Vertigo

Vertigo = sensation of self or room spinning (hallucination of motion)
-vs presyncope (lightheaded, faint)
-vs instability
-vs other (malaise, viral illness, anemia, depression)

Affected pathway:
3 sensory mechanisms (visual, proprioception, vestibular) –> vestibular nuclei in brainstem –> cerebellum

History: time and rate of onset, duration of symptoms
-change in mental status is red flag

Exam:
-nystagmus: downbeating, torsional, or nonfatiguable = central
-skew deviation (cover one eye):

Vertigo ALgorithm Rosens

CENTRAL CAUSES

Cerebellar Stroke
-red flags: sudden onset, occipital headache, severe gait ataxia…difficulty speaking
-risk factors: age, cardiovascular disease (HTN, CAD, smoking)

Cerebral Artery Dissection 
-carotid artery – anterior neck pain
-vertebral artery – posterior neck pain

Vertebrobasilar Insufficiency
one cause is subclavian steal syndrome
-check pulses and systolic BP in both arms

Acoustic Neuroma
-gradually progressive unilateral hearing loss and tinnitis
-vertigo rare!

 

PERIPHERAL CAUSES

BPPV
-normal at rest, onset with head movement

Vestibular Neuronitis
episodic, severe, lasting hours, symptom-free episodes

Meniere’s Disease
-vertigo, hearing loss, tinnitis

Labyrinthitis

Vestibulitis

 

 

Diffuse Abdo Pain

SBO
-simple obstruction
-closed loop obstruction = 2 points of obstruction (ex: 2 adhesions or a loop of bowel within a hernia sac) that prevent anterograde or retrograde flow of contents
—-rapidly progresses to ischemia and infarction
—-loop often twists on itself –> occludes large arteriesG
-can still have BMs with a complete SBO as residual stool is emptied

Pancreatitis
-exam may be impressive – may have acute abdomen
-3x nl lipase, peaks within 12-36h, NOT representative of severity
-if nl, consider early or acute-on-chronic –> CT
-fluid resuscitate! May need 10L/d
-abx (-penams) only for the sickest, ie severe sepsis or septic shock
-CT if diagnosis unclear or sick (eval for complication: necrotizing pancreatitis, pseudocyst)
-RUQ US to r/u surgical cause
-Complications: hypoCa, DKA, AKI, ARDS, pleural effusions, ?GIB

AAA
-elderly pt with new “renal colic” (back pain, hematuria), syncope + abdo pain, hip weakness/neuropathy (retroperitoneal rupture –> compression of femoral/obturator nerve)

Mesenteric Ischemia

ED Thoracotomy

West trauma guidelines
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-repair heart with 3-0 nonabsorbable running suture

Technique

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If hypotension persists following thoracotomy and pericardotomy, the descending thoracic aorta should be occluded to maximize coronary perfusion and to decrease the required effective circulating volume to facilitate resuscitation. Typically, the thoracic aorta is cross-clamped inferior to the left pulmonary hilum; alternatively, it can be clamped above the lung in the more proximal descending aorta. Blunt dissection with one’s thumb and fingertips can be performed to isolate the descending aorta. If the aorta cannot be easily isolated from the surrounding tissue, digitally occlude the aorta against the spine to effect aortic occlusion.

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After performing the thoracotomy and pericardotomy, the patient’s intrinsic cardiac activity is evaluated; patients in asystole without cardiac tamponade are declared dead.

Bimanual internal massage of the heart is initiated; this should be performed with a hinged clapping motion of the hands, with the wrists apposed, sequentially closing from palms to fingers. The ventricular compression proceeds from the cardiac apex to the base of the heart. Intracardiac injection of epinephrine may be administered into the left ventricle, using a specialized syringe, which resembles a spinal needle. Typically, the heart is lifted up slightly to expose the posterior left ventricle, and care is taken to avoid the circumflex coronary during injection. The heart is vigorously massaged to enhance coronary perfusion. After allowing time for vasopressors to circulate, the heart is defibrillated (30 J) using internal paddles. Following several minutes of such treatment, as well as generalized resuscitation, salvageability is reassessed; we define this as the patient’s ability to generate a systolic blood pressure of greater than 70 mm Hg with an aortic cross-clamp if necessary.

FYI
-Air embolism (West guidelines*): Treatment for bronchovenous air embolism demands immediate pulmonary hilar cross-clamping to prevent further propagation of pulmonary venous air. Placing the patient in the Trendelenburg’s position traps air in the apex of the left ventricle; then with an open pericardium, needle aspiration is performed to remove intracardiac air. In addition, aspiration of the aortic root may be required to alleviate any accumulated air. Vigorous cardiac massage may promote dissolution of air already present in the coronary arteries, and direct needle aspiration of the right coronary artery with a tuberculin syringe may be lifesaving. The production of air emboli is enhanced by the underlying physiology–there is relatively low intrinsic pulmonary venous pressure caused by associated hypovolemia and relatively high bronchoalveolar pressure from assisted positive-pressure ventilation. This combination increases the gradient for air transfer across bronchovenous channels. Although more often observed in penetrating trauma, a similar process may occur in patients with blunt lacerations of the lung parenchyma.

Sources:

*http://www.trauma.org/index.php/main/article/361/

*http://westerntrauma.org/documents/PublishedAlgorithms/WTACriticalDecisionsResuscitativeThoracotomy.pdf

Traumatic Arrest

Many patients die because of inappropriate interventions in the prehospital or ED phase, because of delay in performing thoracotomy, and due to poor peri-operative management.

ACLS algorithms DO NOT APPLY to traumatic arrest.The primary causes of traumatic arrest are HOTT: Hypovolemia/Hemorrhage, hypOxia, Tension pneumothorax, and cardiac Tamponade. Hypoxic arrests respond rapidly to intubation and ventilation. Hypovolemia, tension pneumothorax and cardiac tamponade are all characterized by loss of venous return to the heart.  External chest compressions in trauma controversial and not well-studied, in theory they may cause blunt cardiac injury and obstruct access for performing definitive maneuvers (i.e. thoracotomy and aortic cross clamping, relief of  tamponade, repair of myocardial laceration; needle decompression; MTP).

The administration of inotropes and vasopressors such as epinephrine to the hypovolemic patient (who is already maximally vasoconstricted) causes profound myocardial hypoxia and dysfunction.

Management of Traumatic Arrest

Treat the cause of the traumatic arrest.

Hypoxic Arrest

Endotracheal intubation is mandatory and should be secured immediately. Ventilation with 100% oxygen should rapidly reverse hypoxic traumatic arrest without the need for further interventions. This is especially true of pediatric head injuries.
If pt awake, use ketamine and/or fentanyl induction agents for RSI; even etomidate can worsen hypotension significantly.

Tension Pneumothorax

Relief of tension pneumothorax should be accomplised rapidly either by needle chest decompression or preferably bilateral thoracostomies. Bilateral tension pneumothoraces may exist and the classic signs of a tension (tracheal deviation, unilateral hyperresonance) may not be present. Tension pneumothoraces should therefore be presumed and bilateral decompression undertaken in ALL cases of traumatic arrest.

Massive Hemorrhage

Performing bilateral thoracostomies has the advantage of identifying major hemorrhage and which side of the chest the major injury is on. This will determine the side of the chest incision for the thoracotomy.????????

The treatment of massive thoracic hemorrhage is control of hemorrhage, not intravenous fluid therapy. Fluid therapy prior to hemorrhage control worsens outcome in penetrating thoracic trauma (and perhaps all penetrating trauma patients). If there is no response to a small (500ml) fluid challenge, fluid administration should be halted until hemorrhage control is achieved.

Cardiac Tamponade

The classic signs of distended neck veins and muffled heart sounds are almost universally absent in traumatic cardiac tamponade. Needle pericardiocentesis may also fail as a diagnostic measure due to blood in the pericardial sac being clotted. FAST ultrasound scan, if available, will indicate the presence of pericaridal fluid. The pericardium may be felt through the left thoracostomy to assess for the presence of tamponade.

Next Steps

Patients will be cold and profoundly coagulopathic. Blood and component therapy should be warmed and administered rapidly AFTER hemorrhage is controlled. ????The use of epi (or other pressors) is contraindicated in the presence of hypovolemia. Inotropes may be required AFTER control of hemorrhage and cardiac repair. Direct myocardial injury, ischemic myocardial injury, acute cardiac dilatation, pulmonary hypertension and mediator release due to global tissue ischemia can all lead to cardiogenic shock which may require inotropic support.

Lethal Triad of Trauma
= acidosis, coagulopathy, hypothermia
-etiology is massive hemorrhage: 1st 1-2 units uncrossmatched fridge, remaining crossmatched
-use MTP to permissive hypotension to prevent clot destabilization

Indications
-PENETRATING trauma: arrest in ED or within 15 min? prior to arrival

Goals
-to look for and relieve cardiac tamponade (cannot see it, so always cut the pericardium)
-to look for aortic rupture and cross-clamp proximally
-to look for exsanguination into lung and repair lacerated vasculature and myocardium

Signs of life (per East trauma guidelines) = pupillary response, spontaneous ventilation, presence of carotid pulse, measurable or palpable blood pressure, extremity movement, or cardiac electrical activity.

West trauma guidelines
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-repair heart with 3-0 nonabsorbable running suture

Penetrating trauma:
-NEVER assume the pt only has the injuries you can see. Assume there are more.

 

Sources:

*http://www.trauma.org/index.php/main/article/361/

*http://westerntrauma.org/documents/PublishedAlgorithms/WTACriticalDecisionsResuscitativeThoracotomy.pdf

 

ICH

Traumatic:
-subarachnoid
-subdural
-epidural

Spontaneous:
-subarachnoid
-intraparenchymal

Airway management in patients with suspected increased ICP:
-pretreat with fentanyl to prevent increase in ICP during airway manipulation
-paralytics: conflicting studies re whether sux or roc have higher risk of further increasing ICP
-provide good analgesia and sedation post-intubation to avoid sympathetic surges with airway pain/manipulation (no suctioning!)

Syncope

Syncope PLUS” syndromes = high risk
+ headache = SAH or ICH
+ neuro deficit = stroke/TIA or ICH Syncope
+ confusion = seizure
+ chest pain = MI, PE, or aortic dissection
+ back/abdominal pain in elderly = AAA or thoracic dissection if upper back
+ pregnancy = ectopic

-exertional syncope = dysrhythmia (tachycardia- or ischemia-induced) or cardiac output obstruction

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Also noncardiogenic causes, for example neurologic syncope (includes SAH, brainstem ischemia, and basilar artery migraine).

Mnemonic: ABCDEFGHII

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^Strayer’s algorithm

High Risk EKGs

Wellens Syndrome

  • deeply inverted or biphasic T waves in V2-3, which is highly specific for a critical stenosis of the left anterior descending artery (LAD).
  • Patients may be pain free by the time the EKG is taken and have normally or minimally elevated cardiac enzymes; however, they are at extremely high risk for extensive anterior wall MI within the next few days to weeks.

https://lifeinthefastlane.com/ecg-library/wellens-syndrome/

aVR Elevation

  • Widespread horizontal ST depression, most prominent in leads I, II and V4-6
  • ST elevation in aVR ≥ 1mm
  • ST elevation in aVR ≥ V1

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ST elevation is aVR is postulated to result from two possible mechanisms:

  • Diffuse subendocardial ischaemia, with ST depression in the lateral leads producing reciprocal change in aVR due to a process causing generalized coronary ischemia (triple vessel disease, post cardiac arrest)
  • Infarction of the basal septum, i.e. a STEMI involving aVR. aVR records electrical activity from the RVOT and the portion of the septum closest to the base (supplied by a proximal branch of the left main)

https://lifeinthefastlane.com/ecg-library/lmca/

VT vs block with tachycardia:
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Anomalous left coronary artery from pulmonary artery syndrome –> SCD

magnet –> converts pacemaker to fixed rate pacing

Congenital Heart Disease

Ductal-dependent lesions
-Most important to recognize in early neonatal period (ductus closes within 3 weeks of life)
-Subdivide into cyanotic and noncyanotic lesions based on presentation
Cyanotic lesions = obstruction of right heart flow to lungs – patent ductus needed to get blood to lungs
Noncyanotic lesions = obstruction of left heart flow to body – patent ductus needed to get blood to body

Note: if pt has known PDA, find out if isolated or along with other lesions

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Diagnosis:
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Exam: cool shock presentation + crackles and hepatomegaly

Pulse Delay or Absence: Decreased or absent femoral pulses may suggest coarctation of the aorta

Brachial-femoral pulse differential: pulses should arrive at the brachial and femoral pulse simultaneously, if there is a brachial-femoral delay there may be an issue

Blood pressure differential: Difference between preductal (i.e. right arm) blood pressure and lower extremity blood pressure of > 10 mmHg, think of an obstructive process to the lower extremities.

O2 saturation differential: Difference in O2 saturation > 3% between right upper and right lower extremity, <94% in lower extremities, or < 90% in any extremity are considered clinically significant

Labs:

  • Blood glucose (ABC Don’t Ever Forget Glucose)
  • Electrolytes (to assess for adrenal insufficiency)
  • Septic work-up
  • Methemoglobin if cyanosis without respiratory distress
  • Ammonia (metabolic diseases)
  • TSH
  • BNP: ongoing debate about usefulness of this test, particularly in the ED setting.
    • BNP < 100pg/mL to identify significant congenital heart disease had a sensitivity of 100% and specificity of 98%
    • BNP > 132.5pg/mL to detect hemodynamically significant left-to-right shunts had a 93% sensitivity and 100% specificity
    • BNP > 40pg/mL to differentiate cardiac from pulmonary causes of respiratory distress had an accuracy of 84%

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-compare PaO2 of ABG drawn from right radial artery (preductal) before and after 10m of supplemental O2
-CHD pts do not have significant increase (post hyperoxia PaO2 unlikely over 150mmHg), whereas pts with pulmonary disease will  have some improvement of V/Q mismatch

*The hyperoxia test: A simpler method involves using a pulse oximeter before and after the patient receives 100% oxygen (or as close to a 100% FIO2 as possible) for 5-10 minutes and noting whether or not the oxygen saturation improves. If the oxygen saturation improves then the underlying cause of the oxygen desaturation favours a respiratory etiology, whereas if the oxgygen saturation does not improve, a cardiac cause is favoured.

Caution! 100% oxygen is a pulmonary vasodilator and could worsen respiratory distress in a patient with ductal-dependent lesions, by decreasing PVR and increasing pulmonary blood flow, leading to pulmonary over-circulation

With bedside ECHO, ask yourself 3 simple questions:

  1. Is the global cardiac function poor?
  2. Are there four chambers of the heart?
  3. Is the septum intact?

Management of Blue Babies:
-if clinically suspect ductal-dependent lesion, give prostaglandin E1 immediately at 0.05-0.1 mcg/kg/min to maintain patent ductus arteriosus
-be prepared to intubate (apnea common) and support hemodynamics as a result of administration and in preparation for transport to hospital with peds cardiac surgery
-use etomidate or fentanyl for induction (do NOT use ketamine – the increase in afterload may cause decompensation!). Use low PEEP settings.
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Any neonate in distress should be presumed to be septic until proven otherwise. Early empiric antibiotics should be started as soon as possible.

Be judicious with fluids. Use 5-10 cc/kg NS boluses to improve preload, and encourage further opening of the PDA and pulmonary blood flow through the duct. Give Oxygen. Aim for an oxygen saturation of 85% (depending on diagnosis and lesion). The use of sodium bicarbonate is controversial. It may be given empirically based on the blood gas, as acidosis aggravates hypoxic pulmonary vasoconstriction. Inotropes/vasopressors may be necessary to maintain adequate systemic perfusion and encourage pulmonary perfusion in consultation with a pediatric intensivist.

*The tachypneic infant who appears to be struggling to breath (i.e. increased work of breathing) usually has an underlying respiratory cause vs. the infant who is displaying ‘silent tachypnea’, without increased work of breathing is usually secondary to metabolic acidosis from a cardiac or metabolic cause.

The big 4 Causes of Neonatal Cyanosis

  1. Congenital Heart Disease
  2. Sepsis
  3. Respiratory disorders (i.e., pneumonia, ARDS)
  4. Hemaglobinopathy (i.e., polycythemia, methemoglobinemia)

To distinguish central cyanosis from peripheral cyanosis, look for bluish discoloration inside the mouth – tongue, mucous membranes and lips.

 

Pink Perfused Babies (1-6mo/o):
-consider CHF for wheezing baby!

The most sensitive and specific clinical findings for acute CHF in infants

  • < 3 ounces of formula per feed or > 40 minutes per breast feed
  • Respiratory rate > 60 breaths per minute or irregular breathing
  • Hepatomegaly – Start palpation at the iliac crest and slowly move superiorly, and feel for the liver edge. Normally, the liver edge should be < 2 cm below the costal margin. Also percuss for the size of the liver – normally, the liver should be < 8 cm wide.
  • Other clues: poor weight gain & ventricular hypertrophy on ECG

Common causes of CHF in the pediatric patient include structural causes such as VSD, ASD, Aortic Stenosis and PDA as well as other causes such as SVT, AV block, cardiomyopathy and myocarditis.

Management:
-oxygen is a potent pulmonary vasodilator and could worsen hypoxemia in some congenital heart defects. Infants are able to tolerate oxygen saturations lower than adults and so aim for an oxygen saturation of >85% (as opposed to >93% in adults)
-lasix for pulmonary edema
-inotropes or vasodilators (i.e., milrinone, dobutamine) may be indicated in severe CHF in consultation with the pediatric intensivist

Decompensated CHF

3 components of pathophysiology:

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(1) Systemic overload = excess TBW
(2) Acute diastolic dysfunction = sudden increase in LV pressure –> pulmonary congestion. Unrelated to LV contractile function. Occurs via wall stiffening (ex: scarring from old MI) or impaired filling (ex: LVH, tachycardia of any cause).
(3) Low output failure = problem in contractility, leading to poor end-organ perfusion (fatigue, confusion, worsened renal function)

Syndromes:
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DDX/etiology of decompensation:
-abrupt: ACS, PE, ruptured valve or chordae tendinae or papillary muscle, ruptured ventricular septum (above evaluated via echo), arrhythmia
-gradual onset: tamponade, copd, sepsis, acidosis, hyperthyroidism, med/dietary noncompliance

Key history: Chest pain/anginal equivalent? History of CHF (or similar episodes)? History of MI or CAD?

Treatment goals:
-reduce preload??
-improve LV outflow
-maintain myocardial perfusion

Treatment:
dyspnea: sit pt upright, supplemental O2, BiPAP if significant WOB, intubation if altered
chest pain: give ASA, supplemental O2, nitroglycerin SL if hypertensive, PCI if STEMI
pulmonary congestion/ADHF: nitroglycerin if hypertensive to reduce afterload
systemic overload: iv lasix if normotensive and no renal dysfunction, bumex drip if hypotensive or soft pressures or any renal dysfunction
cardiogenic shock/low output failure:  determine etiology if acute (STEMI, valve rupture), consider inotropes*, consider bumex gtt if chronic with concomitant diastolic failure/pulmonary edema

Treatment pathway:
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*from Circulation:
“Patients with decompensated HF unresponsive to diuresis often have diminished concomitant peripheral perfusion, clinically apparent as cool extremities, narrowed pulse pressure, and worsening renal function. They may have markedly elevated SVR despite hypotension due to the stimulation of the renal-angiotensin-aldosterone system, as well as release of endogenous catecholamines and vasopressin. In this setting, reversal of systemic vasoconstriction is often achieved through the use of vasodilators (such as sodium nitroprusside) and inotropes with peripheral vasodilatory properties to improve hemodynamic parameters and clinical symptoms.
The most commonly recommended initial inotropic therapies for refractory HF (dobutamine, dopamine, and milrinone) are used to improve CO and enhance diuresis by improving renal blood flow and decreasing SVR without exacerbating systemic hypotension. Dobutamine stimulation of β1– and β2-receptors can achieve this goal at low to medium doses by modestly increasing contractility with usually mild systemic vasodilation. Unfortunately, β-adrenergic receptor responses are often blunted in the failing human heart. A chronic increase in activation of the sympathetic nervous system and increased circulating catecholamine levels results in a phosphorylation signal that leads to uncoupling of the surface receptor from its intracellular signal transduction proteins (desensitization), as well as increased receptor targeting for endocytosis (decreased receptor density). PDIs such as milrinone, acting through a non–β-adrenergic mechanism, are not associated with diminished efficacy or tolerance with prolonged use. This drug causes relatively more significant right ventricular afterload reduction through pulmonary vasodilation and less direct cardiac inotropy, which results in less myocardial oxygen consumption. Milrinone can cause severe systemic hypotension, necessitating the coadministration of additional pressor therapies. Direct randomized comparisons of milrinone and dobutamine have been small and have demonstrated similar clinical outcomes.”

SCAPE management: BIPAP + high dose NTG drip
https://emcrit.org/emcrit/scape/
http://www.emdocs.net/furosemide-treatment-acute-pulmonary-edema/

Categories of CHF pts (Stevenson profile for CHF):
-warm & dry = healthy CHF (well perfused, adequately diuresed)
-warm & wet = well perfused, needs diuresis
-cold & wet = poorly perfused, needs pressors + diuresis = cardiogenic shock (CCU)
—- or CHF + other etiology shock (ex septic shock)

 

Vasopressors and Inotropes

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Norepi is best first line for most types of shock. Pressors work best for distributive types (septic, osmotic/cirrhotics, but NOT anaphylaxis). Don’t mess around and delay starting pressors if suboptimal response to fluids. Early pressors work well, as they mobilize volume stored in central veins (which act as capacitors). Use weight-based dosing and titrate to central organ perfusion (mental status primarily, which needs MAP>50, but aim for 65), do not go in excess to cause AKI. Note that echo post-pressor may appear to have worse EF. This is due to increased workload; improved coronary perfusion pressure comes at a cost of increased demand.

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