EmergencyMed Flashcards
Causes of cardiac arrest, briefly?
Hs and Ts
Hs: hypovolemia, hydrogen ions, hyper/hypoglycemia, hypo/hyperkalemia, hypoxia, hypothermia
Ts: tablets/toxins, tamponade, tension pneumothorax, thrombosis (MI), thromboembolism (PE), trauma
How can you tx hyperkalemia?
- Ca++ administration to stabilize cardiomyocyte electrochem potentials and thus prevent fatal arrythmias
- Nebulized salbutamol
- IV insulin (usually with glucose and bicarb) to drive K+ into cells
- loop diuretics like furosemide to spill potassium in urine
- sodium polustyrene sulfonate to bind K+ to excrete in stool
- emergent hemodyalisis
How do you treat HYPOkalemia?
Give IV K+
How do you treat hypoxia?
- Give OXYGEN
- Proper ventilation
- Good CPR technique
If cyanide or CO poisoning —> HYPERBARIC OXYGEN
How do you treat hypothermia (core temp < 35ºC)?
- Cadiac bypass
- Irrigation of body cavities with warm fluids
- Warmed IV fluids
How do you treat hypovolemia?
- IV fluid resuscitation (if in hypovolemic shock, use 2 16 gage (large bore) IVs)
- Blood transfusion
- CONTROL BLEEDING
In hyperglycemia that causes DKA and cardiac arrest, how should you treat the patient?
Correct the metabolic acidosis.
How do you treat hypoglycemia (ex. in the scenario of syncope/cardiac arrest)?
Give IV glucose.
Which tablets or toxins can cause cardiac arrest?
- Tricyclic antidepressants
- Phenothiazides
- Beta blockers (antihypertensive, antiarrhytmic)
- CCBs (antiarrhythmic, antihypertensive)
- Digoxin (ionotrope)
- COCAINE
- Aspirin
- Paracetamol/acetaminophen
- Acetaminophen
How do you treat cardiac arrest due to tablets or toxins?
Give fluids for volume expansion
Use specific antidotes
- Give NaHCO3 if TCAs
- Use benzos if cocaine
- Use glucagon or Ca++ for CCBs
As a last resource, cardiopulmonary bypass
How do you treat cardiac tamponade?
Pericardiocentesis
Pericardial window
How do you treat a tension pneumothorax?
Needle decompression thoracotomy, with the largest needle you can get.
LATER: chest tube decompression to definitively drain the (hemo)pneumothorax.
Where should you insert the needle for a needle decompression thoracotomy?
Insert needle in the 2nd intercostal space in the mid-clavicular line.
In obese patients, go through the axilla.
Where do you insert a chest tube to drain a (hemo)pneumothorax?
5th intercostal space, in the mid-axillary line.
Dissect ABOVE the rib, because the neurovascular bundle is just BELOW the rib.
How do you treat a myocardial infarction in the ED (i.e. “thrombosis” in the Hs and Ts mnemonic)?
- Rescucitation (ABC)
- OMI (oxygen, monitors/EKG, and IVF)
- MONA (morphine, oxygen, nitrates, aspirin)
- Antiplatelet therapy (plavix = clopidogrel)
- Thrombolytic therapy
- Percutaneous coronary intervention
How do you treat thromboembolic causes of cardiac arrest (i.e. a hemodynamically significant pulmonary embolism)?
Thrombolytics or thrombolectomy.
Prognosis is POOR.
What is commotio cordis?
A form of CARDIAC ARREST.
An often lethal disruption of heart rhythm that occurs as a result of a blow to the area directly over the heart (the precordial region), at a critical time during the cycle of a heart beat causing CARDIAC ARREST. It is a form of ventricular fibrillation (V-Fib), not mechanical damage to the heart muscle or surrounding organs, and not the result of heart disease.
What are risk factors for acute coronary syndrome?
Smoking HTN DM Hypercholesterolemia Age Family history of CAD in < 55 yo in 1st degree relative Prior personal history of CAD or PVD
How often is ST segment elevation seen on ECG in acute MIs?
50%
Which cardiac markers can you order to aid in the diagnosis of acute coronary syndromes (ACS)?
Is there another type of lab test you would also want to order?
The cardiac markers are:
- CK-MB (creatine kinase)
- Troponin- The most sensitive and specific test for myocardial damage. Because it has increased specificity compared with CK-MB, troponin is a superior marker for myocardial injury.
Troponin isoforms T and I are specific to the myocardium: Tn-I is similar to CK-MB but duration of elevation is 5-10 days; Tn-R is less sensitive, but is an independent marker for CV risk.
ALSO, would want to order a BMP to assess electrolytes and renal function because if the patient is going to the cath lab, they are going to get IV contrast.
What are the drawbacks of CK-MB as a diagnostic marker for acute coronary syndromes?
- It takes a while to elevate. Elevation @3-12 hours, peak @18-24h, and duration is 2 days. Therefore, while it is > 90% sensitive for MI for 5-6h after symptom onset, it is only 50% sensitive shortly after presentation.
- Becomes less specific when skeletal muscle damage is present.
What is the differential diagnosis for cardiac troponin elevation?
- Acute infarction
- Severe pulmonary embolism causing acute right heart overload
- Heart failure
- Myocarditis
Why is aspirin an important medication for preventing and treating acute coronary syndromes?
Aspirin inhibits thromboxane A2.
This inhibition leads to decreasing platelet aggregation.
How do nitrates help in treating acute coronary syndromes?
Nitrates (or nitrovasodilators), are prodrug pharmaceutical agent that cause VASODILATION by donation of nitric oxide (NO) via various mechanisms (many of which are enzymatically mediated).
The most important effect in angina is the widening of veins, which increases their capacity to hold blood and reduces the pressure of the blood returning to the heart (the preload). Widening of the large arteries also reduces the pressure against which the heart has to pump, the afterload. Lower preload and afterload result in the heart needing less energy and thus less oxygen. Besides, NO donated by nitrovasodilators can reduce coronary spasms, thus increasing coronary perfusion.
Why are beta blockers indicated for acute coronary syndromes?
Stimulation of β1 receptors (in the heart) by epinephrine and norepinephrine induces a positive chronotropic and inotropic effect on the heart and increases cardiac conduction velocity and automaticity. Beta-blockers, or beta adrenergic antagonists, block the beta adrenergic receptors in the heart (in particular, beta-1 selective agents are cardioselective, do not act at the other receptors), which does not allow epinephrine and norepinephrine to increase chronotropy and ionotropy in the heart. By not allowing the heart to beat faster and contract harder when faced with a demand, you are reducing the heart’s metabolic demand.
Thus, they slow heart rate, decrease infarct size, CV complications, and mortality.
When should you give fibrinolytic therapy for an acute MI?
When you see ST elevation > 0.1mV in 2+ contiguous leads OR a new LBBB AND time to therapy (read, cath balloon/stent or CABG) is < 12 hours (Class I) or 12-24 hr (Class II).
Of note percutaneous coronary performed within 90 minutes of a patient’s arrival is superior to fibrinolysis with respect to combined endpoints of death, stroke, and reinfarction, but unfortunately, PCI is not widely available at acute care hospitals. Chakrabarti and colleagues noted that any mortality benefit of primary PCI compared with onsite fibrinolysis was nullified when the time delay to primary PCI was 120 minutes or more.
Therefore, THROMBOLYSIS IF CANNOT GET TO PCI IN TIME: In the 2013 STEMI Focused Update, the writing committee recommended fibrinolytic therapy when there was an anticipated delay to performing primary PCI within 120 minutes of first medical contact (FMC). FMC was defined as the time at which the EMS provider arrives at the patient’s side.
Also, THROMBOLYSIS EVEN IF CAUGHT LATE: The benefits of fibrinolytic therapy are well established during the initial 12 hours after symptom onset. The new guidelines mention that you should consider administration of a fibrinolytic agent in symptomatic patients presenting more than 12 to 24 hours after symptom onset with STEMI affecting a large area of myocardium or hemodynamic instability if PCI is not available.
If a patient with a STEMI arrives at your hospital that does not have the capability to perform PCI, what should you do?
ABCs
MONA
Administer Fibrinolysis (alteplase = tPA)
Transfer to hospital that can perform PCI as soon as possible.
In the US, which fibrinolytic agent do we typically use?
Tissue plasminogen activator (tPA), also known by the trade name ALTEPLASE.
This is a fibrin-specific fibrinolytic agent, as compared to streptokinase and urokinase, which are non-fibrin specific
Absolute contraindications for fibrinolysis
Prior intracranial hemorrhage (ICH)
Known structural cerebral vascular lesion
Known malignant intracranial neoplasm
Ischemic stroke within 3 months
Intracranial or intraspinal surgery within 2 months
Suspected aortic dissection Active bleeding or bleeding diathesis (excluding menses) Significant closed head trauma or facial trauma within 3 months Severe uncontrolled hypertension (unresponsive to emergency therapy) For streptokinase, prior treatment within the previous 6 months
How do we treat an MI?
Simply, MONA: morphine, oxygen, nitrates, aspirin.
***OF NOTE, aspirin is the only one the MONA interentions proven to reduce mortality.
STEMIs need to go to the catheterization lab for a PCI within 90 minutes of arrival (door to balloon time).
Why would you get a CXR for a patient with chest pain in whom you suspect an acute coronary syndrome?
To rule out other causes of acute-onset chest pain:
- Aortic dissection
- Pneumonia
- Pneumothorax
- Free air below the diaphragm (abdominal free air)
- Pulmonary effusion
What is the spectrum of acute coronary syndromes?
Stable angina
Unstable angina
Acute myocardial infarction - NSTEMI or STEMI
We use ECG and troponins to differentiate between these different classes within the spectrum.
If the ECG is completely normal, you should consider alternative diagnoses beyond ACS. CXR should help.
If the ECG shows ST-segment elevation (+/- Q waves), the diagnosis is STEMI and you’re set.
If the ECG is abnormal with nonspecific findings, such as ST segment depression, T-wave flattening or inversion, consider Unstable Angina or NSTEMI.
OF NOTE, troponins will only be elevated in patients with NSTEMI and STEMI, but not in patients with unstable angina.
Describe the OH BATMAN mnemonic for all of the treatments to consider for a person presenting with an acute coronary syndrome:
Oxygen Heparin Beta-blocker Aspirin Thrombolysis (tPA) Morphine Anti-platelet agent (Plavix) Nitrates
What is stable angina?
Transient, episodic chest discomfort that is predictable and reproducible (stereotypic). This is caused by fixed atherosclerotic lesions that lead to supply-demand imbalance.
What is unstable angina?
An episode of coronary plaque (atherosclerotic lesion) rupture that leads to narrowing (but not occlusion) of a coronary artery.
What are the symptoms of an acute myocardial infarction?
Substernal chest discomfort > 15 min associated with dyspnea, diaphoresis, lightheadedness, palpitations, nausea, and/or vomiting.
OF NOTE, 12.5% of MIs are clinically silent with no assoc. symptoms.
How does cocaine cause cardiac morbidity?
AMONG OTHER THINGS:
- It causes coronary vasospasms/vasoconstriction, which decreases myocardial oxygen delivery.
- It leads to increased atherosclerosis, which narrows the coronary vessel lumen.
- It leads to platelet activation and a hypercoagulable state.
- It increases HR and BP, which increases myocardial oxygen demand as well as shear stress, which can lead to plaque rupture and thrombosis.
Of patients with cocaine-associated chest pain, 6% have an MI, and 20-60% have transient myocardial ischemia.
How do you treat cocaine-related chest pain?
BENZODIAZEPINES
Also, could give beta blockers, but this is more controversial.
What are big things you CANNOT miss in a patient with chest pain that radiates to the back?
Aortic dissection
Pancreatitis
Perforated ulcer (usually duodenal)
Aside from the classically described “ripping” chest/abdominal pain that radiates to the back, why does aortic dissection have a variable presentation?
Additional symptoms depend on where the dissection is occurring and which aortic branches are involved:
- Carotid arteries: stroke
- Spinal arteries: paraplegia
- Abdominal aorta/renal arteries/iliacs: abdominal/flank pain, renal failure.
- Coronary arteries: aortic insufficiency; pericardial effusion/tamponade
- Laryngeal nerve decompression: hoarseness
- Tracheal decompression: dyspnea/stridor/wheezing
- Esophageal compression: dysphagia
How does aortic dissection present on CXR?
Abnormalities in 85%, including:
-Widened mediastinum
How is delirium defined?
State of disturbed consciousness associated w/
- motor restlessness
- transient hallucinations
- disorientation
- delusions
Patients may be hypoactive or hyperactive.
Patients who are acutely hallucinating or intermittently exhibiting strange behaviors are also delirious.
MOST IMPORTANTLY, delirium always has an organic and reversible cause.
What is a coma?
Any depressed LOC, a complete failure of the arousal system w/ no spontaneous eye opening.
Results from either brainstem dysfunction and/or bilateral cortical disease.
What are some causes of altered mental status to worry about in children?
- Toxic ingestions (i.e. granny’s long-acting insulin. GET A FINGER STICK GLUCOSE)
- Abuse
Describe the role of the baroreceptors in the aortic arch and carotid sinus
They sense hypotension and stimulate peripheral vasoconstriction (“clamp down”) and increase in HR (increase in sympathetic tone).
Describe the role of carotid body chemoreceptors
In response to cellular acidosis, they cause peripheral vasoconstriction and respiratory stimulation (because they sense that perfusion to tissues and brain is low, leading to reliance on anaerobic metabolism and build up of lactic acid).
Briefly, describe the RAAS system
In response to renal hypoperfusion (either from renal artery stenosis, low systemic BP/shock, etc.), the juxtaglomerular apparatus cells secrete renin.
Renin cleaves angiotensinogen to form angiotensin I, which is then converted to the active form, angiotensin II, by angiotensin converting enzyme.
Angiotensin causes peripheral vasoconstriction. It also increases the release of aldosterone and ADH (vasopressin), both of which lead to increased resorption of water to increase intravascular volume (by increasing Na+ reabsorption and by increasing insertion of aquaporin channels into the collecting duct, respectively).
BOTTOM LINE: the RAAS system wants to increase BP by increasing intravascular volume and SVR.
Underlying issue in hypovolemic shock
Decreased preload (i.e. decreased central venous pressure).
Underlying issue in cardiogenic shock
Decreased myocardial function/contractility.
Results in increased preload because blood volume gets backed up/accumulated.
Underlying problem in distributive shock
Drop in SVR leading to functional hypovolemia because intravascular volume is larger.
Underlying problem in neurogenic shock
Loss of sympathetic function leads to loss of vascular tone
Which signs/metrics are included in the SIRS criteria? Which thresholds are used for the values?
Temp: 100.4ºF
HR: > 90
RR: > 20 or PCO2 12, or bands > 10%
How is sepsis defined? How is severe sepsis defined?
Sepsis = SIRS + known infection
Severe sepsis = SIRS + known infection + organ dysfunction (as denoted by elevated creatinine, elevated INR, altered MS, elevated lactate, and hypotension that DOES respond to IVF)
Septic shock = SIRS + known infection + organ dysfunction but NO response to aggressive fluid resuscitation
What is Early Goal Directed Therapy (EGDT) for septic shock?
Achieve the following:
- CVP 8-12 mmHg
- SVC O2 Sat% > 70% (orSvO2 > 65%) — can also use reduction of lactate by ≥ 10% as surrogate.
- MAP ≥ 65 mmHg
- UOP ≥ 0.5 mL/kg/hr
ALSO, early initiation of ABx
A tight/pressing headache that is mild to severe, bilateral, and has no vomiting and no more than one of the following (nausea, photophobia, phonophobia) is most likely a ….
Tension headache.
Can last between 30 min- 7 days
NO evidence of organic disease.
Tx: oral analgesia
A unilateral, pulsating headache that is mod-severe in intensity, lasting from about 4-72 hours if untreated or unsuccessfully treated, and is accompanied by at least one of the following (N/V, photophobia, phonophobia), is most likely….
Migraine w/o aura
Note, these are usually aggravated by physical activity.
Tx: reglan (metoclopramide, dopamine receptor blocker in chemoreceptor trigger zone of CNS and sensitizes tissues to acetylcholine) or compazine, serotonine agonists (triptan), narcotics
What are some causes of secondary headache?
Intracranial hemorrhage (SAH, intracerebral, sub/epidural) Meningitis/encephalitis HTN encephalopathy Ischemic stroke Venous sinus thrombosis Hypoxia Hypercarbia CO poisoning Temporal arteritis Mass lesion (tumor, abscess, AVM) Altitude sickness Metabolic (hypoglycemia, fever, hypothyroid, anemia) Glaucoma Pseudotumor cerebrii (benign intracranial HTN) Trigeminal neuralgia Post-concussion syndrome Sinusitis w/o complication Post-LP headache Diet Medications Fatigue Post-exertional Post-coital
Which features define a heat stroke?
Altered MS w/ core temp > 40.5C (105F). Oxidative phosphorylation becomes uncoupled from ATP-production at ≥42C.
Seen often in pt with compromised homeostatic mechanisms (elderly, small children, chronicall ill/addicted, obese, without AC).
Major complications include ARDS, DIC, rhabdomyolysis, ARF, liver failure, and seizures.
How do you treat a patient with heat stroke?
AGGRESSIVE COOLING IS CRUCIAL(submerge in ice water, hose w/ cold water, ice-soaked towels, wet+windy, iced lavage, endovascular cooling, cold hemodialysis)
Stop cooling when ~39F to avoid overshoot to hypothermia.
Which labs/studies should you get on a person with heat stroke?
- Get ABG/CXR to r/o ARDS
- CBC/Coags to assess DIC
- May see leukocytosis 20-30K with thrombocytopenia.
- Elevated AG from lactic acidosis
- UA to screen for ARF/rhabdo
- Elevated LFTs seen in almost all patients (with AST > 1000 poor prognostic indicator)
- ECG shows QT and ST prolongation, RBBB, sinus tach, afib, SVT, evidence of MI
