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Boards II > cardio > Flashcards

cardio Flashcards

1
Q

Embryo of heart

  • what
  • day fuse
  • day beat
  • whats superior first
  • rotation
  • atrial septal dev
  • closure of foramen ovale
  • bulbus cordis
  • left horn sinous venousus
  • right horn
  • primitive pulm vein
  • primitive atrium
  • primitive ventricle
  • right ant and common cardinal v
  • truncus arteriousus
A
  • endocardial tubes
  • 20
  • 21
  • ventricles superior to atria
  • ventricles curve down and elongate, atria posterior and then move caudally
  • septum primum grow, then splits from endo cardial cushion with ostium primum, then septum primum split 1/3 down with ostium secundum and lower septum primum grows back down to endocardil cushion, then septum secundum grows from top of atria downward forming foramen ovale
  • when born the pressure in the left atrium pushes septrum primum against septum secundum closing the gap, and it eventually fuses
  • left and right ventricle outflow tracts
  • coronary sinus
  • right atrium smooth
  • left atrium smooth
  • left and right atria trabeculated
  • left and right ventricle trabeculated
  • SVC
  • pulm trunk and ascending aorta
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2
Q

cardiac vasc

  • RCA
  • PDA
  • right marginal
  • LCA
  • LAD
  • left circumflex
A
  • RCA 15% of muscle; supply SA and AV node, contains marginal and PDA
  • upper 2/3 of post wall of both ventricles and posterior IV septum
  • lateral portion of RA and RV,
  • lat wall of left ventricle, branches into LAD, LCA
  • ant wall of both ventricles, ant IV septumlower 1/3 of post ventricles
  • left atrium and become left marginal which supplies apex
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3
Q

AVO2

  • equation
  • more extracted
  • normal lowest
  • exercise lowest
  • post prandial
A
  • O2 into tissue - O2 leaving tissue
  • greater AVO2
  • kidney
  • ## skeletal muscle
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4
Q

Symp innervation

  • when
  • what
  • how (3)
A
  • stress
  • NE
  • increase permeability to Na and Ca making depolarization easier; SA node discharge rate increased, contractile force increased
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5
Q

Reflex tachy on standing

- what happens

A
  • stand up -> blood pools to feet -> less blood returning to heart -> less end diastolic vol ->
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6
Q

Reflex tachy on standing

- what happens

A
  • stand up -> blood pools to feet -> less blood returning to heart -> less end diastolic vol -> less stretch to baroreceptors -> baroreceptors slow output -> decrease PS response -> increase in HR
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7
Q

Pulm Capillary Wedge pressure

  • what is it for
  • reasoning
  • why
A
  • indirect estimate of left atrial pressure
  • pressure in left atrium = pressure in pulm v = pressure in pulm a
  • left sided pathology to heart will increase left atrial pressure
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8
Q

Electrical Impulse

- route of conduction

A

SA node (5m/s)-> AV node (.05 m/s)-> bundle of HIS (2 m/s) -> purkinje fibers (4 m/s)

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9
Q

Cardiac Cycle

  • when does aortic valve open
  • what happens when ventricle starts to relax
  • when does aortic valve close
  • iso vol relax
  • what is the increase in pressure after the atria have contracted
A
  • when pressure in ventricle is more than pressure in aorta
  • blood is still being sent out of aorta
  • when pressure in ventricle falls below pressure in aorta
  • both aortic and mitral closed after ventricle has contracted
  • its from the mitral and tricuspid valves buckling as pressure increases in ventricles
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10
Q

Action potential for SA and AV node

  • 4
  • 0
  • 3
A
  • funny channel allows for Na to come in slowly, -60 to -50, from -50 to -40 Ca channels open (t-type), depolarization increase quickly, at -40 more Ca channel open (l-type)
  • at -30 funny and T Ca channels close and lots more L channels open
  • ## K channels open and L channels close
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11
Q

Ventricular Depolarization

  • 4
  • 0
  • 1
  • 2
  • 3
A
  • resting membrane potential, caused by K leak channels
  • fast Na channels open, steep depolarization
  • inital repolarization because K channels open
  • plateau because Ca channels open
  • K channels open to repolarize
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12
Q

ECG

  • p
  • qrs
  • t
  • u
  • QT
  • ST
  • RR
  • height
  • width
A
  • atrial depolarization, .12-.20
  • ventricular depolarization, .08-.10
  • ventricular repolarization
  • repolarization of purkinje fibers
  • 1 ventricular cycle, 0.4-0.43
  • time between end of ventricular depolarization and start of repolarization; if elevated or depressed means ischemia
  • 0.6-1.0
  • voltage; increased = hypetrophy
  • duration; increased = further impulse had to travel for depolarization
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13
Q

Congenital QT syndrome

  • mutation to
  • increases risk of
A
  • gene coding to Na or k channel

- developing torsades -> can deteriorate into vtach or v fib

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14
Q

Long QT syndrome

  • amount
  • manage
  • avoid
A
  • 13 diff types
  • Beta blockers, ICD, cut symp innervation to heart
  • high intensity sports (anything that would cause tachy) and QT prolonging drugs
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15
Q

Jervell and Lange Nielsen

  • what is it
  • mutation
  • diff from romano ward
A
  • LQT syndrome + sensorineural deafness
  • AR
  • AD, LQT syndrome
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16
Q

HTN

  • AA
  • caucasian
  • elderly
A
  • CO * TPR
  • caused by stroke vol (too much Na retention) give thiazide
  • caucasian its heart rate -> Beta blocker
  • cause by total peripheral resistance -> vasodilator, ACE i or ARB
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17
Q

Changes of Aging Heart

  • left ventricle
  • ventricular septum
  • myocytes
  • accumulate
A
  • decreases in dimension
  • sigmoid shaped; gives wall motion abnormalities w/ tachy
  • atrophy with interstital fibrosis
  • lipofuscin pigment
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18
Q

Lipofuscin

  • composed of
  • caused by
A
  • lipid polymers and protein complexed phospholipids
  • free radical injuryand lipid peroxidation
  • yellow/brown, granular
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19
Q

Shock

  • what is it
  • pulse
  • BP
  • cap refill
  • types
A
  • state of hypoperfusion of organs
  • low, or non
  • low or non
  • none
  • hypovol, ardiogenic, septic, neurogenic
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20
Q

Cardiogenic shcok

  • occurs
  • decrease
  • increase
  • caused by
  • sxs
  • management
A
  • when heart doesn’t pump enough forward
  • CO
  • TPR -> try to vasconstrict to get little amount of blood to periphery
  • left or right sided heart failure
  • crackles (LHF), increased JVP, hepatomegaly, pedal edema (RHF)
  • O2, diuretics, DA, ACEi, digoxin
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21
Q

Hypovolemic

  • problem
  • central venous pressure
  • CO
  • compensation
  • managment
A
  • fluid not returning to heart
  • decreased, bc no blood
  • decreased, bc no vol
  • vasoconstrict and tachy
  • fluids, stop source of bleeding
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22
Q

Septic

  • caused by
  • TPR
  • sxs
  • management
A
  • gram - because endotoxin will release NO and cause massive vasodilation
  • decreased bc to vasodilation
  • warm and well perfused, elevated WBC, fever
  • vasoconstrictors, fluids, antibiotics
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23
Q

Neurogenic shock

  • caused by
  • sxs
  • management
A

injury to spine -> nerves shocked -> lose symp control -> unopposed PS

  • vasodilated, brady cardia, low CO, warm and well perfused
  • vasoconstrictors
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24
Q

anaphylatics

  • caused by
  • sxs
  • manage
A
  • release of histamine
  • vasodilation, increased vasc perm, bronchosontriction
  • epi
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25
Q

Cardiogenic shock meds

  • dopamine: what is it, affects, kidney,
  • dobutamine: what is it, affects, BP, lungs, heart, indication
A
  • catecholamine, alpha/ beta/ dopa agonist, renal blood flow improves at low dose; shock and renal failure
  • synthetic cate; only beta 1/2 and alpha; neutral to BP; reduce cap wedge pressure; increase inotropy, cardiac failure and ischemic LVF
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26
Q

Hemo dynamic of shock

  • hypo
  • cardiogenic
  • septic
  • neurogenic
A
  • inc TPR, inc HR, dec CO
  • inc TPR, dec HR, dec CO
  • dec TPR, inc HR, inc CO
  • dec TPR, inc HR, inc CO
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27
Q

Venous return curve

  • mean systemic pressure
  • increase pressure
A
  • where wenous return meets the x axis -> right atrial pressure when there is no venous return
  • decrease venous return to heart -> harder to get blood in
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28
Q

AV fistula

  • what is it
  • sequelae
  • what happens to resistance
  • symp response
  • CO
  • RAAS
A
  • take a and connect to v
  • dilate vein and make it thick so you can use it for dialysis
  • decrease resistance -> increase steady state for CO and venous return
  • vaso constrict -> bring back down to normal
  • increases because of increase in EDV
  • since there is not as much blood in artery, RAAS activates -> increase resistance bc of vasoconstriction AND aldosterone causes reabsorption of water -> increases venous return
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29
Q

HTN

  • chronic causes
  • what is released
  • defined by
  • managment
A
  • left ventricular diastolic dysfunction -> causes hypertrophy of left ventricle -> lose compliance of LV -> pressure increases -> vol overload -> ventricle starts to dilate
  • ANP and BNP released to decrease vol in heart, vasodilate
  • BP over 130/80
  • thiazide, ACEi, ARB, CCB
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30
Q

ANP

  • why is it released
  • kidneys
  • adrenals
  • blood vessels
A
  • heart overstretched
  • vasodilate afferent
  • restrict aldosterone secretion
  • relaxes SM in arteries and veins and increases permeability
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31
Q

Isolated atrial amyloidosis

  • what is it
  • where else
A
  • deposition of abnormally folded ANP derived proteins

- thryoid, pancreatic islet cells, pit, cardiac atria, cerebrum and cerebral blood vessels

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32
Q

Comorbid management

  • CHF + HTN
  • Post MI + HTN
  • DM
  • CKD
  • Recurrent stroke
  • High risk CVD
A
  • thiazide, BB, ACEi, ARB
  • BB, ACEi, Aldosterone ant
  • thiazide, ACEi, ARB, CCB
  • ACEi, ARB
  • Thiazide, ACEi
  • Thiazide, BB, ACEi, CCB
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33
Q

HTN med contra

  • BB
  • ACEi
  • Diretics
  • K+ sparing diuretics
  • Thiazides
A
  • COPD -> bronchospasm, and pts who exercise a lot
  • Preg (renal tubule dysgenesis), bilateral renal a stenosis (only thing allowin perfusion to kidneys is RAAS)
  • gout
  • renail failure -> worsen hyperkalemia
  • diabetics -> precipitate hyperglycemia
34
Q

Malignant HTN

  • urgency: what is it; manage
  • emergency: what is it; management, how much
  • leads to
A
  • BP greater than 180/120 w/o end organ damage, oral BP meds
  • w/ end organ compromise (headaches, blurred vision, edema, renal failure, hematuria) -> admitted and treated
  • Na-nitroprusside -> IV and BB; never lower more than 1/4 at first
  • hyperplastic arteriosclerosis -> onion skinning
35
Q

Pulm Artery HTN

  • what is it
  • genetic cause; 1 hit vs 2; leads to; tx
A
  • anything over 25 mmhg
  • BMPR2; 1 hit -> pulm vasc dx, 2nd hit -> activated vasc SM proliferation; RHF, exertional dyspnea; vasodilators, PDE i (SM relaxers), competitive endothelin receptor antagonist
36
Q

Progression of Atherosclerosis

  • starts with
  • fat
  • then
A
  • endo dysfunction
  • fatty streak formation
  • stable or unstable plaque formation under endo
37
Q

CAD

  • leads to
  • most common place
  • risk factor
A
  • sudden cardiac death -> vfib
  • aorta, coronaries, popliteal, int carotids, circle of willis
  • hypertension and diabetes -> deposit eosinophilic hyaline material in intima and media of small arteries
38
Q

Metalloproteinases

  • importance with CAD
  • how is it incorporated
A
  • helps with plaque stability

- firbous cap -> made from collagen and macrophages secrete metalloprotease which causes degradation of collagen

39
Q

Reperfusion injury

  • when
  • mechanism
A
  • once bloodflow has been restored

- free O2 radicals, irreversible mito damage and inflammation

40
Q

Hibernation

  • how
  • what happens
A
  • repetitive ischemia of myocytes results in chronic, reversible loss of function
  • reduction of myo energy metabolism but still enough ATP to prevent contracture
41
Q

Stable angina

  • what is it
  • sxs
  • dx
  • management: acute
  • management: chronic
  • management: curative
A
  • fixed plaque that obstructs 75% or more of lumen of coronary a
  • during exercise
  • EKG normal, stress test/ chemical, stress echo
  • sublingual nitro -> acts as ven dilator to decrease pre-load -> decrease myo O2 demand -> improves angina; hydralazine and minoxodil as
  • aspirin: reduce risk cardio events by 30%, BB and Ca channel blocker: reduce frequency of attack
  • PCI and CABG
42
Q

Unstable Angina

  • sxs
  • synonymous
  • cause
  • EKG
  • labs
  • risk: low, mod -> manage
  • risk: high -> manage
A
  • more frequent and with less exertion
  • same thing as NSTEMI -> subendocardial infarction due to severe ischemia
  • transient clotting
  • ST segment depression or T wave inversion
  • positive cardiac enzymes
  • rest pain, lasting less than 20 min; rest pain lasting more than 20 min; isosorbide dinitrate
  • rest pain more than 20 min thats ongoing, ST depression; add heparin, nitro drip
43
Q

Prinzmetal Angina

  • what is it
  • EKG
  • when do episodes occur
  • where
  • meds
A
  • coronary artery vasospasm
  • ST elevaation, looks like acute MI
  • at rest and early morning hours
  • near sites of atherosclerosis -> result in transmural ischemia w/ ST segment elevation on EKG
  • Nitro for pain relief and cath
44
Q

STEMI

  • what is it
  • sxs
  • EKG
  • post therapy
  • complication
A
  • infarct secondary to acute thrombosis in atherosclerotic vessel
  • crushing substernal pain not relieved by rest, diaphoresis
  • ST elevation
  • thrombolytics: reduces mortality, aspirin: reduce risk of infarction related death by 30%, BB: reduce risk of death after MI, help with myo wall stress and size of infarction
  • left ventricular failure or rupture
45
Q

STEMI micro changes

  • 0-4 hrs
  • 4-12 hrs
  • 12-24 hrs
  • 5-10 days
  • 10-14 days
  • 2 wks to 2 mnths
A
  • minimal change
  • coag necrosis, edema, hemm and wavy fibers
  • coag and marginal contraction
  • macro phago, dead cells
  • granulation tissue, neovasc
  • collagen deposition, scar formation
46
Q

Diff Dx of ST elevation

  • MCC ST elevation
  • pericarditis
  • ventricular aneursym
A
  • early repolarization; j point; young men -> normal
  • diffuse ST segment elevation, diffuse PR depression
  • ST elevation w/o signs MI
47
Q

Dresslers Syndrome

  • what is it
  • sxs
  • meds
  • prognosis
A
  • pericarditis occurring 1 week - several months after MI
  • sharp, pleuritis CP exacerbated by swallowing, relieved by leaning forward
  • aspirin and ibuprofen
  • transient
48
Q

Heart Block

  • 1st
  • 2nd, 1
  • 2nd, 2
  • 3rd
  • LBBB
  • RBBB
A
  • normal sinus rhythm with PR interval greater then .2; asymptomatic
  • PR interval prolonged from beat to beat until it drops; wenckeback
  • fixed PR interval w/ reg non-conducting p wave leading to drop beats
  • no relationship between P and QRS
  • QRS greater than 3 small boxez, rabbit in v5,6
  • QRS greater than 3 small boxez, rabbit in v 1,2
49
Q

Axis Deviation

  • left: MCC
  • right: MCC
A
  • left ventricular hypertrophy, inferior MI

- right ventricular hypertrophy, WPW, PE, COPD

50
Q

A fib

  • rate,
  • caused by
  • pulse
  • sxs
  • complications
A
  • atrial rate 250-350
  • HTN, EtOH consumption, increase symp tone
  • irregularly irregular
  • palpitations, chest discomfort, tachy, hypotension
  • atrial mural thrombi -> embolize and travel to brain
51
Q

A flutter

  • rate
  • stability
  • classic - rate with ratio
A
  • slower than a fib
  • less than a fib; causes ventricles to beat more
  • 300 bpm; 2:1
52
Q

Multi-focal a tach

  • what is it
  • rhythm
  • most common
  • EKG
  • management
A
  • presence of several pacemaker in atria
  • irregularly irregular
  • COPD
  • tachy cardia w 3 distinct p waves
  • verapamil
53
Q

SVT

  • what is it
  • what happens
A
  • tachy arrythmia in atria

- several pacemakers work together at any single time

54
Q

V tach

  • what is it
  • progresses to
  • stable
  • unstable
A
  • 3 or more consecutive premature ventricular contractions with rate higher than 100 bpm
  • vfib
  • able to talk -> give amiodarone
  • unstable -> shock
55
Q

V fib

  • what is it
  • presentation
  • management
A
  • fibrillations of ventricle
  • syncope, severe hypotension, sudden death
  • 1st defib, 2nd amiodarone/ lidocaine
56
Q

Torsades De Pointes

  • what is it
  • meds: class II, III, antibiotics; depression
A
  • unique form of vfib where axis shifts or twists

- procainamide ;sotalol, amiodarone; erythromycin, quinidine, clarithromycin; fluoxetine;

57
Q

WPW

  • most common cause of
  • what is it
  • sequelae
  • EKG
A
  • palpitations in teenagers
  • accessory pathway from SA node to right ventricle
  • bypasses AV node
  • narrowed GRS w/ delta wave
58
Q

Anti arrythmics: Class I

  • MOA
  • I-a
  • I- b
  • I- c
A
  • NA channel blocker
  • Na and K block -> depolarization and repolarization take longer; prolonged PR, QRS, QT; quinidine, procainamide, diacylpyramide
  • mild Na channel blockade; shorten action potential duration -> suppresses activity in post MI arrythmia (v tach); lidocaine
  • marked Na channel blocker; much slower depolarization; prolonged PR and QRS; flecanide
59
Q

Anti arrythmics: Class II

  • MOA
  • patho
  • EKG
  • suffix
A
  • beta blocker
  • decrease cAMP -> decrease Ca -> decrease contraction and block SA node action potential -> slow HR
  • increase PR interval
  • olol
60
Q

Anti arrythmics: Class III

  • MOA
  • examples
A
  • blocks K channel

- sotalol and amniodarone

61
Q

Anti arrythmics: Class IV

  • drugs
  • MOA

-adenosine

A
  • verapamil and diltiazem
  • block Ca channel -> decrease velocity in AV node
  • hyperpolarization of cells (used for SVT -> stop heart and reset)
62
Q

CHF right sided

  • cause
  • sxs
  • progression
A
  • left sided heart failure -> increased pooling of blood upstream of heart
  • edema, hepatic congestion, increased JVP, fatigue, cyanosis, Afib
  • profression of cor pulmonale to lethal arrythmia
63
Q

CHF management

  • goal
  • contraction drugs
  • reduce workload
A
  • reduce workload and improve contraction
  • digoxin (increase Ca influx into myocardial cells), amrinone (block cAMP degradation in heart) dobuamine (increase cAMP production through stimulation of beta 1), BB
  • ACEi, furosemide, spironolactone
64
Q

Dysfunction

  • systolic
  • diastolic
A
  • too much dilation, cannot contract

- too much hypertrophy, impaired relaxation, LV stiffness

65
Q

Dilated Cardiomyopathy

  • what happens
  • caused by
  • sxs
  • management
A
  • systolic dysfunction
  • viral myocarditis, alcoholism, toxin, AI, pregnancy
  • right/left sided heart failure, S3 gallop, mitral regurg
  • stop offending agents
66
Q

Hypertrophic Cardiomyopathy

  • what happens
  • caused by
  • MCC death
  • characteristics of muscle
  • histo
  • management
A
  • diastolic dysunction
  • genetic, AD; aging, htn
  • vfib
  • aymmetric ventricular septal hypertrophy w/ LV outflow obstruction
  • myofiber disarray w/ interstitial fibrosis
67
Q

Hypertrophic Cardiomyopathy

  • what happens
  • caused by
  • MCC death
  • characteristics of muscle
  • histo
  • management
A
  • diastolic dysunction
  • genetic, AD; aging, htn
  • vfib
  • asymmetric ventricular septal hypertrophy w/ LV outflow obstruction
  • myofiber disarray w/ interstitial fibrosis
  • beta locker, ban from intense activity, keep plasma vol elevated
68
Q

Restrictive cardiomyopathy

  • caused by
  • sxs
  • EKG
A
  • collagen vascular disease, amyloidosis, hemochromatosis, sarcoidosis
  • S4 gallop, pulm HTN
  • demonstrate a decrease in QRS voltage
69
Q

Constrictive pericarditis

  • what happens
  • caused by
  • sxs
A
  • thickening of pericardium
  • TB, radiation therapy to chest, hx of cardiac surgery
  • progressive dyspnea, chronic edema, and ascites
70
Q

Constrictive pericarditis

  • what happens
  • caused by
  • sxs
  • point
A
  • thickening of pericardium -> inhibits normal filling
  • TB, radiation therapy to chest, hx of cardiac surgery
  • progressive dyspnea, chronic edema, and ascites
  • kussmaul sign, pulsus paradoxus, with breath sounds equal
71
Q

Pericarditis

  • what is it
  • caused by
  • sxs
  • EKG
  • DX
  • Tx
A
  • pericardial sac less than 2 mm thick but filled with fluid
  • fungal, viral, bacterial, RA, SLE, scleroderma
  • retrosternal pain, pericardial friction rub
  • ST elevation in all leads
  • clinical and confirm with echo
  • Nsaids for viral and antibiotics for bacterial
72
Q

S3

A
  • dilated ventricle ->vol problem
  • decreased contraction -> decreased EF
  • only normal in adolescent female
73
Q

S4

A
  • due to atria contracting against stiff ventricle -> elevated pressure
  • pressure over load and atrial kick; gallop caused by atherosclerosis
74
Q

opening snap

A
  • heard by forcing through an open valve during diastole -> stenotic
75
Q

ejection click

A
  • heard by forcing through open valve during diastole -> aortic valve and pulm stenosis
76
Q
  • Loud S1
  • Soft s1
  • soft s2
  • loud s2
A
  • stenosis or high pressure in front of valve
  • mitral or tricuspid valves is not closing or not there
  • aortic or pulm not closing or atresia
  • aortic or pulm stenosed or slamming shut
77
Q

max sound of murmur

  • respiration
  • Valsalva
  • standing
  • squatting/sitting:
  • handgrip:
A
  • right sided get louder with inspiration and left sided get louder during expiration
  • should diminish (MVP increases)
  • murmurs diminish (MVP increase)
  • murmurs increase (IHSS and MVP softer)
  • increase afterload -> MR, VSD, AR louder and IHSS decrease
78
Q

midsystolic click

A
  • high velocity blood slaps mitral valve
79
Q

During systole what is

  • open
  • close
  • what can you have
A
  • open: aorta and pulm
  • closed: mitral and tricuspid
  • aortic and pulm stenosis or mitral and tricuspid regurg
80
Q

Systolic

  • crescendo decrescendo systolic
  • holo
  • late click
  • click after s1
A
  • crescendo decrescendo systolic: innocent/ physio aortic/pulm stenosis
  • holo: mitral/tricuspid regurg
  • late click: mitral valve prolapse
  • click after s1: aortic/pulmonic valve dx
81
Q

Diastolic

  • early decrescendo
  • mid decrescendo
  • opening snap and diastolic rumble
  • s3
  • s4
A
  • early decrescendo: aortic regurg
  • mid decrescendo: miral/tricuspid stenosis
  • opening snap and diastolic rumble: mitral stenosis
  • s3: right after s2, low pitch
  • s4: right before s1, low pitch
82
Q

Austin flint

  • what is it
  • sxs
A
  • mid diastolic murmur associated w/ severe aortic regurg

- widened pulse pressure, pounding pulses, waterhammer pulse, head bobbing

Boards II (20 decks)

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