Week 5 CVD & ACS Flashcards
Jugular venous pressure
A reflects pressure in the right atrium.
B Is best estimated from the carotid artery.
C should be measured with the patient positioned at 90 degrees.
D is often higher than arterial pressure.
A reflects pressure in the right atrium.
Pressure in the jugular veins reflects right atrial pressure giving clinicians an important clinical indicator of cardiac function and right heart hemodynamics. JVP is best estimate from the right internal jugular vein. It should be measured with the patient at 60 degrees. Systemic venous pressure is much lower than arterial pressure.
A left-sided S4 heart sound in a 50-year-old female with hypertension suggests which of the following?
A This is a physiologic finding
B Decreased compliance of the ventricular myocardium
C Opening of a stenotic mitral valve
D Turbulent blood flow from the left ventricle into the aorta
B Decreased compliance of the ventricular myocardium
S4 heart sound (atrial gallop) may be heard in trained athletes or older age groups. More commonly, it is due to increased resistance to ventricular filling following atrial contraction resulting from decreased myocardial compliance. Causes include hypertensive heart disease, CAD, aortic stenosis, and cardiomyopathy.
Lateral displacement of the point of maximal impulse (PMI) can be seen with which of the following?
A Mitral valve prolapse
B Heart failure
C Aortic dilation
D High diaphragm
B Heart failure
Lateral displacement occurs from cardiac enlargement. Upward displacement can occur from a high diaphragm.
Exam findings in a patient with peripheral arterial disease (PAD) of the leg include which of the following?
A Pitting edema and decreased sensation
B Cyanosis with cold exposure and rubor with rewarming
C Hair loss and paleness
D Varicosities and stasis dermatitis
C Hair loss and paleness
Pitting edema, varicosities and stasis dermatitis occur with venous insufficiency. Cyanosis with cold exposure and rubor with rewarming occurs with Raynaud’s phenomenon.
Which of the following patient populations often experience atypical symptoms of myocardial ischemia or infarction? (Select all that apply)
A Men between ages 35 and 50
B Women
C Diabetics
D Patients with hypertension
E Obese patients
B Women
C Diabetics
Women usually have non-chest pain symptoms such as nausea, lightheadedness, dyspnea and jaw pain. Patients with type 2 DM may have a silent MI due to autonomic neuropathy. Elderly also have atypical symptoms.
Which of the following best describes classic anginal pain?
A Substernal tightness or pressure
B Sharp, localized left sided pain
C Right-sided chest soreness radiating to the right shoulder
D Chest pain that is worse with inspiration and movement of the left arm
A Substernal tightness or pressure
Classic anginal pain occurs anywhere between the epigastrum and mandible and is described as tightness, heaviness, squeezing, pressure or grip like.
The nurse practitioner refers a patient to the emergency department with symptoms of acute ST-segment elevation MI (STEMI). The nearest hospital that can perform percutaneous coronary intervention (PCI) is three hours away. What does the nurse practitioner expect the initial treatment to be for this patient?
A Intravenous heparin
B Oral beta blocker
C Fibrinolytic treatment
D Transfer of the patient to a PCI-capable institution
C Fibrinolytic treatment
Fibrinolytic therapy should be administered to any patient with evolving STEMI within 30 minutes of the time of first medical contact. Patients more than 120 minutes away from a PCI-capable hospital should be given fibrinolytic therapy since PCI should be performed within 90 minutes if possible. Giving heparin or beta blockers is not helpful.
A 65-year-old male walks into the clinical for acute chest pain and dyspnea. A STAT ECG is performed and it reveals 3 mm ST segment elevation in lead II, III, and AVF. The nurse practitioner calls ALS for transport because he suspects:
A Acute ischemia of the posterior wall
B Acute infarction of the lateral wall
C Acute infarction of the inferior wall
D Acute ischemia of the septal wall
C Acute infarction of the inferior wall
Leads II, III and AVF view the inferior wall of the heart. 2mm or greater ST segment elevation in 2 or more contiguous leads suggests STEMI. ST segment depression and T-wave inversion suggest ischemia.
A patient with stable CAD who has not undergone coronary intervention should be managed with which of the following first-line agents?
A Warfarin, aspirin, and digoxinW
B Beta blocker, aspirin, and nitroglycerin
C Thiazide diuretic, calcium channel blocker, and clopidogrel
D Long acting nitrate, ACE inhibitor, and beta blocker
B Beta blocker, aspirin, and nitroglycerin
All patients with stable CAD should be managed with a beta blocker and aspirin unless contraindicated. Nitroglycerin can be used on an as needed basis.
A patient experiencing heart failure with reduced ejection fraction will have which of the following?
A Increased cardiac contractility and stroke volume
B Impairment of ventricular filling and relaxation
C Left ventricular stiffness and reduced chamber size
D Pump failure from left ventricular systolic dysfunction
D Pump failure from left ventricular systolic dysfunction
Heart failure with reduced ejection fraction results in pump failure from ventricular systolic dysfunction. Heart failure with preserved ejection fraction may have milder symptoms and is associated with impairment of ventricular filling and relaxation. Cardiac contractility and stroke volume are decreased in HFrEF. Ventricular remodeling and dilation occurs.
Which of the following class of medication is the considered the cornerstone of heart failure medical management unless there is an absolute contraindication?
A Hydralazine-isosrorbide
B Angiotensin-converting enzyme inhibitor (ACEI)
C Calcium channel blocker
D Ivabradine
B Angiotensin-converting enzyme inhibitor (ACEI)
ACEI therapy improves mortality in patients with HFrEF and improves overall clinical status. They decrease systemic and pulmonary vascular resistance. ACEI remain the cornerstone of management and should be considered priority in all patients unless there is an absolute contraindication. CCB’s should not be used in HF.
An elderly adult patient without prior history of cardiovascular disease reports lower leg soreness and fatigue when shopping or walking in the neighborhood. The primary care nurse practitioner notes decreased pedal pulses bilaterally. Which test will the nurse practitioner order initially to evaluate for peripheral arterial disease based on these symptoms?
A Digital subtraction angiography
B Doppler ankle, arm index
C Magnetic resonance angiography
D Segmental limb pressure measurement
B Doppler ankle, arm index
The Doppler study may be performed easily to indicate the likelihood of PAD. Other tests are performed only if indicated.
A patient who has been diagnosed with heart failure for over a year reports being comfortable while at rest but experiences palpitations and dyspnea when walking to the bathroom. Which classification of heart failure is appropriate based on these symptoms?
A Class I
B Class II
C Class III
D Class IV
B Class II
Patients with Class II heart failure (HF) will have slight limitation of activity and will be comfortable at rest with symptoms occurring with ordinary physical activity. Patients with Class I HF do not have limitations and ordinary physical activity does not produce symptoms. With Class III HF, less than usual activity will produce symptoms. With Class IV HF, symptoms are present even at rest and all physical activity worsens symptoms.
A patient is diagnosed with peripheral arterial disease (PAD) and elects not to have angioplasty after an angiogram reveals partial obstruction in lower extremity arteries. What will the nurse practitioner recommend to help manage this patient’s symptoms?
A Daily aspirin therapy to prevent clotting
B Statin therapy with clopidogrel
C Walking slowly for 15 to 20 minutes twice daily
D Walking to the point of pain each day
D Walking to the point of pain each day
Studies have demonstrated that an exercise program involving walking to the point of pain is as effective as angioplasty. Medications are useful to prevent progression of plaque formation and to prevent myocardial infarction (MI).
An 18 yo patient is here for a cardiac screening appointment to see if they can play sports in college. The diagnostic test best suited to detect hypertrophic cardiomyopathy or idiopathic left ventricular hypertrophy is
a. Echocardiogram
b. Electrocardiogram
c. Arteriogram
d. Stress test
a. Echocardiogram
Your 59 yo patient has a history of hyperlipidemia, and is presenting with signs/symptoms of unstable angina. The best course of management is
a. Start aspirin therapy and schedule an exercise stress test next month
b. Initiate lipid lowering agents
c. Hospitalize the patient, with EKG monitoring and pharmacologic control of the ischemia, arrhythmias, and thrombosis as appropriate
d. Prescribe a Holter monitor and start her on a beta blocker
c. Hospitalize the patient, with EKG monitoring and pharmacologic control of the ischemia, arrhythmias, and thrombosis as appropriate
You are seeing a new patient, recent move to the area, who has a diagnosis of congestive heart failure. Which of their medications should be discontinued?
a. Nifedipine (Procardia XL), taken for long term management of chronic stable angina
b. Hydrochlorothiazide (HydroDIURIL) for their hypertension
c. Enalapril (Vasotec) for his hypertension
d. Butalbital (Esgic) for his headaches
a. Nifedipine (Procardia XL), taken for long term management of chronic stable angina
Which communication is your first priority when counseling a patient with ischemic arterial ulcers?
a. Increasing coffee intake will stimulate the heart rate and circulation
b. Decreasing water intake slightly will improve blood viscosity
c. Reducing risk factors will help improve tissue perfusion
d. Tell them to begin an intense aerobic exercise program to improve perfusion
c. Reducing risk factors will help improve tissue perfusion
Your patient has chronic ischemic heart disease and is taking a beta blocker, which results in
a. An increase in high-density lipoprotein cholesterol
b. A reduced heart rate
c. A decreased diastolic filling time
d. An increase in oxygen demand
b. A reduced heart rate
Which symptom is noted with occlusive arterial disease?
a. Pain occurring in the calves or thighs when walking, with relief upon resting
b. Pain when standing that is not relieved by sitting or lying down
c. Severe pain at rest that requires the client to raise the legs into the air to obtain relief
d. Redness and pronounced superficial veins
a. Pain occurring in the calves or thighs when walking, with relief upon resting
Mr. J is a 54-year-old man who presents to primary care clinic for an initial evaluation as a new patient. He has not seen a doctor in years, because he “hasn’t needed one” and takes no medications. His chief complaint today is fatigue. He describes progressively worsening dyspnea when walking briskly and climbing stairs. He must rest several times in order to complete mowing his lawn, whereas 6 months ago he could easily complete this task without resting. He feels fine at rest. He finds himself awakening frequently at night feeling “congested” but this has improved somewhat after putting bricks under the head of his bed. He denies any chest discomfort or palpitations. He has never smoked, but he drinks “a few beers” every night. He is unaware of any family history of heart disease. On exam, he is overweight (BMI 31 kg/m2)), heart rate is 83 bpm, and blood pressure (BP) is 184/98 mm Hg. Jugular veins are nondistended without hepatojugular reflux. Lungs are clear. The point of maximal impulse (PMI) is displaced laterally. Heart sounds are regular with a 2/6 systolic murmur at the apex without gallop. Liver is nonpulsatile, and there is no lower extremity edema.
What do you suspect the dx is?
Suspected dx is heart failure
Major preventable causes of HF inlcude CAD, HTN, myocardititis, infiltrative dx, peripartum cardiomyopathy, HIV, connective tissue dx, substance use, chemotoxic cardiomyopathy, and idiopathic cardiomyopathy
Mr. J is a 54-year-old man who presents to primary care clinic for an initial evaluation as a new patient. He has not seen a doctor in years, because he “hasn’t needed one” and takes no medications. His chief complaint today is fatigue. He describes progressively worsening dyspnea when walking briskly and climbing stairs. He must rest several times in order to complete mowing his lawn, whereas 6 months ago he could easily complete this task without resting. He feels fine at rest. He finds himself awakening frequently at night feeling “congested” but this has improved somewhat after putting bricks under the head of his bed. He denies any chest discomfort or palpitations. He has never smoked, but he drinks “a few beers” every night. He is unaware of any family history of heart disease. On exam, he is overweight (BMI 31 kg/m2)), heart rate is 83 bpm, and blood pressure (BP) is 184/98 mm Hg. Jugular veins are nondistended without hepatojugular reflux. Lungs are clear. The point of maximal impulse (PMI) is displaced laterally. Heart sounds are regular with a 2/6 systolic murmur at the apex without gallop. Liver is nonpulsatile, and there is no lower extremity edema.
What tests should you order?
● A chest x-ray (CXR) should be obtained to look for findings of HF as well as for other potential causes of the patient’s dyspnea.
● Echocardiogram
● An electrocardiogram (ECG) should be obtained to assess for evidence of structural heart disease and conduction disease. A normal electrocardiogram nearly excludes the diagnosis of systolic heart failure.
● Laboratory testing should include a hematocrit to exclude anemia and thyroid function tests to exclude thyroid disease.
● A fasting lipid profile and fasting glucose with or without hemoglobin (Hg) A1c should be obtained to assess cardiovascular risk and screen for hyperlipidemia, metabolic syndrome, and diabetes mellitus.
● A urinalysis (UA) and basic metabolic profile (BMP) should be obtained with anticipation of initiating pharmacotherapy, which will be influenced by renal function and baseline electrolyte values. Significant proteinuria may suggest an infiltrative process, although mild proteinuria is often seen in heart failure.
● A plasma brain natriuretic peptide (BNP) level can be useful in patients in whom diagnosis of HF is in question. Whereas BNP can often be elevated in processes other than HF, a normal BNP makes a diagnosis of systolic HF very unlikely.
Meds to AVOID in HF
NSAIDs
CCBs (diltiazem and verapamil)
pharmacologic tx for HF
meds that have demonstrated mortality benefit and offer symptomatic relief
ACE-I or ARBs
beta blockers (carvedilol, bisoprolol, long-acting metoprolol)
Aldosterone antagonists
newer drug - sacubitril/valsartan
isosorbide dinitrate and hydralazine benefits black pts
diuretics and digoxin offer symptomatic relief, no improvement in survival
Treatment should be tailored to both the symptoms and stage of HF
Non-pharmacological tx for HF
smoking cessation minimize or abstain for alcohol use salt restriction 3g/day exercise mild-mod 30 mins/day if stable HF (not during exacerbation) weight loss cardiac rehab monitor daily weights immunizations
AHA goals of tx for HF
control symptoms improve health-related quality of life patient education prevent hospitalization prevent mortality
Patient w/ new dix of HF, echo results show left ventricular (LV) systolic dysfunction. The LV ejection fraction (LVEF) is 40% with global hypokinesis. The end-diastolic dimension is moderately increased. There is concentric left ventricular hypertrophy (LVH) and mitral annular dilatation with mild mitral regurgitation. The left atrium is mildly enlarged.
Are there any additional tests that you would recommend at this point?
Exercise testing should be performed as part of the initial evaluation of systolic heart failure. This can assess for ischemic heart disease and can provide additional prognostic data. Serial evaluation can assess changes over time.
Occult CAD is a common cause of systolic HF. All patients with new systolic HF and angina should be evaluated with coronary angiography. Patients without angina who have not had previous evaluation of their coronary anatomy should also be considered for coronary angiography because of the high prevalence of CAD among the older adult population. Noninvasive imaging has not yet been demonstrated as an acceptable alternative to exclude CAD in this group of patients. Additionally, angiography can exclude coronary anomalies in younger patients.
Patients who have had recent prior angiographic exclusion of CAD presenting with new HF and without anginal symptoms do not need to be reevaluated by coronary angiography.
Pt with HF returns to clinic after 6 months of regular visits and titrating medications. He is now on lisinopril, carvedilol, furosemide, and spironolactone. His dyspnea has improved, and he has used the bricks under his bed to stabilize the stationary exercise bicycle he bought with the money he saved by not drinking beer. His BP is 118/73 mm Hg. The remainder of his exam is unchanged. He met a patient in the waiting area who has a “shock box,” and he wants to know if he should get one.
What recommendations can you make now?
Implantable cardiac defibrillators (ICDs) have clearly demonstrated mortality benefit in select patient populations with increased risk for sudden cardiac death. While these populations continue to be more clearly defined, ICDs are currently recommended for patients with LVEF below 35% on optimal medical therapy, or who have had ventricular arrhythmias.
Patients with left ventricular dyssynchrony may benefit from cardiac resynchronization therapy (CRT). Also termed biventricular pacing, CRT has demonstrated improvement in quality of life, functional capacity, and mortality in patients with advanced HF. Current guidelines recommend CRT for patients with LVEF less than 35%, moderate to severe symptoms, and QRS duration greater than 140 ms. These patients generally have advanced HF and will have already been referred to a cardiologist who should follow these patients and guide decisions regarding CRT.
At present, this patient would not be a candidate for an ICD or CRT. He can be reassured that his risk of sudden death remains low. Symptoms of arrhythmia, such as syncope or palpitations, should be specifically elucidated at follow-up visits.
What should follow up visits with a pt with HF involve and what should you monitor?
Regularly scheduled follow-up visits should include a careful history to assess changes in the patient’s functional status, weight gain or fluid retention, dietary habits, salt intake, tobacco, alcohol and drug use
. Physical examination should include assessment of volume status. Regular laboratory monitoring of renal function and plasma potassium levels should be performed. Plasma potassium levels should be kept between 4 and 5 mEq/L.
Routine reevaluation of LVEF is not necessary, but noninvasive reassessment of LVEF is reasonable when a patient has a change in clinical status suggesting worsening HF.
A 71-year-old man presents to the urgent care with a sudden onset of substernal chest pain 1 hour ago. He describes the pain as a heavy pressure sensation that radiates down both arms and is 10 of 10 in intensity. His pain started while he was walking and improved, but did not resolve, with rest. His medical history is significant for diabetes mellitus. He has smoked 1 pack of cigarettes per day for the past 50 years. His mother died of a myocardial infarction (MI) at age 56 years. On examination, there are both an S4 gallop and bibasilar fine crackles. His electrocardiogram (ECG) shows 3-mm ST-segment elevations in leads II, III, and aVF.
What your diagnosis and how would you manage?
Acute coronary syndrome (ACS) includes unstable angina, non–ST-elevation MI, and ST-elevation MI; all result from myocardial ischemia caused by thrombosis at a site of coronary atherosclerosis. There are other causes of MI, but ACS is the most common. This patient has typical chest pain, meaning substernal, “pressure” or “squeezing,” exertional, and relieved by rest or nitroglycerin. Radiation to the arms correlates strongly with cardiac chest pain. To evaluate a patient with chest pain, first determine the likelihood of ACS as its cause; then stratify the risk for mortality to ensure timely intervention in high-risk patients. Here the history alone strongly suggests ACS. The patient is deemed to be at high risk because of the ST elevations on ECG. Administer aspirin, O2 and Transfer to another facility for PCI within 90 minutes or else fibrinolytic therapy.
What are some differential diagnosis for a patient complaining of acute chest pain?
Unstable angina without MI Aortic dissection Pulmonary embolism Tension pneumothorax Pericarditis Esophageal rupture
What are the laboratory, imaging, and procedures are included in the work up in acute myocardial infarction?
Laboratory Tests
- Troponin I, troponin T, and quantitative CK-MB (creatine kinase myocardial band) elevations are seen as early as 4 to 6 hours after onset; they are almost always abnormal by 8 to 12 hours.
- Troponins may remain elevated for 5 to 7 days or longer and are not generally useful for evaluating suspected early reinfarction.
- High-sensitivity troponin assays
• When positive, help enable myocardial infarction to be detected earlier
• When negative, may be useful in excluding myocardial infarction in patients with chest pain
Imaging Studies
- Chest radiograph: signs of heart failure, often lagging behind the clinical findings
- Echocardiography: assesses global and regional LV function, wall motion
Diagnostic Procedures
- ECG: classic evolution of changes is from peaked (“hyperacute”) T waves to ST-segment elevation to Q wave development to T wave inversion; this may occur over a few hours to several days.
- Cardiac catheterization and coronary angiography can demonstrate coronary artery occlusions and allow PCI.
- Echocardiography or left ventriculography can demonstrate akinesis or dyskinesis and measure ejection fraction.
Patients with a drug eluting stent should be on aspirin and clopidogrel for a minimum of how long?
A minimum of 12 months.
A 55-year-old man presents to the clinic complaining of chest pain. For the past 5 months, he has noted intermittent substernal chest pressure radiating to his left arm. The pain occurs primarily when exercising vigorously and is relieved with rest. He has no associated shortness of breath, nausea, vomiting, or diaphoresis. His medical history is significant for hypertension and hyperlipidemia. He is on atenolol and a low-fat diet. His father had died of a myocardial infarction (MI) at age 56 years. He has a 50-pack-year smoking history and is currently trying to quit. His physical examination is normal except for a blood pressure of 145/95 mm Hg; his heart rate is 75 beats/min. He is currently asymptomatic.
What are your differential diagnosis?
When evaluating a patient with chest pain, first determine if the pain is acute in onset (or progressive) with features concerning for acute coronary syndrome (ACS), pulmonary embolism, aortic dissection, pneumothorax, or another emergency.
Most patients with chest pain, however, do not require emergent evaluation. This patient’s chest pain has characteristics of typical angina, including substernal location, exertional onset, radiation to the arm, and relief with rest. Risk factors for coronary artery disease (CAD) are weighed along with history, examination, and electrocardiogram (ECG). Although other causes (esophageal spasm or musculoskeletal pain) are possible, the symptoms, long smoking history, and family history confer a high pretest probability of CAD.
major CAD risk factors
Age sex family history tobacco use diabetes mellitus hypertension low high-density lipoprotein [HDL] cholesterol high non-HDL cholesterol
A 55-year-old man presents to the clinic complaining of chest pain. For the past 5 months, he has noted intermittent substernal chest pressure radiating to his left arm. The pain occurs primarily when exercising vigorously and is relieved with rest. He has no associated shortness of breath, nausea, vomiting, or diaphoresis. His medical history is significant for hypertension and hyperlipidemia. He is on atenolol and a low-fat diet. His father had died of a myocardial infarction (MI) at age 56 years. He has a 50-pack-year smoking history and is currently trying to quit. His physical examination is normal except for a blood pressure of 145/95 mm Hg; his heart rate is 75 beats/min. He is currently asymptomatic.
What will you include in your diagnostic work up of this patient?
ECG (baseline status, evidence of prior MI, LV hypertrophy), CXR, ETT, echocardiogram.
Consider CTA
CBC, CMP, lipids, CK (if considering statin), TSH
How is stable angina managed, both pharmacologic and nonpharmacologic?
ASA beta blocker statin therapy nitro prn Lifestyle modifications (diet, exercise, alcohol in moderation, no smoking, etc)
Adult male presents with fever, chills, and malaise that are associated with subungual hemorrhages (splinter hemorrhages on nail bed) and tender violet-colored nodules on fingers and/or toes (osler’s nodules). Palms and soles have tender red spots on skin (Janeway lesions). Heart murmur present. Patient has hx of prosthetic valve, congenital heart dx, cardiac device, IV drug use, and recent dental surgery.
What is the dx?
infective endocarditis
infective endocarditis (IE) RF
valvular/structural heart abnorms arrhythmias IV drug abuse hemodialysis implantable devices immunosuppressed hx of infective endocarditis recent dental or surgical procedure
infective endocarditis (IE) most common pathogen
staph aureus
MSSA or MRSA
infective endocarditis (IE) presentation
fever, chills, fatigue, weight loss, poor appetite, cough, SOB, edema, new murmur, CHF, emboli
roth spots, osler’s nodes, janeway lesions , petechaie, renal failure, arthralgia, myalgia
FROM JANE (IE)
F- fever
R- roth spots
O- osler’s nodes
M - murmur
J- janeway lesions
A- anemia
N- nails - splinter hemorrhages
E - emboli (vegatative)
IE diagnostics
blood cultures (3 sets BEFORE antimicorbial tx)
CBC, CRP, ESR
EKG
TTE, TEE, CT
Duke’s criteria IE
major criteria:
- (+) blood cultures
- evidence of endocardial involvement
minor criteria:
- predisposing factor
- temp > 38C
- vascular phenomena
- immunologic phenomena
- microbiologic evidence
definite IE: 2 major OR 1 major + 3 minor
IE management
refer to ED for hospitalization & IV abx
consult ID & cardio
endocarditis prophylaxis recommended in
previous hx IE
prosthetic heart valves
unreparied/repaired cyanotic congenital heart dx
cardiac transplant with valvulopathy
invasive dental procedures (routine dental cleaning, tooth extractions, dental abscess drainage, etc)
invasive resp tract procedures (incision or biopsy of resp mucosa)
surgical procedures involving infected skin or MSK structures
endocarditis prophylaxis med
1st line = amoxicillin single dose 30- 60 mins before procedure
PCN allergy = clindamycin, clarithromycin, or cephalexin
CAD RF
age gender ethnicity family hx genetics obesity smoking DM HLD HTN
CAD clinical presentation
asymptomatic (stable)
STABLE angina - tightness, pressure, heaviness w/ exertion, stress, large meals, cold weather; lasts less than 5 mins and relieved w/ rest or 1 nitro
predictable pain
Levine sign
CAD atypical presentation
occurs in women, DM, older
indigestion
dyspnea
jaw pain
CAD diagnositcs
ECG
exercise tolerance test (gold standard), if inconclusive stress test w/ ECHO, SPECT
coronary angiography
exercise tolerance test (stress test) when to perform and how
stress test should be performed within 72 hours of presenting symptoms of CAD
exercise using Bruce protocol vs pharmacologic
stress test w/ bruce protocol
start at slow speed/low incline
gradually increase speed every 3 mins
goal = heart working at 85% of its maximal capacity
if test stopped early = inconclusive
pharmacologic stress test
administer adenosine or regadenson, puts physiologic stress on heart
positive exercise tolerance test
ECG changes consistent w/ ischemia
horizontal or down-sloping ST depression of 1mm or more at 60- 80 msec after J point
ST segment changes are indicative of viable cardiac muscle being supplied by narrowed coronary artery
stress test should NOT be performed in
HF exacerbation uncontrolled cardiac arrhythmias severe HTN unstable angina acute MI critical aortic stenosis
Duke’s treadmill score (DTS) what is it
predicts 5-year mortality w/treadmill stress test w/ standard Bruce protocol
based on duration of exercise, ST deviation, presence/severity of angina during test
DTS = exercise time (mins) - (5x ST deviation in mm) - (4x angina index)
duke’s treadmill score categories
low risk: score > 5; 5- year survival 97%
intermediate risk: score 4 and (-) 11; 5 year survival 90%
high risk: score < (-) 11 5 year survival 65%
CAD labs
lipid profile HbA1c CBC - anemia, polycythemia renal function BNP - check for evidence of HF
CAD AHA/ACC secondary prevention
PREVENT major coronary event smoking cessation BP < 140/90 DM control a1c < 7% (metformin) physical activity weight management lipids: - < 75 y.o. high intensity statin - > 75 y.o. mod or high dose statin
ASA: daily, clopidogrel if contraindicated
BB: MI, ACS, LV dysfunction, HF
ACE-I: LVEF <40%, HTN, DM, CKD
flu vaccine
stable angina tx
sublingual nitro if NO HF q5 mins x3 doses, no relief 15 mins = ER
BB - 1st line
symptoms not controlled: CCB & long acting nitrate
persistent angina, fail med tx = PCI or CABG
CAD follow up
co manage with cardiology
every 4-6 months within 1st year , then every 4- 12 months depending on clinical situation
Pt w/ stable CAD, when would they require dual antiplatelet tx ?
recent stent placement
dual antiplatelet therapy (ASA plus P2y12 receptor agonist)
continue for 12 months
PAD RF
HTN DM CKD HLD smoking family hx
PAD S/S
intermittent claudication - pain in calves when walking, relieved by rest sparse/absent hair LE shiny LE skin pallor when LE elevated depend rubor when LE dangling
PAD diagnositcs
resting ABI
serum glucose, lipid profile, CRP, homocysteine
ankle brachial index (ABI) when to perform
used in patients with one or more of the following:
- exertional leg symptoms
- nonhealing LE wounds
- hx consistent with PAD in pts > 65 y.o.
- symptoms in pt >/= 50 y.o. w/ DM or smoker
ABI
compares systolic pressure at brachial artery with dorsalis pedis and posterior tibial arteries
should be lower in affected extremity than normal one
ABI = 0.9 = PAD
ABI 0.75- 0.5 = claudication
ABI < 0.5 = rest pain and/or tissue loss
ABI > 1.4 = abnormal, can indicate calcified vessels
normal ABI results
1- 1.4
if normal but high clinical suspicion of PAD, consider treadmill exercise test
PAD management
smoking cessation
EXERCISE
low carb, low fat diet
tx HTN, DM, compression stockings (ABI > 0.8)
ASA or clopidogrel
PAD red flags
severe claudication resting pain gangrene non healing wounds absent/diminished pulses blue, cold limb
- prolonged pain, sudden color changes, numbness = medical eval
PAD complications
AAA
renal artery stenosis
diabetic foot ulcer
infection
acute coronary syndrome (ACS)
thrombus that forms in coronary arteries on plaque & occludes blood flow to areas of heart leading to muscle death
life threatening condition
ACS presentation
chest pain
- no reproducible, not stabbing or localized, usually occurs t rest w/ minimal exertion lasts longer than 20 mins
- can radiate to jaw, neck, back, arm, shoulder
nausea, lightheadedness
SOB
ACS atypical presentation
occurs in diabetics, women, older
indigestion pleuritic pain dyspnea nausea lightheadedness jaw/neck pain epigastric pain
ACS immediate workup
EKG within 10 mins VS ASA nitro O2 if < 90% REFER TO ED
ACS diagnostics
EKG
troponins, peaks 3- 4 hrs; serial draws 3-6 hrs
CXR - r/o other causes
Echocardiogram - detects wall motion abnorms
coronary angiography
consider: BNP for HF, CBC to exclude anemia, Mg, K, NA, BUN, Cr, TSH
ACS ddx
aortic dissection PE MI spontaneous pneumo costochondritis PNA pulmonary HTN aortic stenosis MVP pericarditis cardiomyopathy GERD Acute cholecysitits shingles
STEMI
ST segment elevation of 2mm or more in M; 1.5 mm in F in 2 contiguous leads = infarction
new onset LBBB
NSTEMI
ST-segment depression with symmetrically inverted T waves = ischemia
generally present w/in mins of acute ischemic event
STEMI management
reperfusion tx (PCI) vs fibrinolytic tx
dual anti platelet tx
anticoag: heparin 2-8 days
NSTEMI management
dual antiplatelet tx up to 12 months
anticoag: heparin
PCI with stenting or CABG if medical management fails
PCI must be done within
within 90 mins
unstable angina vs. NSTEMI
both: anginal pain persists AND evidence of myocardial tissue damage (+ trops/ST depression or T wave inversion)
persistence of ST segment depression > 1mm for longer than 48 hours = NSTEMI
rehospitalization risk ACS
1st 30 days
pericarditis
inflammation of pericardium
pericarditis causes
idiopathic
preceded by viral URI, bacterial infection, autoimmune dxw/ MI, meds (isoniazid or hydralazine), malignancy
most common in men aged 20- 50
pericarditis presentation
fever, sharp chest pain worse w/ breathing
retrosternal chest pain can radiate jaw/neck, worse when supine/breathing; relieved by sitting up/leaning forward
pericardial friction rub - heard full breath cycle, loudest on L sternal border
pericarditis diagnosis
2 needed:
- sudden onset pleuritic chest pain
- diffuse ST elevation/EKG changes
- pericardial friction rub
- new or worse pericardial effusion on echo
pericarditis evaluation
CXR (water bottle sign, liquid collects on bottom)
ECHO
EKG (ST elevation, PR depression, inverted T wave)
CBC, ESR, troponin
refer to ED
pericarditis tx for low risk pt
outpatient management
stable, small effusion, no fever
NSAIDs @ max dose titrate over 3-4 weeks (ibuprofen, indomethacin)
f/u regularly: monitor inflammatory markers/symptoms should decrease
NO improvement within 7 days = refer cardio ? hospital
What EF is diagnostic of HFREF?
EF < 40%
what are the two classic presenting symptoms of HF?
dyspnea and fatigue
WHAT ALWAYS NEEDS TO BE RULED OUT FIRST IN A PATIENT PRESENTING WITH NEW ONSET SYMPTOMS OF HEART FAILURE?
R/o ACS with EKG first
PATIENT WITH KNOWN HF HAS LV WALL THICKENING ON HIS MOST RECENT ECHO AND AN EF OF 45%. HE IS ASYMPTOMATIC. WHAT STAGE (A,B,C,D) IS THIS PATIENT IN?
STAGE B – STRUCTURAL CHANGES WITH NO SYMPTOMS
PATIENT PRESENTS TO THE CLINIC WITH NEW ONSET COUGH AND +1 LE EDEMA. HE HAS FINE BILATERAL CRACKLES ON AUSCULTATION. HIS VITAL SIGNS ARE STABLE AND HE IS IN NO ACUTE DISTRESS. EKG IS NORMAL.
WHAT SHOULD THE NP DO NEXT? ADMINISTER PO LASIX AND MONITOR VS REFER TO THE ER?
ER – HOSPITALIZATION CRITERIA INCLUDES NEW ONSET HF CONGESTION SYMPTOMS, ACS/MI, PULMONARY EDEMA (PINK FROTHY SPUTUM), NEW ARRHYTHMIA W/ HEMODYNAMIC INSTABILITY, SPO2 <90, COMPLICATING DISEASE STATE, ? SAFE HOME MANAGEMENT, SYMPTOMS REFRACTORY TO PO TREATMENT OR HOME MANAGEMENT PLAN
WHAT EKG FINDING WOULD YOU EXPECT IN A PATIENT WITH SUSPECTED PERICARDITIS?
DIFFUSE ST ELEVATION
PATIENT PRESENTS TO THE CLINIC COMPLAINING OF NEW ONSET CHEST PAIN THAT HAS BEEN PRESENT FOR 15 MINUTES AND IS NOT ALLEVIATED WITH REST. EKG SHOWS ST DEPRESSION > 1 MM. THE PROVIDER CALLS 911. WHAT ARE 2 THINGS THAT THE PROVIDER CAN DO IN THE OFFICE WHILE WAITING FOR EMS? (TREATMENT WISE)
ADMINISTER ASA CHEWABLE TABLET AND NTG TABLE (IF NOT CONTRAINDICATED)
HF RF
CAD HTN valvular heart dx aging obesity DM metabolic syndrome CKD smoking CHD
systolic HF
HF w/ reduced EF (HFREF) = EF < 40%
enlarged ventricles able to fill with blood but unable to pump it to the body, thinning of ventricular walls
pump dysfunction
diastolic HF
HF w/ preserved EF = EF > 50%
stiff, thickened ventricles fill with less blood than normal
normal CO, less amount of blood being pumped out
filling dysfunction
Left sided HF presentation
fatigue, dyspnea
orthopnea, paroxysmal nocturnal dyspnea
cough, S3 or S4
displaced apical pulse, crackles if pulmonary edema
LEFT think LUNGS, so signs of congestion
right sided HF presentation
usually results from advanced L-sided HF
lower extremity edema, fatigue, exercise intolerance, JVD
nocturia, ascites, hepatomegaly, decreased appetite, nausea
S3
RIGHT think REST of the body, so starting to affect other body systems - lower extremities, liver, etc
HF diagnostics
ECHO! calculates EF & structure of heart
EKG (infarction, ischemia, LVH, arrhythmia)
CXR (cardiomegaly)
Labs:
- BNP - sensitive test can r/o HF
- electrolytes, Ca, Mg
- CBC
- BUN, Cr
- UA
- glucose
- lipids
- LFTs
- TSH
BNP vs NT-proBNP
if pt taking an ARNI, will need to check NT-proBNP b/c BNP is not accurate in these patients
Framingham criteria for diagnosis of HF
At least 2 major or 1 major and 2 minor criteria present:
Major:
- acute pulmonary edema
- cardiomegaly
- hepatojugular reflux
- JVD
- paroxysmal nocturnal dyspnea/orthopnea
Minor:
- ankle edema
- dyspnea on exertion
- hepatomegaly
- nocturnal cough
- pleural effusion
- tachycardia > 120 bpm
Meet criteria = ECHO
+ BNP, but do not meet criteria = ECHO
ACC/AHA HF stages
Stage A: at risk, no structural abnorms, no symptoms
Stage B: structural heart defects but no symptoms
Stage C: structural heart dx w/ prior or current symptoms
Stage D: advanced structural dx w/ symptoms at rest requiring advanced interventions
ACC Stage A HF
at risk, no structural abnorms, no symptoms
ACC Stage B HF
structural heart defects but no symptoms
ACC Stage C HF
structural heart dx w/ prior or current symptoms
ACC Stage D HF
advanced structural dx w/ symptoms at rest requiring advanced interventions
NYHA functional classification of HF
Class I: asymptomatic
Class II: symptoms with moderate exertion; walking up stairs, fine at rest
Class III: symptoms with minimal exertion; making bed, washing dishes, etc , ok at rest
Class IV: symptoms at rest
NYHA Class I HF
asymptomatic
NYHA Class II HF
symptoms with moderation exertion
NYHA Class III HF
symptoms with minimal exertion
NYHA Class IV HF
symptoms at rest
HF complications
cardiogenic shock biventricualr HF, arrhythmias end organ damage liver damage - congestive hepatopathy exacerbations
HF tx goals
relief of S/S
prevent further myocardial injury
prevention of recurrence of clinical failure
improvement in prognosis
management depends on stage and class and which type of HF (preserved vs. reduced EF)
Stage A HF management
lifestyle changes
meds to control HTN, DM, HLD
BP < 130
ACE-I/ARB statins as appropriate smoking cessation salt reduction regular exercise limit alcohol consumption
Stage B HF management
consider screening with BNP
ACEI/ARB & BB
valve repair if needed
Stage C HF management
lifestyle changes daily weights sodium restriction reduced exercise during decompensation cardiac rehab
AVOID CCB & NSAIDs
pharm: 4 classes
- diuretic
- ACE-I/ ARB/ ARNI
- BB
- aldosterone antagonist
hydralazine w/ isosorbide in AA if cannot tolerate ACE/ARB
selected pt: CRT, ICD, revascularization
Stage D HF management
control S/S, improve QOL
managed by cardiology
inotropes - digoxin
palliative care
when to refer to cardiology in HF
- S/s refractory to standard tx
- onset of arrhythmias, coronary ischemia or MI
- young patient with ischemic or nonischemic DCM, HCM
- worsening EF
- NYHA class 3 or 4
- need for ICD or resynchronization
- HF advanced therapies eval
HF hospitalization considerations
- new onset HF w/ symptoms of congestion
- evidence of ACS/MI/ischemia/infarction
- pulmonary edema or acute decompensated HF
- O2 < 90%
- severe medical complications - PNA, renal failure
- anasarca (generalized swelling throughout body)
- symptomatic hypotension/syncope
- hemodynamically significant arrhythmias
- HF refractory to max outpatient PO tx
- needed home support for safe management
Acute HF decompensation tx
mnemonic: POND
Position upright/ positive pressure ventilation (BiPAP)
Oxygen
Nitrates
Diuretics
when is an ICD appropriate in HF pt
Select pts between stage B or D who have an EF < 35% who are on max med therapy
