challenging complex case studies handout 2017 part ii · 4/22/2017 1 sharpening your critical...

4/22/2017

1

Sharpening Your Critical Thinking Skills with Challenging Case StudiesPart II

[email protected]

www.cherylherrmann.com UnityPoint Health- PeoriaHeart of IL AACN – President

Class C150M610

Case Study # 4

BB

Bradycardia Case StudiesBradycardia Case Aelective Transesophageal echocardiogram/ cardioversion

PMH

▪ Atrial fibrillation

▪ Cardiomyopathy with severe LV dysfunction

▪ CHF- Euvolemic at this time

▪ Obesity/ possible sleep apnea

Labs

▪ Sodium 139

▪ Potassium 4.2

▪ Chloride 102

▪ C02 31

▪ BUN 29

▪ Creatinine 1.47

▪ GFR 35

▪ Magnesium 2.0

Home medications

▪ Alendronate (Flosmax) 70 mg daily

▪ Eliquis 5 mg BID

▪ ASA 325 mg daily

▪ Wellbutrin SR 160 mg BID

▪ Cetirizine (Zyrtec) 10 mg daily

▪ Lasix 40 mg 2 tab in the am & 1 tab at night

▪ Levothroid 150 mcg daily

▪ Lisinopril 20 mg daily

▪ Metoprolol tartrate 50 mg BID ( took 2 ½ hours prior to cardioversion)

▪ Pravachol 40 mg daily

Bradycardia Case BVery Elderly ED with Bradycardia

▪ BP 151/80, HR 40, RR 18, T 36.3 C, SpO2 95%

▪ Sinus Bradycardia

▪ Alert/oriented

▪ PMH

– Hypertension

– Hyperlipidemia

– Depression

– Anemia

– GERD

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medications

Was given

▪ Losartan 100mg

▪ Lopressor XL 300 mg

▪ Nifedipine 60 mg

▪ Sertraline 75 mg

Should have taken

▪ Xanax 0.5 mg HS

▪ Imdur 30 mg daily

▪ Losartan 25 mg daily

▪ Meclizine 25 mg TID

▪ Melatonin 3 mg tabs daily

▪ Compazine 10 mg daily

Bradycardia Case C

▪ EMS called for syncope/altered level of consciousness

▪ HR 29 (Junctional vs Sinus Brady)

▪ Hypotension and unresponsive

▪ Intubated

▪ External pacer

▪ Helicopter to regional hospital for emergent pacer insertion

▪ Cardiac history, unable to get medication list

What is the common cause of the bradycardia in these 3 patients?

A. Hypoxia

B. Sick Sinus Syndrome

C. AV Block

D. Toxicity

E. Hypothyroidism

What is the common cause of the bradycardia in these 2 patients?

A.

B.

C.

D. Toxicity

E.

Back to…Bradycardia Case Studies

elective Transesophageal Echocardiogram/ Cardioversion (TEE)

PMH

▪ Atrial fibrillation

▪ Cardiomyopathy with severe LV dysfunction

▪ CHF- Euvolemic at this time

▪ Obesity/ possible sleep apnea

Labs

▪ Sodium 139

▪ Potassium 4.2

▪ Chloride 102

▪ C02 31

▪ BUN 29

▪ Creatinine 1.47

▪ GFR 35

▪ Magnesium 2.0

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Rhythm post cardioversion (0800)

▪ BP dropped to 78/56

▪ Atropine & Epinephrine given

▪ IV fluids given

12 Lead EKG post cardioversion and atropine (10/9 0813)

Denies dizziness, lightheadedness, chest pain

▪ Continue close monitoring for now

▪ Keep atropine and transcutaneous pacemaker at bedside

▪ Dopamine drip if SBP < 80 mmHg or HR < 35 bpm

▪ Alert/Oriented x 3

▪ May need pacer

– NPO

– Hold anticoagulant

▪ Creatinine ↑ 2.24, GRF ↓ 22

▪ Started Dopamine at 2 mcg/kg/min to keep SBP > 90

– Pt baseline SBP was 100 – 110

Dopamine and Atropine did not increase the heart rate. What else do you want to do?

A. Observe as she is alert/oriented & putting out urine

B. Go for pacemaker

C. Other

Dopamine and Atropine did not increase the heart rate. What else do you want to do?

A. Observe as she is alert/oriented & putting out urine

B. Go for pacemaker

C. Other

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Remember her home meds?What’s concerning?

▪ Alendronate (Flosmax) 70 mg daily

▪ Eliquis 5 mg BID

▪ ASA 325 mg daily

▪ Wellbutrin SR 160 mg BID

▪ Cetirizine (Zyrtec) 10 mg daily

▪ Lasix 40 mg 2 tab in the am & 1 tab at night

▪ Levothroid 150 mcg daily

▪ Lisinopril 20 mg daily

▪ Pravachol 40 mg daily

▪ Metoprolol tartrate 50 mg BID (took 2 ½ hours prior to cardioversion)

Glucagon 1 mg given IV at 1027 on 11-10 (day later)

After

Glucagon

Case BVery Elderly comes to ED with Bradycardia

▪ BP 151/80, HR 40, RR 18, T 36.3 C, SpO2 95%

▪ Sinus Bradycardia

▪ Alert/oriented

▪ PMH

– Hypertension

– Hyperlipidemia

– Depression

– Anemia

– GERD

medications

Was given

▪ Losartan 100mg

▪ Lopressor XL 300 mg

▪ Nifedipine 60 mg

▪ Sertraline 75 mg

Should have taken

▪ Xanax 0.5 mg HS

▪ Imdur 30 mg daily

▪ Losartan 25 mg daily

▪ Meclizine 25 mg TID

▪ Melatonin 3 mg tabs daily

▪ Compazine 10 mg daily

▪ Notified poison control

▪ IV glucagon if symptomatic

– Glucagon was not needed

Bradycardia Case C

▪ EMS called for syncope/altered level of consciousness

▪ HR 29 (Junctional vs Sinus Brady)

▪ Hypotension and unresponsive

▪ Intubated

▪ External pacer

▪ Helicopter to regional hospital for emergent pacer insertion

▪ Cardiac history, unable to get medication list

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▪ Given Calcium and Gluconate IV

▪ Immediate response – sinus rhythm

▪ Extubated

▪ Alert/Oriented/Up in chair next morning

Since the rhythm was not a Heart Block,

Cardiologist was suspicious that it was

medication induced

Calcium Channel Blocker (CCB) and Beta Blocker Toxicity

▪ Manifestations of toxicity are extensions of the therapeutic effects of the drug

– Hypotension

– Bradycardia

– Conduction block,

– Myocardial depression

– Decreased contractility (both negative inotropes)

▪ Amount ingested and underlying cardiovascular health determine the severity

– May be asymptomatic to cardiovascular collapse

Reference: Marraffa, J. Cohen, V. & Howland, M.A. Antidotes for Toxicological Emergencies Am J Health Syst Pharm. 2012;69(3):199-212.

AHA ACLS EP.: 2013

Symptoms CCB & Beta Blocker Toxicity

CCB

▪ Awake & Alert even if profound hypotension and bradycardia

▪ Hyperglycemia– Release of insulin from

pancreatic B cells via calcium-dependent pathway

▪ Dihydropyridine CCB (nifedpine)– Peripheral vasodilator

– Limited effect on cardiac rhythm

Beta Blocker

▪ Altered mental status

▪ Respiratory depression

▪ Hypoglycemia/ Hyperkalemia

▪ Arrhythmias – Torsades, VF, AV block

▪ Propranolol– Seizures

– Widened QRS


Combination of

CCB & BB

toxicity can be

serious & life

threatening

Symptom onset with overdose

▪ Regular Released Preparations

– 2-4 hours after ingestion

– If symptoms don’t present within 4 – 6 hours, moderate to severe toxicity is unlikely to occur

▪ Controlled Released Preparations

– May not be seen until 6 – 18 hours after ingestion

Don’t forget --- Symptoms may also occur with

accumulative effect of prescribed medications


AHA ACLS EP.: 2013

TreatmentCCB & Beta Blocker Toxicity

▪ IV fluids 500 - 1000 ml bolus for hypotension

▪ Atropine for bradycardia

▪ Calcium

▪ Glucagon

▪ Hyperinsulinemia–Euglycemia Therapy (HIET),

▪ Vasopressors

▪ Cardiac pacing


AHA ACLS EP.: 2013

Calcium

▪ First line therapy for both CCB & BB toxicity, along with Atropine

▪ Calcium is necessary for automaticity, conduction, contraction, and vascular tone

▪ Works best with mild toxicity; severe toxicity requires additional therapies


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Calcium Chloride vs Calcium Gluconate

10 ml of 10% Ca Cl = 30 ml of 10% Ca Gluconate

Calcium Chloride

▪ Give via central line

– Avoid extravasation

– Extremely damaging to tissues

▪ Start with 10 ml with additional doses every 15 – 20 minutes

Calcium Gluconate

▪ Okay to give via peripheral IV

– Less damaging to tissues

▪ Start with 30 ml with additional doses every 15 – 20 minutes


Both: After 3 does, monitor ionized calcium to avoid hypercalcemia

Other Calcium pearls

▪ Hypercalcemia may lead to

– Ileus

– Myocardial depression

– Hyporeflexia

– Altered mental status

▪ Avoid calcium administration with digoxin toxicity

– May lead to asystole


Glucagon

▪ Increases cAMP (cyclic adenosine monophosphate)

– Enhances inotropy (contractility) and chronotrophy(conduction)

▪ Used for BB toxicity.

▪ May also be used with CCB toxicity as many times CCB and BB toxicity occur together

▪ Rapid action, short duration (15 minutes)

▪ Dosage 50 mcg/kg or 3 – 5 mg up to 10 mg

– Continuous infusion may be used if favorable results are seen


Glucagon Side Effects

▪ Side Effects

– Nausea & vomiting � risk for aspiration

▪ Give antiemetics (metoclopramide and serotonin antagonists

– Hyperglycemia, followed hypoglycemia (rare)


Hyperinsulinemia–EuglycemiaTherapy (HIET)

▪ HIET possibly enhances carbohydrate use & energy production by myocardial cells = increased contractility

▪ High doses of insulin = inotrope

▪ Glucose-Insulin infusion

▪ Slow acting 15 – 60 minutes

▪ Use after fluids, atropine, calcium, glucagon… and yet start early– Rule of thumb, if thinking vasopressor, start HIET

– If started early, may not need vasopressors

▪ Monitor closely for hypoglycemia and hypokalemia


Case Study # 5

HPTH

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presents to ED for 2nd consecutive day for c/o left flank pain

▪ PMH– Hypertension, recent diagnosis, currently on Lisinopril and HCTZ

– Hypothyroidism, currently on Levothyroxine

– Sarcoidosis

– Obstructive sleep apnea

▪ Intermittently severe left flank pain that she thought was similar to "kidney stone pain" that she had experienced previously.

▪ CT scan two days ago � left upper quadrant vascular abnormality, no ureteral stones or hydronephrosis– Treated with Toradol

– Given Norco and Flexeril to take post discharge

▪ Continued to have increasingly severe pain– Plan: IV contrast CT scan

– Creatinine 1.7 Admitted for aggressive IV hydration prior to IV contrast CT scan

Admission Assessment

Vital Signs

▪ BP 180/92, HR 45, RR 16, T 97.1

▪ Sp02 98% on room air

Abnormal Labs

▪ Creatinine 1.6 ↑

▪ Bun 29 ↓

▪ GFR 34 ↓

▪ TSH 165 ↑– Thyroid Stimulating

Hormone

Admission What is the cause of the bradycardia?

A. Pain medications

B. Sick Sinus Syndrome

C. AV Block

D. Toxicity

E. Hypothyroidism

What is the cause of the bradycardia?

A.

B.

C.

D.

E. Hypothyroidism

And the rest of the story….

▪ TSH was 165

– Normal TSH 0.358-3.740 uIU/ml

▪ One month ago, when getting refilled prescription, Levothyroxine 25 mg was prescribed rather than her typical dose of 125 mg daily

▪ Restarted on 125 mg Levothyroxine. TSH was back to normal when rechecked one month later

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Bradycardia Pearls

▪ Is the patient stable or unstable?

▪ What is the rhythm?

– Sinus Bradycardia

– Junctional Rhythm

– AV Block

▪ LOOK for causes

– Medications

– Disease processes

– Electrolytes/other abnormal labs

▪ TREAT the cause

Case Study # 6

HP

Young pt comes to ED with SOB

▪ About 1 ½ weeks ago, became more SOB which limited his activity.

▪ Unable to walk for even short periods of time without becoming SOB.

▪ Last night the SOB had gotten to the point where he could not take it any more so came to the ED.

▪ Dry hacking nonproductive cough

▪ Denies fever

▪ Smokes 1 – 1 ½ packs per day x 15 years

▪ BP 161/116, HR 83, RR 20, T 97.8

▪ SpO2 = 93% on room air

▪ Respirations easy & regular

▪ No acute distress

▪ Clear lung sounds on left

▪ Diminished lung sounds on the right from nipple line down

▪ Ht 6’ 4”, Wt 105 kg

Admission CXR 7-9

7-9 adm7-9 adm lat

What do you think?

A. Atelectasis

B. Tumor

C. Pleural Effusion

D. Pneumothorax

7-9 adm

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What do you think?

A. Atelectasis

B. Tumor

C. Pleural Effusion

D. Pneumothorax

What do you think?

A.

B.

C. Pleural Effusion

D.

7-9 adm

CXR after drained 1600 ml with thoracentesis

7-9 post thoracentesis 1600 ml

Normal Echo of another pt

Breno Pessanha, MD

ECHO on 7-9

▪ Pericardial Effusion

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More History

▪ Video-assisted thoracoscopy (VAT) with biopsies 8 months ago– Negative for malignant cells

– Positive for histoplasmosis

▪ Started on Sporanox – oral antifungal

▪ Right subclavian stent placed for superior vena cava syndrome

▪ Was discharged from correctional facility three weeks ago– Stopped taking Sporanox due to inability to pay

HistoplasmosisCave disease, Spelunker’s Lung, Darling's disease,Ohio valley disease, Reticuloendotheliosis,

▪ An infection transmitted by airborne spores from soil that contains a fungus called Histoplasma capsulatum.

▪ The spores are extremely light and float into the air when dirt or other contaminated material is disturbed.

▪ Generally affects the lungs-- may spread to other organs or tissues

High Risk Populations

▪ Farmers

▪ Landscapers

▪ Construction workers

▪ Especially in the Ohio & Mississippi River Valleys

▪ People who have contact with bird or bat droppings

Types of Histoplasmosis

• Asymptomatic primary histoplasmosis– Most common form

– Usually causes no S/S --- just small scars in the lungs

• Acute symptomatic pulmonary histoplasmosis– Occurs in healthy people who have had intense exposure to H.

capsulatum.

– Reactions may range from brief period of not feeling well to serious illness

• Chronic pulmonary histoplasmosis– Affects people with underlying lung disease such as emphysema

• Disseminated histoplasmosis– Occurs primarily in infants and people with compromised immune

systems

– May affect nearly any part of the body

• Eyes, liver, bone marrow, central nervous system, skin, adrenal glands and intestinal tract.

– Untreated disseminated histoplasmosis is usually fatal.

SymptomsIf S/S occurs, it is usually 3- 17 days after exposure

▪ Fever

▪ Muscle aches

▪ Headache

▪ Dry cough

▪ Chills

▪ Chest pain

▪ Loss of appetite

▪ Sweats

Complications

• Enlarged lymph nodes

• Fibrosing Mediastinitis

– Severe scarring

– A rare, severe late complication

• Pericarditis or Pericardial Effusion

– Develop because the immune system responds to the fungus with an unusual amount of inflammation.

• Arthritis

• Adrenal insufficiency

• Meningitis

Source: http://www.mayoclinic.com/health/histoplasmosis

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Treatment

▪ One or more antifungal medications

– Amphotericin B (Fungizone IV)

– Itraconazole (Sporanox).

More history

▪ Denies IV drugs

▪ At some point in his life had a methamphetamine lab and used to snort coke and smoke methamphetamine.

CXR after drained 1600 ml with thoracentesis

7-9 post thoracentesis 1600 ml

CXR 7-10One day post thoracentesis

Plan

▪ Start back on Sporanox 200 mg bid

▪ Infectious disease & pulmonary consults

CXR 7-112 days post thoracentesis

SM 7-11

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CXR 7-112 days post thoracentesis --

SM 7-11

CT scan 7 -11Pleural Effusion

CT scan 7 -11

Pleural Effusion & Pericardial Effusion

CXR 7-14Postop

▪ Inserted Right CT and drained 3 liters

▪ Went to OR for pericardial window – drained 800 ml from pericardial effusion

CT Scan 7-14 Post op? If the subclavian stent was bleeding in the pericardial space.

SM 7-14 CT scan post pericardial window and Chest tube

7-15

▪ CT #1 (left) output = 200 ml

▪ CT # 2 (right) output = 590 ml

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7-17

7-16

• CT #1 output = 480 ml

• CT # 2 output = 670 ml

7-17

• CT #1 output = 0 ml

• CT # 2 output = 580 ml

7-17

7-18

▪ CT #1 output = 50 ml

▪ CT # 2 output = 570 ml

7-18

7-19

▪ CT #1 output = 10 ml


SM 7-19

7-20

▪ CT #1 d/c


SM 7-20

7-21


SM 7-21

7-22

• Due to continuous large chest tube output, went for VAT and decortication (talc pleurodesis)

• Decortication

– Surgical removal of the surface area of the lung

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DC 7-25 CXR 8-4

Case Study # 7LAST BUT NOT LEAST!

CH-TA

▪ Chest discomfort that radiated up into her neck and jaw.

▪ Very tight discomfort in her upper chest.

▪ Patient thought this was strange as she had just used her inhaler.

▪ Chest tightness and squeezing intensified and worsened with deep breaths.

▪ On admission patient was not particularly SOB and able to take deep breaths.

Middle aged pt presents to ED with chest pain

▪ BP 214/81. HR 55, RR 18, T 98

▪ Potassium 3.1

▪ Hemoglobin 9.7

▪ Troponin 0.02

▪ BNP 36

Prolonged QT

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What do you think?

1. Pneumothorax

2. Pulmonary Embolism

3. Cardiomyopathy

4. Thoracic Aneurysm

ANSWER

What do you think?

4. Thoracic Aneurysm

Thoracic Type A Aneurysm Normal Size of Aorta

Size in CM

Root 3.5–3.91

Ascending 2.86

Mid Descending 2.39–2.64

Diaphragmatic 2.43-2.69

Source: J Vasc Surg 1991:13:452-8 and 2010 Guidelines TAD.

Aortic Aneurysm (AA)

ThoracicTAAThoracicTAA

AbdominalAAAAbdominalAAA

A Silent Disease

▪ 40% of individuals are asymptomatic at the time of diagnosis

– Often discovered on a routine CXR or abdominal sonogram

▪ Only 5% of patients are symptomatic before an acute aortic event.

– The other 95%, the first symptom is often death

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AA Dissection Symptoms“The Great Imitator”

▪ S/S depend where the dissection occurs and what area is not getting oxygen

▪ Confused with:

– Kidney stones

– Gallstones

– Paralysis -- think neuro diagnosis

– Myocardial infarction

AA Symptoms

▪ Abrupt onset of excruciating pain in chest, back, or abdomen

– Ascending Dissection

▪ Retrosternal pain that is not exertional in nature

– Descending Dissection

▪ Interscapsular chest pain

▪ Severe flank pain

▪ Epigastric pain

▪ Ripping, tearing, stabbing and or sharp quality of pain

Aortic Dissection Classification: DeBakey and Stanford Classifications

Note: Figure 20 in full-text version of TAD Guidelines. Reprinted with permission from The Cleveland Clinic Foundation.

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2010 ACCF/AHA/AATS/ACR/ASA/

SCA/SCAI/SIR/STS/SVM Guidelines for

the Diagnosis and Management of Patients

with Thoracic Aortic Disease

Developed in partnership with the American College of Cardiology

Foundation/American Heart Association Task Force on Practice

Guidelines, American Association for Thoracic Surgery, American

College of Radiology, American Stroke Association, Society of

Cardiovascular Anesthesiologists, Society for Cardiovascular

Angiography and Interventions, Society of Interventional

Radiology, Society of Thoracic Surgeons, and Society for Vascular

Medicine.

Endorsed by the North American Society for Cardiovascular

Imaging.

Source: 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STA/SVM Guidelines for TAA

Source: 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STA/SVM Guidelines for TAA

Rate/Pressure Control

Intravenous beta blockadeor Labetalol

(If contraindication to beta blockadesubstitute diltiazem or verapamil)

Titrate to heart rate <60

1

Pain Control

Intravenous opiates

Titrate to pain control

Intravenous rate and pressure control

2

+

Hypotensionor shock state?

No

Yes

Systolic BP >120mm HG?

BP ControlIntravenous vasodilator

Titrate to BP <120mm HG (Goal is lowest possible BP that maintains adequate end organ perfusion)

Secondary pressure control

3

Anatomic based management

Acute AoD Management PathwaySTEP 2: Initial management of aortic wall stress

Acute AoD Management PathwaySTEP 2: Initial management of aortic wall stress

Anatomic based management

Urgent surgical consultation+

Arrange for expeditedoperative management

Intravenous fluid bolus•Titrate to MAP of 70mm HG

or Euvolemia(If still hypotensive begin

intravenous vasopressor agents)

Review imaging study for:• Pericardial tamponade• Contained rupture• Severe aortic insufficiency

1

2

3

Type A dissection

Intravenous fluid bolus•Titrate to MAP of 70mm HG

or Euvolemia(If still hypotensive begin

intravenous vasopressor agents)

Evaluate etiology of hypotension

• Review imaging study forevidence of contained rupture

• Consider TTE to evaluatecardiac function

Urgent surgical consultation

2

3

Type B dissection

1

Thoracic Aneurysm Pearls

▪ Any Chest pain….. ASK if had stabbing, knife like pain

▪ Always think aneursym or you will miss it!

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In Summary…..

Challenging Complex

Case Studies

ALL chest pain is cardiac until proven otherwise

▪ Ask Questions to get a good history!

– Was the chest pain stabbing, knife like?

– SOB – have you traveled anywhere?

▪ Call for decreasing oxygen saturations and increasing oxygen needs

▪ Look for the obvious!

Don’t miss the obvious! And Take Time to Enjoy Life!

Sharpening Your Critical Thinking Skills with Challenging Case Studies

[email protected]

www.cherylherrmann.com UnityPoint Health- PeoriaHeart of IL AACN – President

Class C150M610

challenging complex case studies handout 2017 part ii · 4/22/2017 1 sharpening your critical...

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