week 2- CV 2 Flashcards
• What is malignant HTN?
o Marked hypertension with retinal hemorrhages, exudates, or papilledema.
o Usu diastolic ≥120, but can be 100 if BP increases rapidly
• What is hypertensive urgency?
o Severe HTN
o diastolic BP ≥120 in asx pts
• what hx info gathered for eval of AHTN?
o Current and past MH, risk factors (CAD, HF, stroke, renal dz, dyslipidemia, DM, gout, FHx, smoking, meds, drugs, ETOH, salt and stimulant use, sx of end organ damage, sx ass w/secondary causes of HTN
o Known duration of HTN, previous levels
• What PE is done for eval of AHTN?
o Ht, Wt, waist circumference, fundoscopic, auscultation for neck and abdominal bruits, full CVP (central venous pressure) and neuro exam.
o Palp abdomen for masses, liver and kidney enlargement.
o peripheral pulses and extremities. brachial and femoral pulses palpated simultaneously, screen for coarctation of aorta
• what tests are done for AHTN?
o If new dx:
o UA, resting ECG (if LVH, ST depression, do echo)
o blood tests: creatinine, BUN, K, Na, Mg, Calcium, glucose, lipids, TSH. Consider homocysteine, CRP-hs, fibrinogen, fractionated lipids.
o Consider limited echo for LVH.
• When should you look for causes of secondary AHTN?
o if: onset prior to puberty, acute rise in someone well controlled, severe and nonresponse to therapy (3 drugs including diuretic), age <30 not obese, no Fhx, non-African American or malignant HTN
• what testing is done for 2nd AHTN?
o Renal: Abn BUN, creatinine, UA and urine micro, IV pyelogram, MRA with gadolinium or angiography for renal artery stenosis- most common cause of 2nd HTN- 10-45% of white pt’s with severe-malignant HTN
o Endocrine: electrolytes, glucose, calcium, UA, 24 hr urine K, VMA, metanephrine
o Neuro: no good screen; use hx and PE
o Metabolic and drug factors: hx and chem screen
o Scleroderma, SLE, polymyositis: hx, PE and other sxs
• What is etio and risk factors for atherosclerosis and CAD?
o Obesity, dyslipidemia, HTN, insulin resistance, prothrombic states, pro-inflammatory states, smoking, hyperhomocysteinemia, elevated CRP
o Increased subendothelial uptake of oxidized LDL: inc pro-inflammatory cytokines in arterial walls (atheroma formation)
o Angiotensin II inc cytokines and pro-thrombic factors
o DM inc advanced glycation end-products, injure endothelial cells and inc cytokines
• What are ssx of atherosclerosis and CAD?
o mb asx for decades
o Sx depend on location of plaque
o Eventually: angina, TIAs, IC
o Then, unstable angina, stroke, limb pain at rest, even sudden death
• What screening is done for dx of atherosclerosis and CAD?
o depends if symptomatic or not
o Hx, risk factor: Lipid profile, Lp(a), lipid fractionation, blood sugar, homocysteine, CRP-hs, fibrinogen, platelets – won’t give you a dx, but important to know risks
o Exercise or Nuclear Stress testing
o Imaging: Fast CT w or w/o angiogram; Carotid artery ultrasound; Cardiac catheterization
• What causes angina pectoris (a sx of CAD)?
o Ischemia: clinical presentation is chest pain
o Leading cause of death in industrialized countries, usu dt atherosclerosis
o Insidious onset; major complications of CAD are angina, MI and sudden death
• How is angina classified? What HPI Q’s do you ask?
o according to Canadian Cardiovascular Classification System
o characteristics of pain/discomfort (PQRST), other sxs, provoking factors
• what are ssx of angina pectoris?
o usu brought on by exertion, relieved by rest.
o may radiate to lower jaw/teeth, neck, left shoulder, subscapular areas, down left arm
o Usu 2-5min, < after meal, w anxiety, in cold or contact w cold air
o inc HR and BP
o St at night and during rest (makes MI more likely to occur).
o Patterns usu consistent in an individual.
o Unstable angina - Changes in a person’s usual
o Heart sounds more distant, diffuse apical pulse
o SOB, belching, nausea, indigestion, diaphoresis, dizzy, lightheaded, clammy, fatigue
o Mb abn heart sounds, S4 gallop
o Women usu diff from men
• What is variant angina?
o Aka Prinzmetal’s angina; dt coronary artery spasm
o ST elevation rather than depression on EKG.
o Occurs at rest, usu same time each day.
• What is microvascular angina?
o usu not seen on angiogram.
o Typical angina sxs, but normal arteriogram.
• What is silent ischemia?
o CAD w/o sxs, usu in diabetics.
o Important to screen your DM patients for CAD!
• What is found on PE for angina?
o Dec peripheral pulses or bruits in femoral or carotid arteries
o Xanthomas (lipid-rich deposition on skin)
o tachycardia, new mitral regurg murmur, elevated BP, S4
o EKG usu normal bw attacks; during episode mb visible Q waves or T wave inversion; mb ST depression; mb smaller R wave, bundle branch disturbance
• What is ddx of angina?
o can be difficult to differentiate from other causes of chest pain.
o Radiculopathy, cervicothoracic spine abnormalities, costochondral separation, costochondritis, nonspecific chest wall pain, pericarditis
o dyspnea, pulmonary disease, GI disease, aortic dissection, mitral valve prolapse
o psychological
• what are the acute coronary syndromes?
o Unstable angina: prolonged rest angina, new onset of at least class III, increasing angina; Transient ECG changes, no change in cardiac enzymes
o Non-ST segment elevation MI (NSTEMI): myocardial necrosis W/O acute ST elevation of Q waves, inc cardiac enzymes
o STEMI: myocardial necrosis with ST elevation on ECG (may show Q waves)
• What causes the acute cornonary syndromes? Common Ssx?
o acute obstruction of artery, consequences depend on degree of obstruction
o Usually dt thrombus in coronary artery
o Ssx are Similar in all 3 conditions except sudden death
• What are ssx of unstable angina and NSTEMI?
o same sxs for both, like angina pectoris, but mb more intense pain and longer duration, less exertion required to bring it on, may progress in intensity.
o Often indistinguishable in ER if enzymes have not yet inc
• What are ssx of STEMI?
o mb prodromal, days to weeks before event.
o Deep substernal pain, 20% MIs “silent”.
o Intolerable intense pain may radiate like angina, with nothing easing the pain (nitro)
o Pt is restless and apprehensive.
o usu dyspnea, diaphoresis, N/V
o Women may interpret pain as indigestion, and will more likely present atypically.
o Skin – mb pale, cool, diaphoretic, possible cyanosis.
• How are the acute coronary syndromes diagnosed?
o ECG and serologic cardiac markers (elevated CK-MB and Troponin I) is diagnostic for NSTEMI and STEMI.
o PE: pt mb cold and clammy
o BP usu hi unless there is shock.
o may see basilar rales, murmurs, S4 gallop, fixed or paradoxically split S2, soft heart sounds, tachycardia, bradycardia, peripheral and central cyanosis, fever, thready pulse, papillary murmur, shock or pulmonary edema.
o Ventricular arrhythmias are common
• What testing is done for the acute coronary syndromes?
o ECG, w/i 10 mins of presentation.
o Cardiac markers (done serially): Troponin I (mb hi in ischemia w/o infarct), CK-MB (less specific), myoglobin (less specific but helpful in triage)
o Others: CBC (hi WBC, left shift), ESR (inc)
• What does ECG show in acute coronary syndromes?
o inverted T wave
o ST elevation (acute)
o Q waves > 1 mm wide or 1/3 QRS height (but not necessary for dx!)
o show in V1-4 with anterior infarct
o in I and AVL with lateral infarct
o in II, III and AVF with inferior infarct
o ST depression with acute posterior infarct
• What is px of acute coronary syndromes?
o 30% unstable angina pts have MI w/in 3 mos.
o STEMI and NSTEMI: mortality ~30%
• What are complications of MI?
o Sinus node disturbances o Atrial or Ventricular arrhythmias o Heart failure o Papillary muscle d/os o Myocardial rupture o Ventricular aneurysm o Hypotension, cardiogenic shock o RV ischemia and infarction o Recurrent ischemia o Mural thrombosis o Post-MI syndrome - pericarditis, pleural effusion, pneumonitis, fever
• What is CHF? Causes?
o Syndrome of ventricular dysfunction, reduced pumping action of heart.
o Causes: structural abnormalities/cardiomyopathies, valve disease, MI, ischemia, CAD, HTN, PDA, VSD, arrhythmias
o LCHF causes RCHF and renal insufficiency, liver dz, aggravating the initial problem
o Volume overload (PV-loop, renal failure) causes HTN and CHF.
• What is LCHF? Causes?
o CO dec, pulmonary venous pressure rises, fluid leaks into interstitial and alveolar spaces, causes edema and difficulty breathing
o Causes: CAD, Ischemia, MI, HTN, aortic stenosis, cardiomyopathy, PDA, VSD, mitral or aortic regurgitation, arrhythmias
• What are ssx of LCHF?
o DOE, tachycardia, fatigue on exertion, intolerance to cold.
o PND/orthopnea, cough
o mb bronchospasm and wheezing (cardiac asthma)
o Right sided pleural effusions common with basilar rales
o Palpable and audible S3 and S4
o Displaced apical impulse
o Possible Central or peripheral cyanosis
o Abn serum proteins
• What are complications of LCHF?
o acute pulmonary edema:
o Pallor, extreme dyspnea, cyanosis, tachypnea, restlessness and anxiety, sweating
o Thready pulse, difficult to obtain BP
