CV2-Cardio Flashcards

Question

what are the 7 presentations of a patient that would suggest they are experience HF?

Answer 1

**1. dyspnea** **2. orthopnea** **3. paryoxysmal nocturnal dyspnea** **4. abdominal symptoms** 5**. cerebral symptoms** (decreased profusion to brain) 6. **unexplained weight gain from swelling in the legs** **7. acute pulmonary edema \*\*\*MEDICAL EMERGENCY WORST POSSIBLE SITUATION....patient drowning in their own fluid backing into the alveoli!!!\*\*\*\***

Answer 2

**\*\*\*THIS IS A MEDICAL EMERGENCY\*\*\*\*** pt is drowning from the inside out!! _pulmonary capillary wedge pressure via right heart cath_ \>20 mmHg: concerned with interstitial edema **\>25 mmHg: concerned with pulmonary edema**

Answer 3

1. _tachycardia common_ _2. crackers_ _3. S3 gallop low in pitch in early diastole (associated with HF)_ _4. increased JVP_ _5. hepato-jugular reflex_ (push on liver JVD goes up) _6. cardiac cachexia "wasted appearance"_ _7. pleura effusions with high levels of pulomary pressure!!_

Answer 4

**1. CXR:** _CARDIOMEGALY_ _KERLEY B LINES_ (DISTENSION OF PULMONARY VEINS) **2. ECHO DOPPLER #1 best non invasive tool** **3. BNP:** used for acute ventricular dysfunction or symptomatic heart failure, *helps to distinguish SOB between cardiac and pulmonary cause* **\>100 COMMON WITH HF**

Answer 5

2. treat underlying cause 3. reduction of cardiac workload (preload/postload) 4. control excessive Na/water retention 5. early initiation of ACEI/ARB (hydralazine in blacks) 6. enhancement of cardiac contractility

Answer 6

**\<4 g Na diet or less** **NO SALT ADDED.**

Answer 7

**when patient no longer is responsible to any RX** **1. LV assist devices (implantable pump device connected to external power supply)** - decreases cardiac workload to buy time for transplant - can leave the hospital while waiting - often used since not enough heart donors * complications: thrombis formation, infection* **2. cardiac transplant** *complications: rejection, infection, CHD in donor heart*

Answer 8

70%!!!!! thats pretty good costs minimally $200,000

Answer 9

**1. direutics** - loop dieurtics most potent (furosemide, torsemide) - MUST monitor BUN, creatine, UA, and glucose - can cause _hyperurcemia and metabolic acidosis_ - k sparing dieuretics **2. nitrates**

Answer 10

**afterload:** - always increase in HF bause of the neural and humoral influences that constrict PV and increase SVR - increase in SVR decreases CO and causes back flow to lungs **treat with vasodilators:** **decrease SVR** **increase CO** **decrease pulmonary capillary wedge pressure** **decrease symptoms** **decrease mortality**

Answer 11

**1. ACE inhiborts** -caution *hypotension, dry cough* **decrease mortality by \>25%** **decrease remodeling (fibrosis, wall thinning, cell death)** **2. angiotensin II receptor blockers** less protection against remodeling than ACE but don't cause cough **3. sacubitril** _neprilysin inhibitor_ degrades vasoactive peptides

Answer 12

**CONSIDER AS FIRST LINE TREATMENT FOR HF INSTEAD OF ACE OR ARB ALONE FOR HF!!!!!** 1. slowed HF progression better than a ACE alone 2. se: hypotension, angioedema, hyperkalemia

Answer 13

**if QRS \>.12 _and_ severe refractory CHF** improves symptoms and quality of life and EF this is called "cardiac resynchronization therapy

Answer 14

indications: _secondary:_ **resuscitated cardiac arrest/vfib or hemodynamically unstable Vtach** _primary:_ **EF \<.35 with mild to moderate HF sym,ptoms**

Answer 15

bacteria cause infection on a cardiac valve or an endocardial surface and cause a _VEGETATION "small growth" that moves with the valve_ **-skin, oral cavity, GI, upper respiratory** **-dental work, flossing, cleaning, central lines** \*\*most are due to bacterial infections, however some are fungal\*\*\* organisms: **_staph aureus most common_, virdians group D streptococci, enteroccocus faecaslis** can lead to permanent damage including: 1. valve damage 2. HF (usually left sided) 3. strokes from emboli to the brain 4. damage elsewhere from emboli

Answer 16

50% of people provides are source of turbulent flow that makes it easier for the bacteria to pool there ex: IV drug user

Answer 17

usualy a DISASTER! 1. rheumatic valve disease 2. aortic stenosis/sclerosis/regurg 3. mitral stenosis/regurge/prolapse 4. congenital heart defect

Answer 18

**aortic valve and mitral valve** vegetation occurs on the _low pressure_ side of the valve 1. mitral it occurs on the atrial side 2. aortic it occurs on ventricular side vegetation made of: **platelets, fibrin, colonies of bacteria**

Answer 19

**tricuspid involvement in 85% of cases** pulmonary valve in 15% **_only in the setting of IV drug use!_** causitive agent usually **_STAPH aureus_**

Answer 20

1. febrile 2. symptoms of infectious emboli spreading elsewhere 3. _petechiae on palate or conjunctive_ (from micro emboli) 4. _subungal "splinter" hemmorages_ _5. **olsers nodes-**_**painful raished lesions on fingers and toes** **_6. janeway lesions_: painless red lesions on palms or soles** **_7. roth spots_-exudative lesions in retina** **_NEW OR CHANGING REGURGITANT MURMERS_**

Answer 21

**1. Blood cultures 3 sets 1 hour apart** 2. **TEE-90% sensitive**

Answer 22

**1. acute** **staph aureus and other virlulent organisms** acute with rapid progressing destruction and infection early emboli **2. subacute** **virdans streptococci, enterococcus** gradular valvular destruction

Answer 23

Major: 1. 2+ blood cultures 2. abnormal TEE 3. new/changing regurgitant murmer Minor: 1. IV drug use 2. prior valve abnormality 3. fever 4. systemic emboli 5. immunologic lesions (janeway, olsens, roth) **_Definite DX:_** **2 major** **1 major 3 minor** **5 minor**

Answer 24

**prosthetic heart valve** **prior episode of endocarditis** **complex cyanotic congenital heart disease** other valvular lesions whether congenital or acquired do not require endocarditis prophylaxis before procedures for _dental procedure use amoxicillin_ 2 grams 30-60 mins before surgery

Answer 25

_viridans_ streptococci: _penicillin G_ x 4 hours q 4 weeks _empiric_ tx while awaiting culture results: _vancomycin and ceftriaxone IV_

Answer 26

**50 million americans** only 25% are adequately controlled

Answer 27

HTN \>140/90 eldery: \>150/90 ideal \<120/80

Answer 28

**essential hypertension:** aka idiopathic/primary 95% of cases, etiology unknown **secondary hypertension:** 5% of cases 1. estrogen use increases RAAS 2. intrinsic renal disease (any form of chronic renal parenchymal disease) 3. renovascular HTN 4. endocrine HTN 5. pregnancy

Answer 29

2 types of _renal artery stenosis_ that increase the production of _renin_, cause decreased BF to the kidneys _increasing BP_ **1. fibromuscular hyperplasia (FMH)** - young adults - BP increases renal function preserved tx: angioplasty to increase BF to kidney **2. atherosclerosis of renal artery** - older patients - elevated BP not responsive to meds - renal function impaired, intervention may or may not help

Answer 30

genetics environmental factors sympathetic nervous system hyperactivity renin-angiotensin-aldosterone system defect in natriuresis (getting rid of Na in the body) intracellular Na and Ca insulin resistance

Answer 31

obesity Na in diet cigarette smoking increases NE NSAIDS excess alcohol

Answer 32

**1. HEART** - RF for _CHD_ - _LVH diastolic dysfunction_ POWERFUL PREDICTOR of morbidity and morality, in 50% of people with HTN - _HF_ over time **2. CEREBROVASCULAR** _the major predisposing cause of STROKE_ _rupture of micro hemmorages_ from increase BP correlate closely with SYSTOLIC BP **3. PVD** **4. RENAL DISEASE** _nephrosclerosis_: narrows kidney arterioles causing glomerular damage and decreased function, HTN accelerates this procress, common in _Blacks_

Answer 33

1. SOB, DOE from LVH 2. TIA, stroke, hemmorage 3. MI, angina, HF

Answer 34

BP **\>140/90** requires tx in those **\<60**, including those with _DM or CKD_ BP **\>150/90 \>60 year old,** a little more liberal with the elderly

Answer 35

1. narrowing of the arterioles _A/V \<5._ 2. _A-V nicking_ (arteriosclerosis where artery looks like it is crossing the vein) 3. **silver or copper wired appearance** 4. hemorrhages or exudates 5. **papilledema** 6. bruits

Answer 36

1. _creatine, BUN_ 2. electrolytes Na and _K_ (want to check K cause you will likely put them on a dieuretic and this can cause hypokalemia) 3. lipid levels: TC, LDL, HDL, triglycerides

Answer 37

thiazide and/or CCB

Answer 38

1. ACE 2. ARB if can't tolerate ACE _use these regardless of race or diabetes status if they have CKD!!!!!!! big hint there!!_

Answer 39

combine BB with ACE/ARB BB are no longer reccomended for HTN but they can help in adjunct in patients post MI even though it doesn't actually help treat the HTN

Answer 40

almost always require 3 drug regimen 1. ACE (or ARB if can't tolerate) WITH 2. thiazide OR CCB

Answer 41

decrease **endpoints** including **_MI, Stroke, LVH, PAD, all cause cardiac mortality, HF, and renal failure_** **_try to find drugs that treat more that one co-morbidity_** **_focus on SYSTOLIC BP as the most important aspect for reducing morbidity and mortality_**

Answer 42

SYSTOLIC BP!

Answer 43

diet weight reduction, aerobic activity decrease alcohol, Na intake DASH DIET smoking cessation

Answer 44

thaizide dieuretic

Answer 45

1. 1st line therapy and should be included in ANY drug therapy 2. more potent in _blacks, elderly, obese_ 3. avoid in patiens with _hyponaturemia and gout_ 4. _LOW DOSAGE_ 5. can cause _hypokalemia, hyperurcemia,_ _hyperglycemia, abnormalities of lipids_

Answer 46

used as a 2nd or 3rd line drug because of increased risk for _stroke_ 1. decreases CO 2. helpful in pts with other comorbid disorders like: - angina pectoris, post MI, migrain headaches, essential tremors 3. SE: _exacerbation of bronchospasms in nonselective, bradycardia, worse acute HF, masks signs of hypoglycemia in diabetics!!_

Answer 47

inhibits bradykinin degradation significant efficacy improvement when combined with diuretic SYNERGISTIC RELATIONSHIP ANTI-HTN DOC in **_diabetics, CKD, LV dysfunction, HF_** and **prevents remodeling**!! SE: _dry cough in 20%, angiodema_

Answer 48

losartan like ACE but no cough! renoprotective in diabetics

Answer 49

aliskren i. binds with renin, stopping it from working and blocking the initiation of RAAS ii. increased cost vs ACE but similar in efficacy

Answer 50

preferrable in _blacks and elderly_ **1. dihydropyridine** _reflex tachycardia, headaches, periphreal edema_ **2. nondihydropyridines** **used for arrythmias** _can exacerabte HF so don't use in HF patients, bradycardia, don't use with BB_

Answer 51

relax smooth muscle and decrease SVR _tachyphylaxis_ common with _prazosin_ SE: _postural hypotension and syncope following 1st dose_, palpitations, headache useful in BPH _(prostatic hypertrophy)_

Answer 52

methyldopa, clonidine stimulate CNS presynaptic alpha-2 receptors _reducing efferent peripheral sympathetic flow_ _postural hypotension_ but benefits they come in a _patch_ and are effective for 7 days

Answer 53

initial tx: thiazide dieuretic exception: diabetic, move right to the ACE and add dieuretic later, multiple agents are often needed here

Answer 54

1. Initial rx: thiazide diuretic with some exceptions if diabetic start on ACE then use thiazide diuretic later, multiple agents often needed 2 . initial low dose and follow up in 4-6 weeks 3. titrate up to moderate/high dose before adding a second agent exception: i. if the first drug is a thiazide, low dose is sufficient and shouldn’t increase the dose so add the second med instead of increasing the dose 4. second drug would be BB, ACEI, or Ca blocker Exception: ii. if **BP is \>160/90 can start dual Rx** at the same time 5. most patients will be controlled with 2 drugs, but if need three, usually diuretic, ACE and CCB

Answer 55

**1. Holter monitor** - 2 lead EKG - 24 hours **2. external event monitor** - most patients use this now - allows for monitoring for _weeks or more_ - helpful when the experiences are _spread out and infrequent symptoms_ - when patient has symptoms they push a button and it stores the information **3. implantable loop recorders** - monitoring for up to _3 years_ - hold up to the _phone and the receiver_ the cardiologist has interprets it - continuous

Answer 56

1. arrythmia detection and correlating it with patient symptoms 2. evaluation of syncope 3. arrythmia tx effectiveness

Answer 57

1. _CP/angina pectoris_ 2. functional ability in _CHD_ 3. screening of _high risk_ individuals with atypical symptoms 4. response to intervention (cath, CABG), check them before they are released 5. screening for patients with certain occupation requirements

Answer 58

age, gender, characteristic of CP 1. substernal? 2. brought on by exertion? 3. relieved by NTG?

Answer 59

1. _asymptomatic_ men and women of all ages 2. _women \<50 with atypical CP_ avoid stress testing in this group!! high rate of false positives and then you are stuck with the results and have to work them up!

Answer 60

1. men of all ages with _atypical chest pain_ 2. women _\>50 with atypical chest pain_ 3. women _30-60 with typical CP_ stress tests warrented in this group for DX of CAD!

Answer 61

1. men \>40 with typical CP 2. women \>60 with typical CP might provide _prognostic value_ in this group, may want to consider _coronary angiograph instead because high risk!_

Answer 62

1. evidence of _ishchemia with ST depression of T wave inversion_ 2. achieve target _HR of 85-90%_ of predicted maximal HR (220-age) 3. dangerous _arrythmia_ 4. _decreasing BP! STOP!_

Answer 63

must achieve 85-90% of maximal predicted HR!!! otherwise you can't say the test was negative!!

Answer 64

**1. _adenosine_**: dilates coronary arteries used in _nuclear imaging_ **_2. dypyridamole:_** dilates coronary arteries used in _nuclear imaging_ **_3. regadenoson_** dilates the coronary arteries \*\*\*MOST COMMONLY USED\*\*\*give _bolus injection_ works like adenosine **_4. dubutamine:_** increases HR and contractility used in _echo!_

Answer 65

_combine both imaging and EKG_ increases specificity to 90% downside: cost

Answer 66

treadmill stress test!

Answer 67

downward or horizontal sloping ST depression or T wave inversion

Answer 68

1. high incidence of _false positivites_ in young healthy women w/o risk factors and atypical CP ## Footnote 2. decreased sensitivitiy in women with CHD because they are more likely to have 1 vessel disease 3. _ORDER STRESS WITH IMAGING FOR THESE PEOPLE!_ young without RF or atypical CP

Answer 69

1. **ischemic hearts: decreased or absent contraction seen on echo** **if large ischemia get _large heart with decreased EF_** in normal hearts: contracts normally, heart gets smaller with exercise and EF increases!

Answer 70

**thallium or _TC99 SESTAMbib_** distributes these to heart via blood flow and then through _Na/k pump_, active areas light up, _inactive show defect_ compare resting and stress images for areas of _reversible ischemia_ aka lit up area originally that then turns dark

Answer 71

1. LVH 2. LBBB 3. Digoxin 4. WPW abnormality!! \*\*DON'T READ THEM, YOU'LL LOOK DUMB!!!\*\*

Answer 72

noninvasive 2D tests with doppler options: transthoracic echo or TEE Tells about: 1. _LV function and EF_ _2. hypertrophy, dilation_ _3. endocarditis via TEE_ _4. HF, valvular insufficiency/stenosis_ _5. effusion_

Answer 73

1. enters _central vein_ 2. right atrium, right ventricle, pulmonary artery, pulmonary capillary wedge _invasive monitoring for critically ill patients_ records: pressure and oximetry complications: pneumothorax, arterial puncture, infection, thrombis

Answer 74

1. enters _artery_ 2. aorta, aortic valve, LV, LA _CORONARY IMAGING DONE FROM THIS SIDE!!!!_ - contrast injected into coronary arteries to identify stenosis/occlusions complications: death, stroke, bleeding, thrombis/emboli

Answer 75

left heart cath to do coronary angiography ## Footnote do in: high risk individuals with classic ischemia symptoms

Answer 76

3D imaging of coronary arteries using contrast dye _lacks sensitivity and specificity compared with contrast coronary angiography_ **indications:** 1. intermediate risk for CHD 2. atypical CP with low to moderate risk 3. unclear/inconclusive stress test

Answer 77

complete occlusion of the coronary artery 1. progressive narrowing via _atherosclerosis_ 2. _sudden occlusion_ via ruputure, erosion, fissuring of plaque with superimposed thrombosis

Answer 78

1. history and physical 2. cardiac enzymes 3. EKG

Answer 79

rise 4-6 hours after MI, so when pt is in the ED with symptoms and ST elevation, it is expected the first set would be negative, keep this in mind, if taken 4-6 hours post MI then you will see these as positive

Answer 80

**1. CK MB** **rises in 6 hours after infarct** **2. troponin (cTn)** rises _2-3 hours earlier than CK-MB_ so slighty better

Answer 81

_\>1mm ST depression_ that is _horizontal_ or _downward_ sloping that persists for _.08 sec past J point_ ## Footnote \*\*only needs to be in 1 lead!!\*\* compare the PR segment and the ST segment using the J point **2 other causes:** hypokalemia, digoxin

Answer 82

The end of the QRS and the begining of the ST segment

Answer 83

1. LVH 2. LBBB 3. digoxin 4. WPW

Answer 84

**1. T wave peaking followed by T wave inversion** first couple hours "ischemia" **2. ST elevation at the J point in two or more _contigious leads \>1mm_** after a couple hours "injury" **3. Q wave formation \>.04 seconds wide and \>1/3 the height of the R wave** "death"

Answer 85

aVR these Q waves are never significant!!!

Answer 86

1. ischemia but NOT dianostic for MI 2. first couple hours then they invert 3. "hyperacute T waves" 4. potentially reversible if blood flow is returned, T wave will return to normal

Answer 87

1. occurs after a couple hours 2. _ST elevation at the J point \>1 mm in two or more **contigious** leads_ 3. can be in limb or precordial 4. INJURY beyond ischemia!!! occurs in acute MI but can return to normal if blood flow returned tells you that a true infarction has occured and that it will evolve into death unless there is immediate intervention

Answer 88

ventricular aneurysm

Answer 89

1. some people have regullarly elevated ST segment 2. common in young healthy individuals 3. ST returns to baseline during exercise How to differentiate from MI: 1. _t wave remains an independent waveform, aka the ST segment doesn't blend with T wave_ 2. _in MI: ST merges with T wave_

Answer 90

1. occurs 2-3 days later 2. _\>.04 seconds wide and \>1/3 height of R wave_ 3. "death" has occured, not reversible 4. diagnostic of MI 5. by the point Q waves develop, ST returns to baseline 6. persist for lifetime of pt

Answer 91

when mycardium dies, it is **_electrically silent_** and all the electrical stimulation is conducted **_AWAY_** from it, so that is why you get a **_DEEP NEGATIVE DEFLECTION Q wave_**

Answer 92

left lateral leads V5, V6, aVL and I

Answer 93

leads at a **_distance_** from those showing ST segment elevation may show changes that are **_opposite_** those in the infarct leads: **_ST depression and T wave inversion_** \*\*think about it, as the tissue starts to die, the current is directed to other areas of the heart, so these new leads now see the current comming TOWARDS them so you will get **_tall R waves, ST deoression and T wave inversion\*\*_** keep in mind, not all of the reciprocal leads need to show changes, might only see it in 1 or not at all, totally depends!

Answer 94

1. left anterior descending=anterior heart and interventricular septum ## Footnote 2. left circumflex artery=lateral heart (left ventricle)

Answer 95

**right coronary artery** **changes in inferior leads II, aVF, III** **reciprocal: lateral leads I and aVL** **\*\*\*If there are changes in V1-V3 as well where the _R is super tall_ consider this person is having a posterior MI as welll since the right coronary arter also feeds the posterior wall!! DONT CONSIDER THESE RECIPROCAL CHANGES!!\*\*\*\***

Answer 96

II, aVF, III reciprocal if present in lateral leads! I and aVL

Answer 97

**left lateral circumflex artery** **changes: I, aVL, V5, V6 (lateral leads)** **reciprocal in: inferior leads!**

Answer 98

changes: aVL, I, V5, V6 reciprocal changes in inferior leads!

Answer 99

**left anterior descending artery** **changes: any precordials esp V1-V4** this can be easy to pick out with poor R wave progression **reciprocal: inferior leads**

Answer 100

**left main coronary artery** **changes: I, aVL, all precordials** **reciprocal changes: inferior leads** \*\*think about it....the left main coronary supplies both the anterior and the lateral branches so therefore it makes sense you would have changes in both of these!

Answer 101

anterior infarction V1-V4 shows anterior heart

Answer 102

**90% of patients are supplied by right coronary artery** **changes: _instead of ST elevation you see ST DEPRESSION and TALL R WAVE IN V1,_** this is a mirror image of anterior infarcts because you don't have leads that overly the posterior back 1. must distinguish between this and right axis deviation because in RAD you will also have tall R wave so need to check V6 for large S wave 2. often occurs with INFERIOR MI because they are from the same blood supply of the right cornary artery in the pic...note tall R waves in V1, to rule our RAD, look at V6, there are tall R instead of deep S so this is posterior MI

Answer 103

often occurs with inferior MI because they are from the same blood supply of the right coronary artery

Answer 104

through the entire thickness of the wall of the heart causing Q waves

Answer 105

only through a portion of the thickness of the heart

Answer 106

the only EKG finding with non-q-wave infarctions are **_T wave inverisons and ST segment depressions (not elevation)_** lower mortality rate higher rate of reinfarct \*\*\*\*\*\*\*\*\*in this case you check cardiac enzymes because if elvate this would suggest MI, where as if they were normal it would mean ischemia\*\*\*\*\*

Answer 107

in non Q wave mi the indication is: ST dpression and T wave inversion which is the same as ANGINA **to tell the difference:** 1. order _cardiac enzymes_, elevated in MI 2. ST depression and inversion _will return to normal when angina ends_ (nitro), but non Q wave MI the depression and inversion will stay down for _48 hours_

Answer 108

angina that causes ST elevation from spasms ST segments return quickly to baseline when patient is given antianginal medication

Answer 109

magic number is 3 3 seconds pause, if longer than this the heart doesn’t get blood to the organs, usually the brain is the first noticeable one so you get syncope, dizziness, and lightheadedness

Answer 110

most common in ELDERLY the pause followed these can cause _syncope, dizziness_ **_Sinus Arrest:_** SA node doesn't fire **_Sinus block:_** SA node fires but the signal is blocked so it doesn't cause _atrial depolarization_, usually caused by _scar tissue_ \*\*\*you can't determine between these on a EKG have to insert a cath to distinguish between the presense of an impuslse and the lack of impulse\*\*\* drug causes: _bb, NCCBs_ person might need a pacemaker!

Answer 111

**_Junctional escape rythmn:_** Narrow QRS 40-60 bpm **_ventricular rythmn:_** Narrow QRS with 30-45 bpm

Answer 112

**_PR interval \>.2 seconds!_** _want to look at the limb leads for this, think of it like a "delay"rather than a block_ can be in normal or dieased hearts caused by _prolonged delay at AV node or bundle of HIS causing a longer PR interval_

Answer 113

**sinus arrest with alternations of paroxysms or atrial tachycardia and bradyarrythmias and clearly related to _sinus node dysfunction_** (hence the name, duh) "SA node dysfunction with symptoms"..most commonly cause by aging 40% will have AV node dysfunction _1. afib:_ controled or slow rate _in the absence of meds_ _2. brady-tachy synddrome:_ artial tachyarrythmias and symptomatic bradycardia DX: 24 hour holter monitor **tx: permanent dual chamber pacer with auto ICD**

Answer 114

not every atrial impulse is able to pass through the AV node into the ventricles more QRS than P waves since not all of them make it through **Mobitze Type 1 second degree block: Wenchebach** **Mobitz Type II second degree block**

Answer 115

**_WITHIN the AV node_** usually benign and rarely goes on to third degree HB NEVER SEE MORE THAN ONE DROPPED BEAT IN A ROW, IF YOU SEE THIS THEN IT IS A MOBITZ TYPE 2 **_lengthening of PR interval_** and then **_p wave without QRS_**

Answer 116

**_BELOW AV NODE IN BUNDLE OF HIS_** dangerous and pt usually needs a pacemaker, can progress to third degree AV block presence of a dropped beat **_WITHOUT lengthening of the PR_** interval, **_RANDOM dropped QRS,_** **_CAN HAVE MORE THAN ONE IN A ROW_**

Answer 117

"complete heart block" MEDICAL EMERGENCY!!!! ALWAYS NEED PACEMAKER no atrial impulses make it through to stimulate the ventricles **_each are beating INDEPENDENTLY!! the block prevents the atria and ventricles from communicating_** \*\*QRS are wide and bizarre looking almost like PVCs since they are from ventricular origin\*\* AV dissociation where the ventricular rate is slower than the atrial rate atria: 60-100 junctional: 40-60 ventricular: 30-45 THEY MARCH OUT INDEPENDENTLY!!

Answer 118

1. lyme disease...so check titers ## Footnote 2. congenital heart block, they are born with it where their junction rythmn has been sufficient to supply blood so they are asymptomatic

Answer 119

degenerative disease of the conduction system

Answer 120

**_1. QRS \>.12_** **_2. V1 and V2 have R-S-R' with rabbit ear appearance_** reciprocal changes in lateral leads with _DEEP S wave!_ Handlers explaination: in RBBB, the left bundle branch still works so the conduction runs down the left side, usually on a EKG you only see the left ventricle contraction which gives you the R wave, however, in RBBB the left ventrcile is reponsible for causing the right ventricle to depolarize so the conduction goes from the _left side over to the right_ cell by cell which is _why depolarization has a longer duration and a R’ spike in V1 and V2, the R’ is the right ventricle depolarizing_. this process is a _left to right depolarization_

Answer 121

**_1. \>.12 QRS_** **_2. Broad/notched QRS in V5/V6_** **_ALWAYS WILL HAVE DOWNWARD Q or RS in V1_** reciprocal in: V1/V2 with wide deep S wave

Answer 122

the left bundle branch is made up of _two fasicles, so either of these can become individually blocked_ _1. left anterior fasicle_ _2. left posterior fasicle_ they cause axis devation they have NORMAL QRS, and _must rule out other reasons for axis deviation_ (aka LVH, RVH)

Answer 123

occurs on the left bundle branch!! MOST COMMON HEMIBLOCK IN NORMAL AND DISEASED HEARTS! **1. NARROW QRS** **2. left axis deviation \> (-30)** **3. NO OTHER CAUSES OF LAD** **STEPS:** **1. determina LAD via I and aVF** **2. should also be negative in II** (headed away and more neg) rushes down the posterior fascile and swoops down and up traveling in a inferior superior, and right to left direction!! think about it

Answer 124

LEFT ANTERIOR FASICLE HEMIBLOCK

Answer 125

**_SICK HEARTS ONLY_** **1. narrow QRS** **2. RAD** **3. no other reason for RAD (like RVH)** **4. tall R waves inferiouraly, deep S waves laterally** runs down the anterior fasicle traveling superior to inferiorly and left to right depolarization

Answer 126

**temporary reduction of blood flow to an organ, potentially reversible, caused by mechanical, electrical, and valvular dysfunction** can be reversible or peremanent depending how long it has been happen for, can lead to _infarction_ this can cause angina when there is increased activity Contributory factors: significant LVH, aortic stenosis, tachyarrythmias like afib/aflutter **symptomatic:** **1. angina pectoris** **1.** O2 demand in the presence of fixed stenosis - VASOSPAM and significant narrowing **1. prolonged decreaed O2=unstable angina or infarction** **-**acute thrombis likely present

Answer 127

**1. death within 1 hour after onset of symptoms usually within minutes** **2. malignant arrhytmia commonly present** common presenting manifestation of CHD, frequent end point in patients with CHD propr to MI and imparied LV function

Answer 128

**1. atypical symptoms: pain radiating to _right arm_**, _arm pain along_ 2. many women produce false negative stress tests since single vessel disease more common **3. elderly or diabetic womeon complain of general malaise, loss of appetite, vague abdominal pain** so if they have RF, GET EKG!!

Answer 129

chest discomfort described as **tightness, pressure, aching, choking that is often REPRODUCIBLE WITH ACTIVITY that *resolve after cessation of activity, relaxation, or NTG*** positive _levine sign substernal to left sternum, with crescendo/decresendo pattern 1-5 mins_, less likely to happen in AM (lower threshold) can be brought on by: exertion, exercise, emotional stress,cold weather, cigarettes, sex physical exam may be normal between episodes, may see _xanthomas from hyperlidemia, AV nicking from HTN/DM, s4 gallop during angina, changes in BP_

Answer 130

**1. EKG:** normal between episodes **ST segment depression/T wave change during angina** then normalize after angina passes **2.** **Stress EKG: most helpful non invasive tool** -increase workload with meds or exercise, compare resing and stress EKG for ischemia, may consider *adding image to make it more specific, ability to detect dermines the amoutn of vessel involvment* **3. coronary angiography- Gold standard for CAD** -tells which vessels are involved, degree of stenosis, and LV function

Answer 131

sublingual NTG ## Footnote _reduces LV volume preload and decreasing O2 consumption_ does this by causing venodilation, so that it decreases the amount of blood heading back to the heart, decreasing the volume and decreasing O2 demands

Answer 132

**1. beta blockers ATENOLOL, METOROLOL: decreases HR, contractility, and BP improving exercise tolerance** \*\*\*\*\*REDUCE MORTALITY IN POST MI AND HF PATIENTS\*\*\* **2. long acting nitrates isosorbide dinitrate** \*\*\*\*DONT TAKE THIS WITH VIAGRA!!!!\*\*\*\*\* \*\*\*\*can develope nitrate tolerance so need to dose in intervals!!\*\*\*\* **3. Non dihydropyridine calcium channel blockers** dilate ARTERIES, decreasing afterload, decrease myocardial O2 consumption **4. dyhydropyridine calcium channel blockers****amlodipine, nifedipine** dilate ARTERIES, decrease afterload and myocardial O2 consumption \*\*\*best used in combination with a BB, reduce risk of HYPOTENSION\*\* **5. diltiazem and verapamil** used with nitrates, dilates arterioles decreasing afterload, decrease HR, and O2 consumption \*\*\*don't use in HF patients!!\*\*\* **6. ranolazine** chronic angina that isn't controled with the above \*\*increase QT interval, but won't cause arrythmia\*\* **7. antiplatelet drugs** **_USED IN ALL PTS WITH CHD, PAD, AND CAROTID, DECREASES INCIDENCE OF CARDIAC DEATH AND MI_**, low dose asprin

Answer 133

diltiazem and verapamil

Answer 134

NITRO isosorbide dinitrate

Answer 135

nonselective beta blockers Use selective beta blocker!!

Answer 136

Beta blockers Atenolol and metoprolol

Answer 137

**1. patients with unacceptable symptoms controlled with meds** **2. 3 vessel CAD with LV dysfunction _OR_ left main coronary stenosis that compromises Left anterior descending (LAD)** LEFT main artery consider CABG!! **3. patients post MI with ongoing ischemia** **4. acute MI**

Answer 138

angioplasty restenosis rate: 30-40% angioplasty with stent placement: 15-20% **drug eluting stents restenosis: 5-8%** 1. single or 2 vessel disease 2. 3 vessels disease in pt that doens't qualify for operative drug eluting stents helped decrease rates of restenosis a lot, however probles with _late thrombosis so requires intense anti-platelet RX of **ASA and clopidogrel**_

Answer 139

coronary arteries are bypassed using arteries or veins, low mortality if LV preserved **saphenous veins and mammary arteries most commonly used** **_internal mammary artery graft has highest patency rate over time_**\*\*BEST OPTION WHEN POSSIBLE because arteries last longer than veins\*\* mortality increase with age and EF

Answer 140

can be in normal cornary arteries or superimposed o atherosclerotic ones, the **spasms cause the artery to close** often induced by _cold, emotional stress, meds, and cocaine_ _angina at rest with ST elevation_ \*\*can progress to MI if symptoms don't resolve\*\*

Answer 141

**coronary ishchemia from _vasospasms_** symptoms at rest, usually in AM women\> men ateriography shows normal looking arteries Tx: nitrates and calcium channel blockers (dihyrdopyridines)

Answer 142

20% will remain unstable and need revascularization 80% will get better clinicallly and need to get stress test once stable, if they produce a positive test then it might be an indication for *revascularization*

Answer 143

angina _at rest with minimal activity \>10 minutes_ GET VERY CLOSE TO HAVING A MI BUT DONT, RIGHT AT THE BRINK OF CELL NECROSIS BUT TISSUE HASN'T DIED YET, _high risk for developing MI in following days/weeks so much treat aggressively and quickly_ VERY SIMULAR TO NSTEMI, except in unstable angina negative cardiac markers **new onset:** angina **accerating or cresendo angina in pt with previously stable angina** (gets worse doing less activity) DX: **NEGATIVE CARDIAC ENZYMES** **EKG: ST depression, T wave inversion** Tx: 1. HOSPITALIZE THEM!! BEDREST!! 2. **_full anticoagulation and antiplatelet therapy_** **-HEPARIN +ASA+** **prasurgrel/ticagrelor/clopidigrel OR glycoprotein IIb/IIIa** **3. nitrates, Beta blockers, and Ca-blockers to decrease MVO2**

Answer 144

50% so worry about the 50% that have a normal one, still might need to work them up

Answer 145

cardiac enzymes ## Footnote ck-creatine kinase MB troponins these indicate cell death and that the scale has tipped over the point of unstable angina and cell death is occuring, this is a myocardial infarction

Answer 146

**infarcts caused by prolonged ischemia** CAD to plaque rupture to platelets to clotting to thrombus _small infarcts that are **unstable** and could go on to cause a bigger infarct_ so that is why we treat aggressively "incomplete infarcts" with lower initial mortality but _high risk of re-infarction with HIGH MORTALITY_ DX: like unstable angine **with POSITIVE CARDIAC ENZYMES**

Answer 147

stress test!! low level then maximal stress 6 weeks post MI want to make sure they can saftely return home

Answer 148

increase risk of reccurent MI by 50% post 1st MI. ## Footnote includes ALL nsaids, short and long term use!!

Answer 149

10-15% determined by the size of the MI

Answer 150

1. recurrent ischemic pattern 2. nonSTEMI infarct 3. HF 4. low level stress test causing ishcemia 5. high grade ventricular arrythmia

Answer 151

prolonged ischemia resulting from inadequate tissue profusion leading to _cell death and necrosis_ total occulsion CAD to plaque to rupture to platelets to clotting, to _occlusive thrombus_ "elephant sitting on my chest and the worst pain I have felt in my life" often early in the AM since coronary tone, SEVERE PAIN, **anxious, diaphoretic, and distress, LV dysfunction** variable pulse and BP, _S4 gallop,_ _apical mitral regurgitation_, cold, cyanotic, low CO, _ST elevation_ DX: 1. **Creatinine kinase (CK) ALWAYS ELEVATED!** check **CK-MB,** specific to damanged heart muscle **2. troponins cTnl** represents muscle breakdown, sensitive to small infarcts **3. leukocytosis** **4. EKG _ELEVATED ST_** **5. echo** left ventricular function, identify mitral regurge

Answer 152

**1. percutaneous coronary intervention to reprofuse tissue (CATH)** - _goal: open artery within 3 hours of onset of symptoms_ _goal: open atery within 90 mins presenting to hospital_ \*\*\*If within hour and a half of hospital that does this, consider transfer!!! Must also have CABG CAPABILITY\*\*\*\* **2. thrombolytic (finbrinolytic) therapy: done if no access to cath lab, t-PA (altepase)** -done when _ST elevation \>1 mm in tow or more adjacent leads_ 50% reduction in mortality if given withint 1-3 hrs of symptoms **3. post thrombolytic management** **a. ASA ongoing** **b. heparin 24 hours**

Answer 153

1. morphine sulfaste 2. aspirin in ED 3. nitro IV

Answer 154

**absolute contraindications:** 1. uncontrolled HTN 2. **stroke within 1 year** **3. cerebral hemmorahage** **4. recent head trauma** **relative contraindications:** 1. abdominal or thoracic surgery within 3 weeks

Answer 155

1. rapid resolution of pain 2. ventricular arrythmia (PVCs, VT, AVIR) 3. rapid evolution of EFG (often q waves)

Answer 156

percutaneous coronary intervention....CATH

Answer 157

transferring them!! instead of giving them thrombolytics!

Answer 158

**1. _BETA BLOCKERS_**: decreases wall tension preventing MI complications, decreases morality! **2. nitrates** **2.5 heparin** **3. asprin/clopidigrel** **4. ACE inhibitors:** ***i_mprove short and long term survival, decrease LV remodeling post MI,_** great for **large infarcts*** **5. alosterone blockers** **6. statins LDL goal**

Answer 159

1. atrial and ventricular arrythmias 2. **left ventricular dysfunction** **3. mitral regurgitation, murmer from papillary muscle dysfunction** **4. hyptension and shock** 5. ventricular aneurysm formation

Answer 160

1. full anticoagulation and antiplatelet therapy **-HEPARIN +ASA+** **prasurgrel/ticagrelor/clopidigrel _OR_ glycoprotein IIb/IIIa** 2. **nitrates** **3. Beta blockers** **4. Ca-blockers**

Answer 161

allows you to score the risk of a patient who you think is having a ACS scores of \>3 are high risk

Answer 162

rise: **4-6 hours** peak: 1**6-24 hours** fall: **2-3 days**

Answer 163

rise: **4-6** peak: **8-12** remains elevated: **5-7 days** dianostic if \>.1, abornal if \>.05 This test is the most specific and sensitve, can test for small MI

Answer 164

Left sided: DOE, orthopnea, PND, weakness, fatigue, peripheral edema, etc. Right sided: unexplained weight gain, peripheral edema, abdominal fullness (hepatomegaly, ascites).

Answer 165

**MOST commony type of cardiomyopathy, esp in black men** often caused by _post infectious-myocarditis_, toxix alcohol, endocrine, "ischemia cardiomyopathy" _reduced strength of ventricular contraction_, causing dilation of left ventricle, _left or biventricular failure_ causing dyspnea, _s3 gallop, pulmonary crackles_, _increase JVP_ _cardiomegaly, PMI displaced laterally, TR murmer_ causes: genetic abnormalities (25-30%), alcohol consumption, postpartum, idiopathic DX: - do echo/doppler - EKG, nonspecific changes _excludes other diagnosis_ CXR: cardiomegaly Tx: 1. ACE to decrease afterload 2. Beta blockers 3. dieuretics/nitrates 4. anticoag unless contraindicated

Answer 166

Dependent on length of Sx and functional class. If onset recent, some recovery of ventricular function can occur. Class IV patients: 50% one year mortality Cardiac Transplantation: \>70% 5yr. survival **Only meds that may improve survival are ACEI (or ARB’s), ß-Blockers and Spironolactone.**

Answer 167

**massive hypertrophy, \*\*_usually of septum (assymetric septal hypertrophy)\*\*,_ left ventricle** unrelated to pressure overload, present at birth, _diastolic dysfunction, suddent death in athletes!_ (small left ventricle so can't get enough blood and the leaflet blocks the outflow tract) OFTEN ASYMPTOMATIC IN CHILDREN patients present with **dyspnea and angina, syncope and _arrythmia like Afib that can lead to sudden decompensation and sudden death may be the first presentation in young athletes during strenous activity!!!!!_** on exam: sustained PMI, _loud s4 and S3_, **_loud harsh aortic outflow murmer_** **_cresendo-decreshendo is charactericstic (INCREASED MURMER WITH VALSALVA AND STAND, DECREASED SQUATTING!!!) KEY!!_** variable systolic murmer, jugular venous pulsations _bisferiens pulse with double/triple pulse_ because the ventricle is contracting against the obstuction of the aorta by MV leaflet DX: EKG: might show LVH echo: **key!! show LVH, asymmetrical septal hypetrophy and small left ventricle, and _diastolic dysfunction_** **tx:** 1. **_Beta blockers,_** **_calcium channel blockers (verapamil)_** 2. **_myomectomy_** (to remove extra septal muscle) 3. **_ablation_**, **_ICD_**, **_dual chamber pacers_** and mitral valve replacements as needed

Answer 168

Genetically transmitted in \>50% of cases. Autosomal dominant with high penetrance Must perform echocardiography on all siblings and offspring of a patient with HCM. Genetic counseling is essential

Answer 169

"handler: the area right below the aorta outflow tract narrorws because the intraventricular septum grows and it closes off, so the mitral valve leaflets move abnormally towrads the intraventricular septum and blocks this area so the blood can't get out of the left ventricle, this is _dynamic_ meand the amount of blocking depends on the activity you are doing" obstruction: MV moves abnormally towards the intraventricular septum obstructing the Left ventricular outflow tract **_myocardial fiber hypertrophy and disarray_** **_mitral valve often thickens causing abnormal movement blocks the blood getting out of the heart_**

Answer 170

**fibrosis/infiltration of the ventricular wall because of collagen defects like** **causing the ridgid walls to prevent diastolic filling** characteristic: abnormal diastolic function pts present with **dereased exercise tolerance, in sever get right sided HF, _pulomary hypertension usually present, jugula venous distension, S3/S4, inspiratory increase in venous pressure (KUSSMALS SIGN)_** DX: echo!!! may need endomyocardial biopsy see LV wall thickening decreased diastolic relaxation tx: diuretics and cardiac transplant in extreme, CCB might help with symptoms

Answer 171

90% can't treat it, just help with symptoms CCB might help in some patients

Answer 172

Amyloidosis Hemochromatosis Fabry Disease Gaucher Disease Endomyocardial Fibrosis-Loeffler Endocarditis-hypereosinofilia syndrome

Answer 173

**LDL:** carries lipid to the arteries after being oxidized **HDL:** removes lipids from the arteries \*\*together these contribute the the managing of atherosclerosis\*\* role of tryglycerides is unknown

Answer 174

liver and intestines exogenously: diet

Answer 175

**_converting HMG CoA to mevalonic acid by HMG CoA reductase_** \*\*this is where statins work\*\* when you increase intake of dietary cholesterol_: down regulation of LDL receptors and elevation of LDL cholesterol_

Answer 176

1. significantly reduce mortality and mobidity of coronary heart disease ## Footnote 2. slow progression of atherosclerosis

Answer 177

5-7x greater!

Answer 178

4-6 times greater

Answer 179

TRICK QUESTION...there are no goal levels anymore, it is based on _intensity of statin therapy!!!_

Answer 180

lower we can lower the LDL the better we are at preventing ASCVD and progression get it down and keep it down

Answer 181

**irritation of the parietal pleura adjacent to pericardium** **often following _autoimmune disorders SLE, post MI, \*\*viral infections most common COXSACKIE B VIRUS\*\*, neoplasm_ _chest irriation_, dresslers syndrome** **retrosternal/left precordial pain, may radiate to _tip of left shoulder_** **"KNIFE LIKE STABBING"** that is severe! provoking: breathing, changing positions, laying down, swallowing palliating: _leaning foward_

Answer 182

CP, _pericardial friction rub scratching, grating_ from epicardium and pericardium grating on each other _usually heart two components (Systolic/diastolic)"evanesence" here today gone tom"_ venricular systole and early diastole ## Footnote provoking: _pain is worse laying supine, with inspiration, coughing, swallowing, laughing, pain just as bad as MI_ _Palliating: leaning forward, sitting up_ _**\*\*\*YOU GET ST ELEVATION IN ALL LEADS EXCEPT AVR and V1!!!!!!\*\*\***_ **_(must distinguish from early polarization with healthy individuals which causes ST elevation)_** **ECHO** _**EVERY PATIENT MUST HAVE THIS DONE**!!!!_: may see small **_pericardial effusion and make sure they don't have tamponade cause if this progresses could be dangerous_** also tells you if there is abnormal LV size and function which would indicate MYOCARDITIS as well, in pericarditis you DONT see this!!!

Answer 183

1. bedrest until pain and fever resolve, most treated as out patient 2. **NSAIDS for pain VERY EFFECTIVE!!! (opposit as myocarditis)** **3. DONT USE ANTICOAGULATION** 4. takes 2-4 weeks to recover

Answer 184

**most severe and dangerous side effect of acute heart failure** 1. hypertension and back up causes pressure to increase in capillary bed 2. fluid moves into the alveoli causing stiffness and preventing the lungs from expanding 3. hemoglobin not oxygenated resulting in SOB and cyanosis grasping for air, _rapid pulse_, skin _moist and cool_, lips and nails cyanotic, confusion, stupor, _frothy pink cough, crackles_

Answer 185

the pulmonary circulation is usually a low pressure system pulmonary hypertension: increase in pressure of the pulmomary system, usually the _pulmonary arteries_ this system is _selfperpetuating, once you have pulmonary hypertension, you get structual abnormalities that include smooth muscle hypertropy and proliferation of vessel intima making the problem worse_ 1. secondary pulmonary hypertension (most common) 2. primary pulmonary hypertension

Answer 186

**increase in pulmonary pressures due to secondary cause** most common: cardiac or pulmonary causes Challenges: 1. if from back flow from cardiac issues: the HTN causes the arteries SM hypertrophy and proliferation of intima...perpetuating the problem 2. if from respiratory and hypoxia: the vessels constrict more, perpetuating the problem \*\*\*YOU CAN'T WIN EITHER WAY!!\*\*\* **1. mitral valve/left ventricular dysfunction:** increased LA pressure, backs into pulmonary venous to pumonary arterial, leads to _thickening of pulmonary arteries, perpretuating the problem and causing sustained HTN_ **2. pulmonary thromboemboli** **3. hypoxemia from COPD/interstital lung disease**: for some strange reason the pulmonary arteries constrict under hypoxic environment unlike regular arteries, this perpetuates the problem **4. high altitudes/sleep apnea** DX: radiographic, echo, US Tx: treat underlying cause

Answer 187

elevation in pulmonary arterial pressure in the absense of an identified cardiopulmonary reason **abnormal proliferation and contraction of vascular SM, coagulation abnormalities, and marked intima fibrosis leading to obliteration and obstruction of pulmonary arteries and aterioles** **leading to _progressive right sided HF__, low CO, and death_** autosomal dominant can be associated with appetite suppressing drugs _fenfluramine_ and _HIV!!!!!_ reduced levels of _NO and prostacyclin_ which are potent vasodilators sob with marked periphreal edema Tx: CCB, prostacyclin analogs, endothelin antagonist, PDE5 inhibitors

Answer 188

**when the heart fails to pump blood sufficiently to meet the needs of the body** _hypotension, hypoprofusion, hypoxemia_ despite adequate volume **Most common cause: AMI** also: myocardial contusion, acute mitral valve regurg to papillary muscle rupture \*\*since there isn't enough profusion, causes activation of the sympathetic and renin-angiotensin system which makes the problem worse because it _increases afterload and preload overwheling the heart_\*\*

Answer 189

1. lips, nails, and skin become cyanotic 2. mean arterial and systolic pressure drop due to poor stroke volume 2. 5 narrow pulse pressure 3. normal diastolic pressure 4. rise of pulmonary capillary wedge of 15 mmHg 5. neurologic changes because of low CO and brain profusion

Answer 190

**pharm goal: increase contractility without increasing HR** _1. dopamine #1 choice_ 2. dobutamine or NE **non pharm: mechanical intraaortic balloon pump via cath** 1. pumps in synchrony with the heart 2. inserted into decending aorta 3. inflates during diastole and pushes the blood along, relaxes during systole 4. _enhances coronary and systemic profusion and decreases afterload_ _and myocardial oxygen demands since not working as hard_

Answer 191

1. vascular injury like smoking DM facilitates the uptake of lipoproteins 2. increase in LDL (oxidized) directly leads to vascular damage and premature atherosclerosis 3. LDL oxidation is nessacary for endothelia damage 4. _HDL_: cardioprotective and prevents the oxidation of LDL, reverse transporter of cholesterol

Answer 192

1. **_athlerosclerosis_** disease like PVD, CHD 2. **_eruptive xanthomas_:** can be seen on the buttocks with extremely high levels of triglycerides 3. **_tendinous xanthomas_:** very high LDL, nodules on tendons most commonly on achilles, back of hand, and patella 4. **_xanthelasma_**: yellow plaque on the skin around the eyes

Answer 193

diet, lifestyle and genetics often detected in _asymptomatic adults during routine blood screening_ 1. DIABETES MELLITUS 2. nephrotic syndrome 3. Chronic renal failure 4. hypothyroidism

Answer 194

dyslipidemia

Answer 195

**primary prevetion:** lowering cholesterol/LDL will _prevent NEW ONSET CHD_, they don’t have it yet and you want to prevent them from getting it! **secondary prevention:** lowering cholesterol/LDL will prevent _recurring_ coronary events, they already have it so you want to prevent progression goal: _decrease total mortality in presences of existing disease_

Answer 196

**_lack LDL receptors or they are defective so the LDL isn't taken up by the liver to be degraded_** _heterozygotes:_ have _total cholesterol at birth \>350_ with high LDL _homoxygotes:_ have _total chonesterol \>700_ with high LDL PE: _tendon xanthomas, xanthelasma, cutaneous xanthomas_

Answer 197

1. has separate equations for men and women, whites and blacks 2. inputs 9 RFs to calculate risk 3. can’t calculate for \<40 year olds so must use clinical judgement 4. uses SYSTOLIC BP!! 5. for other ethnicities use sex appropriate white patient equation

Answer 198

basically anyone over 63

Answer 199

Hispanic american and asian america lower risk than whites american indian higher than whites

Answer 200

family hx of premature ASCVD high sensitivity CRP \>2 Coronary calcium score \>300 ABI \<.9 \*\*you need to use clinical judgement!!\*\*

Answer 201

lowers LDL by 50% atorvastatin, rousuvastatin

Answer 202

lowers LDL by 30-50% simvastatin, pravastatin, lovastatin or lower dose of atorvastatin, rousuvastatin

Answer 203

\*\*\*always use statins first unless for some reason the pt can’t tolerate them!\*\*

Answer 204

risk for developing CAD is controversial, however, may play a role when _LDL is also elevated_ associated with **_Very low density lipoprotein (triglycerides)_** inverse relationship between VLDL and HDL….so therefore _treat hypertriglyceridemia \>200_ associated with _obesity, T2DM, metabolic syndrome_ TX: 1. **very sensitive to diet, weight reduction and exercise** 2. **fibrinic acid or niacin**

Answer 205

CARDIOPROTECTIVE: facilitates removal of cholesterol in tissues, so has direct protective effects _reduced amount in:_ smokers, inactivity, and obesity _increases in:_ increases with: weight reduction, exercise, smoking cessation, estrogen therapy _strong inverse relationship between HDL and CV events,_ more HDL the less CV events

Answer 206

drugs that raise HDL-C do not reduce CV events--its the particle not its cholesterol that makes the HDL anti-atherogenic

Answer 207

1. smoking cessation 2. decrease intake of saturated fats 3. decrease total calories 4. increase physical activity 5. decrease sodium intake

Answer 208

diet is a major contributor to lipoprotein disorders **\<30% fat** **\<7% saturated fat** **\<200 mg cholesterol** **replace fats with carbohydrates**

Answer 209

minimum 10% weight reduction

Answer 210

rate limiting step in cholesterol synthesis; up regulates LDL receptors 1. low dose gives you the most bang for your buck, increasing dose you see less effective 2. can cause _chemical diabetes_ but the benefits outweigh the risks 3. _myalgia_ _4. myositis and rhabdomyolysis_

Answer 211

**_myalgia:_** : most common and benign, have then stop taking _measure CK_, usually normal and can usually _start again at a lower dose_ **_myositis/rhabdomyolysis:_** rare but life threatening, _muscle pain/weakness with increased CK \>10x the normal limit_ causing the kidneys to block up and can lead to _death_ DC THE DRUG!!!

Answer 212

stimulate the conversion of cholesterol to bile acids in the liver and upregulate bile acids in the liver decreases LDL constipation, GI issues

Answer 213

decrease VLDL lowers triglycerides raises HDL 20-30% GI DISRESS, flushing/itching (pretreat with ASA start with low dose and work upwards don’t use with statins, increase risk for myopathy!!

Answer 214

when added to a _statin_ there was additional LDL _lowering up to 25% and likely has synergistic effect_ this plus low/moderate dose statin is more effective in lowering LDL than doubling the dose of a statin!!! no in hepatic disease inhibits intestinal absorption

Answer 215

**PCSK9**: an enzyme that binds to LDL receptors on the liver and promote receptor degredation preventing LDL-C clearance from the blood this drug: **monoclonal antibody** given SQ _lowers LDL by 40%_ or more in pts already taking maximal tolerated doses of statins “get extra burst to lower it even more!! indications: **_heterozygous familial hypercholesterolemia_** OR **_patients with ASCVD already taking max doses of statin_**

Answer 216

STATIN FIRST, increased to maximum as necessary if unable to use statins (myopathy) consider non-statins

Answer 217

1. gemfribrozil (fibrinic acid), fenofibrate (fibrinic acid), niacin **_2. must control diabetes, reduce smoking, ETOH, and lose weight_** 3. Still elevated: add statin if LDL remains above goal

Answer 218

**usually occurs in pts with injuries at T4-T6 and above and is related to the interruption of descending control of sympatetic outflow to blood vessels in the extremities and abdomen** 1. pooling of blood impairs the return of venous blood to the heart, causing a decrease in cardiac output along with a drop in _arterial pressure_ dizziness, palor, excessive sweating, blurred vision, possible fainting tx: prevented by slow changes in position and measures to improve venous return

Answer 219

**abnormal drop in BP that occurs when a person stands after a long period of being seated or supine** blood temporarily shifted to the lower part of the body, with an _accompaning decrease in central blood volume and arterial pressure_ **_def: systolic drop of 20 mmHg and diastolic drop of 10mmHg after 3 mins of standing_** in orthostatic HTN: _absense of normal circulatory reflexes or BV so blood pools in the lower extremity causeing **cardiac output drop, BP drop, and BF to brain to decrease**_ dizziness, syncope TX: 1. gradual ambulation to allow patient time to adjust 2. avoid situations that cause excessive dilation (alcohol, exercising) 3. avoidance of excessive dieuretics 4. TEDS/abdominal support brace

Answer 220

**1. drug induced hypotension: HTN and psychotropic drugs most common** **2. getting old: esp after 7o,** have arterial pressure instability and postural hypotension **3. bedrest and immobility: esp after 3-4 days** **4. Automonic nervous system disorders: parkinsons, Shy-drager syndrome** DX: 1. taking orthostatic BP 2. tilt table method

Answer 221

**accumulation of fluid in the pericardial cavity from inflamatory or infectious process that includes pericarditis _\>50ml_** also from: 1. neoplasms 2. cardiac surgery 3. trauma small pericardial effusions: can be asymptomatic **sudden acclumination of 200mL may raise intracardiac pressure enough to signiciantly limit venous return to the heart** DX: echo Tx: depends on extent 1. **diuretics, NSAIDS, colchicine or corticosteroids** to help minimze fluid accumulation 2. **pericardiocentesis, initial _tx of choice for large pericardial effusion_**

Answer 222

can occur with **_pericarditis_** symptoms if present: hiccups, nasues, coup, chest pressure CXR: cardiomegaly \>250 ml EKG: **_decreased WRS voltage_** echo: **_best technique to identify TAMPONADE_** Tx: depends on if pt is hemodynamically stable or not

Answer 223

**_compression on the heart_** due to the acccumulation of fluid or blood in the pericardial sac **LIFE THREATENING** 1. trauma 2. rupture of the heart post MI 3. complication from a cath 4. aortic dissection 5. PERICARDIAL EFFUSION _increased intracardial pressure limits ventricular filling and reduces stroke volume and cardiac output_ \*\*heart doesn't fill properlly with blood\*\* elevated venous pressure, increase JVP, fall in systolic BP, narrowed pulse pressure, circulatory shock, \*\*_pulsus paradox\*\*_ (drop **\>10 mmHg in the systolic BP during _Insppiration_ this occurs because the left ventricle is more compressed because of fluid inthe sac so left ventricle has signifcantly less filling and stroke volume)** \*\*appeare acutely ill\*\* since less blood getting ot the body, the _sympathetic_ system is stimulated which prepetuates the problem

Answer 224

**increasing pericardial fluid raises intrapericardial pressure resulting in compression of the heart** _limits ventricular fillling and reduces stroke volume_ _FATAL IF NOT RECOGNIZED EARLY_ causes CARDIAC TAMPONADE, compression of the heart: **1. equilibration of LV and RV diastolic pressure** **2. marked decrease in CO** 3. **_BECKS TRIAD: decline in arterial pressure, elevation of venous pressure, quiet heart_**

Answer 225

DX: _primarly echo_ can add computed tomography and MRI as adjunct TX: closed pericardiocentesis

Answer 226

during normal inspiration _venous return increas and thre is a slight incres in RV volume_ this normally causes a slight *right to left shift of the heart and compressing the left ventricle* and _decreasing LV output by a normal 2-3%_ **Pulsus paradoxus: marked exageration of this process increase in intrapericardial pressure so RV and LV volumes are decreased. _inspiration causes a marked decrease in LV volume resulting in a systolic BP drop \>10_** **_TAMPONADE with pericardial effusion_**

Answer 227

"broken heart disease" stress cardiomyopathy, outpouring of catecholamines in response to stress...causes LV insult 90% in women \*\*presentation mimics STEMI!\*\* modest elevation of troponins **_absence of obstructive CAD when they go in to do a cath or angiography...all the arteries clear_** DX: echo- significant LV dysfunction with **_anterior, apical, and inferior wall ballooning resembling a fishing pout "the apex doesn't move making a balloon appearance"_**

Answer 228

**a primary inflammatory process of the myocardium, most often caused by infectious agent** _**viral origin most common**: **coxsackievirus B, A, HIV, CMV etc**_ bacterial fungal: _aspergillos, candidiasis_ parasitic: _trypanosoma cruzi "changas"_ _Rickettsial_ tx: supportive antimicrobial if identified agent biopsy guided _AVOID NSAIDS, can make it worse!_

Answer 229

**_PRODOMAL VIRAL SYNDROME followed by symptoms of mycarditis_** (CP, dyspnea) **_HF MAY BE THE INITIAL PRESENTATION!!!_** Tachycardia, muffled heart sounds, elevated temp DX: difficult to confirm diagnosis **viral titer** **endomyocardial biopsy may isolate virus (rare) or show characteristic pathology of myositis-inflammatory infiltrate**

Answer 230

pericarditis: NSAIDS...respond within a couple hours **NORMAL LV FUNCTION and SIZE** myocarditis: NO NSAIDS EVER....MAKE IT WORSE **DECREASE IN LV FUNCTION AND INCREASE SIZE** \*\*\*must do a echo to look for the presense of myocarditis....

Answer 231

ST elevation in all leads with the **exception of aVR and V1 sometimes aVL** \*\*\*\*\*big hint here...**_.people don't infarct their whole heart like this!!_** they would be completely dead and it just doens't happen....so if alive and you see this entire ST elevation....you see it throughout!!!! they also have a **_different type of chest main_**\*\*\*\*\*\*

Answer 232

initial episode of pericarditis transitions to a **chronic stage with fibrosis and calcification and THICKENING of the pericardium** RESTRICTION OF FILLING failure of blood to get into the heart because of the contricted pericarditis obliteration of the pericardial space with _fusion of_ _pericardium to the epicardium_ picture the outside of you heart wrapped in ductape that you havd such stiffening of the walls that it is unable to relax properally so you get _elevation of diastolic pressures in all cardiac chambers, decrease stroke volume, get less blood to the body_ _activates the RAAS exacerbating the probelm and appeares like right sided heart failure_ causes: radiation, TB, uremia, neoplastic, **postpericardotomy (post heart surgery)**

Answer 233

1. pedal edema 2. abdominal ascites 3. hepatomegaly 4. **_elevated JVP KUSSMAULS SIGN (distension of neck veins during inspiration_**) 5. _KNOCK HEARD ALONG left sternal border_: diastolic sound that is the sudden cessation of ventricular filling CXR: calcification 50% EKG: low QRS voltage **echo: _pericardium densely thickened, immobile, dilation of hepatic veins_**

Answer 234

supportive other than pericardiectomy

Answer 235

accessory patway through _bundle of kent_ VIA **REENTRY** **associated with arrythmias like PSVT and Afib that can induce vfib** qualifications: 1. **_delta wave "slurring/upstroke on QRS"_** **_2. shortened PR \<.12_** **_3. widened QRS_** \*\*cant read the presense of: Q waves for MI LVH ischemia\*\*

Answer 236

VERY IMPORTANT!! **_IF REENTRANT PSVT ONLY with WPW:**_ _**accelerates conduction leading to Vfib_** use drugs that block AV node conductions 1. adenosine 2. BB 3. diltiazem 4. verapamil **_IF AFIB/AFLUTTER with WPW:_** **looks a lot like vtach but WPW is** I**_IRREGULAR!!! so its not vtach!!!_**the **_ABOVE DRUGS COULD CAUSE THEM TO GO INTO VFIB!_**!!! THIS WILL BE AN EXAM QUESTIONS!!! accelerates the conduction 1. **procainamide** **2. amiodarone** **\*\*\*If these don't work....CARDIOVERT THEM!!\*\*\*** _tx of choices for most patient ablation to the accesssory pathway! 90% effective and currative_

Answer 237

If PSVT/WPW treat with a drug that slows AV conduction: _adenosine, BB, diltiazem, verapamil_ ## Footnote if Afib/Aflutter/WPW: DO NOT USE THE ABOVE DRUGS IN THIS PATIENT!!!! the ventricular rate is already normal, so slowiing it even more you will cause them to go into vfib

Answer 238

look at the ventricular rate ## Footnote if greater than 200 ventricular rate likely is _WPW syndrome_

Answer 239

look at the R-R ## Footnote 1. ventricular rate \>200 2. Look at the R-R to see if regular or irregular afib: irregular R-R PSVT: regular R-R \*\*\*since the EKGS look funny since so fast you have to use this method to determine if WPW is suposected and guide the treatment between the two\*\*\*

Answer 240

the AV node in WPW with afib actually keeps the ventricular rate lower than if the accessory pathway alone. if you slow the av node you are allowing more impulses down the accessory pathway and it speeds up ventricular rate too much that it can cause the person to go into dangerous vtach/vfib

Answer 241

James fibers bypass track Qualifications: **_1. PR interval \<.12, NO DETLA WAVE_** **_2. QRS not widened_**

Answer 242

narrow therapeutic to toxic ration potent stimulator of arrythmia increases _automaticity_ can cause any arrythmias but _Multiform PVCs most common that can turn into VTACH_ - atrial tach with AV block - accelerated junctional rythmn - 1\* HB, 2\* HB **_ST CHANGES WITH SCOOPING/LADLE appearance_**

Answer 243

Qualifications: 1. ST depression 2. flattening of the T wave 3. _U wave presence after the T wave_

Answer 244

can lead to Vfib and death STEPS: 1. _diffus T wave peaking throughout EKG_...this is different than the peaking you see in a MI because MI is only in the leads you would get a infarct....don't get infarct in all the leads indicated with diffuse T wave peaking 2. PR elongates, _drops the P wave,_ _continues peaking_ 3. QRS _WIDENS TO **SINE WAVE which can turn into vfib**_ first pic is the peaked t waves second pic is the sine waves

Answer 245

1. QT interval should not exceed 50% of the R-R, doesn't apply once HR\>110 ## Footnote 2. QT=square root of RR normal \<.41

Answer 246

1. hypocalcemia.hypercalcemia 2. hypokalemia 3. digoxin 4. macrolides 5. antifungals 6. class IA, IC, III antriarrythmics 7. _TRICYCLIC ANTIDEPRESSANTS_ _8. LVH_

Answer 247

1. **jervell and lang-neilsen syndrome: autosomal dominant and associated with _deafness_** **2. romano-ward syndrome: autosomal dominant**

Answer 248

can cause dangerous arrythmias

Answer 249

ST ELEVATION IN ALL OF THE LEADS ...eventually this goes down and the T waves invert \*\*think about it, pts don’t infarct the entire heart all at once so this indicates it is likely from another cause like pericarditis\*\* DO CARDIAC ULTRASOUND and treat with NSAIDS!!! ONLY TREAT WITH ANTIINFLAMMATORIES…..3-4 hours the pain should go away!!\*\*\*

Answer 250

**normal** variant that causes ST elevation in YOUNG men more than women see a little ST elevation in young healthy person in multiple leads! they are at increased risk for sudden death becuase more likely to enter arrythmia with this variant \*\*\*DONT DO ANYTHING WITH THEM...(she wrote this down\*\*\* no one really knows what to do with these pts

Answer 251

mimics ischemia with T wave inversion, need pt hx

Answer 252

rate? **slight irregularity of sinus rythmn** rythmn? **slightly irregular** p waves? **yes** QRS? **narrow** **1. phasic speeding up with inspiration and slowing down with expiration or _reponse to variety of stressors_** **2. variation in vagal tone as result of _herring breuer reflex_** **TX: doesn't warrant Rx therapy, tx underlying cause**

Answer 253

rate? rythmn? **regular** p waves? **yes** QRS? **narrow** causes? common rythmn seen in early stage of acute MI 1. **may be seen during sleep when vagal tone takes over rate can drop into 40s** **2. can be accompanied by pauses ~2 seconds in sleep** **3. normal in _well trained athletes_** 4. can be caused by meds _beta blockers, diltaizem, verapamil_

Answer 254

**ATRIAL RE-ENTRY or increase AUTOMATICITY, premature atrial depolarization** ## Footnote rate? **single beat** rythmn? **premature complex** p waves? **yes, but looks different than a regular p wave** QRS? **narrow** other? **1. if early coduction can be blocked at AV node** **2. if there is no preceeding p wave then it is called _junctional premature beat_** (only difference) \*\*can initiate supraventricular tachycardias in suseptible individuals PSVT, Afib, Aflutter\*\* precipitory factors: _ETOH, TABACCO, CAFFEINE, ADRENERGIC STIMULATANS_ tx: remove precipitating

Answer 255

**RENTRY CIRCUIT around annulus of tricuspid valve** **250-350 flutter waves** **regular** **no p waves, flutter waves** **QRS narrow** 1. **_most common presentation is 2:1 AV block with QRS ~150 bpm_** 2. SAW TOOTH APPEARANCE in **II, III, aVF** 3. **_after meds given to slow AV conduction given, most common form of bloc_**_k is **4:1 with ventricular rate ~75**_ (only this if have been treated with meds, usually 2:1) 4. **carotid masage can help slow VR down, allowing flutter waves to be seen** underlying heart disease ALWAYS present TX: **_-DC cardioversion_** **_-ablation_** -may need meds to prevent occurance

Answer 256

**MULTIPLE REENTRANT CIRCUITS IN THE ATRIA** rate? **400-600 atrial contractions** (blocked at AV by refractory period) rythmn? **irregullarly iregular supraventricular** p waves? **NO!!! undulating baseline** QRS? **narrow QRS** other: 1. **in new/untreated onset without med control: _ventricular rate is very fast 120-180 bpm_** 2. can be paryoxsmal or persistent

Answer 257

can be in _healthy individuals_ without heart disease caused by _emotional stress, post surgery, ETOH **"holiday heart"**_ can be "lone" without any precipitating factors _95% in presence of cardiac or pulmonary disease_ first goal: access hemodynamic stablilty by pulse ...if not stable _DC cardioversion_ excessive ventricular rate can cause _hypotension, pulmonary congestion, CP_

Answer 258

48-72 hours

Answer 259

**electrical disturbance in the _absence of cardiac or systemic disease_** paroxysmal episodes of symptomatic afib that revert to NSR spontaneously with brief course of meds _natural history:_ increased frequency of episodes over time and becomes harder to maintain NSR with meds Tx: dependent of frequency of episodes

Answer 260

look for underlying cardiac, pulmonary, and systemic disease Dx: Ekg echo (to check for heart abnormalities) throid function test **(hyperthroidism can cause afib)** TX: **1. first goal: acute/rapid _rate control_ in ED is initial goal: IV _diltiazem_ or** **_Beta blockers_** **2. ibutilitde Type III for recent onset \*\*THIS IS A PHARM CARDIOVERTER\*\*\*** **3. if these don't work than proceed to CARDIOVERSION**

Answer 261

anticoag for _3 weeks_ before cardioversion with coumadin, dabigatran \*\*\*\*\*if the patient can't tell you exactly when it started you MUST DO THIS AND DELAY CARDIOVERSION!!!! don't put them on a BB just put them on a anticoagulation......the only way to get around this is to do a TEE to check for a clot if the person needs to be converted sooner\*\*\*\*\*\*

Answer 262

1. rythmn control 2. rate control \*\*\*\*both rythmn control and rate control are acceptable long term strategies to prevent morality, stroke, and quality of life, choice of tx strategy is based on SYMPTOMS!! risk of bleeding, and side effects of the anti-arrhymics\*\*\*

Answer 263

goal: _cardiovert to NSR and use drug to maintain SR_ (often young people so that way they have no limitations) benefits: increase cardiac output/function negatives: side effects of meds and reccurances if you can't cardiovert with med 1. **_DC cardioversion after being on antiarrythmic_**: 90% successful 2. if recurrence: **_DEFINITIVE RX: ABLATION VIA CATH_** (eliminates Pacs that initiate afib) _drugs to maintain SR once cardioverted_ 1. Type IC fleocainide 2. type III **_amiodarone_** 50% WILL HAVE RECURRANCE RATE

Answer 264

goal: leave in afib and _anticoagulate with warfarin_ benefit: no cardioversion bad: increase risk of bleeding from anticoagulant _chronic rate control with drugs_ **1. _diltiazem_** **_2. beta blockers_** **_3. digoxin in eldery/sendentary_** **PLUS** _LIFE LONG ANTICOAGULATION WITH WARFARIN TO PREVENT EMBOLISM,_ use ASA in elderly

Answer 265

most common ventricular rythmn reentry more than automaticity **premature QRS complex that is _wide and biazarre_** **no p waves** **WIDE QRS \>.12** **irregularlly iregular, or regularly irregular (trigeminiy)** **often followed by a pause** **uniform or multiform** **healthy and diseased hearts** **bigeminy and trigeminy**

Answer 266

common in healthy and diseased hearts _in the presense of underlying heart disease they are associated with **suddent death and LV dysfunction**_ PE: palpatations, _fullness in the neck_, or asymptomatic TX: if no cardiac disease: don't do anything in cardiac disease: new studies show that even though there is increased risk of sudden death....new studies show treating the PVCs increased mortality case and point, never treat these

Answer 267

**3 or more consective PVCs at _rate \>100_** sustained: \>30 seconds more often uniform and regular, but can be irregular like torsades _seen in presence of structual cardiac pathology_ _rarely hemodynamically stable, syncope and collapse_ _deteriorates into vfib_ occurs with: **CHD/mi (first 24-48 hours), cardiomyopathies, drug admin** and often reflects **_severe LV dysfunction_**

Answer 268

ischemia, acute MI, electrolyte imbalance, drug toxicity

Answer 269

if hemodynamically _stable_: 1. _amiodarone_ 2. synchronized cardioversion if hemodynamically _unstable_: **_1. DC cardioversion_** **_ablation/antiarrythmic AMIORDARONE DOC_** **_implantable ICD for significant LV dysfunction_**

Answer 270

consider afib with WPW syndrome ## Footnote \*\*\*\*\*don't see Delta wave here so determined based on the rate!!!\*\*\*\*

Answer 271

assess hemodynamic stability ## Footnote most patients are stable which would cause you to do a DC cardioversion (electrical shock)

Answer 272

**terminal arrhythmia associated with death** most common cause of cardiac death, often in _early AM_ **DEFIB ASAP (if you are outside the hospital pt will likely die but if happens at the hospital, the pt will likely live depending on how long it takes you to defib them)** causes: sometimes occurs following administration of antriarrythmic drugs esp with patients with _prolonged QT interval_ UNDILATIONS ONLY, choatic oftren preceeded with vtach **_rarely seen in pts with structually normal hearts_**

Answer 273

inherited cardiac disease with abnormal Na channels _predisposed to dangerous arrythmia_ 1. coved ST elevation in V1-V3 2. RBBB 3. T wave inversion

Answer 274

1. correct metabolic abnormalties 2. treat underlying cause **3.** absence of MI, active ischemia, metabolic abnormalities, drug or other reversible causes **_warrants ICD placement +/- antiarrhythmics_** many recent trials have shown _ICD to be the ONLY EFFECTIVE long term intervention_ that improves long term mortality

Answer 275

**AV NODAL REENTRY!** **abrupt onset and termination** **carotid massage may help terminate** **150-220** **regular** **not usually present** **narrow QRS** 1. most in young healthy people without cardiac disease, can tell you the second it started and stopped. 2. _try valsalva or carotid massage to convert patient out of it_ _3. cardiovert with adenosine 90-95% of the time if carotid massage doesn't work_ _4. selective ablation to part of AV node using radio frequency_ to prevent PSVT if the meds don't keep the patient in PSVT 2. can be caused by coffee, alcohol, and excitement

CV2-Cardio Flashcards

(308 cards)