Cardio Test #2 Flashcards
NYHA Class I
No activity limitations
Ordinary activity causes no fatigue, palpitations, dyspnea, or angina
NYHA Class II
Slight activity limitations
Asx @ rest
Ordinary activity causes fatigue, palpitations, dyspnea, angina
NYHA Class III
Marked activity limitations
Usually Asx @ rest
Less-than-ordinary activity causes fatigue, palpitations, dyspnea, angina
NYHA Class IV
Inability to carry out any physical activity w/o discomfort
Sx @ rest
Increased discomfort w/ any physical activity
ACC/AHA Stage A
Patient is high-risk for heart failure development in future
Currently no function/structural heart disorder
ACC/AHA Stage B
Structural heart disorder
No sx at this stage
ACC/AHA Stage C
Previous/current sx of heart failure w/ underlying structural heart problem
Sx are managed w/ medical treatment
ACC/AHA Stage D
Advanced disease
Pt requires hospital-based support, heart transplant, or palliative care
Drugs that improve left ventricular relaxation
ACEI
CCB
Drugs that regress LVH
ACEI/ARB
Aldosterone antagonists
BB
CCB
Drugs that manage tachycardia
BB (preferred)
CCB - 2nd line
Digoxin
Systolic heart failure
Heart contraction force decreases/pump function failure
Heart can initially dilate to compensate
Hear S3 w/ this
Get pulmonary and systemic edema
Diastolic heart failure
Heart becomes stiff w/ age
Ventricles unable to relax to fill
Pt is more prone to tachycardia
Hear S4 unless pt is in A-fib
Causes elevated pressures/edema
Pulmonary HTN major sign
Dry cough
Viral myocarditis causative agent
Coxsackievirus most common
Excursion
Ejection fraction
Heart can dilate to compensate for contraction
Electromechanical delay
Delay between ventricular depolarization and repolarization
Systolic dysfunction causes
Impaired contractility
Volume overload
Impaired contractility causes
MI
Transient MI
Chronic volume overload - mitral/aortic regurge
Dilated cardiomyopathy
Volume overload causes
(increase in preload)
Mitral insufficiency
Aortic insufficiency
Atrial/Ventricular septal defect
Diastolic dysfunction causes
Impaired ventricular relaxation
Increased afterload
Impaired ventricular relaxation
LVH
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Transient MI
Increased afterload
(Pressure overload)
Mitral stenosis
Pericardial constriction/tamponade
Aortic stenosis
Uncontrolled HTN
CHF causes
*homeostatic imbalances of cardiac output*
Coronary atherosclerosis
Persistent HTN
Dilated cardiomyopathy
Valvular heart disease
Coronary atherosclerosis
fatty buildup clogs coronaries -> myocardial ischemia
Myocardial ischema causes diastolic and systolic dysfunction
Get angina pectoris +/- MI
Persistent HTN
Increased peripheral pressure cause myocardial hypertrophy and progressive weakening from stress
Get concentric or eccentric hypertrophy
Dilated Cardiomyopathy (DCM)
Ventricles stretch, become flabby w/ myocardial deterioration
Increased workload increases Ca in cardiac cells and causes activation of the heart enlargment gene
Right heart failure “backwards failure”
Systemic capillary congestion
Left heart failure backwards failure
Pulmonary vasculature congestion
Acute decompensation
Immediate goal
Nitro, diuretics, NIPPV
Head bob w/ each systolic pulsation
deMusset’s sign
Severe chronic Aortic regurgitation
“Pistol shot” pulses over femoral artery
Corrigan’s pulses
Severe Chronic Aortic Regurgitation
Pulsation of the uvula
Mueller’s sign
Severe Chronic Aortic Regurgitation
Systolic/diastolic bruit over femoral artery
Duroziez’s sign
Severe Chronic Aortic Regurgitation
Capillary pulsations seen in the nailbeds
Quincke’s pulses
Severe Chronic Aortic Regurgitation
Pulsation of retinal arteries and pupils
Becker’s sign
Severe Chronic Aortic Regurgitation
Popliteal BP > Brachial BP by >60mmHg
Hill’s sign
Severe Chronic Aortic Regurgitation
Systolic murmurs
Aortic stenosis
Mitral insufficiency
Mitral valve prolapse
Tricuspid insufficiency
Diastolic murmurs
Aortic Insufficiency
Mitral Stenosis
CHADS2
CHF
HTN
Age >75
Diabetes
Stroke (TIA)
>=2 = anticoagulation unless CI
Only applies to pts w/o valve dx -> those get anticoags regardless
Class I agents and MOA
Block sodium channels
Quinidine
Procainamide
Disopyramide
Lidocaine
Mexilitine
Flecainide
Propafenone
Class II agents and MOA
Beta blockers
Decrease automaticity
Prolong AV conduction
Prolong refractory period
Class III agents and MOA
Block potassium channels
Amiodarone
Dronedarone
Sotalol
Dofetilide
Ibutilide
Class IV agents and MOA
CCB
Decrease automaticity and AV conduction
How does digoxin work?
Where is it used the most?
Inhibits the sodium/potassium ATPase pump
This prolongs AV conduction and refractory period
Used to help rate control pts w/ A-fib/flutter
When is adenosine indicated and what is the dose?
How does it work?
Used for rapid treatment of symptomatic atrial tachycardias
6 mg, then 6 mg, then 12 mg
Works by blocking the AV Node
PEA causes 6 H’s
Hypoxia
Hypovolemia
Hypoglycemia
Hydrogen Ion (acidosis)
Hypothermia
Hypo/hyperkalemia
PEA causes 6 T’s
Toxins
Tamponade
Trauma
Tension pneumothorax
Thrombosis - cardiac
Thrombosis - pulmonary
HACEK
Haemophilus sp
Actinobacillus
Cardiobacterium
Eikenella
Kingella
Osler’s Nodes
More specific for infectous endocarditis
Painful and erythematous nodules
On pulp of fingers and toes
More common w/ subactue IE
Janeway Lesions
More specific for Infectious endocarditis
Erythematous, blanching macules
Not painful
Located on palms and soles
Roth spots
More specific for infectious endocarditis
Pale retinal lesions surrounded by hemorrhage
“target spots” usually near optic disk
Major Duke’s Criteria
Positive blood cultures w/ appropriate organism
Echo finding
New valvular regurgitation
Minor Duke’s Criteria
High risk, hx IVDA
Fever
Vascular phenomena
Immunologic phenomena
Serologic studies
Blood cultures/echo not meeting major criteria
Vascular phenomena
Arterial embolism
Septic pulmonary infarct
Mycotic aneurysm
Intracranial hemorrhage
Janeway lesions
Immunologic phenomena
Osler’s nodes
Roth spots
Glomerular nephritis
Rheumatoid factor
Modified Duke’s - Definite IE
Microorganisms (culture or histology) in valvular/embolized vegitation or intracardiac abcess
Histologic evidence of vegetation/intracardiac abscess
Modified Duke’s Possible IE
2 major
1 major + 3 minor
5 minor
Modified Duke’s - Rejected IE
Resolution of illness <5 days of Abx
Empiric Therapy for infective endocarditis
NVE acute - Vanco (staph) Or Nafcillin + gentamycin (no staph)
NVE Subacute - PCN + gentamycin
PVE - Vanco + gentamycin + Rifampin
Fungal - Amphotericin B w/ valve replacement
IE prevention w/ proceduce
Dental procedures
Tonsillectomy
Surgery of GI, Respiratory, Urinary, Gallbladder, I and D
Esophageal dilation
Cystoscopy/urethral dilation/urethral catheter w/ infection
High risk IE lesions
Prosthetic valve
Prior IE
Cyanotic congenital heart dx
Surgical systemic-pulmonary shunt
PDA, VSD, coarctation
AR/AS/MR/MS w/ MR
Antimicrobial prophylaxis
Recommended in high-risk pts
Prosthetic valves
Previous IE
RHD/aquired valve dysfunction
Hypertrophic cardiomyopathy
MVP (esp w/ murmur)
Crawford Classification of TAA
I: L subclavian to renal arteries
II: L subclavian to iliac bifurcation
III: Midthoracic to infrarenal
IV: Distal thoracic to infrarenal
6 P’s of acute limb ischemia
Pain
Pallor
Pulselessness
Paresthesia
Paraparesis (paralysis)
Poikilothermia (cold limb)
Virchow’s triad
Venous stasis
Vessel wall injury
Hypercoagulable state
Systolic dysfunction
Pump function failure
Usually from myocardial dysfunction/destruction (MI)
Hear S3
Diastolic dysfunction
Ventricles are stiffened and cannot relax
Inadequate filling causes elevated pressures
Pt is prone to bouts of tachycardia (a-fib)
Hear S4, but never w/ a-fib
Acute decompensation
Immediate goal: reestablish perfusion/oxygenation
Tx: Nitro, diuretics, NIPPV
Carcinoid syndrome
Carcinoid tumor in small bowel/appendix
1st mets -> liver, serotonin released straight to the heart
2nd mets -> lungs, cause left-side abnormalities
Commonly causes tricuspid regurge/stenosis
Annular dilation
Most common R heart dx in adults
Tricuspid regurge w/ anterior and posterior sides dilating while septal side remains the same -> uneven dilation
Causes tricuspid regurge
Aortic dissection
Tertiary syphilis
Carcinoid syndrome
Annular dilation
Rheumatic disease
Endocarditis
Ebstein anomaly
Cause tricuspid stenosis
Carcinoid syndrome
Rheumatic disease
Ebstein’s anomaly
Congenital defect
Posterior tricuspid leaflet deformed -> causes TR
Usually concomitant w/ ASD/WPW
High V wave w/ JVD
High-pitched systolic murmur - blowing/coarse/muscial
Tricuspid regurge
Usually functional cause - HTN, Chordae malfunction
High A wave w/ JVD
Low-pitched, rumbling, presystolic murmur w/ loud S1
Tricuspid stenosis
Hyperdynamic PMI
Visible carotid/nailbed (Quincke) pulsations
deMusset’s sign
Diastolic, blowing, faint murmur right after S2
Aortic regurgitation
Sustained PMI w/ palpable heaves
Murmur between S1 and S2, harsh rough murmur
Prominent S4
Aortic Stenosis
Pansystolic, blowing, high-pitched musical murmur
Possible mid-systolic clicks
Prominent S3 if severe
Mitral Regurgitation
Diastolic low-pitched, rumbling murmur
Merges w/ loud S1
Palpable S2 @ 2nd intercostals
Mitral stenosis
Tricuspid valve disorder treatment
Fluid restriction
Diuretics
Rhythm disturbances
Treat symptoms
Pulmonary regurgitation
Treatment is difficult
Congenital -> abnormal cusp number development/complete lack of valve
Acquired -> Pulmonary HTN, Annular dilation w/ structural distortion
Pulmonary Stenosis
Congenital - most common
Acquired -> Rheumatic heart dx, Carcinoid syndrome, IE (fungus grows rapidly, occludes opening)
Mitral Chordae tertiary stands/head
10
Each papillary muscle has 6 heads
Gerbode defect
VSD around AV node
Shunt created between LV into RA
No pressure abnormalities
Mitral stenosis
Usually caused by Rheumatic fever, also congenital, carcinoid, amyloid
Progressive, lifelong dx - 20-40 yr onset, 10 yr to disabled
Left side failure, A-fib common
Orthopnea, PND
Mitral stenosis grading and treatment
MVA = 1.5-2.5 cm2 w/ minimal sx = Mild
MVA = 1.0-1.5 cm2 w/o sx @ rest = Moderate
MVA < 1.0 cm2 = Severe
Tx: Diuretics, BB/CCB (a-fib), Anticoags (a-fib)
Balloon valvuloplasty, surgical repair/replacement
Mitral Regurgitation
Abnormality to any component of mitral valve
Dyspnea, orthopnea, PND, fatigue
Can cause A-fib
Mitral valve prolapse
Congenital, Marfans, Ischemic sequela
Hear a click w/ a late systolic murmur
Hemodynamicly unstable if also have MR
Chronic Mitral Regurgitation
Monitor if asx
Aggressively treat HTN (ACEI) and A-fib (BB, anticoag)
Preload reduction: diuretics
Afterload reduction: vasodilate
Acute mitral regurgitation
Abrupt decline in stroke volume w/ increase in LA volume/pressure => drastic increase in pulmonary pressure
Pt goes into cardiogenic shock, rapidly fatal
Acute severe dyspnea, CHF, HOTN w/ loud S1
Tx: O2, Positive inotrope, DO NOT OVERLOAD W/ FLUID
Aortic stenosis
Disruption of LV outflow, increases pressure w/ hypertrophy and diastolic impairment
Heart cannot increase stroke volume on demand
Cardinal symptoms, sudden death w/ arrhythmias, bruit heard in carotids
Tx: All symptomatic until valve replacement
Cardinal symptoms of severe aortic stenosis
Dyspnea
Angina (increase O2 demand)
Syncope (vasodilation w/ fixed C.O.)
Aortic regurgitation
Leaflet dysfunction/aortic root dilation (Marfans)
LV has both pressure and volume load increase, can be chronic or acute
Decompensation when LV systolic fails and dilation occurs
Wide pulse pressure, bounding pulse, early diastolic murmur
Tx: Vasodilate, diuretics, digoxin
DO NOT SLOW HR
Austin Flint murmur
Mitral valve
Mid-late diastole
Valve pushed closed by aortic jet (AR)
Infective endocarditis
Acute: usually staph on tricuspid, rapidly destructive
Subacute: usually Strep, on damaged valve, indolent nature
IV drug use: Staph, fungus, pseudomonas
Venturi effect
Creation of low pressure sink w/ a jet from valve regurgitation
Bacteria tend to settle on opposite side of valve in sink
Pediatric IE
Almost all cases occur w/ underlying valve defect
Neonate: Staph aureus, coagulase-negative staph, group B strep
Older: usually staph or Strep
Infectious endocarditis signs
Acute: Toxic, high-grade fever and chills, SOB, arthralgias, Abdominal pain, pleuritic chest pain
Subacute: low-grade fever, anorexia, weight loss, fatigue, abdominal pain, nausea/vomiting
Fever, heart murmur (not w/ IVDA), splenomegaly, petechia, splinter hemorrhages, clubbing, neuro changes
IE diagnostic tests
TTE = 1st line for suspected IE w/ native valves
TEE = 1st line for prosthetic, intracardiac complications, inadequate TTE, fungal/staph/bacteremia
IE treatment
Parenteral Abx - high concentrations and prolonged therapy
Empirical therapy (covers staph) = Vancomycin
Viridans = PCN
Fungal = Ampho B + replacement/repair
Should see fever reduced w/in 7-10 days - think wrong bug or mets if not
Acute pericarditis
Sudden inflammation
Usually viral, sometimes metastatic, meds, radiation, Dressler’s syndrome
Pleuritic chest pain w/ fever, Troponin elevated longer
Widespread STEMI w/ PR depression
Tx: ASA, NSAID, Colchicine
Dressler Syndrome
2-3 weeks post-MI
Develop necrosis which inflames the pericardium
Chronic/Recurrent Pericarditis
6 weeks - 18 months after acute
Usually AI
Tx: NSAIDS, colchicine, steroids, activity restriction until echo clean
Pericardiectomy as last resort
Beck’s Triad
Sign of cardiac tamponade
Hypotension
JVD
Muffled heart sounds
Kussmaul sign
JVD doesn’t resolve with inhalation
Pericardiocentesis
Supine pt w/ HOB @ 30-60 degrees
1: 5th-6th intercostal space @ LSB @ left lung cardiac notch = Parasternal approach
2: Infrasternal angle = Subxiphoid approach
Moenckeberg medial calcific sclerosis
Calcium deposits in tunica media
Genetic predisposition
Poor prognosis
Form of Arteriosclerosis
Rheumatic fever
Group A strep - Strep pyogenes/pharyngitis
Antibody cross-reactivity
Strawberry tongue, petechia, beefy red tonsils w/ exudates
Tx: ASA/NSAIDs (kids), PCN/Clarithromycin
Also treat heart failure - ACEI, diuretics, BB, steroids
Rheumatic fever major criteria
Migratory arthritis
Carditis/valvulitis - CHF w/ SOB, pericarditis w/ rub, new onset murmur
CNS involvement
Erythema Marginatum
Syndenham’s Chorea
Sydenham’s Chorea
Rapid arm and face movements without purpose
Late stage Rheumatic fever
Rheumatic fever minor criteria
Fever 100.8-102
Joint pain w/o swelling
Elevated ESR/CRP
Leukocytosis
EKG: Heart block w/ prolonged PR
Previous hx rheumatic fever
Buerger’s Disease
Thromboangitis Obliterans - finger gangrene
Medium vessel
Young, male smokers - recurring progressive inflammation
Tx: Smoking cessation, CCB for vasospasms
Type 1 PAD
Least common
Younger/smokers/hyperlipidemia
Aorta and common iliacs
Type 2 PAD
Aorta, common and external iliacs
Type 3 PAD
Most common
Multi-level disease
Aorta, iliac, femoral, popliteal, tibial
PAD diagnosis and treatment
ABI - <0.8 = claudication, < 0.4 = severe
-not accurate w/ diabetics - no vessel elasticity left
Tx: ASA, Cilostazol (stop platelet aggregation), lifestyle, surgery
Dilated Cardiomyopathy and treatment
IDC, pregnancy, CHF, alcoholism
Tx: Diuretics, ACEI, nitrates, positive inotropes
Allow 6 months to heal on its own - then transplant
Limit salt intake, digoxin will make them feel better
Hypertrophic cardiomyopathy and treatment
Thick septum, aortic valve obstruction
Harsh, blowing murmur, resolves w/ Valsalva maneuver
Sudden death may occur
Tx: BB, vasodilators, diuretics, inotropes
Restrictive cardiomyopathy
Looks like constrictive pericarditis
Right-side problems, dyspnea, edema, ascites, hepatomegaly, JVD, S3, S4
Tx: perfect volume balance - use diuretics, vasodilators, CCB
Constrictive pericarditis history
History of trauma, TB, pericarditis, collagen-vascular disorders
