Substernal or epigastric; squeezing or pressure- like; exertional or at rest; radiating; post-prandial ; postural changes; spasm
What relieves GERD pain?
Antacids / NTG
Why is GERD pain similar to cardiac CP?
Innervation for heart, esophagus & stomach are similar, so symptoms may be similar
How does esophageal perforation present?
Acute, severe, unrelenting & diffuse pain in chest, neck or abdomen (“worst pain of life”). May radiate to back or shoulders & swallowing may exacerbate pain
How does a Mallory Weiss tear present?
hematemesis with or without prior vomiting episode
What is a Mallory –Weiss tear?
A laceration in the mucus membrane of the lower part of the esophagus or upper part of stomach – usually from vomiting or coughing
What are SS of PUD?
burning epigastric pain, post-prandial sx, relieved with food; , may present as N & V, wt loss, anorexia & bleeding (especially in geriatric pts)
How does cholecystitis present?
epigastric/RUQ “visceral” pain + fever, chills, N & V, anorexia…may radiate to back or scapular region
What are SS of pancreatitis?
midepigastric, piercing pain, constant, radiates to back, associated with N & V, abdominal distention & exacerbation in supine position; Low- grade fever, tachycardia & hypotension may be present
How does musculoskeletal CP present?
Sharp pain, worse with movement/palpation (also 5-10% of MI pts have reproducible chest wall tenderness…be aware!)
What is musculoskeletal pain typically relieved with
NSAIDs
This can present with fleeting chest pain, variable onset/duration (usually > 30 min & persistent) & often reproducible on palpation (but not with exertion)
Panic disorder / anxiety
What is the “typical” presentation of an acute MI
New, sudden onset CP/pressure with associated SOB, nausea, diaphoresis
When should an EKG be performed
Goal is within 10 minutes
What other diagnostic studies should be performed for angina?
LV and valvular function, WMA (wall motion abnormalities), effusion/septal defects
Who goes to CPU (chest pain observation units)
Patients at low risk of acute MI
What do you do monitor in CPU?
Rule out MI with serial ECGs & cardiac biomarkers (CK/MB, Troponin levels)
Continuous telemetry monitoring
Is myoglobin specific?
No
Which are the most helpful cardiac markers?
Troponin and CK-MB
Which is released first: troponin or CK-MB?
troponin
Who usually presents with atypical cardiac symptoms?
Elderly, women, diabetic
What is the definition of angina pectoris?
chest discomfort or other related symptoms caused by myocardial ischemia
What is stable angina?
Deep, pressure-like pain in substernal region, may radiate to jaw, neck or left shoulder/arm, Frequently associated SOB, Transient – lasting 2-30 minutes, Precipitated by physical exertion or emotional stress, Responsive to rest or SL NTG
Is the physical exam in stable angina usually normal or abnormal?
Normal
What are some possible PE findings secondary to risk factors?
Would cardiac enzymes be elevated in stable angina?
NO- should be normal – there is blockage but still perfusing
Would an CXR be normal in stable angina?
Yes, often normal
What are some EKG findings in stable angina when no CP is present ?
1/3 normal / non specific changes, Non specific ST-T wave changes (elevation = closer to MI), Q waves = evidence of prior MI, Conduction abnormalities: *LBBB (high association with CAD), RBBB (can be normal), fascicular blocks (*stronger association)
What would you see in unstable angina during angina in an EKG?
ST segment depression/possibly elevation, *T wave inversion
What is the treatment of stable angina?
Lifestyle modification!, 81 – 325mg ASA daily – dose depends on other comorbidities, Beta blocker, ACE Inhibitor – low LV fx or diabetic, Nitrates (PRN or long acting), Statins/Lipid Agents, Consider Revascularization (PCI/Stent vs. CABG) palliative
What are acute coronary syndromes?
Unstable angina: NSTEMI, STEMI
What is the presentation of a NSTEMI/ USA?
New, sudden onset CP/pressure with associated SOB, nausea, diaphoresis. Chest Pain at greater frequency, severity or with less activity. Chest Pain at rest or nocturnally. Chest Pain previously controlled with nitrates, now refractory
What are the EKG findings in NSTEMI/ USA
EKG similar to stable angina but more likely to show acute ischemic changes (ST depression & T wave inversion)
Are cardiac enzymes positive in USA?
No, they are negative
Are cardiac enzymes positive in NSTEMI
YES
What does MOAN stand for?
Morphine, O2, ASA, NTG
What is the diagnosis and treatment of USA/NSTEMI
Admit/monitor, bed rest. MONA (Morphine, O2, NTG, ASA). Serial EKG & cardiac enzymes. ASA, Beta Blocker, NTG, ACE & anticoagulation (heparin/LMWH vs Platelet GP IIb/IIIa Inhibitors). Cardiac risk stratification with cardiac catheterization preferred. Plavix (clopidigrel) following cath
What causes acute STEMI?
thrombotic obstruction of epicardial coronary arteries
Sudden onset CP associated with nausea, diaphoresis & SOB
CP persists > 30 min; may not respond to NTG
What are PE findings of STEMI?
HTN or hypotension, Tachycardia or bradycardia, S3 or S4 or both, Signs of CHF, Systolic murmurs (MR, VSD), Friction rub (usually day 2 or 3)
Why are EKG’s performed on STEMI
To id the site of infarct vessel
What are EKG findings in a STEMI?
Early Peaked T waves (0 – 6 hrs), ST segment elevation (0- 18 hrs), Q waves (takes ~ 18 hrs to “Q” out) & may remain lifelong or later disappear, Extent of ST deviation & QRS duration correlate with risk of adverse outcomes
What EKG findings are indicative of an MI
ST elevation at the J point in 2 or more contiguous leads
Do EKG’s always indicate Acute MI?
NO, Initial ECG is negative or non-diagnostic in up to 40% of patients having an AMI. Repeat ECG…if possible during CP episode
What leads correspond with an inferior MI
II, III, AVF
What leads correspond with an anterior MI?
(V2-V5) or (V1-V4)*
Lateral MI?
(I, aVL, V5-V6)
Inferolateral
(II, III, aVF, I, aVL)
Anterolateral?
(V4-V6, I, aVL)
When is PCI the treatment of choice for a STEMI?
Emergent PCI preferred if early presentation (< 3 hr from sx onset) & skilled team available (door to balloon time < 90 minutes
When are lytics the preferred Rx of choice?
Lytics within 12 hr of onset & no PCI option
What are the ABSOLUTE contraindications to lytic therapy?
any prior intra-cranial hemorrhage, cerebral AVM, malignant neoplasm, active bleeding, suspected aortic dissection, ischemic CVA in past 3 months or closed head trauma, severe uncontrollable HTN
unexpected non-traumatic death in clinically well or stable patients who die within 1 hour after onset of symptoms
What is the most causative rhythm in SCD?
ventricular tachycardia except in the setting of acute ischemia or infarction (then VF arrest)
When do most SCD’s occur?
Early am
What is CHD mostly contributed to in Western cultures?
CHD
What are PE findings of MVP?
Mid-systolic click, inverted T waves inferior leads; unclear etiology of associated CP; myocardial ischemia vs increased systemic arterial pressure
What are PE findings of aortic stenosis?
Systolic ejection murmur transmitted to carotids. LVH on ECG
What are PE findings for aortic regurgitation?
Diastolic murmur transmitted to carotid arteries, wide arterial pulse pressure, ECG may show LVH
Who is at increased risk of aortic dissection?
Men, preggers, patients with connective tissue dz (Marfans), HTN, Bicuspid Aortic Valve or Coarctation of the Aorta
What is an aortic dissection?
Intimal tear in aorta creates a false lumen between media & adventitia.
May be acute or chronic in nature.
Where do AD’s occur?
>95% occur in the Ascending aorta just distal to aortic valve or just distal to the left subclavian (fixed points)
What are the two classification systems for AD?
Debakey, Stanford
What is the difference between debakey and sanford?
Debakey – 3 parts. I Ascending aorta extending to distal (entire length). II. Ascending aorta only (before left subclavian). III. Descending aorta only (after left subclavian); Sanford – 2 parts: A. Any involvement of ascending aorta. B. Not involving ascending aorta
What are SS of AD?
Sudden onset retrosternal and back pain. May see infarct pattern on ECG, neurologic deficits/CVA, limb ischemia, syncope, shock, hypertensive. Pulse discrepancies, tamponade possible. Acute AI indicates aortic root involvement. Beware patients with Marfan’s syndrome
What would you see on a CXR for AD?
Widened Aortic silhouette. Widened mediastinum. Left pleural effusion. 10%-20% normal
When is a CT helpful for AD?
In acute presentation
When is MRI useful in AD?
For serial follow up
What would you see on an EKG in AD?
LVH, non-specific or inferior abnormalities (dissections preferentially extend into Right coronary ostium)
What is the most sensitive & specific diagnostig study for AD?
achieve relative hypotension & bradycardia) beta blocker first, then nitroprusside to maintain SBP of 100 -120 mmHg
How do you treat type A AD?
Surgically (maybe valve replacement)
How do you treat type B AD?
Medically- except for: Rupture, Limb or visceral ischemia, ongoing pain, Saccular morphology uncontrolled HTN, Marfan’s, or AI (rare)
What is the clinical picture of a AAA?
Majority are asymptomatic. Prominent aortic pulsation. Pain (if present) described as epigastric fullness or lower back & hypogastric region. Gnawing, hours to days in duration, not positional. Severe back or abdominal pain & hypotension indicate rupture.
When should AAA patients have an emergent vascular surgery consult?
If diagnosis of rupturing is clear clinically
What test do you use if hemodynamically stable pt?
US
How do you manage AAA patient?
Large bore IV, type & cross, monitor closely
What are TAA clinical findings?
40% of patients are asymptomatic at diagnosis, symptoms dependent on size & position of aneurysm. Pain (if present) substernal, back/neck . Rupture: worsening of pain to severe. Vascular sx: CHF, ischemia, thromboembolism. Mass Effect: SVC syndrome, tracheal deviation, cough, hemoptysis, dysphagia, hoarseness
Is CXR diagnostic?
Chest X-ray is NOT diagnostic alone (need CT or MRI if suspected & CXR-); stability of patient crucial. CXR + Must differentiate from anterior mediastinal mass (ie thymoma, lung CA)
How do you manage TAA?
Same as AAA- Large bore IV, type & cross, monitor closely
An inflammation of the pericardium is usually associated with effusion is…
Acute pericarditis
What is AP due to?
~85% associated with viral or “idiopathic” etiology; remainder are associated with TB/bacterial/fungal infections, neoplastic dz, uremia or collagen vascular dz, or following MI cardiac surgery or irradiation
What does excessive anticoagulation cause?
hemorrhagic effusion
What are clinical findings of AP?
Pleuritic, sharp, stabbing CP that radiates to shoulders, back, neck that is worse on deep inspiration or movement, worse supine & relieved by sitting up & leaning forward. Low grade fever, dyspnea, friction rub LLSB & sometimes palpitations or dysphagia
What is seen on EKG of AP?
Upsloping ST segment
What would be seen on CXR of AP?
Usually normal- r/o other dz
What labs would you order?
CBC with diff, BUN/creatinine to r/out uremia, serologies (strep, ANA, viral studies), thyroid to ID underlying cause
What would an echo reveal?
may reveal effusion
T/F – pericardiocentesis is necessary
False - usually not necessary
Who would you do a pericardiocentesis on?
Patients with tamponade. Confirm / exclude purulent pericarditis
Rx for AP?
Stable pts Rx as OP with NSAIDs for 1 to 3 weeks. Treat underlying cause if identified
Who should be admitted for AP?
Any pt with myocarditis, uremic pericarditis, enlarged cardiac silhouette on CXR or hemodynamic compromise should be admitted for observation
Why does tamponade occur?
Tamponade occurs when the pressure in the pericardial sac exceeds normal RV filling pressure, resulting in restricted filling & decreased cardiac output
What are conditions that lead to tamponade?
Malignancy induced pericarditis. Aortic dissection. MI with Ventricular rupture. Pacemaker perforation during implant
What are the symptoms of cardiac tamponade?
Shortness of breath & weakness more likely than CP, tachycardia
What would you see on PE when evaluating cardiac tamponade?
Distended neck veins, pulsus paradoxus
What is the diagnostic gold standard for tamponade?
ECHO – large pericardial effusion
What would you see on EKG in tamponade?
Electrical alternans an/or low voltage. El Alt = beat to beat variability in the amplitude of the P & R waves unrelated to inspiratory cycle…really only see ~ 20% of time, but is diagnostic if present
When is the only time CXR is helpful for tamponade?
If you see a large cardiac silhouette
Is cardiac tamponade an emergency
YES! - Tamponade is a True Emergency
What are SS of cardiac tamponade?
Becks triad: hypotension, elevated systemic venous pressures, small quiet heart
What is the difference between hypertensive urgency / emergency
Emergency has target organ damage (TOD!!)
What is the Rx for hypertensive urgency?
Short term Rx with labetalol, clonidine or captopril with outpatient follow up within 72 hrs is recommended
What are the most common causes of hypertensive emergencies?
CHF with pulmonary edema, cerebral infarction
What is treatment for hypertensive emergencies?
Goal of treatment is to achieve a controlled, gradual lowering of BP. 10% decrease in first hour, then 15% over next 3 – 12 hrs to BP of no less than 160/110 mmHg. Rapid correction of BP to norm levels puts pt at high risk for worsening cerebral, renal or cardiac ischemia
Malignant htn is a form of hypertensive emergency or urgency
emergency
Who is malignant HTN more common in?
Most common in young adults, prior renal dz, AA males, pregnancy or in collagen vascular dz.
