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Internal Medicine - Guazon Case Disclosure: Important Legal Information
Internal Medicine - Guazon Case Disclosure: Important Legal Information
CHEST PAIN IN MYOCARDIAL INFARCTION
• Due to imbalance in oxygen supply from obstructed coronary vessels and oxygen demand from cardiomyocytes
• Hypoxia leads to shift from aerobic respiration to anaerobic respiration à pyruvate shifted to lactate formation à lactic acid buildup
à pain sensation
INITIAL WORKING IMPRESSION
Acute Coronary Syndrome in cardiogenic shock (Killip IV)
1. r/o Aortic Dissection
Peptic ulcer disease r/o perforation
Hypertension II in relative hypotension
Obesity
DIAGNOSTICS
Items written in bold are considered essential items.
DIAGNOSTIC RATIONALE EXPECTED FINDINGS
• STEMI: ST elevation in contiguous leads
• NSTE-ACS: ST-segment depression, transient
ST-segment elevation or T wave inversions
• To check for changes consistent with ACS (ST-segment • Pericarditis: widespread ST elevation and PR
12L-ECG and T wave changes), rhythm disturbances, LVH depression with reciprocal changes in aVR
(signifies chronicity of HPN) • Pulmonary embolism: S1Q3T3 (large S wave in
lead I, Q wave in lead III and inverted T waves
in lead III), sinus tachycardia, T wave inversion
in leads V1-V4, RBBB
• Aortic dissection: mediastinal widening (>8-10
• To rule out possible aortic dissection cm)
• To check for enlargement of cardiac silhouette • HPN: LV cardiomegaly
• To assess pulmonary vascular markings for congestion • Pulmonary congestion: cephalization of vessels,
Chest x-ray, upright
• To check for air under the left hemidiaphragm found Kerley B lines, perihilar bat wing pattern (for
when there is perforation of viscus severe pulmonary edema)
• To rule out pneumothorax • Perforated peptic ulcer- air under left
hemidiaphragm
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• Pneumothorax: hyperlucent pulmonary areas,
loss of vascular markings beyond the visceral
pleural line (for tension PTX: mediastinal
structures deviated to the contralateral side)
• Pulmonary embolism: normal, focal oligemia
(Westermark’s sign), peripheral wedge-shaped
density (Hampton’s hump), enlarged right
descending pulmonary artery (Palla’s sign),
pleural effusion, may also be normal
• Central in the diagnosis of myocardial infarction
• Elevated levels distinguish patients with NSTEMI from
UA
CORRELATE: TROPONINS
• Due to imbalance in oxygen supply from obstructed
coronary vessels and oxygen demand from
cardiomyocytes
• Acute MI: wall motion abnormalities
(hypokinetic/dyskinetic areas)
• The check for wall motion abnormalities, check • Cardiogenic shock: low ejection fraction
2D-echocardiogram
ejection fraction • Pulmonary embolism: RV overload,
hypokinesia of RV free wall but normal motion
of RV apex
Cardiac
• Stenosis/occlusion of coronary arteries in MI
catheterization/coronary • Check for occluded coronaries and possibly intervene
angiogram • Vasospasm in Prinzmetal’s angina
• Hypokalemia, hyperkalemia, hypomagnesemia,
Serum electrolytes (Na, • To check for electrolyte abnormalities that lay lead to
hypermagnesemia, hypocalcemia and
K, Cl, Mg, Ca) arrhythmia
hypercalcemia may predispose to arrhythmia
• Levels may be elevated due to stress
RBS/CBG/FBS • To check for glucose levels hyperglycemia, but unequivocal elevations may
point to possibility of DM
• To check for presence of anemia or leukocytosis
Complete Blood Count • To check baseline level of platelets • ACS: may present with leukocytosis as high as
with blood typing • Blood typing for anticipatory care (bleeding is a 15,000
common side effect of most ACS meds)
• To check baseline coagulation parameters (especially
PT/PTT • UFH is adjusted according to PTT results
if UFH will be started)
• Hypoperfusion from shock will lead to
metabolic acidosis from lactic acidosis
Arterial blood gases • Assess renal function and check for HPN complications
• A degree of hypoxemia is expected due to
pulmonary congestion
Urinalysis • Identify additional cardiovascular risk factors • HPN nephropathy: usually bland urine
• In MVP – may show abnormal position or
Lipid profile • To check baseline liver status
prolapse of the mitral valve leaflets
• May have small degree of elevation due to
AST, ALT • To check for abdominal aneurysm, GI pathologies, CKD
hypoperfusion
• Pancreatitis: peripancreatic fluid collection,
pancreatic swelling
• GB disease: visualization of stone, ductal
Holo-abdominal UTZ • To rule out pancreatitis dilations
• HPN nephropathy: small kidneys with poor
corticomedullary differentiation/decreased
cortical thickness (if CKD)
Lipase • Assess renal function and check for HPN complications • Acute pancreatitis: at least 3-fold elevation
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DIAGNOSTICS RESULTS
DIAGNOSTIC TEST RESULTS INTERPRETATION
Please see tracing
• Regular sinus rhythm, left axis deviation, left
12-L ECG Write your interpretation on the paper provided atrial abnormality, acute massive ST-elevation
myocardial infarction
Trop I 9.0 ng/mL (N: <0.1)
• Elevated, consistent with myocardial
infarction
• Consistent with massive myocardial
2D-echo Hypokinetic anterolateral wall, (-) thrombus, EF 37% infarction, also corresponds with massive
STEMI on ECG
• Consistent with acute pulmonary congestion
from LV dysfunction from acute myocardial
CXR Cardiomegaly, LV form; pulmonary congestion
infarction; cardiomegaly most probably from
long-standing hypertension
Parameter Patient Values
CBG 100 mg/dL
FBS 97 mg/dL
Na 140
K 4.5
Cl 101
• Normal FBS and electrolytes
Mg 2.0 meq/L
• BUN:creatinine ratio = 29.7 (consistent with
Ca 2.2 mmol/L
pre-renal azotemia)
Serum Chemistry BUN 31 mmol/L • GFR = 36 mL/min
Crea 258 umol/L
• The patient has dyslipidemia (elevated TG,
TG 170 mg/dL
LDL and TC; low HDL
LDL 152 mg/dL
HDL 35 mg/dL
TC 280 mg/dL
Compute for the BUN:Creatinine ratio and the GFR using the
Cockcroft-Gault formula
Write your formula and answer on the paper provided
Hb 120 g/L
Complete Blood Hct 0.39 • Leukocytosis with segmenter predominance
Count WBC 12.1 compatible with ACS
Platelet 285 (PMN 78%, Lym 18%)
Yellow, clear
pH 5.5, SG 1.025 • Bland urine compatible with HPN
(-) CHO/CHON nephropathy
Urinalysis (-) ketones • Elevated SG indicates intact concentrating
0-1 RBC, 0-1 WBC ability (consistent with pre-renal azotemia)
(-) casts/crystals
Patient 10.7 secs
PTT Control 10.3 secs
• Within limits
pH 7.45
pCO2 30
Arterial blood gas • Respiratory alkalosis with metabolic acidosis
pO2 58
on room air HCO3 16 and hypoxemia
O2sats 89%
Normal ultrasound of the liver, pancreas, spleen and kidneys
Holoabdominal • Normal HA-UTZ, no signs of CKD, suspected
(cortical thickness 1.4 cm)
ultrasound Abdominal aorta aneurysm suspected. abdominal aneurysm
REVISED IMPRESSION
Acute massive STEMI, Killip IV (in cardiogenic shock)
Acute respiratory failure, type I from pulmonary congestion
from acute LV dysfunction
Acute kidney injury from renal hypoperfusion (low cardiac
output)
Suspected abdominal aneurysm
Metabolic Syndrome
Hypertension II
Dyslipidemia
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MANAGEMENT
Items written in bold are considered essential items.
EXPECTED RESPONSE/
MANAGEMENT RATIONALE
COMPLICATIONS
A. INITIAL MANAGEMENT AT THE ER
• Patient is in respiratory distress • Maintain O2sats >90%
• Respiratory support decreases the demands on the • WOF: traumatic intubation,
Intubate the patient and hook to myocardium by decreasing both preload and barotrauma, nosocomial
mechanical ventilation on AC mode afterload pneumonia
with FiO2 100% • Beneficial effects on pulmonary edema by
redistributing lung water from intra-alveolar to the
extra-alveolar sites à avoidance of atelectasis
Insert NGT, place patient on NPO • For drug delivery and for feeding while intubated
except for meds • WOF: sinusitis
• To monitor urine output
Insert foley catheter
• WOF: nosocomial UTI
• To assess fluid status and monitor central perfusion
Insert CVP line
• WOF: site infection
Refer/admit to MICU • For closer monitoring and nursing care
• Anti-platelet therapy with ASA is effective in reducing
Aspirin 160-320 mg • WOF: Bleeding
AMI mortality
Clopidogrel 300-600 mg PO (or
• Clopidogrel therapy reduces mortality among patients
prasugrel 60 mg/ticagrelor 180 mg PO • WOF: Bleeding
with AMI
when the patient will undergo PCI)
• Recommended in all patients during first 24 hours of
admission irrespective of patient’s cholesterol levels
High-dose statins (rosuvastatin 20-40 • Also recommended to be given before emergency PCI
mg or atorvastatin 40-80 mg) to reduce periprocedural inflammatory response, to
reduce myocardial dysfunction, and to prevent
contrast-induced nephropathy
• Norepinephrine is a potent vasoconstrictor and
inotropic stimulant that is useful for patients with
Vasopressor/Inotrope: cardiogenic shock
Norepinephrine infusion (2-4 • As first line therapy, it is associated with fewer
mcg/min, titrated as necessary), may adverse events including arrhythmias (compared to WOF: arrhythmia, further
add dobutamine infusion once BP picks dopamine) decrease in urine output
up (70-100 mmHg SBP with NO signs of • Dobutamine has positive inotropic action and minimal
shock) chronotropic activity at low disease (its vasodilating
activity at higher doses precludes its use when a
vasoconstricting effect is required)
• Achieve PT 1.5-2.0 times
that of control
• PT monitoring should be
Unfractionated heparin (UFH) 60
done for both because the
units/kg bolus then 12 units/kg/hr drip
• Also reduces mortality from STEMI patient has altered
or low-molecular weight heparin
pharmacodynamics (obese,
(LMWH) 1 mg/kg SC q12
renal insufficiency)
• Should be given for 48 hours
• WOF: bleeding
• In this patient, invasive strategy is preferable since the patient is in cardiogenic
shock (KIllip IV). If this is not available in the institution, the next best strategy is
fibrinolysis.
FIBRINOLYSIS INVASIVE STRATEGY
Generally preferred if: • Skilled PCI laboratory is available with
• Early presentation with a delay to surgical backup (medical contact-to-
an invasive strategy balloon or door-to-balloon < 90 minutes;
• Invasive strategy is not available door-to-balloon minus door-to-needle is
• Delay to invasive strategy < 1 hr)
Reperfusion (Refer to CVS) (prolonged transport; door-to- • High risk from STEMI (cardiogenic
balloon minus door-to-needle time is shock, Killip >3)
> 1 hr; medical contact-to-balloon or • Contraindications to fibrinolysis
door-to-balloon time is > 90 • Late presentation (symptom onset > 3
minutes) hours ago)
• Diagnosis of STEMI is in doubt
Fibrinolysis is still reasonable if
symptom onset is within 12-24 hours
as long as there is evidence of ongoing
ischemia (although primary PCI is
preferred for this population).
Stop losartan, avoid nitrates • Patient in shock
Consider pulmonary catheter and intra- • Invasive hemodynamic assessment allows for a more precise assessment for patients
arterial pressure monitoring with complications of STEMI such as heart failure or hypotension
Consider circulatory assist devices (e.g. • To maintain adequate perfusion
IABP)
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B. FURTHER PHARMACOLOGIC MANAGEMENT
• Inhibits cyclooxygenase (the first step in
• Continued indefinitely
Aspirin 80-100 mg/day biosynthesis of prostaglandins and
• WOF: GI upset, bleeding
thromboxanes)
• Blocks binding of ADP to a specific
platelet P2Y12 thereby inhibiting • Maintained for at least 14 days up to 1
Clopidogrel 75 mg/day
activation of glycoprotein IIb/IIIa and year
platelet aggregation
• WOF: hypotension, bladder distension,
Morphine 2 mg IV • As needed for severe pain
pruritus
Furosemide drip • To relieve congestion • WOF: hypotension, hypokalemia
Proton pump inhibitors • Stress ulcer prophylaxis
Stool softener • To avoid/lessen straining and coughing • WOF: diarrhea
C. NON-PHARMACOLOGIC MANAGEMENT
Diet:
TCR 35 kcal/kg
CHO 50-55%
CHON 1 g/kg
Fats 25-30%
Sat fats <7%
TC <200 mg/day
Daily assessment of extubation parameters
Start cardiac rehabilitation
Head of bed elevation at 30o inclination
Daily assessment of extubation parameters
D. ANTICIPATORY CARE
Monitor vital signs, oxygenation status and urine output q1
Hook to cardiac monitor
ECG q1 post-procedure for 2 hours then q2-6 hours then daily
Monitor renal status (may require dialysis if AKI not addressed by reversal of cardiogenic shock alone)
• Reduces mortality
• Reduces ventricular remodeling after
infarction
CORRELATE: ARNIs
• Angiotensin receptor – neprilysin
inhibitor
• an ARB (valsartan) with an
Once out of shock: start low-dose ACE endopeptidase inhibitor (sacubitril)
WOF: cough, hyperkalemia, hypotension
inhibitors/ARBS • tested in the PARADIGM-HF trial as an
alternate to optimally dosed ACEI
• demonstrated an incremental
improvement in survival when
compared to ACE-i alone
• Most guidelines now advocate switching
ACE-i to this drug as a standard in
patients with mild-moderate systolic
heart failure
• Reduces infarct size by diminishing
Once out of shock and out of WOF: bradycardia, congestion,
oxygen demand
congestion: consider beta-blockers hypotension
• Reduces in-hospital mortality
Patient may be discharged after 5 days if no significant arrhythmias, recurrent ischemia or congestive HF
Exercise testing early after discharge (within 2 to 3 weeks) or late after discharge (within 3 to 6 weeks) for prognostic,
activity prescription, evaluation of medical therapy
Influenza vaccination
D. PATIENT EDUCATION
Weight reduction
Physical activity
Advise complications of metabolic syndrome and component diseases
Advise on behavioral modifications: reducing stress, etc.
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