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193 Cards in this Set
- Front
- Back
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What are the three cardinal symptoms of heart failure?
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1) fatigue
2) dyspnea 3) edema |
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The most common cause of heart failure?
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Left Ventricular Systolic Dysfxn (60%)
Caused by CAD or idiopathic dilated cardiomyopathy, valvular HD, toxins, congenital |
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What is the clinical syndrome of HF caused by?
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1) pump failure
2) inadequate tissue/organ perfusion |
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What are the goals of HF therapy?
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1) improve ejection fraction (increase contractility, decrease afterload)
2) alleviate pulmonary edema (decrease preload) 3) reduce cardiac remodeling (ACE-I, BBs, aldost antag) 4) reduce mortality |
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What is the body's response to HF?
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- SNS increases HR and contractility to increase CO.
- Circulates catecholamines to increase vasoconst. to shunt blood to brain |
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Why does fluid retention occur in HF?
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- the RAAS is activated
- ADH is released by hyopthalamus causing reabsorption of water in renal CD |
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Explain abnormal lab findings in HF
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CBC- anemia
TSH- thyrotoxicosis CMP- electrolytes LFTs Na- hyponatremia Creat- increased due to hypoperfusion BNP- elevated pH- acidotic p02- hypoxic |
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Discuss findings of CHF on CXR
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cardiomegaly
kerley B lines cephalization of vessels pleural effusions alveolar edema |
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What are the stages of the NYHA HF classification system?
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I- no symptom limitation with ordinary physical activity
II- ordinary phys activity somewhat limited by dyspnea III- exercise limited by dyspnea at mild work loads IV- dyspnea at rest of with very little exertion |
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What are the three distinct arrhythmia mechanisms?
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1) triggered
2) reentry 3) automaticity |
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What can dig toxicity lead to and why?
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DADs, because of a intracellular overload of Ca
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What kinds of drugs can provoke or unmask sinus node dysfunction?
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1) Beta blockers
2) Ca channel blockers (Verapamil/Diltiazem) 3) Digoxin (less common) |
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What are the 2 requirements for reentry to occur?
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1) slow conduction
2) unidirectional block |
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What are the two hallmarks on EKG of AV nodal reentrant tach?
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1) pseudo S wave
2) pseudo R prime- p wave activated in retrograde direction |
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What are the types of Atrial Fib?
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1) Paroxysmal, episodic that converts to NSR spont
2) Persistent- episodic that terminates only after intervention 3) Permanent- resists attempts to restore NSR 4) Lone AF- reserved for pts <60yrs with no underlying cardiac abnormality |
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What is the CHADS score?
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assesses risk of thromboembolism in patients with non rheumatic AFIB. The higher the score, the higher risk of stroke.
-CHF -HTN -Age >75 -DM -Stroke Each are one point. 2 points for hx of stroke. |
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What is the target in ablation of atrial flutter?
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we target the cavotricuspid isthmus to cure the circuit
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What needs to be true if you want to cardiovert AFIB?
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pt needs to be on anticaogulant therapy for 3 weeks to prevent any clots in heart to cause a stroke
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What is the difference bt nonsustained and sustained VT?
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nonsustained VT- more than 3 consecutive beats faster than 100/min
sustained VT- must be longer than 30 seconds or is hemodynamically intolerable |
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What is the only anti-arrhythmic drug that can suppress ventricular ectopy and/or nonsustained VT but have a neutral effect on survival in patients with structural heart dz, myocardial ischemia, and impaired ventricular fxn?
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Amiodarone!
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What are the 7 risk factors of the TIMI Risk score?
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1) age over 65
2) more than 3 risk factors for CAD 3) documented CAD at cath 4) ST deviation more than .5mm 5) more than 2 episodes of angina in last 24 hrs 6) aspirin use within the prior week 7) elevated cardiac markers |
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What are some high risk clinical features for acute coronary syndrome?
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pulmonary edema
new or worsening MR murmur S3 or new/worsening rales hypotension, bradycardia, tachycardia age over 75 |
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When is it appropriate to put a stent in a coronary artery?
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only at >70% stenosis
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What patients do the 2007 ACC?AHA UA/NSTEMI guidelines recommend CABG as the preferred revasculation strategy?
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Pts with:
-sig left main disease (>50% stenosis) - 3 or 2 vessel dz who have sig proximal LAD stenosis, and either treated DM or LV dysfxn |
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What are the 2 patient-centered goals for reperfusion therapy?
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1) first medical contact to balloon time < 90 minutes
2) first medical contact to needle time < 30 minutes |
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What is the timing of a free wall rupture post MI?
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peaks 5th day
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What is the murmur with VSD post MI?
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loud holosystolic murmur
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What is the timing of right ventricular infarction post MI?
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first 24 hours
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What is the murmur of papillary muscle rupture?
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often soft or inaudible holosystolic murmur
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What artery is usually occluded in patients with inferior STEMI?
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RV fed by right marginal artery
ST elevation seen in leads V3 and V4 |
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What are the three phases of cardiac arrest?
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1) Electrical- lasts 4 minutes after initial collapse, high degree of responsiveness to early defib
2) Circulatory- lasts 4-10 min. Good quality CPR is of paramount importance with emphasis on O2 delivery to brain and heart before defib. 3) Metabolic- after 10 minutes |
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What are the big indicators for ICD implantation?
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- For patients who survived cardiac arrest due to VFib or hemodyn unstable sustained VTach
- In patients with LVEF less than 35% due to prior MI who are at least 40 days post MI and are in NYHA class II or III |
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What is the most common cause of myocarditis?
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Viral infections, specifically enteroviruses (Coxsackie virus A and B) and adenovirus which are both main causes of neonatal myocarditis, while Coxsackie B is most freq cause of adult myocard.
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What are some non-viral causes of myocarditis?
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Any bacterial agent can cause myocardial damage due to release of inflamm mediators via activation of TLR2 and TLR4 on mphages in heart.
occurs in 5% of lymes dz pts AIDS patients hypersensitivity reactions Systemic immune dzs: RA, SLE |
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What are the causes of neonatal myocarditis? Mortality rate?
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60-70% from mother
30-40% from hospital staff (nosocomial) most commonly aquired from common cold (adenovirus). Mortality is 50-75% in first week! |
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What is the clinical presentation of myocarditis?
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broad symptoms- fatigue, dyspnea, palpitations, precordial discomfort, fever
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What do you see on micro in myocarditis?
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diffuse lymphocytic infiltrate most common
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What is the pathophysiology of myocarditis?
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Three phases:
Viral Phase- virus enters the host GI or resp system via the Coxsackie-adenoviral receptor (CAR), which is highly expressed in the heart, brain and gut. This is why it is so dangerous in neonates. Immune Response- virus causes acute injury leading to cardiac damage and exposure of intracellular antigens Cardiac remodeling- cardiac injury followed by immunologic response (inflamm) that may destroy heart tissue acutely or linger and produce remodeling leading to cardiomyopathies, HF, or death |
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What is the autoimmune component of myocarditis?
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Virus activates innate immune syst. via TLRs stimulating release of interferons (IFN alpha and beta).
Macrophages and NK cells activated Helper T cells, Effector T cells, B cells join the fight T cells and ABs can react with viral proteins that mimic those of the host- this is termed molecular mimicry and it triggers autoimmunity Autoimmune mechanisms caused by viral release of sequestered heart antigens. Antibodies cause lots of damage. |
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What the diagnostics and tx for myocarditis?
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Adult M: heart biopsy. Tx = supportive care, bed rest, cardiac mon, anti-arrhythmic agents
Neon M: Dx =tachypnea, tachycardia, diaphoresis, anorexia. Tx = supportive care, fluids, digoxin, diuretics. |
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What is the gold standard of Dx of myocarditis?
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Biopsy- look for presence of inlfamm cells with evid of myocyte degeneration or necrosis on same section of specimen!
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What are signs, symptoms, and epidem. clues that support Dx of Chagas disease?
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Headache, fever, weight loss, malaise, Romanas sign (eye swollen shut), conjunctivitis, travel in rural South America
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Explain most common routes by which humans acquire Chagas dz
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Triatomid insect = kissing bug which lives in mud, thatch, adobe homes in rural areas of south america
Transmission occur from feces of bug on face of person, parasites enter. Or transmission through blood as well |
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Why can you have symptoms of megacolon, constipation, dysphagia, megaesophagus in chronic Chagas dz? (10-30 years)
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Parasite can affect GI tract by damaging enteric neurons that controls GI muscles, loss of normal peristalsis
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What are the clinical, gross, micro features of Dilated Cardiomyopathy?
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gradual four chamber hypertrophy and dilation.
May occur at any age as slow, progressive CHF. Can be due to genetic defects, alcohol tox, peripartum cardiomyopathy, post-viral myocarditis Gross- cardiomegaly, mural thrombi, endocardial thickening Micro- nonspecific. 75% have diffuse myoctye hypertrophy and interstitial fibrosis, 25% have none |
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Clinical, gross, micro of hypertrophic cardiomyopathy?
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clinical- usually young adults: dyspnea, angina, near syncope, CHF, but may be asymptomatic. Increased risk of sudden death in athletes.
>50% are autosomal dom gross- disproportionate thickening of septum vs LV free wall. LV cavity is compressed by thickened intervent. septum |
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Clinical, micro of restrictive cardiomyopathy?
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Clinical- restriction of ventricular filling and decreased cardiac output
Micro- Hemochromatosis with Prussian blue stain showing excessive iron deposition in heart Can also see amyloid which can cause RCM. Can see amyloid on Congo Red stain |
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Clinical and micro of Myocarditis?
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Clinical- broad spectrum, from asymptomatic to abrupt onset of arrhythmia, CHF or sudden death. Most thought to be viral origin
Micro- myocardial inflamm infiltrate with myocyte necrosis or degeneration. Lesions are focal. Viral infections show isolated myofiber necrosis with interstitial edema and mononuclear cell infiltrate, little necrosis. |
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What are some benign tumors?
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Hemangiomas
Glomus tumors Vascular ectasia (Nevus flammeus, sturge-weber syndrome, spider telangiectasias) Bacillary Angiomatosis Simple lymphangioma Cystic hygroma (neck) |
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Kaposis sarcoma (4 types, clinical)
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4 types based on epidemiology
1) Chronic/Classic/Euro- elderly men of eastern european decent. multiple red to purple plaques and nodules on lower exts 2) Lymphadenopathic/African- as above but in younger men, mainly in lymph nodes, aggressive 3) Transplant associated- pts on immunosuppressive therapy- goes away after therapy ends 4) AIDS related |
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What is the deal with the Glomus tumor?
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Benign, extremely painful tumor of smooth muscle cells arising from the glomus body. Found in distal phalanges, especially beneath nail beds
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What is the most common primary cardiac tumor in kids?
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Rhabdomyoma
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What is the most common primary adult tumor?
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Myxomas. Usually single. 90% are in area of fossa ovale in atria.
L>R (4:1). cause symptoms by physical obstruction, peripheral emboli, or "wrecking ball" trauma to the valves |
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What are some pediatric differences when it comes to EKGs?
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Right axis predominance in infants
RAD inverted T waves in V1-V3 usually shorter intervals usually faster rates |
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What is a good systematic approach for pediatric EKGs?
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1) Rhythm
2) Rate 3) P waves- are they there? How are they related to the QRS? 4) Intervals (PR and QRS) all increase as kids age |
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How common are PVCs in kids? In adults?
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5-10% of normal children
60% of adolescents and adult men 10% will have MVP |
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What must be ruled out with PVCs?
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HCM
Long QT syndrome Right Ventricular dysplasia |
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Any patient with PVCs and syncope or idiopathic seizures MUST have _____
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EKG with QTc measurement
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What is the PVC workup?
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EKG
Echo Exercise stress test - benign PVC- suppressed by exercise - exercised induced PVCs have poor prognosis |
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What are some false positive EKG findings in athletes?
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LVH (skinny minny more likely to have false LVH)
nonspecific ST-T wave changes Q wave changes low resting heart rates |
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If you see a kid with Sinus Tach during sleep or at rest, think:
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CHF
Fever thyrotoxicosis myocardial dz shock |
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If a baby <4 mos of age has SVT, is it likely to remain long term?
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NO. 93% cease having SVT by 8 months
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If SVT in a kid >5 years old, is it likely to remain long term?
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YES. 83% will have recurrence
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What are some vagal maneuvers>
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1) diving reflex (ice)- glove filled with ice over entire face for up to 20 sec. ALWAYS RECORD RHYTHM STRIP BEFORE, DURING, AFTER
2) Valsalva- gentle rectal stimulation, gag reflex NO EYEBALL PRESSURE |
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What is a contraindication to rectal exam/stimulation?
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Increased intracranial pressure- can vagal out and cause brain herniation!
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What is adenosine? What does it do?
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slows sinus heart rate
causes transient AV block onset in 15-20 seconds works great for stable SVT |
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When is synchronized electrical cardioversion used?
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for unstable child/infant unresponsive to adenosine or ice
need pre and post 12 lead EKG rhythm strip |
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What is the treatment for SVT in infants? Older children/adol?
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Infants- IV adenosine, diving reflex if no IV access. IV digoxin
Older children- IV adenosine. IV verapamil (NEVER GIVE TO INFANTS) |
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How do you treat WPW?
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Digoxin
Propanolol |
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Would you ever give CCB in WPW?
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NO! Unless you want a lethal arrhythmia
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What is the top cause of an infant's HR drop?
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Apnea!
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What is Beneficence?
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obliges persons to benefit or help others
requires positive action (to prevent harmful or promote good) |
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What is Justice?
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fair distribution of benefits and burdens
requires that persons recieve that which they deserve appears in decisions to allocated scarce healthcare resources |
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What is Nonmaleficence?
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refrain from harming others
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What is Causitry?
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a case-based approach to ethical decision making. Focuses on practical decision making in particular cases and compares to paradigm cases for comparison
weakness- does not provide clear rules or principles |
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What is Narrative based ethics?
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emphasis on learning patients story
learn patients perspective of their illness and the meaning to the patient |
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What is the difference between sepsis, sepsis syndrome and septic shock?
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Sepsis- systemic inflamm response syndrome due to infection
Sepsis syndrome- sepsis plus evidence of hypotension, or altered organ perfusion: hypoxemia, elevated lactate, oliguria, altered ment stat Septic shock- sepsis syndrome with refractory hypotension |
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Identify some likely settings for development of sepsis
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Nursing home, ICU, Neonatal ward
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List major cardiovascular alterations in pts with septic shock
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Initial vasodilation and capillary leakage result in decreased SVR, compensatory cardiac output. Not getting blood to vital organs
Marked hypotension Coag abnormalities, generalized CV insuff from endothelial damage, hypoperfusion |
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List the most likely bacterial agents of sepsis in the following settings
a) nursing home b) ICU c) deep tissue wound d) postpartum e) UTI |
nursing home- S. pneumoniae
ICU- Pseudomonas deep tissue wound- bacteroides, clostridium Postpartum- group B strep UTI- E. Coli, Klebsiella, other gram negs |
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Briefly explain some unique aspects of septic shock cause by Pseudomonas aeruginosa, along with some important characteristics of the organism
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Gram Neg bacilli
ubiquitous, opportunistic oxidase positive pigments and toxins- sputum can be tinged with color Immunocompromised neutropenic pts (Neutrophil is most important defense against Pseud) higher mortality rate notoriously resistant to antimicrobials |
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List at least 5 of the host factors thought to play a sig role in the development of sepsis syndrome and describe their activities
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Complement activation
cytokines NO tissue factor |
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Briefly describe the coag abnormalities in sepsis
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reduced protein C
increased coag and inflamm: increase proinflamm mediators endothelial injury tissue factor expression thrombin production |
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How do you treat suspected sepsis or sepsis syndrome?
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Immediate empiric antimicrobial IV therapy
Obtain 2-3 blood cultures every 30 minutes Good phlebotomy technique essential surgical drainage of any infection |
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Explain the MOST IMPORTANT considerations and general patient management steps to increase likelihood of positive outcome for patient with severe sepsis.
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Early detection, fluids, early antimicrobials, prevention
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List the data that will help risk stratify patients with syncope
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San Francisco syncope rule: If have one of more of the following, then high risk.
Risk factors- Systolic pressure < 90 SOB EKG non NSR Hx of CHF Hematocrit < 30% Also, patients older than 60 with CV hx are high risk Pts younger than 45 without CV hx or other risk factors are low risk Syncope during exercise in younger pts w.o benign cause are at increased risk |
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List factors which determine when a patient should be hospitalized
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Admit patients with syncope if they have any of the following:
Hx of CHF or ventricular arrhythmias assoc chest pain or Acute coronary syndrome symptoms evidence of CHF or valvular heart dz on Physical EKG findings of ischemia, arrhythmia, prolonged QT, BBB Consider admission if: Age older than 60 history of CAD or congenital heart dz fam hx of sudden death exertional syncope in younger pts |
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List the age dependent causes of syncope
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Pediatric patients- vasovagal, conversion rxns, primary arrhythmias (LQTS and WPW)
Middle age- Vasovagal most common. Orthostasis, panic disorders Elderly- Obstructions to Cardiac output (aortic stenosis, P.E) arrhythmias |
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Determine treatment of patients with syncope
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s
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What are three important parts of a syncope history?
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1) What occured before the event
2) description of the event 3) orientation and LOC after the event (postictal state?) |
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What characteristics from the cardiac exam can help differentiate valvular lesions?
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s
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What are the symptoms of specific valvular pathology?
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s
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Know how to manage specific valvular pathologies and when to refer for intervention.
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s
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What does an S3 sound indicate?
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Overloaded ventricle (CHF, 3rd trimester pregnancy)
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What is the prognosis like for people with an S3 gallop?
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Although normal variant in pregnancy and children, VERY POOR prognosis if present after age 40 or with decreased left heart fxn
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What is an S4 usually indicative of?
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Stiff ventricle
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How do you grade a murmur?
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I- less intense than S1, S2
II- same intensity III- more intense but without palpable thrill IV- grade III but with palpable thrill V- can be heard through solid medium VI- can be heard without stethoscope |
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What occurs to the intensity of most murmurs as you increase flow across the valve?
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they increase in intensity
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What are the two murmurs that decrease with increased preload?
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MVP and HCM
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What can you ask a pt to do to decrease preload?
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Standing
valsalva |
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How can you increase preload?
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Lying down
squatting raising legs |
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Sustained 30 sec hand grip increases or does not change the murmur of ____ but should soften the murmur of ____
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MVP
HCM (Handgrip increase afterload which widens the outflow tract) |
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Right sided murmurs increase with ____
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inspiration (except PS)
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Left sided murmurs increase with ______
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expiration
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What position are S3 and S4 gallops heard best?
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left lateral recumbent
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Fixed split S2 is assoc w _____
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ASD
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If a wave is large on Right, what can be happening?
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atrial pressure is high, so tricuspid stenosis or severe pulmonic regurg, stiff RV is possible
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If a wave is large on Left, what can be happening?
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blood backing up from lungs= mitral stenosis, severe aortic stenosis, complete heart block
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Aortic Stenosis
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Sx- CHF, angina, dyspnea, syncope with exercise
PE- pulsus tardus with sustained apical impulse, SEM at RUSB with radiation into carotids. S4 sec to LVH which can become S3. Ejection Click. Dx with ECHO or left heart cath Worse prognosis of all valve lesions Surgery is best tx, refer as soon as pt becomes symptomatic Use Extreme Caution with diuretics and vasodilators (ventricle needs excess volume to overcome pressure of stenotic valve) |
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Chronic Aortic Regurg
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Sx- CHF, angina, dyspnea, sense of pounding heart beat
PE- pulsus bisiferens, high pitched diastolic mumur at LLSB (best heard sitting up and leaning forward) Dx- ECHO Indications to replace valve: 1) SYMPTOMS AT REST 2) LVES dimension > 5.5 cm2 3) EF decreased during exercise MUGA scan by >10% |
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Acute Aortic Regurg
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due to acute event like endocard, truama, MI
Sx- acute severe pulm edema with cardiogenic shock PE- short diastolic murmur at LLSB Dx- ECHO Rx- emergency valve replacement |
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Mitral Stenosis
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almost always sec to rheumatic heart dz
increased risk of thromboembolic events and endocard Sx- dyspnea, HEMOPTYSIS, frequently causes of AFIB PE- diastolic murmur with opening snap, rumble. EKG with LAH *Pregnant females may present with acute pulmonary edema and AFIB Dx- ECHO MV under lower pressure so vegetations bigger than in aortic stenosis Tx- digoxin if LV fxn is reduced or AFIB. Diuretics if signs of LHF and pulm HTN BBs if resting tach Consider lifelong anticoag if chamber > 5.5cm, prior embolic event, or AFIB Valvuloplasty |
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Chronic Mitral Regurg
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caused by rheumatic heart dz, MVP, LV dilation, PAPILLARY MUSCLE RUPTURE
Sx- SOB, angina, AFIB frequent PE- pansystolic murmur with radiation to axilla, wide split S2, EKG with LAH, CXR shows cardiomegaly Dx- ECHO Rx- diuretics, ACE-I, beta blockers Valve replacem. if EF decreases during exercise MUGA scan by >10% or symptoms at rest Valve reconstruction is preffered to replacem unless: valve too damaged caused by rheumatic dz |
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Mitral Valve Prolapse
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very common (10-20% of teens)
PE- midsystolic click with murmur unaffected by sustained hand grip Dx- ECHO Tx- same as chronic MR. If murmur, use antibiotic prophylaxis |
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Are right sided valvular lesions common? Are they replaced?
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No! Rare
No! Low pressure so diseased valves are rarely removed and NEVER replaced |
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What are common causes of tricuspid stenosis?
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Rare!
rheumatic heart dz staph endocarditis (IV drugs) carcinoid syndrome Sx- systemic venous congestion (dysp or pulm edema = LHF Sx). Abd p sec to hepatic congestion. Fluttering in neck sec to increased JV pressure PE- diastolic murmur LSB, giant a wave, EKG with RAH without RVH Dx- ECHO or RHC Tx- symptomatic support with diuretics. Valvotomy if symptomatic and valve area > 1cm2 |
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What kind of murmur is heart in tricuspid stenosis?
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diastolic murmur LSB, giant a wave, EKG with RAH without RVH
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Tricuspid Regurg
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usually sec to LHF with increased PAH
Also caused by RHEUMATIC HEART DZ, STAPH ENDOCARD, or CARCINOID Sx- generally none, but can have fatigue, systemic venous congestion, neck discomfort PE- holosystolic murmur LLSB with parasternal heave, JVD, v waves Dx- ECHO Tx- treat underlying dz (RF, endocard) VALVE NEVER REPLACED |
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What are 7 causes of large R wave in V1?
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RVH
RBBB- rsR posterior wall MI misplaced leads muscular dystrophy dextrocardia- CXR WPW |
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Pulmonic Stenosis
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always congenital, rarely progresses
Sx- systemic congestion PE- RVH, RAH, a waves Dx- ECHO or RHC Rx- diuretics to reduce congestion valvuloplasty if symptoms severe Almost always a secondary condition resulting from PAH |
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When do you replace valves?
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Left heart valves- consider when pt FIRST BECOMES SYMPTOMATIC
Right heart valves- NEVER REPLACED, consider valvuloplasty if severe |
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Porcine valves
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less durable, but do not require anticoag
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When do you NOT give antibiotic prophylaxis?
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isolated secundum atrial septal defects
surgically repaired ASD, VSD or PDA innocent heart murmurs ASD |
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What are the four classifications of pericardial dz?
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1) nonconstrictive pericarditis
2) constrictive pericarditis 3) relapsing pericarditis 4) pericardial effusions |
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What is the diff between pericarditis and acute coronary syndrome?
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s
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Nonconstrictive pericarditis
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90% idiopathic probably viral
often preceded by viral URI or gastroenteritis Most common pericardial disorder Sx- severe pleuritic chest p (IMPROVES WITH LEANING FORWARD). FEVER. FRICTION RUB EKG- DIFFUSE CONCAVE UP ST ELEVATIONS, DEPRESSED PR SEGs Labs- elevation in CK Tx- stop causative drugs. NSAIDS |
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Constrictive pericarditis
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scarring and loss of elasticity of pericardial sac
usually idiopathic CXR- CALCIFICATION WITHIN PERICARDIAL SAC Dx- CT/MRI finds PERICARDIAL THICKNESS >5MM |
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Relapsing pericarditis
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RARE condition of recurring inflammation of pericardium with severe Chest pain.
autoimmne |
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Pericardial effusion
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accumulation of blood or fluid in sac that can lead to tamponade (compression of the ventricular chambers reducing cardiac output)
Sx- PROGRESSIVE DYSPNEA BECKS TRIAD Dx- usually ECHO for dx however CT/MRI are most accurate EKG- may show LOW VOLTAGE or ELECTRICAL ALTERNANS (beat-to-beat alternation of QRS appearance) - pericardial fluid rarely helps with diagnosis unless etiology is malig. Chronic Per Eff-- can warrant surgical drainage or pericardiocentesis |
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What is Becks Triad?
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hypotension, muffled heart sounds, JVD.
Friction rub may be present. Pulsus paradoxus |
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What should you remember to r/o in PEA pts before stopping code?
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Pericardial effusion!
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What is pulsus paradoxus?
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an exaggerated decline in systemic blood pressure with inspiration, which indicates tamponade. Pressure from the effusion presses on the IV septum, reducing LV filling, decreasing SV and decreasing BP
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Dilated Cardiomyopathy
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Ejection fraction less than 40%
Common causes- Viral, etoh, lymes dz, peripartum, chemotherapy agents, Chagas dx (LEADING CAUSE OF DCM in Central and South Am) High incidence of MURAL AND PERIPHERAL THROMBUS, esp if EF <20% Tx- treat underlying dz. Like HF (diuretics, ACE, fluid restriction, low salt, BBs) If EF <40% and patient has had syncope, VT or sig orthostatic Sxs, consider an AICD |
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What does Chagas dz show on ECG?
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nonspecific changes (RBBB and Left ant hemiblock, PVCs)
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Peripartum Cardiomyopathy
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can occur within last trimester up to 6 mos postpartum
mortality 20-50% prognosis depends if heart returns to normal size strongly advise to AVOID FUTURE PREG |
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Hypertrophic Cardiomyopathy
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IHHS (Idiopath Hypertroph Subaortic Stenosis)
disproport. hypertrophy of LV, septum Assoc w SUDDEN CARDIAC DEATH, especially in kids with FAMILIAL HX Genetic dz but Majority of pts are ASYMPTOMATIC If syncope, three factors assoc w high risk of sudd death: 1) age < 30 2) small LVEDL per ECHO 3) nonsustained VT per Holter monitor PE- often normal. may have S4 gallop. Murmur INTENSIFIED BY VALSAVA (decreasing preload) EKG- LAH, LVH, LAD, lateral Q waves. NORMAL EKG UNCOMMON Dx- ECHO |
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What is the only way to cure HCM?
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heart transplant. No drug improves survival.
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What should you use with extreme caution in HCM?
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anything reduces LV volume (diuretics, nitrates, volume depletion)
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Restrictive Cardiomyopathy
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rare and a dx of exclusion
HISTORY IS IMPORTANT poor prognosis Dx- need endocardial biopsy. Ct to r/o Const Pericard Tx- no specific tx |
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How do you differentiate RCM from constrictive pericarditis?
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EKG with normal voltage
Nondisplaced apical impulse (absent in CP) no evidence of pericardial calcifications |
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4 common causes of artifact
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1) patient movement
2) loose or defective electrodes 3) improper grounding 4) faulty EKG machine Artifact can mimic VFIB |
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What do PVCs look like?
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wide, bizarre QRS
followed by compensatory pause usually no p wave |
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What does junctional escape rhythm look like?
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p waves inverted, absent or after QRS
rate 40-60, unless accelerated (60-100) |
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What does SVT look like?
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cant see p waves
narrow QRS reg rhythm |
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What does aFib look like?
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irreg irreg
no p waves, fib waves instead |
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Which are not shockable rhythms?
Shockable? |
asystole, PEA
Vfib and pulseless Vtach |
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What does Second Degree Block Type I (Wenkebach) look like?
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progressive lengthening, then dropped beat
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2nd degree Type II look like?
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constant PR interval, just dropped beats
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3rd degree block?
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P and QRS are divorced!
Tx: pacemaker |
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Describe proper techniques for obtaining BP in children
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avoid stimulant food or drugs
sitting quietly for 5 minutes right arm supported with cubital fossa at heart level preferred method = auscultation 40% circumference at midpoint of upper arm Dont use machines! need 3 measurements on separate visits |
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integrate historical data and risk stratify pediatric pts for CAD risk
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s
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describe proper tx for different classifications of HTN
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s
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What are the classifications for HTN in kids?
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Normotensive- SBP and DBP < 90th %
PreHTN- 90-95% Stage 1 HTN- 95%-99% Stage 2 HTN- >99% |
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What are the BP standards based on?
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Gender, Age, Height
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If kids BP is <90th% but is still about 120/80, this is considered ____
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preHTN.
THIS BP LEVEL OCCURS FOR SBP AT 12 YRS OLD AND FOR DBP AT 16 |
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Plan for prehtnsive?
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recheck in 6 mos
TLCs- weight management no drugs |
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Plan for Stage 1 HTN?
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recheck in 1-2 weeks if pt is symptomatic
TLCs Drugs based on indications: 1) symptomatic HTN 2) secondary HTN 3) HTNsive target organ damage 4) DM 5) persistent HTN despite nondrug plan |
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Stage II HTN
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Evaluate or refer to source of care within 1 wk or immediately if symptomatic
TLCs Drugs- initiate therapy |
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Why should you ask about sleep history with HTN?
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association with sleep apnea with overweight and HTN
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Overweight and high BP are components of ________, a condition of multiple metabolic risk factors for CVD as well as for type II DM
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METABOLIC SYNDROME
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What does BEARS stand for?
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Bedtime problems
Excessive daytime sleepiness Awakenings during the night Regularity and duration of sleep Sleep disordered breathing |
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T or F: Secondary HTN is more common in children than in adults
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True
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What labs do you get in kids with secondary HTN?
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Renal function (BUN, UA)
CMP (looking for anemia) |
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Fasting plasma glucose and lipids should be performed in prehtnsive children who are ___, ____, ___
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Obese
have fam hx of HTN or CVD have chronic renal dz |
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What is the most prominent clinical evidence of target organ damage caused by HTN in children/adol?
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LVH on ECHO
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What is the goal of pharm therapy in HTNsive kids?
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to get them down to <95% unless concurrent conditions present, then <90%
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What is the most common cause of acquired heart dz in children?
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Kawasaki's dz
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What is Kawasaki's disease?
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acute self limiting vasculitis of unknown etiology
76% in children under 5 boys > girls asians and blacks > whites |
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What are the clinical manifestations of Kawasaki's?
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CRASH and BURN
Conjunctivitis Rash Adenopathy Strawberry tongue Hand and feet edema and BURN! FEVER FOR > 5 DAYS can have coronary artery aneurysms and ectasia in 15-25% of untreated cases. May lead to MI, sudden death, ischemic heart dz |
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What labs are abnormal in Kawasakis?
EKG findings? |
elevated acute phase reactants
elevated ESR elevated platelets elevated WBC elevated LFTs flattened T waves |
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What is the treatment for Kawasakis?
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IVIG
ASA high dose until afebrile, then low dose ASA 6-8 wks until ESR and platelets are normal |
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Kawasakis board buzzwords
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Febrile child, not responding to Antibiotics
Fever of AT LEAST 5 days NO CARDIOMEGALY |
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What is the only reason ever to treat a child with aspirin?
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KAWASAKIS
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What is Kawasakis commonly confused for?
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-drug reactions (no fever)
-JRA (chronic low grade temp, rash when fever peaks) -measles (rash diff, measles has exudative conjunctivitis) |
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What is the second most common acquired heart disease in childhood?
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Rheumatic fever/Heart Dz
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What is the latency period for RF?
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3 weeks
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What causes Rheumatic Fever?
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untreated Group A Beta hemolytic strep of the pharynx
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What are the Jones criteria? How many do you need?
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Need either 2 Maj +1 minor OR 1 Maj + 2 minor
Major- arthritis (large joints, migratory) carditis chorea erythema marginatum (serpinginous border rash on trunk/limbs) subq nodules Minor- arthralgia, fever of 38C, elevated ESR or C reactive protein, prolonged PR interval |
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Diagnosis of RF?
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need evidenc of an antecedent strep infection
history of recent scarlet fever positive throat culture elevated ASO streptozyme test |
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What is the most common valve involved with carditis s/p RF?
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Mitral valve- insufficiency, CHF, stenosis years later.
Aortic insuff less common but more severe |
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RF treatment?
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supportive care, bed rest, treat strep, Aspirin
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When should you consider meds for a kid with an LDL over 190?
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If they have fam hx of early heart dz or two additional risk factors present; or if LDL is higher than 130 if DM present
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When is informed consent required?
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Most times for:
Surgery anesthesia other invasive or complex medical or radiological procedures |
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What should the physician discuss during informed consent discussions?
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the Dx if known
nature and purpose of proposed tx risk and benefits alternatives regardless of cost or insurance coverage risks and benefits of alternatives risk and benefits of not receiving tx |
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What are the main barriers to effective informed consent?
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lack of clinician time
confusion about when IC is needed afraid of giving too much info perception of pts that IC is just legal release Pt unaware they can refuse Pt language/culture poor quality of form Pt inability to understand info clinician inability to detect lack of pt understanding |
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What is it called when surgery is performed without pts consent or it exceeds scope of consent?
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BATTERY
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What is it called if pt suffers consequence from procedure that was not discussed with the pt?
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NEGLIGENCE
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What percentage of patients who receive CPR in the hospital die?
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86% of patients who are rescusitated by CPR dont live to be discharged
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What is a POST form? Who is it for?
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a physician order that can be completed by any provider but must be signed by a MD or DO.
COMPLEMENTS, does NOT REPLACE advanced directives It is for seriously ill or terminally ill patients |
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What question do you ask yourself to see if a pt needs a POST form?
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Would I be surprised if the patient died in the next year?
IF NO, DO A POST! |
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What is the rationale behind the POST form?
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AD might not be available when needed.
AD might not have prompted need discussion, may not be specific enough AD may be overridden by a treating Dr AD does not immediately translate into a Drs order |
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Legality of POST form
|
Must accompany patient!
protects from liability if follow form POST orders are ORDERS legally recognized form of DNR |
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If you would not be surprised patient died in 6 months, consider _______
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HOSPICE
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