Primary 2 - Test 2 - Sheet1 Flashcards
What meds should be included for a 60 yo male with DM and new diagnosis of CAD. Decreased smoking, walks 2 days/weel x20 minutes, LDL 130, triglycerides 210, non HDL 130, HGB A1c 7%
Statin, aspirin, and ACEI
A patient returning to the clinic since his first MI should expect to be ordered…
Beta blocker
Post-stent procedure for an MI includes which preferred antiplatelet treatment?
ASA and Clopidogrel (Plavix)
Beta blockers and ACEI are used in post-acute MI to…
Preserve the contour of the heart
Characteristics of stable angina include…
Occurring with effort
The best diagnostic tool to assess for vague complaints of fatigue with walking and possible angina is…
Exercise stress test
Before counseling partners about sexual activity following a MI, the provider should consider what information?
Depression, loss of interest, spousal reluctance and anxiety may interfere with a client’s resumption of sexual activities.
Which medication is considered essential in the management of heart failure?
ACE inhibitors
What are more common causes of heart failure?
HTN, aortic stenosis, and ischemic cardiomyopathy
What is a less frequent cause of heart failure?
Valvular heart disease
Conditions that result from damages to the heart
Angina pectoris and CHF
Conditions that result from atherosclerosis
Peripheral vascular disease adn most CVAs
The most appropriate coronary heart disease (CHD) recommendations
10 Year Risk Estimator for ASCVD
Determining the risk factor for CHD
Can be calculated using age, sex, total and high-density lipoprotein (HDL) cholesterol levels, diagnosis of diabetes, and blood pressure.
Persons at high risk for CHD via the Omnibus Risk Estimator
Have greater than 20% 10-year CHD risk, and include persons with established CVD, as well as those with CHD equivalents such as diabetes and chronic renal disease
Persons at intermediate risk for CHD via the Omnibus Risk Estimator
Have a 10-20% 10-year CHD risk
Persons at low risk for CHD via the Omnibus Risk Estimator
Have less than 10% 10-year CHD risk
“Optimal risk” of CHD via Omnibus Risk Estimator
Defined as optimal levels of all risk factors and adherence to a heart-healthy lifestyle
Non-modifiable risks for CHD
Gender, ethnicity, age, and genetics.
Homocystein
Amino acid occurs naturally in the body. Does not come from diet. Body changes it into another amino acid. Inability to transform to useful acids leads to hyperhomocysteine (15 umol/L to 100 umol/L).
What causes elevation of homocystein (hyperhomocystein)
Genetic defects, smoking, fibrate and niacin meds, and nutritional defects of vitamin cofactors B1, B6, B12
Hyperhomocysteine
Combines with LDL to produce foam cells that form necrotic centers of luminal plaques. Has prothromboic properties - activates protein C, vactors V and VIIA and plasminogen.
What does hyperhomocysteine impair?
Nitric oxide production, free radical oxidation, leukocyte recruitment, and platelet aggregation.
Treatment of hyperhomocysteine levels
Folic acid 1 mg/daily can decrease levels up to 72%. Although evidence does not fully support this - no benefit or harm for CVD or CVA
C-Reactive Protein
Acute phase protein from the liver influenced by cytokines during inflammation responses. Enhances macrophage phagocytosis and complement binding to foreign damaged cells. Does not cause CVD, but shows evidence of CVD. Used for other markers of inflammation.
C-reactive protein treatment if high
Diet, statins, beta blockers, glitazones all can decrease CRP by 50%
What can increase C-reactive protein?
Now evidence that aspirin and hormones are associated with an increase in CRP
What has C-reactive protein elevation been correlated with?
Future cardiac events (PEACE trial) not a strong correlation
AHA recommendations for C-reactive protein for patients with low CV risk
Low risk = less than 10% in next 10 years. No testing for CRP
AHA recommendations for C-reactive protein for patients with intermediate range risks for CV
Intermediate = 10-20% in 10 years. CPR can help predict a CV event or stroke and help direct evaluation
Lipoprotein (a)
Modified form of LDL. Similiar to plasminogen which is a protein that helps dissolve clots, so this protein competes with plasminogen and promotes coagulation. Also binds to macrophages that form cholesterol deposition in plaques.
What is considered high level of lipoprotein (a)?
10 mg/dl
Who do you test for lipoprotein (a)
Those with no identifiable dyslipidemia but established CVD; strong family history of CVD and not other dyslipidemia. HTN with early target organ damage; hypercholesterolemia refractory to therapy
Therapy for lipoprotein (a)
NOT diet and exercise and NOT statins. In fact, no treatment approved yet in the U.S. Niaspan has some effect.
Who should be tested for cardiac markers according to the Framingham Score?
Yes for everyone.
Framingham Score of <10%
No further testing
Framingham Score of 10-20%
Testing is warranted
Framingham Score of >20%
Testing is not warranted because these patients will be treated aggressively
Presentation of patient with heart failure
Shortness of air, edema, and fatigue
Prevalence of heart failure in U.S.
Afflicts 10 out of every 1,000 persons over age of 65
Percentage of Medicare patients with heart failure who are readmitted within 6 months
44%
Burdens of heart failure
Congestive symptoms, activity limitation, dysrhythmias, hospitalizations, and reduced survival
General lifestyle modification measures to treat heart failure
Weight reduction, discontinue smoking, avoid alcohol, avoid other cardiotoxic substances, and exercise
General medical consideration measures to treat heart failure
Treat HTN, hyperlipidemia, DM, arrhythmias; coronary revascularization; anticoagulation; immunization; sodium restriction; daily weights; and close out-pt monitoring
Provider directed or controlled measures to treat heart failure
Recognize and treat those at risk for developing heart failure. Maximize survival enhancing medications. Decrease risk of new cardiac injury. Administer influenza vaccine yearly and pneumococcal every 6 yr. Reinforce patient and family involvement in care.
What causes heart failure?
The loss of critical quantity of functioning myocardial cells after injury to the heart due to; ischemic heart disease, HTN, idiopathic cardiomyopathy, infections, toxins, valvular disease, and prolonged arrhythmias
5 year survival rate of persons diagnosed with CHF
Less than 50% and less than 25% will be alive in 10 years.
Mortality of older adults with CHF
6 year rate of 80% for older men and 65% for older women
Progression of CHF
Incurable and progressive and symptoms can greatly impair functional abilities and quality of life.
Patient management of CHF
Requires consultation with a cardiologist
Therapy for patients under Stage A and Stage B HTN guidelines
Treat HTN, hyperlipidemia, etc, dietary salt restriction
Drugs for routine use for patients under Stage A and Stage B HTN guidelines
Diuretics, ACE inhibitors, beta blockers and in some patients- dig, aldosterone inhibitors, ARBs, hydralizine/nitrates
Symptoms of left ventricular dysfunction
Dyspnea on exertion, paroxysmal nocturnal dyspnea, tachycardia, cough, and hemoptysis
Physical signs of left ventricular dysfunction
Basilar rales, pulmonary edema, S3 gallop, pleural effusion, and Cheyne-Stokes respirations
Symptoms of right ventricular failure
Abdominal pain, anorexia, nausea, bloating, and swelling
Physical signs of right ventricular failure
Peripheral edema, jugular venous distention, abdominal-jugular reflux, and hepatomegaly
The Donkey Analogy
Ventricular dysfunciton limits a patient’s ability to perform the routine activities of daily living…
Neurohormonal activation of compensatory mechanisms
Many different hormone systems are involved in maintaining normal cardiovascular homeostasis, including: sympathetic nervous system (SNS), renin-angiotensin-aldosterone system (RAAS), and vasopressin (aka antidiuretic hormone, ADH)
Neurohormonal responses to impaired cardiac performance
Salt and water retention, vasoconstriction, and sympathetic stimulation
Short-term effects of neurohormonal responses to imapired cardiac performance
Augments preload, maintains BP for perfusion of vital organs, and incrases HR and ejection
Long-term effects of neurohormonal responses to imapired cardiac performance
Pulmonary congestion, anasarca, exacerbates pump dysfunction (excessive afterload), increases cardiac energy expenditure, and increases energy expenditure
Think FACES - symptoms of heart failure
F - fatigue; A - activities limited; C - chest congestion; E - edema or ankle swelling; and S - shortness of breath
Assessing heart failure
Consider the patient’s history, physical exam, and lab and diagnostic tests
Diagnostic evaluation of new onset heart failure
Determine the type of cardiac dysfunction (systolic vs diastolic), determine etiology, define prognosis, and guide therapy
Initial work-up of diagnostic evaluation of new onset heart failure
ECG, chest x-ray, blood work, ECG
Class I - New York Heart Association functional classification
No symtpoms with ordinary activity
Class II - New York Heart Association functional classification
Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, dyspnea, or angina.
Class III - New York Heart Association functional classification
Marked limitation of physical activity. Comfortable at rest, but less than ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain
Class IV - New York Heart Association functional classification
Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency may be present even at rest
Therapies demonstrated to reduce mortality in heart failue
ACEI; ARB; BB; aldosterone antagonists; hydralazine-isosorbide dinitrate; ICD (lvef 1120 ms, Class III or IV)
ACE inhibitors - how it saves lives
Dilate blood vessels, increase blood flow
Beta blockers - how it saves lives
Help strengthen the herat’s pumping ability, block the response to neurohormonal substances. Slow down the heart rate. Limits the heart’s speed, thus saving energy.
Aldosterone inhibitors - how it saves lives
Primarily used in chronic heart failure as a suppressor of the renin-angiotensin-aldosterone system
Reverse remodeling in HF: Effects of chronic beta-blockage
Decreased chamber size (less EDV and ESV), increased LV and RV ejection fractions, improved geometry (restoration of more elliptical shape), and decreased mitral and tricuspid regurgitation
Initial dose of carvidilol (coreg) - BB
3.25 bid. CR 10 mg qd
Target dose of carvidilol (coreg) - BB
25-50 mg bid. CR 80 mg qd
Initial dose of metoprolol XL - BB
12.5 md qd.
Target dose of metoprolol XL - BB
150 mg/day
Initial dose of bisoprolol (Zebeta) - BB
1.25-2.5
Target dose of bisoprolol (Zebeta) - BB
10 mg qd
Titration of beta blockers
Start low and go slow, double the dose every 2-3 weeks if tolerated. BP >90; HR >60, no signs of decompensation
Diuretics
Optimize their effect before and during initiation of other medication treatments
Diuretics and ACE inhibitors - Donkey analogy
Reduce the number of sacks on the wagon
Captopril dosing (ACEI)
Initial 6.25 TID. Max - 50 tid
Enalapril dosing (ACEI)
Initial - 2.5 BID. Max - 10-20 mg BID
Ramipril dosing (ACEI)
Initial - 1.25 - 2.5 mg qd. Max - 10 mg qd. may be given in divided doses
Quinapril dosing (ACEI)
Initial 5 mg bid. Max - 20 mg bid
Spironolactone dosing (aldosterone antagonists - potassium sparing diuretics)
12.5-25 mg daily
Eplerenone dosing (aldosterone antagonists - potassium sparing diuretics)
25 mg - 50 mg daily
Lab monitoring of aldosterone antagonists - potassium sparing diuretics
Serum potassium and creatining should be monitored closely in the first few weeks of therapy. Creatining should be less than or equal to 2.5 mg/dL in men and 2.0 in women and potassium should be less than 5.0
Aldosterone antagonists - potassium sparing diuretics
Used in class II-IV HTN
Hydralazine and isosorbide dinitrate use
Along with ACEI and/or a BB was shown to be significant benefit int he African American cohert
Dosing of hydralazine/isosorbide
37.5/20 tid. Max 2 po tid.
Diuretics
Decrease fluid retention and reduce swelling. Improve exercise tolerance. Facilitate use of other drugs for heart failure. Pts can be taught to adjust dose based on symptoms. Electrolyte depletion is frequent. Should never be used alone in heart failure. Higher doses associated with increased mortality. Does not slow the progression of heart failure.
Digoxin
Enhances inotropy of cardiac muscles. Reduces activation of SNS and RAAS. Improve circulation by enabling the heart to pump more efficiently. Does not slow the progression of heart failure. Long - term effects - reduces symptoms, increases exercise tolerance, improves hemodynamics, decreases risk of HR progresison, reduces hospitalization, does not improve survival.
Diuretics and heart failure
Patients may become unresponsible to high doses of diuretic drugs if they: consume large amounts of sodium, take agents that can block effects of diuretics, have significant impairment of renal funciton or perfusion
Drugs that block effects of heart failure
NSAIDs, COX-2 inhibitors
Diuretic resistance and heart failure
Can be overcome by iv administration of diuretics and using 2 or more diuretics in combination
Digitalis compounds in relation to Donkey Analogy
Like the carrot placed in front of the donkey
Dosing of digoxin
0.125 mg - 0.250 mg daily. Increases left ventricular ejection fraction. Should be used in conjunction with other standard therapy that includes ACEI, BB, and diuretics
Anticoagulants
Increased risk due to stasis of blood indilated hypokinetic cardiac chambers and periphery. Risk low in clinically stable. No controlled trials evaluating risk reduction. Justified in those in a-fib or with previous embolic events
Monitoring for those taking anticoagulants
Renal function, electrolytes, CBC, thyroid function, Hgb A1C, ECHO/ECG, and device check
3 classes of drugs that can exacerbate the syndrome of heart failure and that should be avoided in most patients
Antiarrhythmia agents - only amiodarone and dofetilide have been shown not to adversely affect survival. Calcium channel blockers - only the vasoselective ones have been shown not to adversely affect survival. NSAIDs
Potential uses of plasma BNP test
Rule out false-positives in CHF. Measure severity of LV compromise. Quantify functional class. Estimate prognosis and predict future cardiac events. Evaluate efficacy of therapy for CHF
Cardiac resynchroniation therapy - regarding the Donkey Analogy
Increase the heart’s efficiency
Cardiac resynchronization Purpose
To improve ventricular synchrony in symptomatic patients
Cardiac resynchronization - benefits
Reverse remodeling, decreased heart size and ventricular volume, improve EF, and decreased mitral regurgitation.
Cardiac rsynchronization - clinical improvements
Increase exercise tolerance, quality of life, and rate of hospitalizations
Cardiac resynchronization therapy - creating realistic patient expectation
Approximately two-thirds of patients should experience improvement (responders vs non-responders). Some patients may not experience immediate improvement
Having patients set own goals regarding cardiac resynchronization therapy
Grocery shopping, decreasing diuretic dose, lying flat to sleep. Encourage them to be part of the group that responds to their therapy
ICDs and CRT/ICD
Rate of sudden death in a person with heart failure is 6-9x the average person. Those at high risk: EF <30%, ischemic CM, history of SVT, history of SCD
A-fib and heart failure
Often coexist (10-30%) and significantly effect prognosis as well as complicate management
Pharmacological therapies for A-fib
Have potentially dangerous side effects.
Catheter ablation for A-fib
Has been established as an effective therapeutic option and is resistant to pharmacologic rhythm control or rate control
Precipitating factors of A-fib
Ischemia, sleep apnea, electrolyte abnormality, thyroid disorder, recent myocardial surgery. Is it a rate control vs rhythm control? Consider paroxysmal A-fib and anticoagulation
Sleep apnea and heart failure
Screen patients for sleep apnea. Ask the following question: Do you snore? Take naps during the day, fall asleep while rising in a car? Feel refreshed upon arising?
Important of exercise
Encourage pt to perform some form of regular exercise on a daily basis. Increase length of time of exercise. “Start slowly and listen to your body”. Set goals together, ideally, 30 minutes a day 5 days per week.
Left ventricular assist devices and Class III and IV CHF
Are important in the care and treatment. These devices can provide a bridge to transplant and allow the other organs a change to recover. Heart transplant is another option.
Elements of a follow up visit - CHF
Assess functional capacity and activity level. Volume status and weight and edema. History of arrhythmia, syncope, palpitation. Careful history of current use of alcohol, tobacco, illicit drugs, sodium intake. Determine understanding of and compliance with medical regime.
Patient-contolled measures - CHF
Limit daily salt and fluid intake. Eat appropriate diet. Check daily weight. Use flexible diuretic regimen. Improve physical conditioning. Stop smoking. Limit alcohol use. What to do if symptoms worsen. Close follow up and monitoring. Control depression and anxiety
Medications known to cause fluid retention
Ibuprofen, Cox-2 inhibitors, Actos, Avandia
5 and 10 year survival rates with persons diagnosed with CHF
50% and 25%
6 year mortality of older adults with CHF
80% men and 65% women
Symptoms of heart failure regarding quality of life
It is incurable and progressive and can greatly impair functional abilities
Primary care providers regarding CHF
Must consult a cardiologist. PCP can provide initial diagnosis, monitoring, and follow-up
Acute coronary syndrome
Used for the disorders of myocardial ischemia - stable angina, unstable angina, variant angina, or MI
ASA for primary prevention requirements for men and women
Men at 45 and women at 55 if they have additional CV risk factors AND they aren’t high risk for bleeding. Use 81 mg.
ASA for primary prevention requirements for diabetics
Save for patients with a 10 year CV risk over 10%. This includes most people if they have risk s like HTN, high lipids, smoke, family hx. Use 81 mg.
Indications for a holter monitor
Evaluation of frequent, transient symptoms suggestive of a cardiac arrhythmia. Evaluation of chronic arrhythmias (a-fib). ST segment analysis for chest pain. Heart rate variability. Continuous 24 ht heart rhythm monitoring
Event cardiac monitor
30 day loop recorder. Symptom specific. For infrequent symptoms. Implantable monitor available if symptoms are rare.
Goals of stress testing
Evaluate exercise capacity. Reproduction of symptoms. HR response- pt with a-rib. Arrhythmias. Comparison to previous studies. Evaluate for MI.
Exercise ECG
Usually treadmill. Usually maximal unit individual cannot exercise any longer or until certain endpoints develop (chest pain, target heart rate reached, arrhythmias, ECG changes). Abnormality usually based on ECG criteria.
Sensitivity of stress ECG for detecting single and three vessel disease
Single - 50%. Three vessel - 85%
Exercise ECG advantages
Relatively inexpensive. WIdely available. Straightforward interpretation. Can be scheduled quickly.
Exercise ECG disadvantages
Moderate sensitivity and specificity. Requires a certain amount of effort and a target HR needs to be achieved. Higher false positives in women, pts with mitral valve prolapse, resting ECG abnormalities such as LBBB or in the setting of certain drugs (Digoxin)
Stress echo imagine
With exercise stress or pharmacologic stress, there is increasing O2 demand by the myocardium. In the setting of significant coronary artery narrowing, the O2 demand exceeds the blood supply and results in a stress related wall motion abnormality.
Transthoracic and transesophageal ECHO
Transthoracic - standard approach with 4 views of left ventricular cavity. Transesophageal - can be used with pharmacologic stress or with pacemaker
Stress ECHO in detecting single and three vessel disease
Single - 58%. Three vessel - 94%
Stress ECHO advantages
Portable. Less expensive. No radiation exposure. Provides cardiac structural info in addition to perfusion information
Stress ECHO disadvantages
Not able to image in all patients (large chest and COPD). Results are not as reproducible and prognostic info is just being developed. Difficult to interpret in setting of previous MI with resting wall motion abnormalities.
Nuclear stress test advantages
Reproducible. Able to obtain images in all patients regardless of size. Exercise or pharmacological. Extensive data supporting reliability of results and prognostic info.
Nuclear stress test disadvantages
Expensive. Requires expensive, sophisticated equipment in fixed location. Requires strict adherence to standards related to radioisotope handling. Radiation exposure.
Limitations to exercise stress testing
PVD. Arthritis/orthopedic. COPD. Extremity amputation. Poor exercise capacity. Beta blocker use (limits heart rate response). Neurologic. Systemic muscular disease.
Pharmacologic stress agents
Primary (direct) vasodilators - Adenosine and persantine. Secondary (indirect) vasodilators - dobutamine
Careful use of dobutamine stress - inotropic
Must be combined with imaging. Can trigger arrhythmias due to catecholamine surge. May be an unsettling sensation for many patients. If HR response is suboptimal, atropine may be given IV.
Side effects of dobutamine
HA, nausea, palpittions, flushing, arrhythmias, and chest pain.
Adenosine stress test
Potent receptor-mediated vasodilator. Increases coronary blood flow 3-5x normal. Short biological half-life (10 seconds). Causes mismatch of perfusion in areas of significant coronary stenosis. Needs accompanying nuclear perfusion. Avoid in pts with significant lung disease as this can trigger bronchospasm.
Side effects of adenosine
HA, flushing, chest pain, nausea, dyspnea, lightheadedness, AV block, high degree AV block in <2%. Severe bronchospasm. Chest pain 90% - non-specific.
Stress testing with left bundle branch block
Frequent “false-positive” exercise studies due to effectson ST/T wave segments. Cannot accurately distinguish coronary artery disease from LBBB artifact. Adenosine stress is study of choice!
Stress testing and caffeine
Must be off all forms of caffeine for 24 hrs
Stress testing and patients with paced rhythms
Frequent “false-positive” exercise studies due to reversible or partially reversible distal septal/inferoapical defects. Cannot accurately distinguish CAD from PM artifact although frequentlydo not fit standard anatomic distributions. Adenosine stress is study of choice!
Left ventricular hypertrophy with strain and stress testing
May also cause false positive exercise stress test results related to abnormal ST depression seen with “strain” pattern on the ECG. Adenosine is the study of choice. If interested in exercise capacity, must add nuclear images to exercise test.
2D echo with doppler
Evaluation of heart function: chamber size and contracility. Evaluation of valves and blood flow. Clinical applications - valvular disease, congenital heart disease, myocardial disease, pericardial disease
MUGA - multiple gated acquisition scan
Can test for right and left ventricular ejection fractions.
PET myocardial view
Current “Gold Standard” for viability. Positional Emission Tomography (PET) is a specialized nuclear imaging technique to assess myocardial perfusion and viability. Differentiates between ischemic tissue and scarred tissue.
Cardiac MRI
Limitations include lack of portability, no permanent pacemakers, no AICDs, high cost
Venous and arterial duplex (Doppler Ultrasound)
Duplex refers to 2 modalities: images and velocity. Used to assess carotids with cerebrovascular symptoms. Primary tool to diagnose DVT.
What to ask chest complaints to differentiate those with ACS
Where, when did it start, how long, what aggravates, what alleviates, does it radiate, associated symptoms, has it ever happened before? If you think it is ACS, then jump into action!
Patients with unstable angina
Should be transported via EMS to a hospital for eval. Give 165 - 325 mg non-enteric coated ASA to all pts. Give O2 and subling nitro and morphine maybe.
ASA and prophylaxis
Consider for all pts with increased risk for CHD.
All patients with CAD should be taking the following meds unless contraindicated
Aspirin, a lipid lowering agent if LDL above target, and a beta-blocker. Long acting calcium channel blockers are useful adjuncts if patients with contraindications to beta blockers.
Types of calcium channel blockers
Dihydropyridines or nondihydropyridines
Med names of dihydropyridines
Amlodipine, felodipine, and nifedipine. Expensive
Med names of nondihydropyridines
Dilitiazem and verapamil
Calcium channel blocker effects
Inotrpic effects - all relax arterial smooth muscle and produce peripheral vasodilation that lowers BP. Affect cardiac contraction by calcium channel blockge and depress cardiac contractility
Negative inotropic effect of calcium channel blockers
The negative effect of depressing cardiac contractility isnot with the dihydropyridines because they are more potent vasodilators. This leads to baroreceptor mediated increase in sympathetic tone and blunts the negative effect. Best used if needed in HF.
CAD is a spectrum
Pts move along the spectrum from stable to unstable angina to NSTEMI to STEMI, to HF. Providers need to know where on the spectrum the patient is currently, and work to treat current stage and prevent progression. Once on the spectrum, treatment is secondary prevention!
Meds post-MI
High intensity cholesterol, ACE, ASA, plavix, beta blocker and nitro
Drug eluting cardiac stents
Have been associated with fewer restenosis (due to overgrowth of smooth muscle cells that block the stent) events initially but may have more late stent thrombosis at the 3 year mark
FNP care post-MI
Make sure pt is on ASA and plavix, usually for 1 year for both after MI. After 1 year, plavix can be discontinued and stay on ASA.
Use of plavix
Even though expensive, it is like a super aspirin. Acts on adenosine phosphate receptor on the platelet cell membrane, which inhibits the activation of platelets.
How aspirin work
Works on the aggregation of platelets.
When can patients typically return to work after MI
Typically when they can walk up a flight of stairs without being out of breath. No set guidelines.
Healing time of cardiac tissue and stent placements
4-6 weeks and usually 1 month
Adverse effect of Norvasc
Doesn’t have negative ionotrophic effect, but is notorious for causing peripheral edema
Meds for patient with heart failure
Diuretics - HCTZ then loop. ACE-I - lisinopril. Beta blocker - metoprolol do not stop abruptly. Aldosterone antagonist - only mod-severe to severe symptoms. Na+ restrictions. Lipids - new guidelines. Daily exercise. Avoid NSAIDS. Prevention - flu and pneumonia vaccine. Education. At every visit assess functional status and recent clinical visits.
Why use diuretics
Reduce symptoms more rapidly than any other class of meds. Critical for maintenance of Na+ balance. Goal is to increase urinary output and decrease clinical evidence of fluid retention. Weight loss will be about 0.5-1.0 ky/day. Loop diuretics preferred.
Why use ACEs
Inhibit RAA system, and modify LV remodeling. If intolerant, use ARB
Why use BBs
Inhibit SNS effect on CV system. Only three approved for HF. Monitor for early fluid retention d/t negative inotropic effect.
Length of time to achieve maximum effects of beta blockers adn ACEIs
May take weks to months
Why use aldosterone antagonists
May have negative effects on structure & function of heart. Require close monitoring of potassium and renal status especially in insulin-dependent DM. Contraindications - elevated creatinine, hyperkalemia, other potassium sparing diuretics. Monitor at 1 day 1 week and 1 month
Why use digoxin
May improve exercise tolerance, quality of life & symptoms. May be added if on diuretic, ACE-I, and BBs
Chronic stable angina
Precipitated by exertion and relieved at rest. Symptoms occur with predictable frequency, severity, duration, and provocation and generally last 1-3 minutes.
Variant angina
History of spontaneous or unprovoked episodes of typical angina. Occurs predominantly at rest and is usually not provoked by exertion.
Side effects of beta blockers
Fatigue, impotence, cold extremities, bronchospasm, worsening claudication, bradycardia, and cardiac conduction disturbances.
Effects of abrupt discontinuation of beta blockers
May precipitate angina symptoms or lead to MI as a result of rebound tachycardia.
Most common cause of systolic heart failure
Coronary artery disease
Common causes of diastolic heart failure
HTN, A-fib, and diabetes
Cardinal symptoms of heart failure
Dyspnea and fatigue
Diagnostic exam of heart failure
Echo
Standard first-line approach to initial testing for CAD
Exercise tolerance test
Venous stasis ulcer
An ulcer that has an irregular border with a red base often with redden, swollen shiny appearing skin located on the medial side of the leg
If an ultrasound indicates an aortic aneurysm of 3 cm in diameter, what is your next step
Monitor with ultrasound every 2-3 years
What is the best initial plan for a 60 year old male diagnosed with mild arterial insufficiency
Encourage walking to the point of pain as often as possible
Instructions to provide to a patient diagnosed with severe arterial insuffiency
Toenail trimming should be done by the podiatrist, comfortable tennis shoes are fine as long as they fit properly, and it is best to examine feet for lesions rather than relying on being able to feel pain.
Raynaud’s phenomenon
A condition in which cold induces vasospasm of the small blood vessels in the fingers and toes causing a characteristic blanching
What would you counsel for a patient diagnosed with ischemic arterial ulcers
Reduce risk factors such as stopping smoking and reducing fat intake, avoiding restrictive garments and trauma, and maintaining adequate hydration but avoiding drinks containing caffeine
An Unna boot is appropriate for….
Venous stasis ulcers
Chronic warfarin therapy for anticoagulation should include maintaining the INR between
2.0-3.0
Does a CHADS2 score of 1 require coumadin therapy?
No
Would routine screening for peripheral vascular disease be part of a work-up?
No, there is no data to support this as beneficial in terms of mortality or morbidity reduction
In a patient without symptoms to suggest PVD, what PVD primary prevention would be included in patient education
Smoking cessation
Differential diagnoses for a patient who complains of pain in legs when walking includes
Cauda equina, acute embolism, and DVT
The most reliable physical finding in patients with PVD includes
Presence of femoral artery bruit
Management of PVD includes
Montoring symptoms because patients with claudication may progress to acute or critical limb ischemia, monitoring degree of pain and pain free walking, and treatment with ASA and exercise to decrease risk of serious vascular events and increased walking time.
Arteriosclerosis obliterans (ASO)
Used to indicate lesions of the aorta, its proximal branches, and the arteries of the legs
Risk factors of chronic arterial insufficiency and aortic aneurysms
Result from arteriosclerosis and have same risk factors of other atherosclerotic conditions. Almost always signal the presence of disease in the coronary and cerebral vasculature as well.
Symptoms of PAD
Calf muscles that shrink (late sign), hair loss over toes and feet (late signs), thick toenales, shiny tight skin, painful non-bleeding ulcers on feet or toes that are slow to heal, and an early sign might be that legs hurt or become tired when walking far.
Intermittent claudication
More than twice as common in men earlier in life and is like angina to the leg muscles
Ischemic leg pain at rest
O2 to the foot is so insufficient that the patient may experience tissue necrosis spontaneously or from minor trauma. Needs to be referred to vascular surgeon urgently.
Other causes of lower leg pain
Joint dysfunction, peripheral neuropathy, spinal stenosis, and lumbar disc disease and must be ruled out in H&P
Treatments for patients with intermittent claudication
Balloon angioplasty, rotary atherectomy, stent placement, or bypass surgery. Usually reserved for patients who have failed at exercise and patients with co-morbidities (MI, CVA, DM)
PAD
May be the first sign of cardiovascular disease. Caused by smoking, diabetes, and obesity. Affects African-Americans more common.
What causes PAD
Atherosclerosis: when the wall of the artery thickens because there is a build-up of fatty material (plaque) such as cholesterol
Who is at risk for PAD
Older (over 50), smoking, diabetes, HTN, high cholesterol, overweight
Symptoms of PAD
Many have no symptoms, pain in legs while walking, pain in foot while at rest (Severe symptoms), and ulcers that fail to heal or Gangrene
ABI procedures to test for PAD
Blood pressure in arm and ankle using a doppler should be equal. Anything less than 90% indicates a problem with circulation.
Exercise ABI testing for PAD
Used when the ABI is normal or borderling but symptoms are consistent with claudication. A drop in ABI post-exercise supports a PAD diagnosis
Prognosis of PAD
Increased risk of for cardiovascular disease. Severity is linked to risk. Those without symptoms have low risk of amputation. Overall 20-30% may require a surgical procedure within 5 years to increase blood flow. Severe disease requires prompt attention and treatment.
Key Features of PAD-related leg pain
Cramping, aching, tightness, fatigue; calf, thigh or buttock muscles; exercise-dependent; consistently brought on by exercise to similiar degree or walking distance; not brought on by simple standing or changes in position; and quickly relieved by rest (standing still)
Critical limb ischemia (CLI) - more severe PAD
Advanced state with severe reductions in blood flow; high risk for amputation if untreated; pain in feet or toes at rest, often at night, relieved by dangling; advanced signs such as discoloration or open sores develop; limb salvage requires procedures to improve blood flow to the foot
Goals of treatment of PAD
Improve limb outcomes and reducing cardiovacular events - decrease morbility and mortality from MI and stroke
General treatment of PAD
Risk factor management - stop smoking, diet and lifestyle changes, and glucose control. Medications to reduce CV events - ASA and plavic, statins and cholesterol lowering drugs, and HTN meds
Treatment of leg of PAD
Exercise - supervised programs. Meds - pletaal may improve walking in some patients. Most pts with mild disease do not require surgerical procedures. Pts with advanced disease may benefit from procedures to open or bypass. See a dedicated vascular specialist.
Diabetes and PAD
Increased risk of amputation, nerve damage and impaired resistance to infection contribute to foot problems, careful attention to preventive foot care, and close monitoring by a vascular specialist - minor foot problems can rapidly worsen and Gangrene much more likely
A-fib
Most common heart rhythm abnormality and is characterized by an irregularly irregular heartbeat.
Great danger of A-fib
Blood clots can develop within the quivering left atrium and be prepared into general circulation with some reaching the brain
Drugs used to convert A-fib into a normal rhythm
Calcium channel blockers - diltiazem and verapamil; small dosease of beta blockers; and less common digoxin.
Coagulation therapy and A-fib
Until normal rhythm is restored, anticoagulation therapy is required. Coumadin is more effect than ASA and can be used together
Coumadin use and A-fib
Not every patient receives coumadin. Now use the CHAD2 scoring system to decide on risk for stroke.
Major risks for abdominal aortic aneurysm
Age >65, male, history of smoking at least 100 cigarettes in a person’s lifetime, first-degree family history of AAA requiring surgical repair elevates a man’s risk but not as clear for women, modest association between risk factors for atherosclerotic disease and AAA
Description of AAA
“Searing pain in my belly that goes right through to my back”
Screening recommendations by the USPTSF
One-time screening using ultrasound in men aged 65-75 whi have ever smoked, no recommendation for men who have never smoked, and women should not be screened
AAA pathophysiology
Arises as a consequence of loss of structural integrity leading to dilation of the abdominal aortia
Occurrance of AAA
More common in men, 6% men older than 65 years, higher in whites
Risk factors for AAA
Atherosclerotic vascular disease, white race, male gender, advanced age, HTN, smoking, COPD, history of hernias, family history of AAA, and presence of other aneurysms
Clinical presentation of AAA
Results from pressure to surrounding structures and 75% are asymptomatic. May see a pulsatile abdominal mass. May see abdominal pain, back pain. “Shearing pain”
Detecting AAA in older men
Palpation is one of the few exams that is EBP
Diagnostic test for AAA
Ultrasound
Differential diagnoses of AAA
MI, esophageal rupture, perforated gastric ulcer, pancreatitis, bowel obstruction, appendicitis, ischemic bowel, back strain, and arthritis
Management of AAA
Prevent aneurysmal rupture while minimizing surgical risk
Factors that dictate elective AAA repair
Size of aneurysm, patient’s medical status, life expectancy
Best predictor of AAA rupture
Size of aneurysm, patient’s medical status, life expectancy
When to refer a AAA
When 4.0 cm or larger to a vascular surgeon. Elective repair - 5.0-6.0 cm. Expansion beyond 10% of diameter per year.
Most common symptom of arrhythmias
Palpitations
Palpitations in A-fib
Usually irregular and may be more sustained
Physical exam of patient with arrhythmia
General appearance, particularly color, diaphoresis, respiratory effort, and anxiety, hydration status, vital signs, and mental status
A-fib on ECG
Normal P wave is replaced by fibrillatory F waves, producing a wavy baseline. Rate estimated between 350-650 beats/min.
Therapeutic goals or treatment of A-fib
Control rate and prevention of thromboembolisms.
Common causes of A-fib
Rheumatic heart disease, mitral valve disease, HTN, CAD, hyperthyroidism, stimulant ingestion, ETOH withdrawal, and acute pulmonary disease
Therapeutic procedure to correct a-fib
Cardioversion; sotalol; digoxin - not used as commonly; ETT
Meds to control A-fib
Sotalol; digoxin; beta blockers; calcium channel blockers; amiodarone; anticoagulation therapy
Anticoagulation therapy for A-fib in low-risk patients
Those younger than 60 without heart disease may use ASA or a combo of ASA and plavix for those who can not take warfarin
Anticoagulation therapy for A-fib in most patients
Warfarin is preferred
CHADS2 score
Used to calculate embolic risk on the basis of a patient’s other comorbid factors
Arrhythmias that require hospitalization
Any that produces hemodynamic decompensation
Referral for arrhythmias
When treatment requires a nonpharmacological agent, such as a pacemaker, catheter ablation, or ICD implant
Peripheral arterial insufficiency
Condition that results when there is insufficient blood flow to the extremities. More common in lower extremities.
Pathyphysiology of chronic arteial insufficiency
Results from diverse systemic conditions that affect arteries found in different parts of the circulatory system, even in the absence of clinical symptoms.
Classic symptom of peripheral arterial insufficiency
Claudication
Claudication
Tightening or cramping pain usually in the calf muscles that is precipitated by exercise and is relieved by rest
Iliac artery obstruction (Leriche’s syndrome)
Claudication that begins typically while in bed and is relieved by dangling the legs over the side of the bed
Physical characteristics of peripheral artery insufficiency
Muscle wasting, loss of hair, and reduced temp in affected limb, absence of pulses, dependent rubor
ABI (Ankle-brachial index)
Most useful tool in assessing peripheral arterial insufficiency
Differential diagnoses of peripheral insufficiency
Peripheral neuropathy, cauda equina syndrome, Buerger’s disease, leg cramps, and musculoskeletal disorders
Cauda Equina Syndrome
Spinal stenosis causing pressure on the nerve roots may result in symptoms of claudication from the hip downward, which can be confused with Leriche’s syndrome. Often must rest longer to relieve symptoms.
Buerger’s disease
Inflammatory occlusive disease of medium and smaller arteries of arms and legs, very common among smokers.
Referring patients with peripheral artery insufficiency
When severe claudication results, rest pain, or gangrene
Acute arterial insufficiency
The sudden onset of the symptoms of ischemia and usually the result of an embolus
Clinical presentation of acute arterial insufficiency
Usually with a history of sudden onset of pain in an extremity.
Physical exam of acute arterial insufficiency
Usually limb is pale and pulseless with absent or diminished cap refill, loss of sensation or immobility. Become gangrenous if untreated.
Management of venous stasis ulcers
Bed rest. Wet-to-dry dressings after debridement. antibiotics. Nonstick dressings may be less painful.
