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PA-S1 Cardiology > Cardiology Clinical Studies > Flashcards

Cardiology Clinical Studies Flashcards

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
Q

What are the genetic tests for hypertrophic cardiomyopathy?

A

autosomal dominant
sarcomere mutations - primary HCM
non-sarcomere mutations - systemic disease caused HCM

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26
Q

Describe hypertrophic myopathy outflow obstruction

A

occurs during exercise
systolic anterior motion (SAM) or mitral valve leaflet prevents blood from leaving the aorta

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27
Q

How would you treat obstructive hypertrophic cardiomyopathy?

A

avoid meds that lower preload (ACE/ARB/ARNI/nitrates/diuretics)

metroprolol or verapamil

intervention:
surgical septal myetcomy
alcohol septal ablation

mavacamten

28
Q

describe dilated cardiomyopathy. What are the causes?

A

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
Q

What is the treatment for dilated cardiomyopathy?

A

same as HFrEF - GDMT

30
Q

Describe restrictive cardiomyopathy

A

rigid ventricular walls with severe diastolic function
- significant biatrial enlargement

can be: infiltrative, non-infiltrative, storage disease, idiopathic

31
Q

what are the causes of restrictive cardiomyopathy?

A

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
Q

What are the treatments for restrictive cardiomyopathy caused by hemochromatosis and cardiac amyloidosis?

A

hemochromatosis - chelation of phlebotomy to decrease iron

cardiac amyloidosis - manage HF symptoms
- congestion with diuretics
- antiarrhythmics
- ACE/ARBs/ARNI contraindicated

33
Q

How do you manage an NSTEMI?

A

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
Q

What do you do if someone is having a STEMI?

A

EMS can send them straight to cath lab for repercussion

if PCI not available - give them Aspirin, supplemental O2, nitroglycerine, morphine

35
Q

what lipid test is the best predictor for CHD?

A

TC:HDL-C ratio

other random labs
- Lipoprotein A - 30+ = High
- ApoB 130+ = high

36
Q

What labs would you see ins someone who has hypertriglyceridemia, hypercholerterimia, and mixed hyperlipidemia?

A

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
Q

Describe aortic stenosis. What are the causes and clinical presentation?

A

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
Q

What is the management of aortic stenosis?

A

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
Q

CXR reveals cardiomegaly, calcified valve, prominent ascending aorta and BNP. There is LVH on echo and reduced aortic orifice. What is the dx?

A

Aortic stenosis

39
Q

What is the pathophysiology of chronic and acute aortic insufficiency?

A

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
Q

What is aortic insufficiency? What are the causes?

A

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
Q

Echo reveals regurgitant jet, valve vegetations, and an enlarged aortic root. What is this dx?

A

aortic insufficiency

42
Q

Describe tricuspid stenosis. What causes it? How is it managed?

A

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
Q

What is the management of aortic insufficiency?

A

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
Q

Describe tricuspid insufficiency. What are common causes? What does the clinical presentation look like?

A

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
Q

What are the treatments for tricuspid insufficiency?

A

medical treatment and surveillance echos
HF = GDMT and diurtetics

surgery - rare
- tricuspid valve repair > replacement
- RV infarct - ischemic revascularization with stent or CABG

46
Q

Describe mitral stenosis. What is the pathophysiology and the clinical manifestations?

A

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
Q

How is mitral stenosis managed?

A

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
Q

Describe mitral valve regurgitation. What are some structural and functional causes?

A

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
Q

How is mitral valve regurgitation medically managed?

A

medical:
congestion - diuretics
vasodilators for symptomatic pts to decrease after load

surgical
- mitral valve repair/replacement
- percutaneous mitral clip

50
Q

Describe rheumatic fever. What is the criteria for diagnosis> What are some complications?

A

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
Q

Describe endocarditis. What is the common clinical presentation? What are some causes?

A

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
Q

Describe the etiology and pathophysiology of pericarditis

A

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
Q

How is pericarditis diagnosed? What would you see on exam, EKG, and echo?

A

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
Q

Describe the etiology and pathophysiology of myocarditis

A

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
Q

How is myocarditis diagnosed? What would you see on exam, labs, CXR, EKG, Echo?

A

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
Q

Describe the location of each in fetal circulation:
foramen ovale
ductus venosus
ductus arteriosus

A

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
Q

Describe the flow of blood in fetal circulation

A

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
Q

Describe atrial septal defects. What is the physiology, clinical presentation, and management?

A

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
Q

Describe venticular septal defects. What is the physiology, clinical presentation, and management?

A

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
Q

Describe patent ductus arteriosus. What is the physiology, clinical presentation and management?

A

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
Q

Describe transpiration of the great arteries. What is the physiology, clinical presentation and management?

A

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
Q

What are the 2 abnormalities in tetralogy of fallot?

A

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
Q

What are the clinical presentation and management of tetralogy of Fallot?

A

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
Q

What are the outcomes for someone with tetralogy of Fallot?

A

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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