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Clin Med Comprehensive > Cardio Diseases > Flashcards

Cardio Diseases Flashcards

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1
Q

clinical presentation of stable angina

A

onset during activity or stress
located substernal or left chest with radiation to L upper extremity
lasts <3 min -15 min
tightness, squeezing, pressure (not pain)
worsened with activity, stress
releived by rest and nitroglycerin

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2
Q

PE findings of stable angina

A 
HTN or hypotension
Apical systolic murmur
Levine's sign
Hyperlipidemia
RF
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3
Q

What diagnostis studies do you order for stable angina?

A

CBC, thyroid fn, hsCRP, ECG, ETT

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4
Q

How do you diagnose CAD?

A 
Gold standard: cardiac catheterization
ETT
Echo stress test
nuclear stress test
coronary CT angiogram
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5
Q

What will ETT show for stable angina?

A

inversion of T waves and typical or atypical chest pain (low intermediate or high on Duke)

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6
Q

What is accelerating angina?

A

change in typical symptoms, greater severity and onset with less physical exertion

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7
Q

Clinical presentation of coronary vasospasm

A

Looks like STEMI
Typical anginal sx
Sx occur AT REST not w/ exercise
Circadian pattern → sx frequently occur in early morning hours
Significant clamping down of vessel and responds readily to nitro

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8
Q

RF of coronary vasospasm

A

RF: smoking, cocaine use, hyperventilation, provacative agents (histamine, serotonin)

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9
Q

What is a specific clinical finding for Atrial septal defect?

A

Wide split S2

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10
Q

Where can you hear murmur for atrial septal defect?

A

Left upper sternal border because volume overload to the pulmonic region

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11
Q

What are the 4 basic mechanisms of heart failure pathophysiology?

A
  1. Increased Blood Volume (Excessive Preload)
  2. Increased Resistance to Blood Flow (Excessive Afterload)
  3. Decreased contractility 4. Decreased Filling
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12
Q

What occurs with increased afterload?

A

CHF, HTN, aortic stenosis

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13
Q

What occurs with decreased afterload?

A

mitral regurgitation, VSD< AV fistula, septic shock

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14
Q

How do you classift heart failure?

A

I - No sx
II – Sx with ordinary activity
III – Sx with slight activity
IV – Sx at rest

A – Risk factors but normal heart and no sx
B – Asymptomatic structural heart disease
C – Symptomatic structural heart disease
D – Decompensated heart failure

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15
Q

Who is considered stage A heart failure?

A 
AT RISK
Hypertension
Known atherosclerotic disease
Diabetes
Metabolic syndrome
Cardiotoxin exposure
Familial history of cardiomyopathy
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16
Q

Who is considered stage B?

A 
Prior MI
Decreased LV EF
Diastolic Dysfunction
LVH
Asymptomatic Valvular Disease
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17
Q

What are symptoms of right sided heart congestion?

A

GI discomfort, edema

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18
Q

What are symptoms of left sided heart congestion?

A

orthopnea, immediate dyspnea, fatigue, trouble concentration

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19
Q

What is elevated JVP a sign of?

A

elevated intravascular volume

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20
Q

How does dehydration present?

A

skin cool and dry

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21
Q

How does volume overload present?

A

skin is wet and warm

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22
Q

How does CHF present?

A 
skin is wet and cool, Fatigue
Altered Activity
Chest congestion
Edema
SOB
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23
Q

What are precipitants of heart failure?

A

calcium channel blockers, beta blockers, NSAIDS, infection, anemia, worsening HTN, dietary indiscretion, arrhythmias

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24
Q

What is the mechanism of action of AVNRT?

A

Reentry

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25
What is the mechanism of shock?
reduced O2 delivery and tissue perfusion, increased O2 consumption or inadequate O2 utilization
26
What are the signs and symptoms of shock?
``` ↓CO ↓SVR tachycardia Dyspnea Restlessness Diaphoresis Metabolic acidosis Hypotension Ogliuria cool, clammy skin ```
27
What is a key feature of distributive shock?
Decrease systemic vascular resistance
28
What makes you highly suspicious of shock?
hypotension, tachycardia, oliguria, AMS, tachypnea, cool, clammy, cyanotic skin, metabolic acidosis, hyperlactatemia
29
What is a PE finding that makes you suspicious of shock in younger patients?
tachycardia
30
What are mechanisms of arrhythmias?
abnormal impulse formation (automaticity or triggered activity) and/or impulse conduction
31
What has late afterdepolarizations?
digitalis toxicity
32
What has early afterdepolarizations
long QT syndrome
33
What happens to HR with conduction block?
bradycardia
34
What happens to HR with reentry?
tachycardia
35
What is a specific finding for atrial septal defect?
fixed split S2
36
Epidemiology of atrial septal defect
MC 10% of all congenital Heart disease
37
Pathophys of atrial septal defect
Septum should close at birth but doesn’t fully and allows blood fo flow from LA to RA
38
Clinical presentation of atrial septal defect
Usually asymptomatic | If larger-fatigue, DOE, wide fixed S2 split, mid systolic, LUSB murmur, recurrent LRTI
39
How to diagnose atrial septal defect
Echo-Doppler study to demonstrate shunt Cardiac cath-to measur O2 saturation (will be higher in RA than expected) Bubble study
40
Epidemiology of ventricular septal defect
MC than ASD but many will heal on own
41
Pathophys of ventricular septal defect
Abnormal opening in interventricular septum Small shunt-small Defect, less left to right shunt Large shunt-large defect, low Pulm resistance
42
Clinical presentation of ventricular septal defect
Asymptomatic if small Heart failure if large defect tachypnes, poor feeding, failure to thrive, frequent LRTI If reversed shunt-dyspnea and cyanosis harsh holosystolic murmur along LSB (smaller defects are louder), systolic thrill, mid diastolic murmur
43
Diagnosis of ventricular septal defect
``` Echo to confirm Cardiac cath (unnecessary but will confirm step up in O2 from RA TO RV) ```
44
Pathophys of pulmonic stenosis
Obstruction of flow across pulmonic valve due to abnormal development of valve or pulmonic artery
45
Clinical presentation of pulmonic stenosis
Usually asymptomatic DOE, exercise intolerance, r sided heart failure sx Prominent JV a wave RV heave and thrill Widely split Sw and sour P2 Crescendo-decrescendo systolic murmur at LSB
46
Diagnosis of pulmonic stenosis
Look at transvalvular gradient (if high need intervention) Echo to confirm and assess pressure gradient Mild <50 mmHg Mod 50-80 Severe >80
47
Pathophys of Patent Ductus Arteriosus
Ductus Fisk’s to close after birth resulting in persistent connection btwn pulmonary artery and aorta
48
Clinical presentation of Patent Ductus Arteriosus
Small asymptomatic larger looks like heart failure Left to right shunt CHF, A fib in L atrial dilatation, continuous machine like murmur best at L subclavian region Eisenmenger syndrome lower extremity cyanosis and clubbing
49
Diagnosis of Patent Ductus Arteriosus
Echo can deter PDA, determine flow
50
Pathophys of Coarctation of Aorta
Place aorta becomes narrowed→LVH
51
Clinical presentation of Coarctation of Aorta
Firm bounding pulse in UE and diminished pulse in LE Femoral pulses are weak or delayed Preductal has differential cyanosis Most cases are asx-postductal
52
Diagnosis of Coarctation of Aorta
Echo: gradient change from high to low across the lesion | CXR-lower rib notching
53
Epidemiology of Tetralogy of Fallot
MC form of cyanotic heart disease after infancy | Toddler
54
Pathophys of Tetralogy of Fallot
Hole in intraventricular septum where AV and PV connect that causes mixing of blood in the aorta Also mimics pulmonic stenosis (outflow tract is messed up)
55
Clinical presentation of Tetralogy of Fallot
RVH & pulm stenosis DOE Mod cyanosis-clubbing of fingers and toes Systolic ej murmur at LUSB Spells: following exertion, feeding, crying→irritability, cyanosis, hyperventilation, syncope, convulsion→ squat relieves
56
Epidemiology of Transposition of the Great Vessels
Rare but MC causes of neonatal cyanosis Will only make it to birth if ductus arterosis in tact
57
Pathophys of Transposition of the Great Vessels
Aorta arises off RV outflow tract and PA arises out of LA | Two closed loops-circulating deoxy blood throughout body and oxy blood through lungs
58
Clinical presentation of Transposition of the Great Vessels
Blue baby | Extremely hypoxic
59
Epidemiology and RF of Coronary Artery Disease
MC males | RF: inc age, diabetes II, smoking, physical inactivity, emotional stress, low intake of fruits and veggies, alcohol
60
Pathophys of Coronary Artery Disease
Development of atherosclerotic plaques over long term stable plaque vs nonstable 75% can no longer compensate
61
Clinical presentation of Coronary Artery Disease
Asymptomatic Angina MI
62
Epidemiology and RF of Stable Angina
At younger ages 45-64 Mc black women >65 all RF: DM, smoking
63
Clinical presentation of Stable Angina
``` Onset during activity substernal or L chest Lasts <3 to 15 min Tightness, squeezing, burning, pressure, gas but not typically pain Worsened with activity, emotional stress and heavy meal Relieved with rest and nitroglycerin Levine’s sign Hyoerlipidemia (xanthelosma) Hypertension or hypotension systolic murmur (mitral regurg) ```
64
Prognosis of Stable Angina
Usually benign CABG improves lifespan PCI does not improve lifespan Severity: number of diseased vessels, location, LV function, arrhythmias, accelerating angina, Duke Treadmill score
65
RF of Coronary Vasospasm or Variant Angina
RF: smoking, cocaine use, hyperventilation, provacative agents (histamine, serotonin)
66
Pathophys of Coronary Vasospasm or Variant Angina
vasospastic disorder that occurs in some patients
67
Clinical presentation of Coronary Vasospasm or Variant Angina
Looks like STEMI Typical anginal sx Sx occur AT REST not w/ exercise Circadian pattern → sx frequently occur in early morning hours Significant clamping down of vessel and responds readily to nitro
68
Diagnosis of Coronary Vasospasm or Variant Angina
Check cardiac biomarkers (troponin, CK, CK-MB) | 12 lead EKG
69
Pathophy of Unstable Angina & NSTEMI
Detachment of stable clot of plaque | partial obstruction by emboli, clot or spasm
70
Clinical presentation of Unstable Angina & NSTEMI
``` Sx of MI at rest Dyspnea, nausea, diaphoresis, syncope Hx of stable angina S3 or S4, transient mitral regurg murmur, arrhythmias 1st clinical presentation of CAD ```
71
Diagnosis of Unstable Angina & NSTEMI
``` ECG-may show T wave inversion or ST depression Labs UA: no cardiac biomarkers NSTEMI: does have release of biomarkers Non-invasive stress test ```
72
Epidemiology of Acute Myocardial Infarction
Males, older, smokers, diabetes, HTN, and obestiy, alcohol
73
Pathophys of Acute Myocardial Infarction
Rise and fall in troponin or CKMB of myocardial necrosis biomarkers due to occlusive thrombosis
74
Clinical presentation of Acute Myocardial Infarction
Look sick, sudden onset chest pain, substernal or L chest with radaiton to L upper extremity, continuous duration, dull pressure, aching pain, nothing makes better but anything makes it worse, severity close to 10 Pale, sweaty, agitated, restless, ↕BP or pulse, JVP, rales, pulm congestion, soft S1, pericardail friction rub (MI several days ago)
75
Diagnosis of Acute Myocardial Infarction
ECG changes: ST elevation (>1 mm limb leads, >2mm precordail leads in 2 or more contiguous leads) or depression, pathologic Q waves Cardiac biomarkers: CKMB, MB index, troponin I CXR: failure or dissection

Clin Med Comprehensive (9 decks)

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