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Angina Pectoris: Case Study and A SOAP Note
Norseen H. Lotfy
Department Of Pharmacy, Galala University
PPP302 : Integrated case-based Learning
Dr. Dina Mansour
Jan 4, 2023
1
Outline
I. Introduction
II. Etiology
III. Diagnosis
IV. Manifestations
A. Stable angina
B. Unstable angina.
C. variant Prinzmetal angina
V. Risk-factors
A. Modifiable
B. Non-modifiable
VI. Treatment
A. Non-pharmacological Therapy (Lifestyle Modification)
B. Pharmacological Therapy
C. Revascularization
VII. SOAP Note
VIII.References
2
Angina (A study of Case)
Introduction
Angina, or chest pain, is the most common symptom of ischemic heart disease, a primary cause
of morbidity and mortality worldwide Prevalence increases with age in both men and women.
Angina pectoris is the symptomatic manifestation of transient myocardial ischaemia. At the most
fundamental level, angina arises when myocardial oxygen demand exceeds the ability of the
coronary circulation to provide adequate oxygen delivery to maintain normal myocardial
metabolic function. It’s common among patients with stable ischaemic heart disease (SIHD)
.Separating cardiac from non-cardiac causes of chest pain and identifying people with acute
coronary syndrome need a thorough history and physical examination. One of the signs of acute
coronary syndrome is angina, which can be stable or unstable (ACS). Stable angina is defined as
having symptoms that only appear after exerting effort. An prompt evaluation and course of
action are required for unstable angina or symptoms that occur when you're at rest. Nearly 9
million people in the US have angina symptoms, and recognising these signs is essential to
improving patient outcomes.
Etiology
Non-cardiac reasons, non-ischemic cardiac illness, and then ischemic cardiac disease can all
produce chest discomfort. Other non-cardiac reasons include lung illness, musculoskeletal issues,
anxiety/panic episodes, and gastric reflux disease. Pericardial illness is one of the non-ischemic
cardiac causes. Most experts agree that coronary artery atherosclerosis and coronary vasospasm
are the causes of chest discomfort brought on by myocardial ischemia. A mismatch between
3
myocardial oxygen supply and demand results from this situation. In unstable angina, the
increased demand also arises while at rest, whereas in stable angina it only happens during effort.
Exercise-induced increases in heart rate, blood pressure, and myocardial contractility are among
the main causes of increased myocardial oxygen demand. Under typical cardiac physiologic
circumstances, an increase in oxygen demand brought on by physical effort is followed by
coronary vasodilation, but in cases of coronary artery atherosclerosis, this function is impeded,
and ischemia and chest pain ensue. Vasospastic angina, otherwise known as variant angina or
Prinzmetal angina, like stable angina, also occurs at rest but is unrelated to coronary
atherosclerosis.
Factors that increase myocardial oxygen demand:
 Arrhythmias
 Fever
 Hypertension
 Cocaine use
 Aortic stenosis
 AV shunts
 Anemia
 Thyrotoxicosis
 Pheochromocytoma
 CHF
Diagnosis
1- Treadmill test TMT: examining ECG of patient while he run on treadmill
2- Coronary angiogram: to see clots in coronary arteries
4
Manifestations
Fig. 1. – Fig. 2.
Different types of angina
There’re 3 types of Anginas:
1. Stable angina
also is known as typical angina or angina pectoris, is a symptom of myocardial ischemia.
Stable angina is characterized by chest discomfort or anginal equivalent that is provoked
with exertion and alleviated at rest or with nitroglycerin.
2. Unstable angina.
The most common cause of unstable angina is due to coronary artery narrowing due to a
thrombus that develops on a disrupted atherosclerotic plaque and is nonocclusive.
3. variant Prinzmetal angina
A less common cause is vasospasm of a coronary artery. Endothelial or vascular smooth
dysfunction causes this vasospasm
5
Fig. 3. – Fig. 4.
Comparison between stable angina and unstable angina
6
Risk factors
Modifiable risk factors
1. Hyperlipidemia
2. Hypertension
3. current or past tobacco use
4. diabetes mellitus
5. obesity/metabolic syndrome
6. Increasing BMI is an independent risk factor for coronary arterial disease (CAD).
Non-modifiable risk factors
1. Age
2. male sex
3. family history of CAD
4. ethnic origin
Treatment
Management is multifactorial and involves lifestyle modifications, risk factor modification, and
medical therapy as essential components of treatment.
Non-pharmacological Therapy (Lifestyle Modification)
1. smoking cessation
2. healthy diet
3. Maintaining or obtaining a healthy weight (defined as body mass index < 25 kg/m2
)
4. Consumption of N-3 polyunsaturated fatty acids, mainly from oily fish rather than from
supplements
7
5. A ‘Mediterranean diet’, supplemented with extra-virgin olive oil or nuts, reduces MACE
in patients at high risk.
6. regular physical activity, undergo moderate intensity aerobic exercise training ≥3 times a
week for 30 min per session
7. Blood pressure (BP) control. Strong evidence supports lowering systolic BP (SBP) to
<140 mmHg and diastolic BP to <90 mmHg
8. Management of hypercholesterolaemia, particularly reduction of LDL-cholesterol levels
with a statin
9. Patients with angina who have symptoms of depression, anxiety, and/or hostility should
be appropriately evaluated and referred for therapy.
Pharmacological Therapy
1. Nitrates - no mortality benefit, but used for chest pain relief. They cause vasodilation,
which decreases preload and left ventricular end-diastolic volume. This reduces
myocardial oxygen consumption. They are contraindicated in cases of hypotension and
previous use of phosphodiesterase inhibitors within the past 48 hours.
2. Morphine - no mortality benefit, used for pain relief when pain relief is not fully
achieved by nitrates. It causes some vasodilation, aside from analgesia.
3. Beta-blockers - reduce mortality. They cause a decrease in heart rate, contractility, and
blood pressure, thereby reducing myocardial oxygen demand.
4. Antiplatelet agents - dual therapy with aspirin and either clopidogrel, ticagrelor, or
prasugrel decreases the risk of cardiovascular events in patients with acute coronary
syndromes— acute myocardial infarction, cardiovascular death, and stroke.
5. Anticoagulants - reduce mortality by decreasing re-infarction rates in combination with
antiplatelet agents. Used intravenously for acute treatment.
8
Table 1.
Summary of angina therapies and different effects.
Reduces MACE Reduces symptoms Further study
Vascular smooth muscle relaxing agents
Nitrates No Moderate effect No
PDE inhibitors Unknown No Yes
cGMP stimulators Unknown Unknown Yes
Rho kinase inhibitors Unknown Mild effect Yes
Calcium antagonists Maybea
Moderate effect No
Metabolic modulation
Trimetazidine Unknown Moderate effect Yes
Perhexiline Unknown Moderate effect Yes
Heart rate reduction
β-Blocking agents Maybeb,c
Moderate effect Yes
Sinus node inhibitors Maybed
Moderate effect Yes
Other agents
Ranolazine Noc
Moderate effect Yes
Amiodarone Noc
Mild effect No
Dronedarone Noc
Mild effect Yes
Arginine No No Yes
Allopurinol Unknown Mild effect Yes
Testosterone May increase Unknown Yes
Omapatrilat Unknown Mild effect Yes
9
Reduces MACE Reduces symptoms Further study
Physical interventions
Revascularization Noe
Significant effect Yes
Spinal cord stimulators No Mild effect No
EECP No Mild effect No
Transmyocardial revascularization No Mild effect Yes
Coronary sinus restrictor No Moderate effect Yes
Acupuncture No No No
Angiogenesis and myocardial
regeneration
Unknown Unknown Yes
Also there’s anatomic assessment of coronary arteries/consideration of revascularization
High-risk patients should be identified with risk stratification methods and considered for urgent
revascularization, such as:
1- Catherzation
2- Angiogram
3- Bypass graft CABG
4- Percutaneous intervention PCI
5- Stent
10
Case ( SOAP Note )
Case: Angina pectoris
Mr. W is a 56-year-old man who comes to your office with chest pain.
Mr. W has a history of well-controlled hypertension and diabetes. He has been having symptoms
for the last 4 months. He feels squeezing, substernal pressure while climbing stairs to the
elevated train he rides to work. The pressure resolves after about 5 minutes of rest. He also
occasionally feels the sensation during stressful periods at work. It is occasionally associated
with mild nausea and jaw pain. Medications are metformin, aspirin, and enalapril.
Mr. W is a middle-aged man with chronic, nonpleuritic chest pain and risk factors for coronary
artery disease (CAD). His symptoms are consistent with stable angina. The pivotal points in this
case are the chronicity, exertional nature, and substernal location of the pain. Given the
seriousness and prevalence of CAD, it must lead the differential diagnosis. Gastroesophageal
reflux disease (GERD) and musculoskeletal disorders are common causes of chest pain that can
mimic angina (exacerbated by activity, sensation of pressure) and thus should be considered. The
chronicity of his symptoms argues against many other worrisome diagnoses (eg, pulmonary
embolism [PE], pneumothorax, pericarditis, or aortic dissection). Pain from a mediastinal
abnormality is possible.
Physical exam is entirely unremarkable except for mild, stable, peripheral neuropathy
presumably related to diabetes. The patient’s ECG is remarkable only for evidence of left
ventricular hypertrophy with strain.
11
A tentative diagnosis of stable angina from CAD is made. Laboratory data are notable for normal
blood counts and chemistries. There is hypercholesterolemia (LDL, 136 mg/dL; HDL, 42
mg/dL). Mr. W is referred for an exercise tolerance test. Because of his abnormal resting ECG,
an exercise myocardial perfusion SPECT was performed. Although chest pain developed during
the test, his results were normal without evidence of myocardial ischemia.
The results of the patient’s exercise test are surprising. Stable angina remains high in the
differential despite the normal stress test but alternative diagnoses must be considered. The
intermittent nature of the pain and the lack of constitutional symptoms both make a mediastinal
lesion unlikely. The absence of a recent injury, change in activity or reproducible pain on
physical exam moves musculoskeletal pain down on the differential. GERD is a common cause
of chest pain and should be considered.
Prior to the stress test, Mr. W’s probability of having CAD was at least 92% (see Table 9-2). It is
important to understand why the exercise test was done in this case. The diagnosis of coronary
disease was essentially made by the history and physical. The exercise test was meant to guide
therapy. Considering a pretest probability of 92%, and a LR– of about 0.15 for the exercise test,
the posttest probability is 60%. This is still well above the test threshold for a potentially fatal
disease like CAD.
Despite the results of the stress test, stable angina was considered more likely than GERD. Mr.
W was given aspirin and a beta-blocker and underwent an angiogram the week after the visit. He
was found to have a 90% stenosis of the mid left anterior descending artery and underwent PCI
with stent placement.
12
SOAP Note
Patient
Name: Mr. W
Date:______________ Age: 56 Sex: man
S; subjective
SUBJECTIVE: (Mechanism of injury (MOI), chief complaint (C/C))
He feels squeezing, substernal pressure while climbing stairs to the elevated train he rides to
work. The pressure resolves after about 5 minutes of rest. He also occasionally feels the
sensation during stressful periods at work. It is occasionally associated with mild nausea and jaw
pain. and has a history of well-managed HTN and diabetes. Pt has a number of CAD risk factors.
_____________________________________________________________________________
O; Objective
OBJECTIVE: (Patient exam findings, Vital Signs, SAMPLE History)
mild, stable, peripheral neuropathy presumably related to diabetes.
Physical exam: The patient’s ECG is remarkable only for evidence of left ventricular
hypertrophy with strain
There is hypercholesterolemia (LDL, 136 mg/dL; HDL, 42 mg/dL).
Although chest pain developed during the test, his results were normal without evidence of
myocardial ischemia
Exercise myocardial perfusion SPEC: normal but with chest pain
13
Pretest probability of CAD: 92% and posttest probability of CAD: 60%
He was found to have a 90% stenosis of the mid left anterior descending artery and underwent
PCI with stent placement.
LR for exercise test: 0.15
Allergies: no
Medications: Pt takes metformin, aspirin, and enalapril
Last Oral Intake:
Events leading to accident:
_____________________________________________________________________________
A; Assessment
ASSESSMENT: (problem list)
Stable angina CAD
left ventricular hypertrophy with strain
90% stenosis of the mid left anterior descending artery
underwent PCI with stent placement
hypercholesterolemia
_____________________________________________________________________________
14
P; Plan
PLAN: (plan for each problem on list, evac route, bivouac location)
1. Aspirin (anticlotting)
2.Angiogram 1 week post-visit
3. Nitrates; tablets and sublingual to be taken during attacks
4. Beta-blocker or CCBs, shift to new generation when causing hypotension
5. Aspirin (antiplatelet)
Form completed by: Norseen Hosam
_____________________________________________________________________________
15
References
Gillen C, Goyal A. Stable Angina. [Updated 2021 Dec 21]. In: StatPearls [Internet]. Treasure
Island (FL): StatPearls Publishing; 2022 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK559016/
Goyal A, Zeltser R. Unstable Angina. [Updated 2022 Sep 18]. In: StatPearls [Internet]. Treasure
Island (FL): StatPearls Publishing; 2022 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK442000/
Hermiz C, Sedhai YR. Angina. [Updated 2021 Dec 21]. In: StatPearls [Internet]. Treasure Island
(FL): StatPearls Publishing; 2022 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK557672/
Winchester, D. E., & Pepine, C. J. (2015). Angina treatments and prevention of cardiac events:
an appraisal of the evidence. European heart journal supplements : journal of the
European Society of Cardiology, 17(Suppl G), G10–G18.
https://doi.org/10.1093/eurheartj/suv054
Fig.3; https://www.issuesandanswers.org/back-to-basics-recognising-different-types-of-
coronary-artery-disease-2/
Fig.4; https://www.issuesandanswers.org/back-to-basics-recognising-different-types-of-
coronary-artery-disease-1/

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Angina + SOAP note.

  • 1. 1 Angina Pectoris: Case Study and A SOAP Note Norseen H. Lotfy Department Of Pharmacy, Galala University PPP302 : Integrated case-based Learning Dr. Dina Mansour Jan 4, 2023
  • 2. 1 Outline I. Introduction II. Etiology III. Diagnosis IV. Manifestations A. Stable angina B. Unstable angina. C. variant Prinzmetal angina V. Risk-factors A. Modifiable B. Non-modifiable VI. Treatment A. Non-pharmacological Therapy (Lifestyle Modification) B. Pharmacological Therapy C. Revascularization VII. SOAP Note VIII.References
  • 3. 2 Angina (A study of Case) Introduction Angina, or chest pain, is the most common symptom of ischemic heart disease, a primary cause of morbidity and mortality worldwide Prevalence increases with age in both men and women. Angina pectoris is the symptomatic manifestation of transient myocardial ischaemia. At the most fundamental level, angina arises when myocardial oxygen demand exceeds the ability of the coronary circulation to provide adequate oxygen delivery to maintain normal myocardial metabolic function. It’s common among patients with stable ischaemic heart disease (SIHD) .Separating cardiac from non-cardiac causes of chest pain and identifying people with acute coronary syndrome need a thorough history and physical examination. One of the signs of acute coronary syndrome is angina, which can be stable or unstable (ACS). Stable angina is defined as having symptoms that only appear after exerting effort. An prompt evaluation and course of action are required for unstable angina or symptoms that occur when you're at rest. Nearly 9 million people in the US have angina symptoms, and recognising these signs is essential to improving patient outcomes. Etiology Non-cardiac reasons, non-ischemic cardiac illness, and then ischemic cardiac disease can all produce chest discomfort. Other non-cardiac reasons include lung illness, musculoskeletal issues, anxiety/panic episodes, and gastric reflux disease. Pericardial illness is one of the non-ischemic cardiac causes. Most experts agree that coronary artery atherosclerosis and coronary vasospasm are the causes of chest discomfort brought on by myocardial ischemia. A mismatch between
  • 4. 3 myocardial oxygen supply and demand results from this situation. In unstable angina, the increased demand also arises while at rest, whereas in stable angina it only happens during effort. Exercise-induced increases in heart rate, blood pressure, and myocardial contractility are among the main causes of increased myocardial oxygen demand. Under typical cardiac physiologic circumstances, an increase in oxygen demand brought on by physical effort is followed by coronary vasodilation, but in cases of coronary artery atherosclerosis, this function is impeded, and ischemia and chest pain ensue. Vasospastic angina, otherwise known as variant angina or Prinzmetal angina, like stable angina, also occurs at rest but is unrelated to coronary atherosclerosis. Factors that increase myocardial oxygen demand:  Arrhythmias  Fever  Hypertension  Cocaine use  Aortic stenosis  AV shunts  Anemia  Thyrotoxicosis  Pheochromocytoma  CHF Diagnosis 1- Treadmill test TMT: examining ECG of patient while he run on treadmill 2- Coronary angiogram: to see clots in coronary arteries
  • 5. 4 Manifestations Fig. 1. – Fig. 2. Different types of angina There’re 3 types of Anginas: 1. Stable angina also is known as typical angina or angina pectoris, is a symptom of myocardial ischemia. Stable angina is characterized by chest discomfort or anginal equivalent that is provoked with exertion and alleviated at rest or with nitroglycerin. 2. Unstable angina. The most common cause of unstable angina is due to coronary artery narrowing due to a thrombus that develops on a disrupted atherosclerotic plaque and is nonocclusive. 3. variant Prinzmetal angina A less common cause is vasospasm of a coronary artery. Endothelial or vascular smooth dysfunction causes this vasospasm
  • 6. 5 Fig. 3. – Fig. 4. Comparison between stable angina and unstable angina
  • 7. 6 Risk factors Modifiable risk factors 1. Hyperlipidemia 2. Hypertension 3. current or past tobacco use 4. diabetes mellitus 5. obesity/metabolic syndrome 6. Increasing BMI is an independent risk factor for coronary arterial disease (CAD). Non-modifiable risk factors 1. Age 2. male sex 3. family history of CAD 4. ethnic origin Treatment Management is multifactorial and involves lifestyle modifications, risk factor modification, and medical therapy as essential components of treatment. Non-pharmacological Therapy (Lifestyle Modification) 1. smoking cessation 2. healthy diet 3. Maintaining or obtaining a healthy weight (defined as body mass index < 25 kg/m2 ) 4. Consumption of N-3 polyunsaturated fatty acids, mainly from oily fish rather than from supplements
  • 8. 7 5. A ‘Mediterranean diet’, supplemented with extra-virgin olive oil or nuts, reduces MACE in patients at high risk. 6. regular physical activity, undergo moderate intensity aerobic exercise training ≥3 times a week for 30 min per session 7. Blood pressure (BP) control. Strong evidence supports lowering systolic BP (SBP) to <140 mmHg and diastolic BP to <90 mmHg 8. Management of hypercholesterolaemia, particularly reduction of LDL-cholesterol levels with a statin 9. Patients with angina who have symptoms of depression, anxiety, and/or hostility should be appropriately evaluated and referred for therapy. Pharmacological Therapy 1. Nitrates - no mortality benefit, but used for chest pain relief. They cause vasodilation, which decreases preload and left ventricular end-diastolic volume. This reduces myocardial oxygen consumption. They are contraindicated in cases of hypotension and previous use of phosphodiesterase inhibitors within the past 48 hours. 2. Morphine - no mortality benefit, used for pain relief when pain relief is not fully achieved by nitrates. It causes some vasodilation, aside from analgesia. 3. Beta-blockers - reduce mortality. They cause a decrease in heart rate, contractility, and blood pressure, thereby reducing myocardial oxygen demand. 4. Antiplatelet agents - dual therapy with aspirin and either clopidogrel, ticagrelor, or prasugrel decreases the risk of cardiovascular events in patients with acute coronary syndromes— acute myocardial infarction, cardiovascular death, and stroke. 5. Anticoagulants - reduce mortality by decreasing re-infarction rates in combination with antiplatelet agents. Used intravenously for acute treatment.
  • 9. 8 Table 1. Summary of angina therapies and different effects. Reduces MACE Reduces symptoms Further study Vascular smooth muscle relaxing agents Nitrates No Moderate effect No PDE inhibitors Unknown No Yes cGMP stimulators Unknown Unknown Yes Rho kinase inhibitors Unknown Mild effect Yes Calcium antagonists Maybea Moderate effect No Metabolic modulation Trimetazidine Unknown Moderate effect Yes Perhexiline Unknown Moderate effect Yes Heart rate reduction β-Blocking agents Maybeb,c Moderate effect Yes Sinus node inhibitors Maybed Moderate effect Yes Other agents Ranolazine Noc Moderate effect Yes Amiodarone Noc Mild effect No Dronedarone Noc Mild effect Yes Arginine No No Yes Allopurinol Unknown Mild effect Yes Testosterone May increase Unknown Yes Omapatrilat Unknown Mild effect Yes
  • 10. 9 Reduces MACE Reduces symptoms Further study Physical interventions Revascularization Noe Significant effect Yes Spinal cord stimulators No Mild effect No EECP No Mild effect No Transmyocardial revascularization No Mild effect Yes Coronary sinus restrictor No Moderate effect Yes Acupuncture No No No Angiogenesis and myocardial regeneration Unknown Unknown Yes Also there’s anatomic assessment of coronary arteries/consideration of revascularization High-risk patients should be identified with risk stratification methods and considered for urgent revascularization, such as: 1- Catherzation 2- Angiogram 3- Bypass graft CABG 4- Percutaneous intervention PCI 5- Stent
  • 11. 10 Case ( SOAP Note ) Case: Angina pectoris Mr. W is a 56-year-old man who comes to your office with chest pain. Mr. W has a history of well-controlled hypertension and diabetes. He has been having symptoms for the last 4 months. He feels squeezing, substernal pressure while climbing stairs to the elevated train he rides to work. The pressure resolves after about 5 minutes of rest. He also occasionally feels the sensation during stressful periods at work. It is occasionally associated with mild nausea and jaw pain. Medications are metformin, aspirin, and enalapril. Mr. W is a middle-aged man with chronic, nonpleuritic chest pain and risk factors for coronary artery disease (CAD). His symptoms are consistent with stable angina. The pivotal points in this case are the chronicity, exertional nature, and substernal location of the pain. Given the seriousness and prevalence of CAD, it must lead the differential diagnosis. Gastroesophageal reflux disease (GERD) and musculoskeletal disorders are common causes of chest pain that can mimic angina (exacerbated by activity, sensation of pressure) and thus should be considered. The chronicity of his symptoms argues against many other worrisome diagnoses (eg, pulmonary embolism [PE], pneumothorax, pericarditis, or aortic dissection). Pain from a mediastinal abnormality is possible. Physical exam is entirely unremarkable except for mild, stable, peripheral neuropathy presumably related to diabetes. The patient’s ECG is remarkable only for evidence of left ventricular hypertrophy with strain.
  • 12. 11 A tentative diagnosis of stable angina from CAD is made. Laboratory data are notable for normal blood counts and chemistries. There is hypercholesterolemia (LDL, 136 mg/dL; HDL, 42 mg/dL). Mr. W is referred for an exercise tolerance test. Because of his abnormal resting ECG, an exercise myocardial perfusion SPECT was performed. Although chest pain developed during the test, his results were normal without evidence of myocardial ischemia. The results of the patient’s exercise test are surprising. Stable angina remains high in the differential despite the normal stress test but alternative diagnoses must be considered. The intermittent nature of the pain and the lack of constitutional symptoms both make a mediastinal lesion unlikely. The absence of a recent injury, change in activity or reproducible pain on physical exam moves musculoskeletal pain down on the differential. GERD is a common cause of chest pain and should be considered. Prior to the stress test, Mr. W’s probability of having CAD was at least 92% (see Table 9-2). It is important to understand why the exercise test was done in this case. The diagnosis of coronary disease was essentially made by the history and physical. The exercise test was meant to guide therapy. Considering a pretest probability of 92%, and a LR– of about 0.15 for the exercise test, the posttest probability is 60%. This is still well above the test threshold for a potentially fatal disease like CAD. Despite the results of the stress test, stable angina was considered more likely than GERD. Mr. W was given aspirin and a beta-blocker and underwent an angiogram the week after the visit. He was found to have a 90% stenosis of the mid left anterior descending artery and underwent PCI with stent placement.
  • 13. 12 SOAP Note Patient Name: Mr. W Date:______________ Age: 56 Sex: man S; subjective SUBJECTIVE: (Mechanism of injury (MOI), chief complaint (C/C)) He feels squeezing, substernal pressure while climbing stairs to the elevated train he rides to work. The pressure resolves after about 5 minutes of rest. He also occasionally feels the sensation during stressful periods at work. It is occasionally associated with mild nausea and jaw pain. and has a history of well-managed HTN and diabetes. Pt has a number of CAD risk factors. _____________________________________________________________________________ O; Objective OBJECTIVE: (Patient exam findings, Vital Signs, SAMPLE History) mild, stable, peripheral neuropathy presumably related to diabetes. Physical exam: The patient’s ECG is remarkable only for evidence of left ventricular hypertrophy with strain There is hypercholesterolemia (LDL, 136 mg/dL; HDL, 42 mg/dL). Although chest pain developed during the test, his results were normal without evidence of myocardial ischemia Exercise myocardial perfusion SPEC: normal but with chest pain
  • 14. 13 Pretest probability of CAD: 92% and posttest probability of CAD: 60% He was found to have a 90% stenosis of the mid left anterior descending artery and underwent PCI with stent placement. LR for exercise test: 0.15 Allergies: no Medications: Pt takes metformin, aspirin, and enalapril Last Oral Intake: Events leading to accident: _____________________________________________________________________________ A; Assessment ASSESSMENT: (problem list) Stable angina CAD left ventricular hypertrophy with strain 90% stenosis of the mid left anterior descending artery underwent PCI with stent placement hypercholesterolemia _____________________________________________________________________________
  • 15. 14 P; Plan PLAN: (plan for each problem on list, evac route, bivouac location) 1. Aspirin (anticlotting) 2.Angiogram 1 week post-visit 3. Nitrates; tablets and sublingual to be taken during attacks 4. Beta-blocker or CCBs, shift to new generation when causing hypotension 5. Aspirin (antiplatelet) Form completed by: Norseen Hosam _____________________________________________________________________________
  • 16. 15 References Gillen C, Goyal A. Stable Angina. [Updated 2021 Dec 21]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK559016/ Goyal A, Zeltser R. Unstable Angina. [Updated 2022 Sep 18]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK442000/ Hermiz C, Sedhai YR. Angina. [Updated 2021 Dec 21]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557672/ Winchester, D. E., & Pepine, C. J. (2015). Angina treatments and prevention of cardiac events: an appraisal of the evidence. European heart journal supplements : journal of the European Society of Cardiology, 17(Suppl G), G10–G18. https://doi.org/10.1093/eurheartj/suv054 Fig.3; https://www.issuesandanswers.org/back-to-basics-recognising-different-types-of- coronary-artery-disease-2/ Fig.4; https://www.issuesandanswers.org/back-to-basics-recognising-different-types-of- coronary-artery-disease-1/