Clin Med Exam 5 Flashcards
Pericarditis causes
Infectious/viral is the most common
Inflammation of pericardium, often occurs in the presence of MI
Acute pericarditis clinical findings
Chest pain- sharp, stabbing
Pain relieved by leaning forward
Intermitten fever, builds over a few days
Dyspnea
Acute pericarditis physicical exam
Possible pericardial effusion
Pericardial friction rub- expiration
Acute pericarditis EKG
Concave up ST elevation, PR segment depression
Constrictive pericarditis
Long term, chronic
Inflammation becomes thickened, fibrotic, adheres to pericardium
Restricts motion of ventricles, reduces diastolic filling
Constrictive pericarditis clinical findings
Dyspnea Fatigue Orthopnea Chronic edema Weakness
Jugular venous distension, ascites, pleural effusion
Constrictive pericarditis clinical findings/diagnosis
Distant or muffled heart sounds
Elevated jugular venous pressure
Pericardial knock
Kussmaul sign (increased systemic venous pressure during inspiration)
Pericardial effusion clinical findings
Pain, dyspnea cough, N/V, fatigue, malaise
Dressler syndrome- fever, chest pain, pericardial friction rub
Pericardial effusion physical exam
Signs of shock or right heart failure (tachycardia, hypotension)
Pericardial friction rub
Low grade fever
EKG findings on pericardial effusion
Electrical alternans- pathognomonic
Cardiac tamponade
Decreased cardiac output from impaired ventricular filling due to the pericardial fluid
For cardiac tamponade, the prognosis depends…
Size and speed of effusion
Cardiac tamponade clinical findings
Becks triad- hypotension, JVD, muffled heart sounds
Pulsus paradoxus
Low voltage QRS
Biggest differentiation between musculoskeletal causes of chest pain and cardiac causes
Palpable tenderness
Most common cause of musculoskeletal chest pain
Costochondritis
Dilated cardiomyopathy clinical findings
Palpitations
Fatigues
Dyspnea
Arrhythmias
Holosystolic murmur, regurgitation
Lower SV
Dilated mardiomyopathy causes
Alcohol abuse is most common!!
Also peripartum cardiomyopathy, infection, genetics
Dilated cardiomyopathy treatment
LVAD
Restrictive cardiomyopathy causes
Amyloidosis, sarcoidosis, radiation of heart tissue, anything fibrosing the tissue
Restrictive cardiomyopathy clinical findings and diagnosis
Less blood filling the ventricle, causing diastolic herat failure
Dyspnea, distant heart sounds, exercise intolerance
Hypertrophic cardiomyopathy clinically
Interventricular septum grows larger, decreased stroke volume
Diastolic herat failure
Crescendo decrescendo murmur
Cause of HOCM
Autosomal dominant inherited
HOCM contraindication
Digoxin
What is the most common cause of death in young athletes?
HOCM
Takotsubo
Acute cardiac syndrome aka broken heart syndrome, presents like ACS
LV apical ballooning
Infective endocarditis general
Infection of heart valves or endothelium
Valvular disease is an important precursor- jet effects disrupt endothelium
Bacteremia prerequisite
Endocarditis microbiology
Staph and strep
HACEK
What is the most common cause of acute endocarditis?
Staph aureus
Bacteremia with strep bovis is strongly associated with…
Colon cancer
Colonoscopy is indicated for these patients
Endocarditis signs/symptoms
Fever
Murmur that is new/changing
Metastatic infection, emboli, immune phenomenon
Skin findings of endocarditis
Petechia/hemorrhage
(Palate, conjunctival, ungal)
Janeway lesions- painless red lesions on palms/soles
Osler nodes- painful, raised lesions on hands and feet
Roth spots
Endocarditis sign- exudative retinal lesions
Duke criteria endocarditis
2 major
1 major and 3 minor
0 major and 5 minor
Abscess and endocarditis
Perivalvular abscess is an important complication of IE
Reduced rate of cure
Prosthetic valve endocarditis
Rare but bad
TEE is diagnostic test of choice
Rheumatic fever
5-15 years age
Systemic immune process that is a sequela to GABHS
ASO titers to confirm
Mitral valve attacked in 75-80% of cases
Jones criteria rheumatic fever
Two major criteria
One major two minor
Major jones criteria for rheumatic fever
Carditis
Erythema marginatum and subq nodules
Sydenham chorea
Polyarthritis
Myocarditis general
Inflammation of heart muscle
Post viral
Hist. Changes of myocarditis
Inflammation and necrosis
Gold standard of myocarditis
Endomyocardial bx
Myocarditis presentation
SOB
DOE
Chest pain
VOLUME OVERLOAD
Aneurysms
EKG and CXR findings for myocarditis
EKG- ventricular ectopy
CXR- pulmonary venous congestion
Severe myocarditis
Left Ventricular assist devices
Impella (short term replacement of pump function)
Then total artificial heart and heart transplant
Frank starling effect
SV rises as end diastolic volume increases
Systolic dysfunction in heart failure
Decreased contractility, flattens frank starling curve
Diastolic dysfunction
Due to stiffened myocardium
Less compliant ventricle, requires more work from the atria to fill the ventricle
Pre/afterload dysfunction
Preload- end diastolic volume/pressure
Failing heart increases preload
Afterload- arterial pressure/systemic vasc resistance
Increased afterload in HF
Broad systolic HF description
HF with reduced left ventricle ejection fraction
Broad classification of diastolic heart failure
Heart failure with present ejection fraction
Abnormal diastolic dysfunction
Why does NE increase in heart failure and what does it say?
Compensating for the decreased pulse pressure and renal perfusion
Poor prognostic sign in HF
RAAS in HF
Increases to increase renal perfusion
ACEIs and ARBs are essential in HF
Increases vasoconstriction and retains fluid and acts like the patient is underperfused, but they are volume OVERLOADED
General heart failure symptoms
Fatigue Dyspnea (most common sx) Exercise intolerance Nocturnal Cachexia
Right heart failure symptoms
Fluid retention- JVD
Dependent edema
HSM, ascites
Fluid backing up into the systemic system
Left heart failure symptoms
Dyspnea- pink frothy sputum/pulmonary edema
Orthopnea
Paroxysmal nocturnal dyspnea
Most common cause of RHF?
LHF
Failing LV, blood backs up into LV then pulmonary system then increases the afterload of RV
Exam findings for HF are…
90% specific but not very sensitive
HF exam findings
Mild
Dyspnea
Variable HR
BP normal to high early on, then low in late HF
Neck exam findings in HF
JVD
Hepatojugular reflux
Pulmonary exam findings HF
Rales/crackles
Pleural effusion
Cardiac exam findings HF
Displaced or prolonged or enlarged PMI
Parasternal lift
S3 (suggests systolic dysfunction)
S4
Murmurs
Abdomen exam HF
HSM
Jaundice (sublingual first)
Extremities exam HF
Cool to touch
Cyanosis
Edema (pitting, dependent)
Untied shoes
High output heart failure
Symptoms of heart failure but increased cardiac output
Eventually will progress to low output HF
Chronic HF
Gradual onset and progressive signs
Generally remains stable
Flash pulmonary edema description
Dramatic presentation of acute, decompensated HF
Increased LV pressure, rapid fluid accumulation in alveoli
Flash pulmonary edema presentation
Severe cough
Dyspnea- pink frothy sputum
Tachypnea
Pulmonary venous HTN CXR findings
Increased pulmonary veins
Cephalization
CXR interstitial edema findings
Interstitial infiltrates
Kerley B lines (short, parallel lines at periphery)
Brain natriuretic peptide
Released in response to ventricular stretch
Helpful in volume overload
Need to know baseline BNP
NYHA classes
1- asymptomatic
2- asymptomatic at rest, symptoms with walking up a couple of blocks or flights of stairs
3- asymptomatic at rest, symptoms with walking up 1 flight of stairs
4- symptomatic at rest
NYHA classes major points
Widely used, class can change and even quickly
Somewhat subjective
ACCF/AHA guidelines
A- at high risk for HF but no structural disease or sx
B- structural heart disease without signs/sx of heart failure
C- structural heart disease with prior or current sx of HF
D- refractory HF requiring specialized interventions
Right to left shunt
Bypasses pulmonary circulation
Cyanosis
Left to right shunt
Increased pulmonary circulation
No cyanosis
Can cause right heart failure from the volume overload
Eisenmenger syndrome
Prolonged left to right shunt causing pulmonary hypertension, then the right ventricle pressure exceeds the left
The shunt reverses, and the left ventricle ejects more deoxygenated blood
Very bad
Ventricular septal defect
Failure of any component of ventricular septum to develop fully
Symptoms depend on size and pulmonary vascular resistance
VSD exam
Loud, pansystolic murmur
Increased flow through the lungs
Left to right shunt
Atrial septal defect (types_
Primum- inferior
Secundum- superior
Sinus venosus defect- around inlet of vena cava, develops into SA node
Left to right shunt
ASD findings
Rarely symptomatic due to low pressure system
Soft systolic ejection murmur, fixed s2 splitting
Patent ductus arteriosus general
Allows blood to flow from the pulmonary artery into the aorta
Left to right shunt with pulmonary hypertension
PDA and NSAIDs
Prostaglandins keep the ductus open during pregnancy- which is why pregnant women cannot take NSAIDs while they are pregnant
Closure can be induced by NSAIDs
Endocardial cushion defect
ASD, VSD, and A-V valve malformations
Left to right shunting
AV valvular insufficiency
CHF, pulmonary hypertension
Needs surgical repair
Pulmonary stenosis
DOE, fatigue, right herat failure if severe
Aortic stenosis
Post stenotic dilation of aorta, LVH as well
Severe stenosis is fatigue, syncope
Systolic ejection murmur
Coarctation of the aorta
Narrowing of aortic lumen, generally near the ductus
PDA reduces symptoms in these patients!
Coarctation of the aorta findings
Baby- poor feeding, resp. Distress, shock
Older- exertional leg discomfort, epistaxis, upper extremity HTN
Systolic ejection murmur
**BP/oximetry screening of multiple extremities
Tetralogy of Fallot
VSD
Pulmonary stenosis
Overriding aorta
RVH
Tetralogy of Fallot findings
Hypoxic “tet” spells
Squat to increase venous return, cyanotic
Transposition of great arteries
Reversal of pulmonary artery and aorta
Desaturated blood returns to right heart and is sent through the aorta to the systemic system
Death occurs rapidly
Transposition of great arteries findings
CXR- egg on a string
Hyperdynamic herat
Quiet tachypnea
Tricuspid atresia
Absent tricuspid valve
Hypoplastic RV
Requires PDA or VSD to perfuse pulmonary artery and ASD needed to allow blood flow to left heart
Tricuspid atresia findings
Surgery is essential, prostaglandins given to maintain ductus until surgery
Truncus arteriosus
Truncus does not separate into aorta and pulmonary arteries
Variable cyanosis
Needs surgical repair
Total anomalous pulmonary venous return
Pulmonary veins drain into right atrium, no oxygenated blood goes to the right heart
Obstruction- severe cyanosis
Surgery essential
Hypoplastic left heart syndrome
Cyanotic disease
Failure of development of mitral or aortic valve/aortic arch
Small left ventricle
Urgent surgery needed
Patent foramen ovale
Foramen ovale does not close, allows for right to left shunting
Increased left heart pressure should close it usually
Often clinically silent
Patent foramen ovale findings
Maybe: Stroke Migraine Hypoxia Risk of atrial fib Decompression illness with air embolism Dyspnea and decreased o2 saturation when upright
Ruling out valvular heart disease- diagnostic approach to a murmur
Careful H&P
EKG to verify rhythm
CXR to rule out pulmonary issues
Echo with doppler flow to visualize blood flow
Best diagnostic for valvular disorders?
Echo
What are the majority of mitral stenosis cases caused by?
Rheumatic fever
More common with multiple infections and multiple bouts of rheumatic fever
Mitral stenosis auscultation findings
Opening snap following s2
Localized diastolic murmur (if disease is farther along)
Best heart at apex
Systemic effects of mitral stenosis
Long asymptomatic phase
Right heart failure and low cardiac output
Sudden increase in HR causing pulmonary HTN/edema
Mechanical prosthetic valves
Last 30-50 years
Can cause endocarditis, paravalvular leaks
**most importantly, thrombosis. Need to be anticoagulated for life
Bioprosthetic valves
Last 5-10 years
Anticoagulation not needed
When do you use a bioprosthetic valve?
Anticoag CI or not desired
Desire to be pregnant
> 70 year old patients
When do you use a mechanical valve?
Patients less than 60 years old that can be anticoagulated
Re operation is dangerous
Mitral regurgitation auscultation
Pansystolic murmur best heard at apex, radiating to the axilla
Mitral regurgitation systemic findings
LV enlargement (reflects severity/chronicity)
Chronic dz can be asymptomatic
Afterload reduction is helpful
What is going on in the heart because of mitral regurgitation?
Increased preload, but decreased afterload
Enlarged left ventricle
Increased ejection fraction
Acute- pulmonary edema
Chronic- LA/V enlargement
What can chronic mitral regurg cause?
Valvular atrial fibrillation
Mitral valve prolapse general
Usually females
Can see arrhythmias
Asymptomatic or SOB, fatigued, palpitations
Auscultation mitral valve prolapse
Mid systolic click
Murmur (could be absent or late/pansystolic, which is severe)
How does valsalve effect mitral valve prolapse?
Increased murmur (if there is one) because of the decreased venous return
What are skeletal/collagen disorders seen with mitral valve prolapse?
Pectus excavatum, scoliosis/straight back
Marfan, ehlers-danlos
Symptoms for tricuspid stenosis
Right heart failure
JVD with a giant “a wave” (aka resistance to R atrial emptying)
Auscultating tricuspid stenosis
Diastolic rumble at LLSB
Tricuspid stenosis EKG/CXR findings
EKG- RA enlargement
CXR- cardiomegaly with normal PA size
What valve is preferred to replace tricuspid stenotic valve?
Bioprosthetic, less risk of thrombosis
Tricuspid regurgitation causes
Valve defects
RV dilation from any cause
Tricuspid regurg signs/symptoms
Asymptomatic
R heart failure
Systolic murmur at LLSB
Obliteration of x descent in jugular pulse wave
Pulmonic stenosis general
Most commonly sen as congenital heart disease, can be valvular, supravalvular or subvalvular
Pulmonic stenosis symptoms
Often asymptomatic
Fatigue, DOE, right heart failure (if severe)
Pulmonic regurgitation causes
High pressure (pulmonary HTN)
Low pressure (valve disorders)
Which ventricle tolerates volume load better than pressure load?
Right ventricle
Signs for pulmonic regurgitation
Split s2, systolic click, right sided gallop, RV lift
Diastolic murmur, graham steel murmur
Aortic sclerosis general
Common in elderly
Atherosclerotic calcification of valve leaflets, **does not effect valve function
Gradual evolution to aortic stenosis
Aortic sclerosis signs
Maybe systolic murmur
Incidental echo finding
Irregular leaflet thickening
Aortic stenosis causes
Uni/bicuspid valve
Degenerative/calcification
Which is the most common surgical valve lesion?
Aortic stenosis
Symptoms of aortic stenosis
Heart failure, angina, syncope (50% 3 year mortality)
LVH
Arrhythmia
Aortic stenosis exam findings
Systolic ejection murmur
Best heart at aortic area, transmitted to neck and apex with patient leaning forward
Maybe preceded by AV click
If severe, s2 split
Gallavardin phenomenon
Aortic stenosis
Musical murmur best heard at apex, maybe vibrations from the stenotic valve.
Handgrip increases arterial resistance and thus decreases the AS murmur
Aortic regurgitation common cause
Aortic root dz (marfan, aortic dissection)
Aortic regurg compensatory mechanisms
Left ventricular dilation increasing the stroke volume
If EF drops, time to replace the aortic valve
Aortic regurgitation symptoms
Usually chronic with no side effects aside from diastolic murmur
LV failure can arise and be sudden
LVH if chronic
Aortic regurgitation exam
High SV with rapid runoff, causing:
Wide pulse pressure
Water-hammer/corrigan pulse
Musset sign
Quincke pulse
Aortic regurgitation murmur
Systolic ejection murmur with increased SV
Diastolic murmur from the regurg
Austin flint murmur- rumbling apical diastolic murmur
When do you treat aortic regurg?
If symptoms, need surgery
What medications help aortic regurg?
Beta blockers to reduce afterload
ACEI to reduce aortic stiffness
What are the 4 major factors that determine myocardial work and therefore oxygen demand?
Heart rate
Systolic blood pressure
Myocardial wall tension/stress
Myocardial contractility
Right coronary artery perfuses mostly…
Lateral and inferior parts of the heart
Left coronary artery perfuses mostly…
The posterior aspect of the heart
Left anterior descending artery perfuses mostly…
The anterior aspect of the heart
Causes of angina:
- Obstruction of coronary arteries
- Structural cardiac abnormalities
- Increased metabolic demands
- Cardiac syndrome X
What is cardiac syndrome x?
Cause of angina
Angina like chest pain with exertion
ST depression on stress test
Normal coronary arteries without vasospasm
What are some hypermetabolic states?
Hyperthyroid Anemia Sepsis/infection Trauma Pregnancy
What is prinzmetal’s angina?
Coronary vasoconstriction occuring as a result of spasm of the large coronary arteries
Spontaneously or from cold, stress, or drugs
Usually women <50, early morning chest pain waking them up, often associated with arrhythmias or conduction defects
What is the time frame for angina versus MI or unstable angina?
<30 minutes is angina
> 30 minutes, consider unstable or MI
Low risk
<10%, watch and follow
Intermediate risk
10-90%, stress test
High risk
> 90%, stress test or heart cath or something!
Silent ischemia
Most common manifestation of CHD
Common in diabetics, elderly, prior MI or revascularization procedures
After stress test, what dictates a worse prognosis?
> 2mm depression at lower workload
Low HR
Hypotension during the test
Positive stress test?
> 1 mm horizontal or downsloping ST segment depression 80 ms after J point
When do you use vasodilators for pharmacologic stress testing? What are the drugs?
Dipyridamole, adenosine
Avoid with bronchospastic dz, HOTN, high degree AV block
Synthetic catecholamine? When do you use it with pharm. stress testing?
Dobutamine
Preferred in stress echo
Avoid in ventricular arrhythmias, recent MI, aortic dissection, LV outflow tract obstruction
Scintigraphy
Myocardial nuclear perfusion imaging
Radionuclide uptake goes to areas of adequate** myocardial blood flow
Good for determining reversible damage or nonreversible infarct
Echo
Higher specificity, lower cost
Assesses cardiac anatomy and function
Wall motion abnormalities with increasing myocardial demand
CTA
Useful for low likelihood of significant CAD, non invasive
EBCT
Quantifies coronary artery calcification
Best for intermediate risk patients
Cardiac MRI
Used more for tissue diseases, like pericardium or neoplasm
Coronary angiography
Gold standard test to diagnose CAD
Used when noninvasive testing is inconclusive or severe CAD
Narrowing of >50%
Hemodynamically and clinically significant
Narrowing of >70%
Ischemia!
Coronary vasospasm diagnostics
IV ergonovine and ST segment elevation on an EKG
USPSTF ASA guidelines
low dose ASA for adults 50-59 with
> 10% 10 year CVD risk
No risk for bleeding
Life expectancy of 10 years
Willing to take for 10 years
Treatment of stable, chronic angina
1st line- beta blockers!
Long acting nitrates
Ranolazine
CCBs (3rd line)
Acute coronary syndromes 3 presentations
- Unstable angina
- ST elevation MI
- NSTEMI
ACS presentation vs. chronic stable angina
Similar symptoms as stable chronic angina, but occur at rest or with minimal exertion
More severe
NTG has little effect
Respiratory distress and edema indicating HF killip classification:
Class 1: absence of rales & S3
Class II: rales don’t clear with coughing less than 1/3 of lung field or presence of S3
Class III: rales do not clear with coughing over >1/3 lung fields
Class IV: cardiogenic shock
NSTEMI diagnostics
Biomarkers of myocardial necrosis positive in addition to at least one of the following:
Ischemic symptoms
Q waves
Ischemic ST segment changes on EKG or imaging or coronary intervention
Cardiac enzymes and biomarkers timing
3 sets, measured at 6-8 hour intervals after the patients presentation
Which biomarkers is quickest to rise and when does it normalize?
CK-MB, normalizes in 24 hours
Which biomarker is latest to peak and how long will it stay elevated?
Troponin I & T, stay elevated for 5-7 days
Acute magement of STEMI
PCI or fibrinolytics
Dual antiplatelet therapy
Anticoagulation therapy
CABG
Patients with stable angina
Rarely performed in STEMI patients, unless failure of previous intervention, shock, or life threatening arrhythmia
After CABG prognosis
Mortality beneficit is most evident in first decade after surgery, then falls off
MI deaths
About half occur before arrival to ED
Neurally mediated syncope
Vasovagal
Situational
Orthostatic hypotension syncope
Hypovolemia
Medication
Underlying disease
Primary cardiac syncope
Structural
Arrhythmia
Decreased CO
What is the most important part in the evaluation of a syncopal patient?
History
Reassuring features of syncope
Prodrome of weakness, lightheadedness, diaphoresis, nausea
Non-reassuring features of syncope
Sudden onset
Prodrome of chest pain and/or palpitations
Physical exam of syncope
Assess for trauma, then look for causes
