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PA-S1 Cardiology > Cardiology Clinical Studies > Flashcards

Cardiology Clinical Studies Flashcards

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1
Q

Describe stable angina

A

ANGINA THAT IS WORSE WITH EXERTION
heart has increased O2 demand
- after load increases = HTN
- HR increases

Dyspnea with exertion
chest tightness
Sweating
pallor
nausea

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2
Q

Describe unstable angina

A

TOTAL OCCLUSION, OCCURS AT REST
chest pain/tightness
dyspnea

subendocardial ischemia - ST depressions

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3
Q

What do EKGs and Troponins show to diagnose unstable angina vs MI

A

EKG
- ST wave depression - unstable angina, NSTMI
- ST wave elevation - STEMI

Troponin
- no increase in unstable angina
- increase in semi
- marked increase in STEMI

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4
Q

Describe Stage B HF

A

Pre-HF
without current/prior symptoms and one of the following:
- structural heart disease
- abnormal cardiac function
- elevated BNP/troponin levels

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5
Q

Describe Stage C HF

A

diagnosed CF
pt with current/prior symptoms
signs of heart failure caused by structural/functional/cardiac abnormalityD

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6
Q

Describe Stage D HF

A

advanced heart failure
Severe signs of HF at rest
recurrent hospitalizations
refractor/intolerant to GDMT
requires advanced therapy
transplantation/mechanical circulatory support

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7
Q

Describe HFpEF and HFrEF

A

HF with preserved ejection fraction
- heart failure with LVEF ?50%
- typically an issue with ventricular contractility

HF with reduced ejection fraction
- heart failure with LVEF <40%
- often an issue with ventricular COMPLIANCE

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8
Q

What are the congestive symptoms of heart failure?

A

Pulmonary congestion
- cardiomegaly
- SOB + tachycardia
- Dyspnea: exertion, paroxysmal (SOB wakes up), orthopnea (SOB when lying), at rest

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9
Q

What are the low perfusion symptoms of heart failure?

A

renal dysfunction - decreased output, volume overload, increased BUN/CR
GI - N/V, constipation
Neurologic : lightheaded, fainting, fatigue, confusion, weakness
cold extremities

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10
Q

What is BNP? Why is it not always the most reliable test for heart failure?

A

brain natriuretic peptide - hormone secreted by cardiac myocytes in response to stress

levels naturally higher in people who are:
women, older, renal dysfunction, have a fib, obese

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11
Q

What are the things you would see on exam with someone who is experience heart failure?

A

jugular venous distention
pitting edema
hepatomegaly
are they able to exercise?
how many pillows to you sleep with?

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12
Q

Describe the outcomes of pts that present as warm/cold and dry/wet (combine them)

A

warm + dry - good = can be monitored out pt
warm + wet = not good, on floor
cold + dry = bad, in ICU
cold + wet = very bad, ICU

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13
Q

What are some devices that can be used in pts with heart failure?

A

cardiac resynchronization therapy - pacemaker for both ventricles
implantable cardiac defibrillator - primary prevention of arrhythmias
cardiomems - implant device in pulmonary artery to monitor pressure

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14
Q

If someone is experiencing decompensated heart failure in the hospital, what would you treat the,?

A

Respiratory insufficiency due to volume overload
- nasal cannula, biPIP, intubate

circulation - not enough perfusion, too much pressure on heart
- preload reduction: diuretics
- after load reduction

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15
Q

What is refractive heart failure?

A

GDMT medical therapy is not working on the pt, must be more invasive (devises, pacemakers, transplant)

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16
Q

Describe cardiogenic shock. How do you treat this pt?

A

low output state that can result in end-organ failure and tissue hypoxia
inotropes - milrinone, dobutamine: increases CONTRACTILITY and CHRONOTROPY (HR)

mechanical circulatory support
- aortic balloon pump
- left ventricular assist device

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17
Q

What are the symptoms of sinus node dysfunction?

A

bradycardia
light headed, fatigue, pre/syncope
symptomatic chronotropic incompetence - HR does not increase when exercising

primary indication for implanted pacemaker

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18
Q

How would you treat someone with atrial flutter?

A

Meds: metoprolol + apixaban
- Ca channel blocker

pacemaker implantation, AV nodal ablation
Atrial flutter ablation - scars tissue so signal cannot go through

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19
Q

What are the treatments for atrial fibrillation?

A

want to protect from thromboembolism
- Vitamin K antagonists - coudamin, warfarin
- DOACs - pradaxa, eliquis, xarelto
- IV/SQ: heparins

radiofrequency ablation

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20
Q

How would you treat someone with second degree AV block - Mobitz I? What about II? What about 3rd degree AV block?

A

Mobitz I: Give pace maker if symptomatic
Mobitz II: give pacemaker to prevent development into heart block

3rd degree AV: pacemaker

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21
Q

How do you treat someone with a ventricular tachycardia?

A

radio frequency ablation
+ magnesium if pt has Torsades

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22
Q

What is sinus sick syndrome?

A

group of disorders where hears it unable to perform pacemaker function
- disease of the SA node
- Rate varies: goes fast, slow and back and froth

symptoms: lightheaded, figure, pre/syncope

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23
Q

describe tachycardia-bradycardia syndrome

A

type of sinus sick syndrome
- complication of SSS characterized by alternating tachycardia and bradycardia
- can present with palpitations

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24
Q

Describe hypertrophic cardiomyopathy. What are the criteria for diagnosis?

A

thickened L ventricular wall without secondary causes
non-dilated L ventricle
histology - myocyte disarray, hypertrophy with fibrosis

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25
What are the genetic tests for hypertrophic cardiomyopathy?
autosomal dominant sarcomere mutations - primary HCM non-sarcomere mutations - systemic disease caused HCM
26
Describe hypertrophic myopathy outflow obstruction
occurs during exercise systolic anterior motion (SAM) or mitral valve leaflet prevents blood from leaving the aorta
27
How would you treat obstructive hypertrophic cardiomyopathy?
avoid meds that lower preload (ACE/ARB/ARNI/nitrates/diuretics) metroprolol or verapamil intervention: surgical septal myetcomy alcohol septal ablation mavacamten
28
describe dilated cardiomyopathy. What are the causes?
enlargement of all cardiac chambers - soft and floppy - can lead to HFrEF causes Ichemic - MI, CAD nonischemic: idiopathic, viral infections - coxsackie B adeno/parovirus, lyme toxic - alcohol, cocaine, chemo peripartum stress
29
What is the treatment for dilated cardiomyopathy?
same as HFrEF - GDMT
30
Describe restrictive cardiomyopathy
rigid ventricular walls with severe diastolic function - significant biatrial enlargement can be: infiltrative, non-infiltrative, storage disease, idiopathic
31
what are the causes of restrictive cardiomyopathy?
cardiac sarcoidosis - middle aged black women - granulomas surrounded by fibrosis hemochromatosis - middle aged, unregulated iron supplementation cardiac amyloidosis - >60, hx carpal tunnel, spinal stenosis, HFpEF w/o HTN - INTOLERANT TO HF THERAPIES - TT tetramers break down and get deposit into heart
32
What are the treatments for restrictive cardiomyopathy caused by hemochromatosis and cardiac amyloidosis?
hemochromatosis - chelation of phlebotomy to decrease iron cardiac amyloidosis - manage HF symptoms - congestion with diuretics - antiarrhythmics - ACE/ARBs/ARNI contraindicated
33
How do you manage an NSTEMI?
acute - in hospital - anti ischemic: nitrate, B blockers, O2 - antithrombotics - dual anti platelet with aspirin and "grel" ≥3 months - consider short course anticoagulation/coronary revascularization long term - risk modification meds - beta blockers, statins, ACE/ARBs, DAPT
34
What do you do if someone is having a STEMI?
EMS can send them straight to cath lab for repercussion if PCI not available - give them Aspirin, supplemental O2, nitroglycerine, morphine
35
what lipid test is the best predictor for CHD?
TC:HDL-C ratio other random labs - Lipoprotein A - 30+ = High - ApoB 130+ = high
36
What labs would you see ins someone who has hypertriglyceridemia, hypercholerterimia, and mixed hyperlipidemia?
hypertriglycemia - TG ≥500 mg hypercholesterolemia - LDL-C >190 (w no risk factors) mixed hyperlipidemia - TGs ≥150 - LDL-C ≥ 130 or non-HDL-C ≥150
37
Describe aortic stenosis. What are the causes and clinical presentation?
aortic valve cannot open properly = pressure overload - L sided hypertrophy = more O2 consumption - increased after load causes - age related calcification - rheumatic fever - congenital abnormalities clinical presentation - SAD backwards order - dyspnea then angina then syncope - systolic ejection murmur: crescnedo-descresendo
38
What is the management of aortic stenosis?
TAVR - transcatheter aortic valve repair - better for older, sicker pt SAVR - surgical aortic valve repair - better for low risk surgery - lasts longer intraoritic balloon pump - femoral artery to aorta = inflates with breaths - only in cardiac ICU
39
CXR reveals cardiomegaly, calcified valve, prominent ascending aorta and BNP. There is LVH on echo and reduced aortic orifice. What is the dx?
Aortic stenosis
39
What is the pathophysiology of chronic and acute aortic insufficiency?
chronic - back flow causes L ventricle to dilate - can lead to HF - increased cardiac pressure on LV and acute HF (shock, pulmonary edema) acute SOB, orthopena (SOB lying), paroxysmal nocturnal dyspnea (SOB wakes up)
40
What is aortic insufficiency? What are the causes?
regurgitation - goes back into L ventricle causes: - valve leaflet destruction due to endocarditis, rheumatic valvular disease, bicuspid valve - aortic root dilation - Marfan's, aortic dissection
41
Echo reveals regurgitant jet, valve vegetations, and an enlarged aortic root. What is this dx?
aortic insufficiency
42
Describe tricuspid stenosis. What causes it? How is it managed?
stenotic tricuspid valve - -back up into R atria - can lead to R sided HF usually only seen in rheumatic heart disease, lupus, cardiac tumor Dx - echo management - decrease R atrial V = salt restriction + diuretics - balloon valvotomy - minimally invasive, improves symptoms - surgical - only pursued if there is another valvular repair necessary
43
What is the management of aortic insufficiency?
regurgitation meds that reduce after load - ACEi/ARBs/entresto, nifedipine, hydralazine surgical - valve repair not recommended - surgical valve replacement for acute/symptomatic aortic insufficiency
44
Describe tricuspid insufficiency. What are common causes? What does the clinical presentation look like?
tricuspid valve does not close properly infective endocartditis, pulmonary HTN (backup from lungs) no symptoms until severe can lead to R sided HF (JVD, edema, hepatosplenomegaly) holosystolic blowing through S1-S2
45
What are the treatments for tricuspid insufficiency?
medical treatment and surveillance echos HF = GDMT and diurtetics surgery - rare - tricuspid valve repair > replacement - RV infarct - ischemic revascularization with stent or CABG
46
Describe mitral stenosis. What is the pathophysiology and the clinical manifestations?
narrowing of the mitral valve - common cause: rheumatic heart disease pathophysiology: - inflammation and scarring - leaflet thickening - fusion of chordae - elevation of L atrial pressure: can lead to pulmonary congestion (RHF) and LA enlargement (A fib) Clinical manifestations: dyspnea, hemoptysis, RSHF, thromboembolism, loud opening snap mid diastolic
47
How is mitral stenosis managed?
rheumatic fever pts get Pen G prophylaxis until 25 meds for symptoms: diuretics, rate control, anticoagulation if in a fib procedures - rheumatic mitral stenosis: percutaneous ballon valvuloplasty - mitral valve replacement - rheumatic and calcification mitral stenosis
48
Describe mitral valve regurgitation. What are some structural and functional causes?
mitral valve does not close properly, blood back flows into L atrium structural causes: - mitral valve prolapse: degeneration of leaflets/cords - rheumatic heart disease functional - altered LV geometry - ischemic heart disease affecting papillary muscle - LV dilation caused by LHF
49
How is mitral valve regurgitation medically managed?
medical: congestion - diuretics vasodilators for symptomatic pts to decrease after load surgical - mitral valve repair/replacement - percutaneous mitral clip
50
Describe rheumatic fever. What is the criteria for diagnosis> What are some complications?
Group A strep infection of the throat - molecular mimicry JONES criteria: Joints, heart (carditis) Nodules, erythema marginatum, Syndeham chorea (flinching) Tx with prophylactic pen G until 25 can lead to permanent heart failure - typically mitral valve disease no permanent damage to joints
51
Describe endocarditis. What is the common clinical presentation? What are some causes?
Fever + new murmur = infective endocarditis - joint pain, roth spots on retina - osler nodes - petechiae, spinner hemorrhages (nails), jane way lesions bacterial causes - S aureus, Streptococci, H influenzae, viridans (subacute) causes vegetations on the valves - damage pyemia - can abscess in the lungs and brain
52
Describe the etiology and pathophysiology of pericarditis
pathophysiology - inflammation of layer covering heart = friction - causes pain - can develop effusion - can lead to shock etiology - infections - HIV, TB, fungal - post infarction/trauma - collagen vascular disease - lupus - radiation - metabolic - neoplastic - breast, lung, melanoma, lymphoma
53
How is pericarditis diagnosed? What would you see on exam, EKG, and echo?
Hx - recent viral infection, acute onset of pleuritic chest pain exam - friction rub - effusion: tachycardia/hypotension, JVD, muffled heart sound EKG - ST elevation with/out PR depression ECHO - rule out MI and evaluate for effusion
54
Describe the etiology and pathophysiology of myocarditis
pathophysiology - inflammation of the myocardium leads to heart muscle damage - inflammatory cardiomyopathy - weakened ability to pump blood etiology - idiopathic in >50% - viral - Coxsackie, echovirus, adenovirus, provirus, EBV, covid - bacterial - autoimmune - drug related - hypersensitivity run - neoplastic
55
How is myocarditis diagnosed? What would you see on exam, labs, CXR, EKG, Echo?
exam - congestive signs: JVD, crackles, peripheral edema - low flow signs: tachy/hypotension, cool/clammy extremities, decreased urine, weak/thready pulses labs - troponin - proportional to damage to muscle CXR - cardiomegaly, pulmonary vascular congestion EKG - T inversion, ST elevation Echo - enlarged heart with decreased systolic fx - mild inflammation can be missed - use MRI
56
Describe the location of each in fetal circulation: foramen ovale ductus venosus ductus arteriosus
foramen ovale - between atria - R to L shunt - bypasses the lungs ductus venosus - inferior VC and hepatic - shunts blood to heart instead of liver ductus arteriosus - aorta to pulmonary artery - R to L shunt - bypasses lungs and goes to systemic circulation
57
Describe the flow of blood in fetal circulation
oxygenated blood from placenta goes thru umbilical vein to liver - goes thru ductus venosus to the IVC - R atria oxygenated blood in R atria mixes with the L via the foramen ovale - can go to the aorta via L ventricle OR ductus arteriosus to the fetal tissue fetal tissue sends blood back via the IVC or goes through umbilical arteries to the placenta
58
Describe atrial septal defects. What is the physiology, clinical presentation, and management?
NON CYANOTIC Physiology - hole btw atria increases blood flow to lungs - shunts LA to RA - enlarges heart, can damage blood vessels in lungs clinical presentation - SOB, exercise intolerant - systolic ejection murmur, wide fixed S2 split management - observation for spontaneous closure - elective closure 3+ - surgical: patch, primary closer - transcatheter - if secundum has sufficient rims
59
Describe venticular septal defects. What is the physiology, clinical presentation, and management?
NON CYANOTIC physiology - shunting from LV to RV - if large, chambers can dilate and lead to pulmonary vascular disease due to high systemic pressure presentation - seen in 4-6 weeks - poor feeding, tachypnea, diaphoresis (sweating) - tachycardia, active precordium - murmur - holosystolic + diastolic rumble + gallop management - observe for spontaneous closure - medical management - anti-congestive - surgical - patch closure - trans-catheter - muscular defects
60
Describe patent ductus arteriosus. What is the physiology, clinical presentation and management?
NON CYANOTIC physiology - ductus arteriosus (btw aorta and pulmonary artery) remains open - doesn't close properly after 1 day - blood gets shunted L to R - oxygenated blood goes back to lungs clinical presentation - continuous murmur - signs of CHF management medical: anticongestives - indomethacin - blocks prostaglandin to help close patent surgical - PDA ligation transcather - coil/device closure
61
Describe transpiration of the great arteries. What is the physiology, clinical presentation and management?
CYANOTIC aorta and pulmonary artery are switched - asymptomatic as fetus due to shunts - no O2 getting into baby system clinical presentation - extreme cyanosis - mottled appearance - tissue hypoxia, acidosis - no murmur management - prostaglandin 1 to maintain patent ductus arteriosus - temporary fix - atrial balloon septostomy - surgical repair in neonatal period
62
What are the 2 abnormalities in tetralogy of fallot?
Cyanotic disease 1. stenosis of R ventricular outflow tract to pulmonary artery 2. RV hypertrophy - boot shaped heart on CXR 3. Large ventricular septal defect 4. Aorta overrides septal defect - gets pushed to R side
63
What are the clinical presentation and management of tetralogy of Fallot?
Exam - cyanotic - early months - Prominent R ventricular impulse/heave - systolic ejection murmur - RA enlargement, RVH management - mild stenosis - observe/elective surgery severe - incompatible with life - Palliative: PT shunt, PDA stent - complete repair = ventricular septal closure + pulmonary obstruction relief
64
What are the outcomes for someone with tetralogy of Fallot?
risk of RV dilation, dysfunction, arrhythmia subsequent surgeries and interventions endocarditis PPX 6 months after surgery life long cardiac follow up - MRI, holter monitor

PA-S1 Cardiology (2 decks)

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