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
• What is ddx of LCHF?
o LCHF (pulmonary edema)
o ARDS
o COPD, IPF, Cancer
o Chronic bronchitis
• What are ssx of RCHF?
o Increasing fatigue, ankle swelling, ascites, mb sense of fullness in neck and abdomen
o JVD
o HM, tender, abdominal discomfort
o Tricuspid murmur, pitting edema of lower extremities
o Peripheral cyanosis
o Systemic HTN with low CO
o Nocturia, cool extremities, postural light-headedness
• What causes RCHF?
o previous LV failure, severe lung d/os (cor pulmonale), multiple PEs, RV infarction, primary pulmonary HTN, TC regurgitation or stenosis, mitral stenosis, pulmonary artery or valve stenosis
• what is ddx of RCHF?
o RCHF (peripheral edema) o Nephrotic syndrome o Idiopathic edema o Myxedema (lower lid and pretibial edema) o Lymphedema o Cirrhosis, liver dz o Peripheral vascular dz o Pericarditis
• What is the New York Heart Association (NYHA) Classification of Heart Failure?
o Class I: no physical activity limitations, no dyspnea, fatigue or palpitations
o Class II: Slight limitation with dyspnea on ordinary physical activity
o Class III: Moderate limitation of activity, sxs w/ less than ordinary activity
o Class IV: severe limitation with dyspnea at rest
• What are the more definitive tests to dx CHF?
o PE and hx
o CXR (Enlarged cardiac silhouette, Kerly-B lines, pleural effusion)
o Echo (LV hypertrophy, reduced wall motion, EF)
o BNP – only blood test used in diagnosis (>100)
• What other tests support, but do not make the dx of CHF?
o ECG: nothing specific to CHF, but may represent underlying cause
o High BUN, mb creatinine, proteinuria
o Liver enzymes mb abn
o Electrolytes useful to see compensation and failure of compensation
o Abn serum proteins
• What is cor pulmonale? Ssx? Dx?
o Enlarged RV 2nd to lung dz
o Ssx: Usu of 1st dz, and signs of right heart enlargement
o Chronic: slight dyspnea at rest, syncope, chest pain, abnormal heart sounds
o Xray may show right heart and proximal pulmonary artery enlargement
o RCHF signs
o Dx: Echo, CXR, BNP. ECG as a supporting test.
• When are cardiomyopathies considered in ddx?
o when valve, hypertensive, and lung dz are ruled out as causes of sxs, and no other explanation for ventricular failure, heart enlargement, or other evidence of heart dz
• what is cardiomyopathy? Causes?
o structural or functional abnormality of myocardium.
o Causes: drug/chem sensitivity, radiation, serum reactions, connective tissue dzs, viruses, bacteria, aging, thyroid dz, anemia, nutritional d/os
• What are the classes of cardiomyopathy?
o Dilated
o Hypertrophic
o Restrictive
• What is dilated cardiomyopathy? Ssx? Dx? Px?
o ventricular dilation and systolic dysfunction
o Sxs: dyspnea, fatigue or peripheral edema
o 25% have atypical chest pain
o Atrial or ventricular tachyarrhythmias
o Dx: Need ECG, CXR and Echo, cardiac markers if acute or has chest pain
o Poor px w/o transplant
• What is hypertrophic cardiomyopathy? Dx?
o Mostly inherited, with abn myocardium
o usu age 20-40, exertional sxs of chest pain, dyspnea, palpitations, syncope (increased risk of death)
o May result in sudden death
o Systolic ejection murmur, increased w Valsalva
o Need ECG and Echo, and CXR (but usu N)
• What is restrictive cardiomyopathy?
o non compliant ventricles resist filling
o Least prevalent form
o Results in PH
o Exertional dyspnea, orthopnea, peripheral edema (in RV dysfunction)
o Atrial and ventricular arrhythmias common, and AV Block
o Angina and syncope uncommon
o Quiet heart sounds, rapid carotid pulse, lung crackles, pronounced neck vein distention
o S4 almost always present, may have S3
o Mb mitral or TC regurg murmur
o Same tools for Dx as others
• What is general cause of arrhythmias and conduction d/os?
o Rhythm disturbances result from abnormalities of electrical impulse FORMATION, impulse CONDUCTION, or BOTH.
• What are arrhythmias? Sxs? Patterns?
o dt inappropriate discharge rates from SA node or from ectopic pacemaker
o sxs: asx, or palpitations, sxs of hemodynamic compromise (dyspnea, chest discomfort, presyncope or syncope), cardiac arrest.
o Rhythms mb regular, regularly irregular (either intermittently irregular as in premature beats, or predictable pattern), or irregularly irregular (no detectible pattern)
• How are arrhythmias diagnosed?
o H&P: Inciting events (sleep, food, body position, stress/anxiety); Palpation of pulse, cardiac auscultation; ABN rhythm
o Tests: 12 lead ECG (preferably during sxs) to see rate/rhythm of atrial and ventricular activation.
o Also serum and intracellular electrolytes, dietary analysis, food sensitivities.
• What is sinus rhythm? 3 types?
o a normal P wave precedes every QRS complex in a 1:1 ratio.
o Sinus bradycardia
o Sinus tachycardia
o Sinus arrhythmias
• What are bradyarrhythmias?
o Rates < 60 bpm. Dec intrinsic pacemaker function or blocks in conduction (usu AV node or His-Purkinje system)
• What are tachyarrhythmias?
o >100 bpm. Usu dt reentry phenomenon, enhanced by shortened tissue refractoriness (dt sympathetic stimulation), lengthened conduction pathway (hypertrophy), slowed impulse conduction (ischemia)
• What is sinus bradycardia? Causes?
o < 60 w normal P wave morphology
o Often benign
o Causes: Inc vagal tone; Myxedema, jaundice, recovery from conditions presenting with tachycardia
• What is sinus tachycardia? Causes?
o > 100 in adult.
o Causes: Dec vagal tone or inc sympathetic tone; Emotion, exercise, anemia, thyrotoxicosis, hemorrhage, infection; CHF, hypoglycemia, prolonged immobilization, drugs
• What is sinus arrhythmia?
o Normal inc HR w inspiration, more pronounced in children.
o Common, usually non-pathological.
• What are the supraventricular arrhythmias?
o Sinus Node Dysfunction (Sick Sinus Syndrome)
o Ectopic Supraventricular Rhythms
o Re-entrant Supraventricular Tachycardias (aka PSVT)
o Atrial Fibrillation
o Atrial flutter
• What is Sinus Node Dysfunction (Sick Sinus Syndrome)?
o SA node dysfunction, refers to several different conditions that produce irregular atrial rates:
o Inappropriate bradycardia
o tachycardia followed by periods of high block
o bradycardia w no P waves
o SA blocks (1st, 2nd, 3rd degree),
o Sinus pauses
• What are ssx of sinus node dysfunction? Cause? Dx?
o Ssx: Slow irregular pulse (most commonly); Cerebral sx of lightheaded, syncope, mb palpitations
o Cause: Idiopathic SA node fibrosis
o Dx: ECG
• What are the extopic supraventricular rhythms?
o begin from ectopic foci usu in atria. o Atrial premature beats o Atrial escape beats o Wandering atrial pacemaker o Multifocal atrial tachycardia o Atrial tachycardia
• What are atrial premature beats (APBs or PACs)? Causes? Sxs? Dx?
o seen in normal hearts or w organic pathology (ischemia)
o Causes: Emotion, fatigue, alcohol, tobacco, coffee, stimulants
o asx or occasionally cause palpitations.
o Dx: ECG: abn premature P waves. QRS complex normal and mb narrow. May or may not conduct to ventricles.
• What are atrial escape beats?
o Occur after long sinus pauses, or arrest.
o Slower HR, abnormal P wave morphology, shorter PR interval
• What is Wandering Atrial Pacemaker?
o multifocal atrial rhythm
o Irregularly irregular, dt random discharge from multiple ectopic foci in atria
o HR < 100 bpm.
o Usu in hypoxic ppl, or lung dz
o ECG: differing P waves from beat to beat (3 or more morphologies)
• What is Multifocal Atrial Tachycardia?
o chaotic atrial tachycardia
o Irregularly irregular rhythm, dt random discharge from multiple ectopic foci in the atria
o HR > 100, Otherwise features same as wandering pacemaker
o Occurs in lung dz
• What is atrial tachycardia?
o Regular rhythm dt consistent rapid, atrial activation from single focus
o HR = 150-200 bpm, but may be slower.
o Rare, least common type of SVT, usu dt structural heart d/o, but also drugs (digoxin), alcohol, toxic gas inhalation
o ECG: P waves of different morphology, mb hidden in previous T wave
• What are Re-entrant Supraventricular Tachycardias (aka PSVT)?
o 50%: AV node (most pts otherwise healthy)
o 40%: bypasses AV node, occurs in accessory pathway (Wolff-Parkinson-White syndrome)
o Young adults: mid-age with sudden episodes of palpitations.
o rapid HR 160-240 bpm.
o ECG: rapid regular tachycardia with variable P waves, usu narrow QRS
o Wolff-Parkinson-White syndrome
o Most common accessory pathway SVT, idiopathic
o Ventricle depolarizes early dt fast accessory pathway
• What is atrial fibrillation? Classification?
o Atria depolarize from variety of foci, resulting in chaotic motion and random re-entry
o Rapid, irregularly irregular
o One of the most common arrhythmias
o Most have pre-existing heart condition
o Great inc risk of thrombus formation
o Classified as 1) Acute (new onset <48 hrs), 2) Paroxysmal, 3) Persistent, 4) Permanent
• What are ssx of atrial fibrillation? Dx?
o Sxs: often asx, palpitations, vague chest discomfort, fatigue, heart failure/shock sxs, stroke sxs
o Dx: ECG: Absent or indiscernible P waves, but not necessarily in all leads, irregular R-R intervals, may have rapid ventricular rate.
o Must also do echo, check thyroid function, consider checking risk for clotting – platelets, bleeding time, fibrinogen.
• What are tx goals for atrial fibrillation?
o Control ventricular rate, convert rhythm to NSR, and prevent thrombus formation.
• What is atrial flutter? Causes? Risk?
o Often dt large re-entrant circuit in RA
o Rapid, regular, less common than AFib. Often also have periods of fib.
o Atrial rate of 250-350 bpm – so only 1/2 the impulses get through (2:1 block)
o Causes: CAD, MI, inflammatory dzs, rheumatic heart dz
o Lower risk of thrombi than Atrial fib
• What are ssx of atrial flutter? Dx? Tx?
o Sxs: depends on Ventricular rate. If low, likely asx. Faster rates have potential sxs similar to A fib
o EKG: identical sawtooth P waves, QRS normal
o Do echo as well, check for underlying inflammatory d/o
o Tx: same goals as AFib
• What are the ventricular arrhythmias?
o Ventricular Premature Beats (VPBs or PVCs)
o Ventricular Tachycardia
o Ventricular fibrillation
• What are Ventricular Premature Beats (VPBs or PVCs)? Sxs? Dx?
o Ectopic beats generated in ventricle and transmitted outside usu conduction system.
o Usu benign
o May have bi-, tri-, or quadrigeminy patterns. Couplet and triplet (V-Tach) patterns.
o Pts often sense skipped, missed beats, “flip flop” sensation
o Sxs with sympathetic stimulation, drugs, caffeine, electrolyte disturbances
o ECG: early QRS widened notched slurred, no preceding P wave, inverted T wave
• What is Ventricular Tachycardia?
o Regular rhythm; broad QRS complexes, rate 120-250
o EKG: Inverted T waves, no P waves (3 PVCs or more in a row)
o Irregular thready pulse, may see jugular waves in neck
o Palpitations and racing heart if long duration.
o Seen most in CAD and MI, with drugs
o Cardiac emergency if prolonged.
• What is Ventricular fibrillation?
o Uncoordinated quivering ventricle with no useful contractions. Dt multiple re-entry pathways
o Rapid rates and disorganized spread. No emptying of ventricles; shock
o Most common rhythm with cardiac arrest
o EKG: erratic voltages without P or QRS waves
o Cardiac emergency
• What are conduction defects? Types?
o = heart blocks= slowed or interrupted depolarization
o 1st deg AV block
o 2nd deg AV block (Mobitz I or Wenkebach phenomenon)
o 2nd deg AV Block (Mobitz II)
o 3rd deg AV Block (complete) with AV dissociation:
o Bundle Branch/Fascicular Blocks
• What is 1st deg AV block?
o delay at the AV node; partial block
o mb dt Inc vagal tone, or organic heart dz
o Asx
o EKG: normal P waves and QRS, long PR interval.
• What is Second degree AV block?
o Aka: Mobitz I or Wenkebach phenomenon
o Progressive delay in PR interval until normal impulse dropped and no ventricular contraction.
o Mb physiologic in younger pts and athletes
o Usu asx
• What is Second Degree AV block?
o Aka: Mobitz II
o Constant PR interval w intermittent dropped QRS complexes (non-conducted beats)
o Intermittent; mb dt organic heart dz
o Asx, or signs of hemodynamic compromise depending on how often missed beat occurs
• What is Third degree AV Block (complete) with AV dissociation?
o Independent irregular impulses generated in SA or AV nodes, or ventricles. No relationship bw atria and ventricles
o Occurs in serious cardiac dz, CAD
o EKG appearance depends on area initiating conducted beats
o Mb Brady- or tachycardia
