cardio Flashcards
(82 cards)
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
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
3
Q
AVO2
- equation
- more extracted
- normal lowest
- exercise lowest
- post prandial
A
- O2 into tissue - O2 leaving tissue
- greater AVO2
- kidney
- ## skeletal muscle
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
5
Q
Reflex tachy on standing
- what happens
A
- stand up -> blood pools to feet -> less blood returning to heart -> less end diastolic vol ->
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
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
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)
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
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
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
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
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
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
15
Q
Jervell and Lange Nielsen
- what is it
- mutation
- diff from romano ward
A
- LQT syndrome + sensorineural deafness
- AR
- AD, LQT syndrome
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
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
18
Q
Lipofuscin
- composed of
- caused by
A
- lipid polymers and protein complexed phospholipids
- free radical injuryand lipid peroxidation
- yellow/brown, granular
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
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
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
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
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
24
Q
anaphylatics
- caused by
- sxs
- manage
A
- release of histamine
- vasodilation, increased vasc perm, bronchosontriction
- epi
25
Cardiogenic shock meds
- dopamine: what is it, affects, kidney,
- dobutamine: what is it, affects, BP, lungs, heart, indication
- 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
26
Hemo dynamic of shock
- hypo
- cardiogenic
- septic
- neurogenic
- inc TPR, inc HR, dec CO
- inc TPR, dec HR, dec CO
- dec TPR, inc HR, inc CO
- dec TPR, inc HR, inc CO
27
Venous return curve
- mean systemic pressure
- increase pressure
- 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
28
AV fistula
- what is it
- sequelae
- what happens to resistance
- symp response
- CO
- RAAS
- 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
29
HTN
- chronic causes
- what is released
- defined by
- managment
- 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
30
ANP
- why is it released
- kidneys
- adrenals
- blood vessels
- heart overstretched
- vasodilate afferent
- restrict aldosterone secretion
- relaxes SM in arteries and veins and increases permeability
31
Isolated atrial amyloidosis
- what is it
- where else
- deposition of abnormally folded ANP derived proteins
| - thryoid, pancreatic islet cells, pit, cardiac atria, cerebrum and cerebral blood vessels
32
Comorbid management
- CHF + HTN
- Post MI + HTN
- DM
- CKD
- Recurrent stroke
- High risk CVD
- thiazide, BB, ACEi, ARB
- BB, ACEi, Aldosterone ant
- thiazide, ACEi, ARB, CCB
- ACEi, ARB
- Thiazide, ACEi
- Thiazide, BB, ACEi, CCB
33
HTN med contra
- BB
- ACEi
- Diretics
- K+ sparing diuretics
- Thiazides
- 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
Malignant HTN
- urgency: what is it; manage
- emergency: what is it; management, how much
- leads to
- 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
Pulm Artery HTN
- what is it
- genetic cause; 1 hit vs 2; leads to; tx
- 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
Progression of Atherosclerosis
- starts with
- fat
- then
- endo dysfunction
- fatty streak formation
- stable or unstable plaque formation under endo
37
CAD
- leads to
- most common place
- risk factor
- 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
Metalloproteinases
- importance with CAD
- how is it incorporated
- helps with plaque stability
| - firbous cap -> made from collagen and macrophages secrete metalloprotease which causes degradation of collagen
39
Reperfusion injury
- when
- mechanism
- once bloodflow has been restored
| - free O2 radicals, irreversible mito damage and inflammation
40
Hibernation
- how
- what happens
- repetitive ischemia of myocytes results in chronic, reversible loss of function
- reduction of myo energy metabolism but still enough ATP to prevent contracture
41
Stable angina
- what is it
- sxs
- dx
- management: acute
- management: chronic
- management: curative
- 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
Unstable Angina
- sxs
- synonymous
- cause
- EKG
- labs
- risk: low, mod -> manage
- risk: high -> manage
- 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
Prinzmetal Angina
- what is it
- EKG
- when do episodes occur
- where
- meds
- 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
STEMI
- what is it
- sxs
- EKG
- post therapy
- complication
- 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
STEMI micro changes
- 0-4 hrs
- 4-12 hrs
- 12-24 hrs
- 5-10 days
- 10-14 days
- 2 wks to 2 mnths
- 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
Diff Dx of ST elevation
- MCC ST elevation
- pericarditis
- ventricular aneursym
- early repolarization; j point; young men -> normal
- diffuse ST segment elevation, diffuse PR depression
- ST elevation w/o signs MI
47
Dresslers Syndrome
- what is it
- sxs
- meds
- prognosis
- pericarditis occurring 1 week - several months after MI
- sharp, pleuritis CP exacerbated by swallowing, relieved by leaning forward
- aspirin and ibuprofen
- transient
48
Heart Block
- 1st
- 2nd, 1
- 2nd, 2
- 3rd
- LBBB
- RBBB
- 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
Axis Deviation
- left: MCC
- right: MCC
- left ventricular hypertrophy, inferior MI
| - right ventricular hypertrophy, WPW, PE, COPD
50
A fib
- rate,
- caused by
- pulse
- sxs
- complications
- 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
A flutter
- rate
- stability
- classic - rate with ratio
- slower than a fib
- less than a fib; causes ventricles to beat more
- 300 bpm; 2:1
52
Multi-focal a tach
- what is it
- rhythm
- most common
- EKG
- management
- presence of several pacemaker in atria
- irregularly irregular
- COPD
- tachy cardia w 3 distinct p waves
- verapamil
53
SVT
- what is it
- what happens
- tachy arrythmia in atria
| - several pacemakers work together at any single time
54
V tach
- what is it
- progresses to
- stable
- unstable
- 3 or more consecutive premature ventricular contractions with rate higher than 100 bpm
- vfib
- able to talk -> give amiodarone
- unstable -> shock
55
V fib
- what is it
- presentation
- management
- fibrillations of ventricle
- syncope, severe hypotension, sudden death
- 1st defib, 2nd amiodarone/ lidocaine
56
Torsades De Pointes
- what is it
- meds: class II, III, antibiotics; depression
- unique form of vfib where axis shifts or twists
| - procainamide ;sotalol, amiodarone; erythromycin, quinidine, clarithromycin; fluoxetine;
57
WPW
- most common cause of
- what is it
- sequelae
- EKG
- palpitations in teenagers
- accessory pathway from SA node to right ventricle
- bypasses AV node
- narrowed GRS w/ delta wave
58
Anti arrythmics: Class I
- MOA
- I-a
- I- b
- I- c
- 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
Anti arrythmics: Class II
- MOA
- patho
- EKG
- suffix
- beta blocker
- decrease cAMP -> decrease Ca -> decrease contraction and block SA node action potential -> slow HR
- increase PR interval
- olol
60
Anti arrythmics: Class III
- MOA
- examples
- blocks K channel
| - sotalol and amniodarone
61
Anti arrythmics: Class IV
- drugs
- MOA
-adenosine
- verapamil and diltiazem
- block Ca channel -> decrease velocity in AV node
- hyperpolarization of cells (used for SVT -> stop heart and reset)
62
CHF right sided
- cause
- sxs
- progression
- 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
CHF management
- goal
- contraction drugs
- reduce workload
- 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
Dysfunction
- systolic
- diastolic
- too much dilation, cannot contract
| - too much hypertrophy, impaired relaxation, LV stiffness
65
Dilated Cardiomyopathy
- what happens
- caused by
- sxs
- management
- systolic dysfunction
- viral myocarditis, alcoholism, toxin, AI, pregnancy
- right/left sided heart failure, S3 gallop, mitral regurg
- stop offending agents
66
Hypertrophic Cardiomyopathy
- what happens
- caused by
- MCC death
- characteristics of muscle
- histo
- management
- diastolic dysunction
- genetic, AD; aging, htn
- vfib
- aymmetric ventricular septal hypertrophy w/ LV outflow obstruction
- myofiber disarray w/ interstitial fibrosis
67
Hypertrophic Cardiomyopathy
- what happens
- caused by
- MCC death
- characteristics of muscle
- histo
- management
- 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
Restrictive cardiomyopathy
- caused by
- sxs
- EKG
- collagen vascular disease, amyloidosis, hemochromatosis, sarcoidosis
- S4 gallop, pulm HTN
- demonstrate a decrease in QRS voltage
69
Constrictive pericarditis
- what happens
- caused by
- sxs
- thickening of pericardium
- TB, radiation therapy to chest, hx of cardiac surgery
- progressive dyspnea, chronic edema, and ascites
70
Constrictive pericarditis
- what happens
- caused by
- sxs
- point
- 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
Pericarditis
- what is it
- caused by
- sxs
- EKG
- DX
- Tx
- 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
S3
- dilated ventricle ->vol problem
- decreased contraction -> decreased EF
- only normal in adolescent female
73
S4
- due to atria contracting against stiff ventricle -> elevated pressure
- pressure over load and atrial kick; gallop caused by atherosclerosis
74
opening snap
- heard by forcing through an open valve during diastole -> stenotic
75
ejection click
- heard by forcing through open valve during diastole -> aortic valve and pulm stenosis
76
- Loud S1
- Soft s1
- soft s2
- loud s2
- 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
max sound of murmur
- respiration
- Valsalva
- standing
- squatting/sitting:
- handgrip:
- 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
midsystolic click
- high velocity blood slaps mitral valve
79
During systole what is
- open
- close
- what can you have
- open: aorta and pulm
- closed: mitral and tricuspid
- aortic and pulm stenosis or mitral and tricuspid regurg
80
Systolic
- crescendo decrescendo systolic
- holo
- late click
- click after s1
- 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
Diastolic
- early decrescendo
- mid decrescendo
- opening snap and diastolic rumble
- s3
- s4
- 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
Austin flint
- what is it
- sxs
- mid diastolic murmur associated w/ severe aortic regurg
| - widened pulse pressure, pounding pulses, waterhammer pulse, head bobbing
