Objectives ?s Flashcards
Extremity rubor usually indicates what?
Chronic arterial insufficiency
Extremity palor usually indicates what?
vasoconstriction, anemia, or ACUTE ARTERIAL INSUFFICIENCY
cyanosis on the extremities usually indicates what
decreased O2 supply - arterial insufficiency, hypoxemia, venous stasis, arterial obstruction
NY Heart association functional classification of heart disease
Class 1: no limitations, no sx.
Class 2: slight limitations of physical activity
Class 3: Marked limitation - comfy at rest but less than ordinary activity causes sx.
Class 4: Unable to engage in any physical activity without discomfort, sx may be present even at reat
Class 5: symptoms that are atypical and can occur either at rest or exertion.
BP goal per JNC7
under 140/90 or 130/80 if CKD or DM
initial treatment for HTN (JNC 7)
- Thiazide (stage 1, 140-159/90-99)
- Drug combo (stage 2, 160+/100+)
JNC 8 recommendations for HTN
For those 60+?
For those under 60?
For those 18+ with CKD?
For those 18+ with DM?
60+: initiate tx at 150 SBP or 90 DBP, treat to les than this. A recommendation.
Under 60, initiate at 140SBP or 90DBP, treat to less than this. Grade A rec for DBP, grade E for SBP and for those 18-29.
18+ with CKD: treat at 140/90 (either), treat to less than this, grade E recommendation
18+ with DM: treat at 140/90 (either #) to less than this, grade E recommendation
JNC8 recommendations for non-black HTN tx?
For black HTN treatment (inc. DM)?
For 18+ with CKD
For non-black: one of - Thiazide, CCB, ACE/ARB –> B rec
For black: Thiazide OR CCB –> B rec (or C for DM)
CKD: ACE or ARB –> B recommendation
What to do if the drug doesn’t work?
- If goal BP not reached in one month, increase dose or add another drug
- If not reached with 2, add one more
- Use other drugs if contraindication or if more than 3 drugs are needed
Can you prescribe an ACE and an ARB together?
NO WAY JOSE
Isolated Systolic Hypertension - definition and typical patient
Systolic > 140, Diastolic less than 90
-Older man with atherosclerosis and DM, obesity, alcohol use, smoking, sedentary
Sx and complications of isolated systolic HTN
Sx: really, non. headaches?
Complications: stroke, MI, HF, kidney failure
Essential hypertension - definition and typical patient
No clear cause, 140/90 BP
more common in blacks than whites
-obesity, salt intake, smoking, alcohol, NSAIDs, metabolic syndrome, sleep apnea
S/Sx of essential HTN
Mostly asymptomatic! HA most frequent. Later HTN can show retinopathy (copper/silver wiring, exudates, hemorrhages, papillidema)
End organ damage possible with HTN
Heart: LV hypertrophy--> heart failure Brain: stroke, TIA, dementia CKD PAD Aortic dissection reinopathy nephrosclerosis (particularly in african americans)
Workup for HTN pt
Hg, UA, Serum creatanine, fasting blood glucose, lipids, serum uric acid, serum electrolytes
(Dr. S - ECG, UA, HCT, K, CBG, GFR, Lipids)
Primary aldosteronism
- cause of secondary hypertension
- adrenal hyperplasia or aldosterone producing adenoma
- risks=fam hx, hypokalemia
- s/sx: mm weakness, polyuria, nocturia
- complications: organ damage (cerebral hemorrage, MI, cardiomegaly, arrhytmia, renal insufficiency), hypokalemia, metabolic alkalosis, supression of renin
CKD
- MOST COMMON cause of secondary hypertension
- increased intravascular volume or increased renin-angiotensin-ald system activity
- risks: elderly, nephrotoxic drugs, DM, CVD, HTN, SLE
- S/sx: sleep disturbances, fatigue, anorexia, N/V
- CAUTION - Kidney failure
- Workup: GFR, albumen, creatine ratio
Renovascular disease
- renal arter stenosis or fibromuscular dysplasia
- decreased renal perfusion pressure, excess renin release
- complications: end-stage renal disease, pulmonary edema, unstable cornary syndromes
Coarction of the aorta:
congenital localized narrowing of the aortic arch just distal to the left subclavian artery. Collateral circulation develops.
RADIAL FEMORAL DELAY.
Cardiac failure usually occurs in infancy, if not, pt is generally asymptomatic until HTN produces LV failure or cerebral hemorrhage.
Continuous murmur on back and left anterior chest.
Pheochromocytoma
Rare - catecholamine producing tumor within adrenal medulla, causes vasoconstriction and leads to a reduction in plasma volume.
- Postural hypotension
- Risks: TCAs, antidopaminergic agents can cause hypertensive crisis.
- S/sx: orthostatic drop of 20/10 mmHg, TRIAD of headachee, sweating, palpitations, glucose intolerance.
- SCREEN those at risk via genetics
Drug induced hypertension
Drugs that can exacerbate HTN, usually due to renal vasocontriction or sodium retention
(nsaids, cocaine, erythropoeitin, stimulants, OCPs, cyclosporine, alcohol).
Thyroid/Parathyroid
familial, acquired, autoimmune.
END ORGAN: CHF, exaggeated with levothyroxine tx.
s/sx - forceful heartbeat, PACs, sinus tac, exertional dyspnea, afib (hyper)
weakness, fatigue, cold intolerance, depression (hypo)
-TSH/T4/T3 echo
Sleep apnea and HTN
Elevated sympathetic activity, CV variability, intrathoracic pressure changes, inflammation, oxidative stress.
PT: male, older age, increased BMI/neck girth, snoring, pauses
CPAP!
complications - CV disease, AAA, HTN, DM
Hypertensive urgency vs. hypertensive emergency
Urgency: 220/125 (either one) usually does not requre emergency therapy unless organ damage is evidence. Reduce within a few hours.
Emergency: BP diastolic >130. Reduce within an hour. HOSPATILIZE! encelopathy, neuropathy, intracranial hemorrhage, aortic dissection, preeclampsia, pulmonary edema, agina, MI.
- Reduce BP by 25% within minutes to hour, then the next goal is less than 160/110 in 2-6h. Don’t drop too quickly.
- use nitroprusside, NG, lalbetalol
malignant hypertension
HTN much like hypertensive emergency–NEEDS HOSPITALIZATION, encephalopathy or neuropathy with accompanying papilledema in addition to htn
Hypercholesterolemia
Reduce saturated fats, cholesterol, increase fiber, lose weight, exercise. Treat with statins for total cholesterol <200mg/dL
Elevated LDL
-diet & lifestyle change, weight loss, quit smoking.
tx goals:
high risk, is >100, treat to less than 100
mod high, goal=130, start tx at 130
mod, goal=130, start tx at 160, lifestyle changes 130
low=less than 160, consider drug therapy at 190
hypertriglyceridemia
can be caused by obesity, DM, alcohol, CKD, COPs, diuretics. Diet is primary therapy. Statin, fibrates
low HDL
reach LDL first, focus on weight and exercise.
Familial hypercholesterolemia
GENETIC, total cholesterol >500 usually. Warning: sudden death can happen. Family hx is important, cut saturated fat from diet, lose weight, exercise. No prevention. Use statins.
Ankle Brachial Index
upper and lower extremity BP comparison, indicates CAI. less than .9 is abnormal, .5 indicates significant disease.
risks of CAI
coronary artery insufficiency - ulcerations, acute ischemia, amputation (worse in diabetics and smokers)
Occlusive cerebrovascular disease
-due to emobli occluding cerebral artery: TIAs
-most emboli originate from the proximal internal carotid (unless Afib)
-Sudden weakness/numbness of extremity, aphasia, dysarthria, unilateral blindness.
-bruit loudest in neck
-can last few mn (or seconds for TIA) to 24 hrs
STENT
Aorta and Iliac Occlusive Dz
- distal abdominal aorta and iliac arteries - atherosclerosis.
- obstruction of blood to lower extremities
- Men 50-60yr, smokers, claudication, dimished femoral pulses, tissue loss
- Pain in low/back buttock!!!, pain with exercise, ED, weak pulses, low ankle brachial index
- No meds, control risk factors. Angioplasty, stenting, antiplatelet therapy.
Mesenteric Insufficiency AKA visceral artery insufficiency
Postprandial abdominal pain, weight loss with “fear of eating,” embolic occlusion of one major mesenteric vessel.
Tx - determine bowel viability, bypass, resection,
for chronic: angioplasty and stenting
Acute arterial occlusion (embolism/thrombosis)
Loss of blood supply to distal extremities due to:
-thrombus formation of a disease vessel (ruptured plaque) –> most common.
arterial emboli: 80% arise from heart, emboli come from another location in the body, secondary to Afib, etc.
acute thromboses: likely if other evidence of chronic obstructive disease present. Thrombus formation of diseased vessel.
5Ps of compartment syndrome and other features of acute arterial occlusion
pain pallor parasthesias pulselessness, pain
veins collapsed
blue toe syndrome
clinical presentation of acute arterial occlusion
50% with sudden onset of severe, unrelenting leg pain
50% have insidious onset of pain over several hours
sharp demarcation between perfused and ischemic tissues
treatment of acute arterial occlusion
HOSPITAL! Heparin, tpa
Thromboangiitis Obliterans (Buerger Dz or TAO)
SMOKING disease, generally in young males
- multiple segmental occlusions of obliterating tibial and pedal arteries, can also affect UPPER EXTREMITIES
- more common in Japan and SE asia
- small/medium arteries and veins, CLOTTING
Superficial thrombophlebitis
- hardening, tenderness, redness along vein
- most commonly from IV placement, can also be trauma, varicose, TAO, or spontaneous.
- Inflammation subsides 1-2weeks and “firm cord remains.
- Usually benign and brief, treated with NSAIDs, but can lead to post phlebitic syndrome if untreated.
DVT
- Pain or aching in affected limb, swollen/red/tender with distended veins, pitting edema, Homan’s sign. 50% asymptomatic in early stages.
- DOPPLER/VENOGRAPHY*/D-Dimer
- Low dose heparin and compression socks (proph)
- Heparin+3 mos oral warfarin (tx)
Varicose Veins
- Hereditary, associated with prolonged standing/lifting, highest incidence after pregnancy
- Dull, aching heaviness
- Compression stockings, elevation, stripping, sclero (better hope you don’t need cardiac surgery!)
Chronic venous insufficiency
- Veins are dilated or valve leaflets scarred/thickened
- can result from trauma, obesity, or secondary to thrombophlebitis
- progressive pitting edema (can be unilateral), brawny pigmentation, taught/shiny ankle skin, ulcerations just above ankle (medial/anterior aspect of leg), fibrous subQ for longstanding cases
- COMPRESSION STOCKINGS and treat any DVT
AAA
- Widening of the AAA (normal is 2cm)
- Normal part of aging, can be caused by inflammation, more common in men
- Most are asymptomatic, pain and tenderness indicate impending rupture
- 90% below renal arteries at bifurcation
- ULTRASOUND and elective repair if >5.5cm or rapidly expanding.
Thoracic Aortic Aneurysm
- Most due to atherosclerosis, CT disorders, trauma
- Most asymptomatic, can cause back/neck pain or pressure on trachea and associated sx
- CXR, CT scan (gold standard)
- Surgical repair if 6cm or larger
Aortic Dissection
- Spontaneous tear in aorta, may be from repetitive torque from cardiac cycle
- SEVERE chest pain, radiating to back. Syncope/hemiplegia/paralysis, diminshed pulses, diastolic murmur in ascending aorta
- LVH on EKG, CT (gold standard)
- Control BP, surgical graft
Stable angina
Under the patient’s control –> predictable triggers and relief
Probable angina
Classic discomfort, not exertional, not relieved by rest/NG
Unstable angina
Out of pt’s control –> more severe episodes, at lower workload, rest, barely relieved by NG
3 determinants of oxygen demand
Heart rate, myocardial contractility, ventricular wall stress
Determinants of oxygen supply
Low ambient O2, inadequate O2 transfer from lungs to blood, inadequate O2 transfer from blood to tissues, inadequate blood supply to myocardium
Labs for angina
CK-MD, troponin, hyperlipiedmia labs. 3 serial cardiac enzyme tests to r/o MI. EKG shows ST degment depression for unstable.
TX for angina
Nitrates, bblockers, aspirin. Treat HTN, avoid triggers.
variant (prinzmetal) angina
Common in smokers, caused by coronary spasm, causes ST segment elevation. Occurs without precipitating factors, early in the AM. Normal labs. Nitrates, CCB to treat.
MI, Two types of MI
MI: rise of cardiac biomarkers with evidence of myocardial eischemia (EKG)
NSTEMI - non-occlusive thrombus with no ST elevation but cardiac enzyme elevation
STEMI - ST elevation with cardiac enzyme elevation
Etiology of MI
COMMON: Occlusive coronary thrombus at the site of a pre-existing atherosclerotic plaque.
Rare: downstream embolus mobilizes, vasculitis, dissection, cocaine (consider if young with no risk factors)
Symptoms of MI
-Unstable angina, JVD, kussmaul, soft heart sounds, S4 sounds, mitral regurg, rales in lungs –> both types
Prolonged chest disconfort with little/no effect of NG, acute death –> STEMI
Labs for MI
Gold standard: troponin I, troponin T, CK-MB, myoglobin, Total CPK, ECG
Managment of MI
ASA, O2, LMWH, thrombolysis for STEMI, beta blockers post MI
Silent MI
occlusive thrombus with no pain, ST elevation, and cardiac enzyme elevation
- more common in women, older, those with DM
- tx directed at underlying problem - CHF usually
tx: ACE/ARBs, other health lifestyle things
Post MI treatment:
1) Cardiac cath if pt has recurrent ischemia, imparied LV function, heart failure, ventricular arrythmias, hemodynamic instability
2) ACE inhibitors, Aldosterone blockade if LV EF less than 40%
3) Lipid management (statins), smoking cessation, BP control, BETA BLOCKERS, antiplatelets (aspirin and clopidogrel), cardiac rehab/exercise
4) Cardiac revascularization in those with LV dysfunciton, NSTMI with high risk, risk factors, those who underwent thrombotic therapy
Right heart failure vs. Left heart failure
Left: Exertional dyspnea, cough, fatigue, orthopnea, PND, cardiomegaly, rales, gallop, pulmonary venous congestion
*symptoms of low cardiac output and elevated pulmonary venous pressure
Right: Elevated venous pressure, nocturia hepatomegaly, dependent edema –> Usually due to LEFT HEART FAILURE
*signs of fluid retention
CHF
Condition in which the blood cannot adequely pump blood to the body, most are a combiation of left and right failure.
-a disease of aging
Systolic dysfunction:
-heart function based on depression of myocardial contractility (most common cause, often MI related), elevated preload of ventricle (valvular regurg, etc), excessive afterload (impeded LV ejection), and heart rate.
Diastolic dysfunction: can lead to heart failure when filling of LV or RV is abnormal (impaired relation, noncompliant chamber)
Tx of CHF
Diuretics+Acei, B-blockers can be added.
Poor prognosis - 5 yr mortality rate of 50%
Endocarditis
- bacterial or fungal infection of the valves/endocardium
- fever, splinter hemorrhages, osler nodes, janeway lesions, roth spots, stroke/emoblic events
- get CXR, echo, 3x blood cultures on hr apart
- vanco+cephtriaxone before specific culture back
- surgery often necessary
myocarditis
Viral and non-viral causes (cocaine, chemicals, radiation, SLE, chemo)
- can present days to weeks after acute febrile
- dyspnea, chest pain, arrythmias, heart failure, sinus tach, cardiomegaly
- EKG, CXR, requires confirmational bx
- Ace inhibitors and Bblockers if LV EF <40%, treat arrythmias, NSAIDs for pain
pericarditis
viral, neoplasm, radiation, drug, dressler syndrome (post surgery), kidney failure
- chest pain, dyspnea, fever, pericardial friction rub
- Complication: Cardiac tamponade
- Elevated WBC,BUN, pericardiocentesis, EKG
- NSAIDs, cholchisine, steroids
Dilated cardiomyopathy
- Idiopathic, alcoholism, myocarditis, postpartum
- sx of HF (dyspnea, elevated JVP, cardiomgealy, edema, ascities), if severe-chene stokes, pulsus alternans, ventricular arrythmias
- S3 gallop, sinus tach, left BBB, arrhythmias
- CXR shows cardiomegaly and pleural effusion, BNP to show severity
- Treat with ACEI, B-blockers, diuretics, digoxin is second line, avoid CCBs
- Pacing
HOCM
Hypertrophic cardiomyopathy, LV hypertrophy unrelated to pressure/volume overload.
- Autosomal dominant, presents in early adulthood with dyspnea/chest pain/post-exertional syncope, arrythmia
- dyspnea, chest pain, syncopy; symptoms related to diastolic dysfuntion, Lous S4 sound, Mitral regurg
- septal hypertrophy, which reduces LV systolic stress, increases EF, and can result in empty ventricle at end of systole.
- Tx: bblockers, CCBs, diuretics, defibrillation, surgical excision
Restrictive cardiomyopathies
Impaired diastolic filling with preserved contractile funtion; rapid early filling with diastolic dysfunction.
- Right heart failure dominates over left heart failure
- pulmonary HTN present, Kussmaul sign
- Amyloidosis is the most common cause
- EKG, diuretics, chemo if amyloidosis
Tako-Tsubo cardiomyopathy
- Occurs after major catecholamine discharge
- Chest pain and shortness of breath, most commonly in postmenopausal women
- Presents as acute MI, imaging reveals left ventricular ballooning - most pts recover completely
- aspirin, bblockers, ace.
Rheumatic fever
Jones criteria - two major or one major/two minor.
major criteria: carditis, erythema, sydenham chorea, polyarthritis
minor: fever, polyarthralgias, reversible PR intervals, elevated ESR/CRP
rheumatic fever can lead to rheumatic heart disease and damage in which valves?
mitral, aortic, tricuspid (high pressure valves affected most). Early lesion is mitral valve regurg, late is mitral stenosis.
