Lecture 6: Sepsis Flashcards
(148 cards)
1
Q
Cardiac emergencies:
* Common or not?
* What is the leading cause of death?
* What makes up 20% of medical malpractice?
A
- Approximately 5 % of all ED visits are for chest pain
* 5 million visits / year - Acute myocardial infarction (AMI) is a leading cause of death in the US
- “Errors in diagnosis account for 20% of medical malpractice”
Chest pain (CP) is one of the most common and most complex of problems presenting to the Emergency Department (ED). More than 2.0 million patients are admitted to cardiac care units throughout the US per year.
2
Q
Diagnostic challenge:
* CAD risk factors better for who?
* _ presentations (i.e. more in who?)
* What is subjective?
* Most tests are not what?
* what is your best tool to sorting out the etiology of chest pain?
A
- CAD risk factors better for asymptomatic patients
- Atypical presentations(i.e. more in females)
- Interpretation of pt’s subjective perception of pain
- Most tests are not helpful in the ED
- History is your best tool to sorting out the etiology of chest pain
3
Q
What are The Big 7 Life-threatening causes of CP in the ED?
A
- Unstable angina
- Acute MI
- Aortic dissection
- Pulmonary embolus
- Spontaneous pneumothorax (Tension)
- Pericarditis (Tamponade)
- Boerhaave’s Syndrome (think if CP after endoscopic exam recently)/Mallory-Weiss tear
4
Q
What are some nonlife threatening DDX?
A
5
Q
History:
* history is what?
* What can history be divided into?
A
History is, by far, your best diagnostic tool
May be divided into three areas:
* Proximate history- show me where pain/discomfort is
* Remote history
* Risk factors
6
Q
The remote history takes into account of what?
A
The remote history takes into account previous episodes.
* Have the patient describe his recent episodes, hospitalizations, consultations, outpatient testing, treadmills, catheterizations.
* Inquire about old EKGs, and compare the present EKG with previous ones.
* Scrutinize the patient for previous admissions. Do not trust the patient if they say they are in good health but do not have a doctor and have not been evaluated medically with labs.
7
Q
Initial evaluation: Remote history
* Previous what? (2)
* Do not create what?
A
8
Q
What are absolute risk factors of MI?(5)
A
family history, HTN, DM, smoking, elevated cholesterol
9
Q
What is contributory risk factors MI?(5)
A
age over 30, male, obesity, sedentary, cocaine (vasoconstriction of all arteries in the body)
COMAS
10
Q
Physical Examination: General Appearance and Vitals
* Look for what? (4)
* Obtain what?
* What is more important than actual physical exam?
A
- Look for tachypnea, diaphoresis, cyanosis, pallor
- Obtain vital signs and blood pressure in both arms
- Appearance of pt is more important than actual physical exam
11
Q
Specific findings: MI
* What can be heard? Why is it useless in the ED? What can you order?
A
New murmur - papillary muscle dysfunction (MVP or rupture)
Extrasystolic sound - useless in ED setting
* Noisy environment
* Could recommend to have an echo done upon admission
12
Q
How to Approach ED Patients
* What do you do first?
A
ABCs, establish safety net: oxygen ?, monitor, IV lines, vital signs
Generally start oxygen if below 94% O2 Sat.
13
Q
What are the sx specific work up in ED?
A
- CXR, EKG, cardiac enzymes
- EKG alone: Low risk patient
- CXR, Chest CT Angio
- CXR, EKG, D-Dimer
- CXR, gastrograffin swallow: esphagal problems
Cannot/should not do all of the above for all patients: depends on issue
14
Q
Generally, in any chest pain, palpitations, SOB, or dizziness – MUST always get what?
A
EKG
Dizziness can be issue metabolic, decrease CO, neuro stoke
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Q
A
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Q
fill in the covered part
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Q
Fill in the covered part
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18
Q
Heart score
* What does it determine?
* Used in Who?
A
- Determines eligibility for admission and delineates mortality risk
- Use in patients >21yo with symptoms suggestive of ACS. Do not use if having EKG changes, hypotension, life expectancy <1year, or found another medical or surgical reason for admission.
19
Q
What are the components of the heart score?(5)
A
- Suspiciousness of history
- EKG changes
- Age
- Risk factors
- Initial troponin value
20
Q
What are the scores of the heart score?
A
Maximum score of 10 to evaluate MACE
* Score 0-3: mortality of <1.7%
* Score 4-6: mortality of <16.6%
* Score of 7+: Mortality 50-65%
Score of 4+ will generally meet admission criteria for observation
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Q
A
22
Q
Timi score:
* Still used by what?
* Estimates what?
* What does score of 0 not requrie?
A
- Still used by some internal medicine teams for risk stratification, Heart score proven to be superior
- Estimates mortality for patients with non-STEMI or unstable angina
- Generally scores of 0 would not require admission and patient may follow-up outpatient
23
Q
18yo female comes in to ED with chest pain. After detailed history, you learn that she also has had cough, sharp pain only on inspiration, SOB and runny nose for 1 day. V/S show temp 99.6, 100%RA, 61bpm, 119/62. Patient is not a smoker, does not use hormones and has no PMHx or FHx that is pertinent. Exam reveals lungs CTA b/l.
* What do you do to r/o life threatening condition?
A
Need to order EKG, covid, flu
24
Q
Cardiac Testing in ED
* What are the enzymes that you look up?
A
Troponin
* Rise in 4-6hrs, peak in 12hrs, Up for 7-10 days
CK
* Rise in few hours, normal in 48hrs
CK-MB
* Peak in 24hrs, Negative after 2-3 days since MI
* Use when repeat visit for CP post MI >4 days, <10 days.
CK-MB/CK index
* Ratio <3= Skeletal, >5= Cardiac
25
Cardiac Testing in ED
* D-Dimer: Could only be used as what? Do not use if what?
* Could only be used as a combination with a correct and validated pre-test clinical probability
* Don’t use if pretest criteria are negative
## Footnote
D-Dimer can be elevated without PE/VTE with pregnancy, age, trauma, cancer, inflammation and several other clinical conditions
26
What are the conditions that can associated with elevated cardiac troponin enzymes in absence of ischemic heart disease?
27
In suspected AMI, what is ordered?
* What are the values to ruled out MI?
* What happens if numbers or inbetweeen
* When is AMI possible?
HS troponin is ordered x 2 (1 hour apart)
* AMI ruled out if: Hour 0 is <6 ng/L AND 1hour △ <3 ng/L
* In between above and below -> observe and consider ordering 3rd troponin
* AMI is possible if
* >99% of upper reference limit (URL) OR 1hour △ >10 ng/L
* URL male 78 ng/L; URL female 54 ng/L
28
What is stable angina?
CP or SOB that is predictable
* Stress or exertion or after eating a big meal
* Goes away when you remove typical offending activity that causes increased heart stress
* >4 weeks
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What is unstable angina?
CP or SOB occurring for the first time or <2 weeks
* New pattern of usual CP (prolonged and more severe, happens more frequently)
* Happens spontaneously at rest or minimal activity
* MAY or MAY NOT go away with NTG or ASA
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Clinical Characteristics: Acute MI (ACS)
* How long is the pain?
* What does it feel like?
Pain longer than 15-30 min, building up to maximum
Dull or pressure-like pain in the midsternal or peristernal areas
* Levine sign (has 80% sensitivity)
* Pressure is equivalent to pain
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Clinical Characteristics: Acute MI (ACS)
* What are the associated sxs?
* Nausea, diaphoresis, SOB, fatigue
* Neck pain, arm pain, jaw pain
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Clinical Characteristics: Acute MI
* Be weary of the five causes of silent / atypical MI presentations?
* D Diabetes
* E Elderly
* A Alcohol
* T Trauma to the thoracic spinal cord
* H Hypertension
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What gender usually has atypical presentation?
FEMALE
Women more commonly than not, have atypical presentations (i.e. . Fatigue, gastroenteritis).
* May NEVER develop CP or SOB
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What are the sxs of atypical presentation?
* Weakness
* Shortness of breath
* Indigestion
* Dizziness
* Fatigue with minimal exertion
* New Onset A-Fibrillation
35
What are the 5 most frequent causes of new onset of a.fib?
* AMI (MC)
* PE
* Hyperthyroid state
* CHF
* Drug use
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54yo male smoker with Hx of HTN/DM/HLD/Obesity/2 stents on Plavix here with substernal chest pressure that is new for 1hr. Chest pain now resolved and patient wants to go home.
* What do you do?
* CBC, CMP, troponin, EKG, CXR
* Admit for observation
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# Risk Stratification for Acute Coronary Syndromes
EKG:
* What are some changes?
* Normal
* Non-specific S-ST changes
* Abnormal but not diagnostic
* Ischemic/strain/infarct that is old, Ischemic/strain/infarct not known to be old
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What are signs on EKG for probable AMI?
39
Unstable angina still a possibility in what?
Unstable angina still a possibility in normal or non-specific ECG (4-23%) - in this case you want to order serial EKG's
40
What is Scarbossa criteria? What are the components?
Utilize Scarbossa criteria in patient with preexisting LBBB or paced rhythms
* ST elevation of >1mm in leads concordant (same direction) as the QRS complex
* ST elevation >5mm in discordant (opposite direction) of QRS complex
* ST depression >1mm in leads V1, V2, V3
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What are the different leads?
42
What is this?
43
STEMI Update
* Plavix if being replaced by what?
* What is the dose?
* Plavix being replaced by Ticagrelor (Brillinta) due to superiority in PLATO study in STEMI patients
* Dose is 180mg
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Chest pain and Probability of ACS: Based on risk stratification
* Very low risk:
* Low risk:
* Possble ACS:
* Evidence of MI/STEMI/NSTEMI:
## Footnote
* PLAVIX OR BRILLINTA NOT USED IF ANY CONSIDERATION OF CABG
* CURRENT THERAPY FAVORS PTCA
45
Plaque rupture leads to what?
Plaque rupture leads to platelet activation and adhesion
46
Antiplatelet Agents
* What are the different agents? What are they used for? What do you need to make sure of?
47
What does antiplateletes agents do?
* INHIBITS CYCLOOXYGENASE NEEDED FOR SYNTHESIS OF THROMBOXANE A2 ( ACTIVATES PLATELET AGGREGATION
* Causes vasoconstriction
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Nitrates:
* What does it reduce?
* Titrate to what? What is the max dose?
* 35% reduction in mortality in AMI if not treated with thrombolytics
* Titrate to chest pain relief/ BP observe
* Up to 500ugm/min IV
49
When do you avoid nitrates?
Avoid in RV (hypotension) Infarct – preload dependent
* 1/3 of Inferior wall MI also have RV infarct
Avoid if on Viagra (even last night)
50
BB:
* Decrease what (2)
* When do you give it?
* Decrease CO (myocardial oxygen demand)
* Decrease mortality
* Give within 12 hours of presentation of STEMI or NSTEMI (metoprolol 5mg IV q 15 min x 3 doses)
51
What are the contraindications of BB?
* Bradycardia, hypotension, poor EF (AS), asthma, COPD, CHF, 2° or greater heart block
* Cocaine use
52
What are the anti-thrombin agents?
* When can you reverse?
* Dose?
* When do you not use? When is it great?
53
Stemi and PCI/PTCA
* What is the first option?
Option 1: PCI – TREATMENT OF CHOICE
* Preferred if time to “balloon” less than 90 mins, cardiogenic shock, or symptoms greater than 3 hours
54
Stemi and PCI/PTCA
* What is the second option?
Option 2: Thrombolytic Therapy (Alteplase/Reteplase/Tenecteplase)
* Inclusion criteria – If symptoms started within 12 hours and PCI cannot be performed in less than 120 minutes
* Exclusions apply to tPA
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Stemi thrombolytics:
* What is last resort? When do you give it
Alteplase (tPA) over 2 hrs – LAST RESORT
* 1 mm of ST elevation in 2 consecutive leads
* Symptoms less than 12 hours
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What are the contraindications of thrombolytics?
* ICH
* CVA within a year
* Intracranial tumor
* Active internal bleeding
* **Suspect aortic dissection or pericarditis**
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Cooling Protocol
* When do you induce hypothermia?
* What rhythms should you and should not do this?
* Improve what?
Induce Hypothermia after cardiac arrest/ROSC (32C=89.6F)
* Asystole – No
* V-Fib – Yes
* V-Tach without pulse – Yes
Improved functional recovery and reduced cerebral histological deficits (becasue decrease metabolism so decrease acidosis)
58
59yo female with Hx of HTN/HLD/NIDDM with FHx of CAD (brother died at age 56 from AMI) In ED with indigestion, diaphoresis and DOE. After initial visit, POC troponin and EKG are normal. Patient tells you she has constant pain that is getting progressively worse.
* What do you do?
* Get a second troponin
* Serial EKG q 10-15 mins
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Clinical Characteristics: Aortic Dissection
* Most common people?
* What is are the sxs? (4)
* Most are hypertensive males 50 – 70 yo
* Infrascapular severe pain with abrupt onset, and worst at onset
* “Ripping, tearing”
* AMI (acending into conorary)
* CVA ( PAIN ) if Abdominal Aortic Dissection
* Pericardial tamponade – if ascending aorta.
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Which aneruyem is more common
Thoracic dissection is 2 to 3 times more common than abdominal AA.
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Specific Findings: Aortic Dissection
* What happens to BP and HR?
* What can be on CXR?
* What happens with the pulse?
* What is another presentation?
* Hypertension and tachycardia
* Hypotension can occur in dissection of ascending aorta
* Abnormal aortic contour on CXR (90%)
* Decreased / unequal pulses in radial, femoral, or carotid arteries (50%) – always do BP in both arms
* Paraplegia / **neurologic presentation** (40% due to loss of volume to brain flow)/ **Ascending Thoracic Aorta**
## Footnote
Patients with aortic dissection are elderly males, with a history of hypertension, atherosclerosis and present with tearing chest pain. On presentation, the BP may be high, usually above 160. Bilateral pressures may be unequal. If the patient is hypotensive, one must consider dissection of the ascending aorta due to impending tamponade or rupture. On CXR, the patient will have a widened mediastinum. When present, these signs are diagnostic for dissection.
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Initial Evaluation: Risk Factors - Dissection
* What is a big factor?
* If they have predisposing conditions, then what do you need to do?
* Hypertension
* Predisposing conditions: If they have it – look for dissections, not ACS with chest pain complaints
* Marfan’s, Ehlers-Danlos syndrome, coarctation of the aorta, trauma
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Aortic dissection:
* What can you see on CXR (4)
* 90% will have an abnormal CXR
* Widen mediastinum
* Deviation of trachea, bronchus
* Pleural effusion
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Aortic dissection:
* What is the gold standard?
* What else can you do?
Aorta angiogram
* “gold standard”, risk of procedure, time delay
CT Angiogram – most likely test to use in real life (next best test)
* Fast
* Sensitive but does not evaluate aortic valve-> Aortic insufficiency (dt prox dissection, decr CO, BP, Pleural Effusion)
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What is this?
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Treatment: Thoracic Aortic Dissection (2-3 x more frequent than AAA)
* What is type 1 and 2? What is the treatment?
Type I: ascending and proximal descending aorta
Type II: ascending aorta only (most lethal)
* Surgery
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Treatment: Thoracic Aortic Dissection (2-3 x more frequent than AAA)
* What is type 3? What is the treatment?
Type III: descending aorta only (most common)
* Medical until 5 cm or greater
* Don’t go to Sx until they show hemodynamic changes
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What is the medical txt of Thoracic Aortic Dissection?
Antihypertensives (control BP and HR)
* B-blockers (esmolol gtt)
* Sodium nitroprusside with B-blockers
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Aortic dissection
* Any presurgical management of AD requires what? Explain
Any presurgical management of AD requires BP control.
* Target SBP of <120 mmHg
* Esmolol, Na Nitroprusside, Cardene (nicardipine)
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Ambulance brings in a 64yo male with tearing chest pain for the last 30 minutes going to his abdomen and back that is not getting better. BP is 199/90, HR 110, O2 99% RA, patient is uncomfortable, diaphoretic. Right arm pressure is less than left by 20mmHg. XR tech shoots a quick CXR which reveals widened mediastinum.
* What do you do?
* BP down
* EKG
* Order CTA with runoff
* Type and screen
* Order rapid blood
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Acute pericarditis:
* What are sxs?
* Chest Pain, better with leaning forward
* Fever, dyspnea, dysphagia
* Friction Rub – present when hold your breath
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Acute pericarditis:
* What does the EKG, CXR and enzymes show?
* EKG: Diffuse ST elevation, PR depression (early)
* CXR: normal
* Enzymes normal unless myocarditis
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Acute Pericarditis
* What is this txt?
* TX: NSAID’s 1-3 weeks
* TX any identified underlying cause
* Post MI – Dressler syndrome
## Footnote
Dresslers – will come 6-8 weeks later. Inflammatory response following AMI. Never give steroids to Dresslers – prevents tissue redevelopment.
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Myocarditis:
* What is mc cause?
* May result in what?
* Typical diagnosis following what?
* Even if there is no symptoms, you should consider getting what?
* Viral etiologies are most common (Coxsackie B)
* May result in heart failure
* Typical diagnosis following viral URI/GI symptoms with chest pain and elevated cardiac markers
* Even if there is no symptoms, you should consider getting an EKG to look for changes if they recently recovered from suspected pericarditis
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What is the gold standard of myocarditis?
Cardiac MRI is gold standard (NOT an ER test)
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Myocarditis
* Should not clear what?
* When do patients get cleared? Why? (3)
Should NOT clear these patients for sports from ER
(Only of you work in outpatient setting) - Cannot clear these patients for sports for at least 6 months
* Linked to sudden cardiac death (based on autopsy findings)
* Depending on severity should repeat ECG, cardiac markers, Holter and cardiac MRI prior to resumption of athletic activities.
* Do not order tests that you do not know how to interpret (see next slide)
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Non-traumatic Cardiac Tamponade (Cancer,Dialysis Pts)
* What are the sxs?
* Dyspnea, exercise intolerance
* Tachycardia, low blood pressure, narrow pulse pressure, **pulsus paradoxus** (more than 10 mm Hg drop in SBP during inspiration in supine position), elevated JVP, distant or soft heart sounds
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Non-traumatic Cardiac Tamponade (Cancer,Dialysis Pts)
* What does the CXR, EKG show?
* What is the txt?
* CXR possibly enlarged cardiac silhouette (4 HEART CHAMBERS EQUAL PRESSURE)
* EKG low voltage; electrical alternans
* TX: pericardiocentesis
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Mitral Valve Prolapse
* What type of syndrome?
* Possibly what?
* What is happening in the heart?
* Click-Murmur Syndrome
* Possibly congenital; common
* Leaflets prolapse into atrium during systole
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Mitral Valve Prolapse
* What are the sxs?
* What does the EKG and CXR show?
* What is the txt for asymptomatic and symptomatic?
* Most patients asymptomatic
* Symptoms: chest pain, palpitations, fatigue, dyspnea (not exertional), and ANXIETY
* EKG and CXR usually normal
* FLAT OR INVERTED T-WAVES LEADS II, III AND AVF
* Tx Asymptomatic: re-assure
* Symptomatic: beta blockers, avoid alcohol, caffeine, tobacco
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Chest Pain Pearls
* A normal EKG does not rule out what?
* Normal enzymes do not rule out what?
* Examine every CXR closely for evidence what?
* Remember bilateral what?
* **A normal EKG does not rule out cardiac etiology**
* **Normal enzymes do not rule out an MI** 8% of AMIs will have reproducible chest wall pain
* Examine every CXR closely for evidence of pneumothorax or aortic dissection
* Remember bilateral BPs - especially in elderly and predisposing conditions
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If you put something in your differential, you need to do what?
If you put something in your differential, you need to prove that you looked for it.
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Hypertensive Urgency
* Also known as what?
* Dx criteria is what?
* What is the basic work up?
* Managed acutely with what?
* Also known as “Malignant Hypertension”, “Hypertensive Crisis” or just “Severe Hypertension”
* Dx criteria is BP >180/110mmHg or MAP >135 **without** end organ damage
* Basic work-up should include chemistry, ECG and troponin (looking for end organ damage)
* Managed acutely with labetalol or nicardipine to target 10-25% in the first hour
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HTN emergencies:
* What is it?
* What are the sxs?
## Footnote
* URGENCY MEANS NO ORGAN SYSTEM INVOLVED
* When DBP>140 – no autoregulation >>> need for chemical intervention
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HTN encephalopathy:
* Implies what?
* Most commonly seen with a BP of what?
* BP exceeds limits of what? What happens?
* Implies mentation change (i.e. GCS less than 15)
* Most commonly seen with BP >220/120mmHg, but required to meet only hypertensive urgency criteria
* BP exceeds limits of autoregulation (MAP>150/DBP>140)
* Cerebral hyper-perfusion
* Posterior reversible encephalopathy syndrome (PRES) is a syndrome characterized by headache, confusion, seizures and visual loss. It may occur due to a number of causes, predominantly malignant hypertension
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What is the onset and sxs of HTN Encephalopathy
Acute onset, progressive over hours
* Reversible
* Headache, nausea, vomiting, AMS, seizures, focal deficits, coma, death
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Treatment of Hypertensive Encephalopathy
* What do you do immediately?
* ABC’s
* Immediate BP reduction: no more than 20-25% in the 1st hour to prevent progression of stroke and lower perfusion to kidneys and heart.
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How do you drop the BP in Hypertensive Encephalopathy
* Nicardipine drip used most frequently - 2mg IVP, 4-15mg/h infusion
* Labetalol
* Nitroprusside 0.3-10 micrograms/kg/min (see in board questions)
* NTG, labetalol (not if Viagra/cocaine user
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HTN with Stroke
* What it is?
* Dx via what?
* What are the two types?
Elevated blood pressure and AMS or other neurological deficits
Diagnosis via imaging, CT without contrast
2 fundamental types
* Thromboembolic
* Hemorrhagic
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Treatment of HTN with Stroke: Thrombo-embolic stroke(85%)
* What is the txt?
Avoid routine reduction in BP
* Lead to increased area of hypoperfusion
* Some studies note to allow permissive hypertension as high as 215 systolic
Diastolic > 140 (need to go to below 120 or so)
* BP/MAP reduction of no more than 20-25%
* Labetalol 20 mg IV over 2 minutes ( may repeat )
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Treatment of HTN with Stroke: Hemorrhagic stroke(15%)
* What is the txt?
* Controversial
* Nimodipine (SAH) 60mg po q 4h – CCB to prevent severe constriction in brain BV that leads to hypoperfusion
* Nicardipine (Cardene®) 2mg IVP, 4-15mg/h infusion
* Labetalol, nitroprusside
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CHF
* Typically what?
* Patients is usually what?
* What are the Sxs?
* What is the general txt?
* Typically systolic failure
* Patient is usually fluid overloaded following holidays
* Symptoms: SOB, pitting/pulmonary edema and DOE
* General treatment consists of Loop diuretics (Lasix 80mg first dose)
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CHF
* Moderate SOB with pulmonary edema responds well to what?
* Usually do not use digoxin due to what?
* If hypotensive, what is last resort and why? what is the alternative?
* Moderate SOB with pulmonary edema responds well to BiPAP and nitroglycerin drip along with Lasix
* Usually do not use digoxin due to lack of survival benefit and even then, can only be used in reduced EF.
* If hypotensive, Dobutamine as last resort --> can cause arrhythmia and beta blockers should be avoided
* Norepi is an alternative
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What do you do for:
* Stable brady:
* Unstable bradycardia:
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Arrhythmias - AV blocks
* If stable:
* If unstable:
* Symptomatic blocks or any 3rd degree blocks require what?
* Generally, should avoid what?
* If stable – monitor the patient
* If unstable – atropine 0.5mg
* Symptomatic blocks or any 3rd degree blocks require temporary transcutaneous pacing in ED and placement of ICD upon admission
* Generally, should avoid atropine is suspicious for ACS
97
Arrhythmias – Atrial flutter
* What is it?
* How do you txt stable?
* Ectopic rhythm, NOT paroxysmal/reentry, so cannot use vagal maneuvers to terminate
* Stable – rate control via BB or CCB (<100bpm) and anticoagulation
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Arrhythmias – Atrial flutter
* How do you treat unstable?
cardiovert with 50J biphasic shock (only if onset within 48hrs and can be proven with an EKG; or they are anticoagulated already for unrelated issue >3 weeks)
* Can get a TEE done but it is time consuming
Otherwise, give them amiodarone gtt
99
Arrhythmias – Atrial Fibrillation
* In terms of ER care, essentially the same as what?
* Stable ones get what? How?
* In terms of ER care, essentially the same as atrial flutter
* Stable ones get anticoagulated and rate controlled
* Rate control with IV bolus and titratable drip **Cardizem** OR Ibutilide OR Amiodarone OR Dronedarone OR Metoprolol OR Digoxin.
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Arrhythmias - SVT
* What do you do first if stable? Avoid what?
* If unstable do what?
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Arrhythmias – Wide complex Tachycardia
* What is this?
* Avoid what?
* Consider giving what?
* What happens if unstable?
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Arrhythmias – Sustained VT
* Typically seen in who?
* What do you give for stable and unstable?
103
Arrhythmias – Monomorphic VT
* If stable, what do you do?
If stable: start with IV fluids and look for source.
* Start Amiodarone 150mg or Procainamide 50mg/min drip
* May give Adenosine 6mg only if regular and monomorphic.
* Could also just do Amiodarone 150mg or Procainamide 50mg/min drip
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Arrhythmias – Monomorphic VT
* If unstable and with pulse:
* If unstable and without pulse with wide rhythm:
* If unstable and with pulse: Synchronized cardioversion at 100J to start
* If unstable and without pulse with wide rhythm: give unsynchronized cardioversion at 200J. AKA Code Blue
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Arrhythmias – Polymorphic VT
* Also known as what?
* How do you txt?
Known as Torsades
* Unsynchronized cardioversion at 200J
* 2g of Magnesium Sulfate to stabilize membrane
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# FYI
How do you run a code blue?
## Footnote
Of course avoid tPA if mediastinum is widened, trauma patient or evidence of hemorrhage
107
Arrhythmias – Asystole/PEA
* Cannot do what?
* How do you txt?
Cannot shock any lack of rhythm
* Treated with Epinephrine 1mg every 3 minutes and quality CPR
* Vasopressin can replace only 1st or 2nd dose of Epi
108
Arrhythmias - WPW
* What do you do for these patients (stable and unstable)?
Typically just monitor however NEVER give AV nodal blocking agents (Digoxin, BB, CCB) because you will block Regular pathway and Accessory pathway will take over.
* Give them Amiodarone OR Ibutilide OR Procainamide if unstable
109
What is the SIRS criteria
Inflammatory state affecting whole body
* tachycardia (heart rate >90 beats/min)
* tachypnea (respiratory rate >20 breaths/min or PaCO2<32mmHg)
* fever or hypothermia (temperature >38 (100.4F) or <36 °C (96.8F))
* Leukocytosis (white blood cells >12,000 per µL, leukopenia (<4,000 µL), or bandemia (bands ≥10%)
| If patient has any 2 of the above, patient screened positive for SIRS
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Sepsis:
* What it is?
* What is the criteria to have sepsis?
* What is the mainstay txt?
* What can impact outcomes?
* Sepsis is the body’s extreme response to an infection which overwhelmed body’s defenses
* 2 SIRS criteria + Source of infection (suspected or known) = Sepsis
* Hemodynamic management and early goal directed infection control with antibiotics is the mainstay of treatment.
* Even minimal delays of fluids and broad-spectrum antibiotics administration can adversely impact outcomes
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Severe Sepsis diagnosis
* What it is?
* What is the criteria?
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What is severe sepsis?
Severe Sepsis is sepsis with impaired blood flow to body tissues (hypoperfusion) or detectable organ dysfunction (e.g., with fever, encephalopathy, renal failure and Lactate >2 *previous slide) and could have normal blood pressure OR hypotension.
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What is septic shock?
Septic Shock is severe sepsis with sepsis-induced hypotension (systolic blood pressure < 90 mmHg (or a drop of > 40 mmHg from baseline) or mean arterial pressure < 70 mm Hg) that persists after adequate fluid resuscitation (30cc/kg).
* Lactic Acid >4 is a septic shock regardless of pressure
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Sepsis Treatment IVF's
* For intravascular fluid resuscitation, various types of intravenous fluids are available, which can be broadly divided into two categories?
(1) crystalloid solutions (normal saline and Ringer’s Lactate) - Much cheaper than #2
- only give 2L of NS before switching to LR due to renal
(2) colloid solutions (albumin, hydroxyethyl starch (HES), dextrans, gelatins, and plasma) - higher incidence of side effects
## Footnote
No significant difference found between fluids in sepsis management but #1 is preferred generally. Normal saline is a typical preferred choice in real life however, Ringer’s lactate has lower chloride concentration than normal saline. Excess chloride can lead to hyperchloremic acidosis.
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Things to Consider
* What do you need to consider with fluids?
Patient must receive some fluids, even a 100cc bolus is ok in following special situations. But you must document exception to full bolus:
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Fill in antibiotics
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Bottom Line
* look at what to evalute for SIRS
* What is sepsis?
* What is sever sepsis?
* What is Septic shock?
* What is MODs?
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Sepsis Bundles
* What do you to five in the first hour?
* Get lactate level
* Obtain Blood Cultures (2 sets) prior to Antibiotics administration
* Give antibiotics based on source and risk factors
* Administer 30cc/kg of IVF's bolus crystalloid solution for hypotension or lactate >4mmol/L
* Document if bolus is too much (CHF, pulmonary edema…)
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Sepsis Bundles
* What do you within Within 3 hours of recognizing sepsis?
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In the event of persistent arterial hypotension despite volume resuscitation (septic shock) or initial lactate ≥ 4 mmol/L (36 mg/dL), what do you do?
* Measure central venous pressure (CVP)
* Measure central venous oxygen saturation (ScvO2)
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Shock types
* What are the different types?
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SIRS and Septic Shock
* What is the txt?
* What population will not have fever?
* What is the MC pathogen?
* Treatment with IV fluids resuscitation and antibiotics
* Elderly and neonates usually have hypothermia, not fever
* Most common pathogens in US causing sepsis are gram-positive bacteria, including streptococcal pneumonia and Enterococcus
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Anaphylactic Shock
* What is it?
* What is released? What does that cause?
Ig-E mediated severe hypersensitivity reaction causing cardiac and respiratory collapse.
Histamine Release
* Vasodilation= HYPOTENSION
* Smooth muscle constriction = DYSPNEA
* Increase capillary permeability = DYSPNEA
## Footnote
0.3-0.5 mg of 1:1000 Sub-Q repeated every 5-10-20 minutes as needed and reassess after 3 doses of Epi for improvement. If cardiovascular collapse - 0.1 mg 1:10,000 IV over 5-10 minutes while watching the monitor for arrhythmias.
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What is the txt of Anaphylactic Shock?
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H1 & H2 Antihistamines
* No studies support what? Why?
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Glucocorticoids
* No studies on what?
* Onset?
* Rationale for use?
* Only use for how long without taper?
* NO STUDIES show effectiveness in anaphylaxis
* Onset of action = several hours
* Rationale for use = prevent biphasic or protracted reactions
* Only use for 1-2 days without taper
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Biphasic Anaphylaxis
* When does it occur?
* Recurrence can be severe enough to warrant what?
* What decreases occurrence?
* Typically occur 4-10 hrs (up to 72 hrs) after resolution of initial symptoms
* Recurrence can be severe enough to warrant intubation and vasopressor administration
* Earlier epinephrine administration decreases occurrence
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What is the doses for Epi IV and SQ?
## Footnote
New evidence to support glucagon administration to promote positive inotropic and chronotropic effects especially for those that are on BBs.
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Angioedema
* Developes when?
* Can be what?
* Laryngeal edema can progress to what?
* What should you do early?
* Angioedema generally develops over **minutes to hours and resolves in 24 to 48 hours.**
* Angioedema can be life-threatening if it involves the larynx.
* Laryngeal edema can progress to airway compromise and asphyxiation.
* Intubate early to protect airway
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What is the txt for angioedema?
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Endocrine shock:
* Caused by what?
* What is the txt?
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Neurogenic shock
* What causes it?
* Seen with what?
* Nerve injury leading to dysregulation
* Seen with upper thoracic and cervical trauma resulting in interruption of sympathetic pathways and decreased global vascular resistance with vagal tone change (Spinal Shock/UMN)
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Neurogenic shock
* What are the sxs?
* What is the txt?
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Spinal Shock
* usually after what?
* Expect what? (incomplete vs complete?)
* Usually following trauma
* Expect areflexia, loss of sensation, paralysis and loss of rectal tone
* Incomplete: usually resolve after few days
* Complete: unlikely to regain function again
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Spinal Shock
* What is the management?
Supportive management is advised but avoid lots of fluids to prevent pulmonary edema
* Hypotension management as per Neurogenic shock
* Give IV steroids and transfer to trauma/surgical intervention
* Methylprednisolone IV (30mg/kg bolus; and 5.6mg/kg/hr for 24 hrs) – although weak evidence from AANSCN
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Cardiogenic shock
* AKA what?
* What should you increase?
* Usually results when?
* Can be seen with what?
* What is high? What are the sxs?
* Avoid what?
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Cardiogenic Shock
* What is the txt?
* Need to get to where?
* What are the DOC (2) for hypotension?
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Obstructive Shock
* Typically seen with what?
* List the causes?
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Hypovolemic shock
* Decreased what?
* What are the two types?
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Hypovolemic shock:
* What do you do?
As in Sepsis, start with fluids (30cc/kg), then if failed, move on to vasopressors
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What are the inopressers?
Epinephrine
* Nonselective beta/alpha agonism -> increased contractility, chronotropy, peripheral vasoconstriction.
NorEpinephrine
* More vasoconstriction peripherally than inotropy
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What are pure vasopressors?
Pure (i.e. peripheral) vasoconstrictors
Phenylephrine
* Pure alpha agonist -> useful in A.fib since it avoids beta cardiac receptor activation
Vasopressin
* No effect on cardiac contractility
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What are the inodilators?
Inodilators (usually in early cardiogenic shock)
* Dobutamine
* Milrinone
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Vasopressors Summary Bottom Line
* What is first line for septic shock management and fluid refractory patients? Add what if needed?
* What is first line for is first choice in cardiogenic shock and CHF? What should you avoid
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* Phenylephrine ideal in what?
* Atropine: Best for what?
Phenylephrine
* Ideal in aortic stenosis (reduces stroke volume) and sometimes A.fib
Atropine
* Best in symptomatic bradycardia or neurogenic/spinal shock
