re doing/why.

Cardiac Tamponade:
200-400cc of fluid usually necessary to cause tamponade, faster accumulation more likely to cause tamponade.
Cardiac path (CA, trauma, etc) -> pericardiac filling -> cycle of heart failure to pump against building pressure
Signs: SOA, CP, fatigue, dizziness, elevated JVD, hypotension, narrow pulse pressure, possible cardiomegaly
-Beck’s triad only 10% of the time
EKG: sinus tach or alternans
Dx: clinically, can use US +/- CXR, EKG
Tx: 1L IVF, pericardiocentesis, window

AAA:
50% increase in normal diameter (normal ~3cm)
Infrarenal is most common location (classified by where it starts/location of most superior aspect)
Smoking and Age are biggest RFs, also fluorquinolones (don’t use em)
Asymptomatic Signs: pulsatile abdominal mass
Symptomatic non-rupture: abd pain, back pain, flank pain, limb ischemia
Symptomatic ruptured: pain, hypotension, pulsatile mass. Pain radiating to back.
Dx: Stable gets CTA (non-con CT for those who can’t do contrast). Unstable gets OR (CT surg or vascular) if known AAA, if unknown then US.
Tx: crossmatch 6U, pain control, esmalol/labetalol/nitroprusside (permissive hypotension 80-100 SBP if conscious), get them to OR
Complications: aortoenteric fistula, aortocaval fistula, limb ischemia, graft infection, inflammatory AAA, endoleak
Beware of thrombolytics since it can break up mural thrombus and send emboli

Aortic Dissection:
Tear in aortic intima. Type A involves ascending aorta, Type B doesn’t
Hypertension is #1 RF, also some sort of prior cardiac path, connective tissue disorders, inflammatory vasculitities
Hx: sudden onset chest pain most common, look for pulse deficit
Paraplegia if it involves the vertebral arteries
Mitral valve complications if involvement of aortic root
Horner’s syndrome if dissection compresses superior cervical ganglion
Dx: BP in both arms, CTA chest
Tx: control HR and BP, as well as pain
-Esmolol (quick on/quick off, good for HR control, titrate to HR 60-70), add cardene if BP still too high once HR controlled (SBP goal 100-110)
-Fentanyl for pain
Surgery for Type A, Type B can be medically managed
Complications: MI, Tamponade, rupture

Air embolism:
Iatrogenic is common, occurs due to pressure gradient (low pressure in venous system allows air from central line to easily enter system)
Central line air embolism 1 in 772
RFs: patient sitting upright, hypovolemic, negative intrathoracic pressure
Lethal dose thought to be 200-300cc of air (3ml/kg)
Signs and symptoms: sudden CNS/Resp/cardiac symptoms with central line placement
-looks like PE with CP, SOB, cough, tachy, syncope, anxiety, possible cardiac arrest, mental status change
Tx: prevent further air, reduce air volume, 100%FiO2, fluids, ionotropic support, hyperbaric oxygen (less so with CVC related), ECMO, L lateral decub positioning (takes embolus out of RV outflow track), and trandelenburg (unless arterial then avoid for cerebral complications)
Prevention: flush lumens and cap hubs prior to placement, adequately hydrate patient, keep insertion site below the heart

SHOCK:
Hypotension doesn’t mean hypoperfusion
Stressor->body compensates->decompensates->end-organ dysfunction->Death
-goal is to treat the stressor
diastolic is good indicator for PVR, systolic is good indicator for the strength of the heart
Shock index: HR/SBP, normal is 0.5-0.7 (HR goes up before BP)
Lactate up in times of lack of blood flow/oxygenation, but also depends on sympathetic nervous system and B-blockade can lead to lower lactate despite how sick patient is
Shock types: Obstructive, cardiogenic, hypovolemic, distributive
Obstructive: decreased CO, increased CVP, increased SVP (trying to shunt blood to heart), cool extremities (from shunting)
-PE, tension pneumo, tamponade, restrictive pericarditis, abdominal compartment syndrome, dissection
Cardiogenic: decreased CO, increased CVP, increased SVR, cool extremities
-MI, arrhythmia, cardiomyopathy, valve disease
-Ionotropes: dobutamine, milrinone, dopamine, epi (below 5-10mcg/kg/min)
-Milrinone solely renal clearance and better in chronic B-blockade, dobutamine is fast on/fast off. Make sure properly fluid resuscitated prior to starting these meds
Hypovolemic: CO normal or decreased, decreased CVP, increased SVR (trying to get blood back to heart), cool extremities (elderly might be a little warm due to slowed response)
-Fluid loss (GI/kidney/skin/DKA/3^rd space) or hemorrhage
-Permissive hypotension (MAP 65-70) has mortality benefit in trauma
-Balanced resuscitation (whole blood, keeping prbcs:ffp:plts 1:1:1)
-Calcium will be low because all the product are in citrate which will bind Ca so make sure to replete
Distributive: Septic, anaphylactic, neurogenic
Anaphylactic: consider delayed sequence intubation, need IM epinephrine (slowly diffuses over hours), consider glucagon if chronically B-Blockade
Neurogenic: Dx of exclusion, MAP>85