Enhancing Thinking & Learning via Mechanism Maps

1. A teaching hospital of Harvard Medical School Enhancing Thinking & Learning via Mechanism Maps Richard M. Schwartzstein, MD David H. Roberts, MD Shapiro Institute for Education and ResearchBeth Israel Deaconess Medical Center HMS Academy Education is at the heart of patient care.

2. After this session, you will be able: • To describe the underlying cognitive theory behind the use of concept maps and mechanism maps • To use mechanism maps to foster linkage of basic and clinical science concepts • To enhance teaching of analytical reasoning in the approach to clinical problems

3. Surface Learning -- New info not linked to previous knowledge -- Knowledge abundant but disorganized -- Focus on memorization and recall -- Learn concepts and facts without reflection Deep Learning -- Relates new knowledge to previous knowledge -- Content organized into coherent whole -- Focus on problem-solving; synthesis, application, transfer -- Link concepts/principles to everyday experience How do we facilitate deep learning?Modified fromHarasym et al. 2008

4. Encoding and Retrieval of Information Influences Learning Karpicke and Blunt, Science Express, 2011 • “Activities that promote effective encoding, known as elaborative study tasks, are important for learning” • “Because each act of retrieval changes memory, the act of reconstructing knowledge must be considered essential to the process of learning”

5. Problem Solving and Neural NetworksAdapted from Jung-Beeman et al., PLoS Biology, 2004 Problem solving relies on cortical networks for access to and use of information Problems without obvious/immediate solutions require engagement of distinct neural and cognitive processes These processes allow solvers to see connections that may have previously eluded them

6. Encourage inductive reasoning to enhance thinking Modified from Pottier et al. Med Ed 2010 Inductive Reasoning Deductive Reasoning

7. What do Concept Maps incorporate?

8. Mechanistic Mapping “The mechanistic case diagram is a student constructed tool whose objective is to trace, in stepwise form, the pathophysiologic mechanisms leading from underlying causes of disease (including genetic, microbiologic, and social) to the clinical signs and symptoms and psychosocial consequences described in a PBL case.” Guerrero APS, Acad. Med. 2001;76:385–389

9. …and now, let’s try one!

10. Chief Complaint PJ is a 51 year old woman with a one year history of intermittent abdominal pain who now presents with nausea, vomiting, and worsening abdominal pain.

11. PMH Type II Diabetes Hypertension Rheumatoid Arthritis Obesity NO history of gallstones, hypertriglyceridemia or prior pancreatitis PSH - Low-transverse abdominal scar c/w possible gynecologic surgery Medications Hydroclorothiazide Metoprolol Amlodipine Cyclobenzaprine Nabumetone Fluticasone History • FH • HTN • No FH GI malignancy/disease • SH • Tob: 1ppd, duration uncertain • EtOH: 2-3 beers/day • Illicits: unknown

12. Initial Presentation • Vital signs notable for tachycardia to 110’s What does this tell you? Is it specific? Sensitive? • Increased sympathetic activity • Compensatory (hypovolemia) • Pathologic (Axis dysregulation) • Parallel (Pain) • Pharmacologic • Decreased parasympathetic activity • Neurologic dysregulation • Pharmacologic

13. Initial Presentation Continued • CT abdomen revealed acute pancreatitis • extensive peripancreatic inflamation • distended GB with no evidence of stones, • diverticulosis • RUQ ultrasound • No stones or biliary duct dilation. • Amylase 183 • Lipase 157 • She was admitted to their medical service, made NPO, and started on IV fluids for presumed mild pancreatitis

14. Deterioration at Outside Hospital • Overnight, developed hypotension, acidemia, hyperglycemia, and extreme fever/hyperthermia • Transferred to the OSH ICU for mechanical ventilation, central line placement, vasopressor support, and insulin and bicarbonate drips

15. Was her Tachycardia an early Warning Sign? Stages of Intravascular Volume Depletion Stage% Vol downCompensation BPUOP 1 <15 Increase SVR Normal Normal 2 15-30 Increase HR, SVR Normal Decreased 3 30-40 Increase HR, SVR <100 Decreased 4 40+ Increase HR, SVR <70 Absent Adapted from Lawrence, Essentials of General Surgery and The American College of SurgeonsATLS guidelines

16. Labs Prior to Transfer 94 125 15 550 38 10 2.8 (0.3) Calcium: 5.5 Phos: 2.0Mag: 4.7 (8.4-10.3) (1.6-2.6) ABG pH 6.97 pCO2 55 pO2 121 AST126 ALT63Alk Phos  95LDH469Alb2.9INR1.2 Amylase783 (from 183)  Lipase2000 ( from 157)  CK1090Lactate9.2

17. Condition on Arrival to BIDMC VS: T: 106.9 HR: 152 BP: 113/61 RR: 21 O2Sat: 93% Glucose 235 On Norepinephrine, bicarb and insulin drips On Ventilator (FiO2 100% RR 24 VT 400 PEEP 10) ABG: pH 7.06 pCO2 90 pO2 121 (from 6.97) (from 55) (stable) Exam notable for: ET tube properly positioned with bilateral breath sounds. Abdomen firm, distended, and dull to percussion. Extremities cool. No edema. Na 145 Cl 110 HCO3 22

18. Admission CXR ABG Trend 23:39 pH 7.06 pCO2 90 pO2 121  (FiO2 100% RR 24 Vt 400 PEEP 10) 00:19 pH 7.09 pCO2 95 pO2 106   (FiO2 100% RR 27 Vt 300 PEEP 10) Bladder pressure 1828

19. What’s going on Here? Problem List: • Hypotension • Hypoxemic, hypercarbic respiratory failure • Anion gap metabolic acidosis with overlying respiratory acidosis • Pancreatitis • Acute Renal Failure…

20. Inflammatory Response, Cytokine Release Concept Map Decreased Chest-Wall Compliance Pancreatitis Increased vasculature permeability Increased abdominal pressures Hypotension Hypercarbic Resp Failure Third Spacing Poor tissue perfusion Anaerobic Metabolism Acidosis

21. Why develop Shock in Pancreatitis? Hypovolemic Component: • intravascular volume decreases by 19% in 2 hours • Decreases by 30% in 6 hours • Patients may require 10L fluid in initial 24 hours Cardiogenic Component: • Initially, CI increases and SVR decreases (sepsis-like) • Later, cardiac function decreases Distributive Component: • Inflammatory cytokines(IL-1, IL-6, TNFalpha)  reduced SVR Early volume-resuscitation lowers mortality Yegneswaran et. al, Cardiovascular Manifestations of Acute Pancreatitis. J Crit Care 2011 Apr;26(2):225 Gardner et al. Faster rate of initial fluid resuscitation in severe acute pancreatitis diminishes in-hospital mortality. Pancreatology 2009;9:770-76