Systems - Cardio
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Describe the 5 phases of the action potential
- phase 0: depolarization - sodium channels open (become active) and Na rushes in
- phase 1: Start of repol - Sodium channels become inactivated, K+ channels open and K+ flows out
- Phase 2: Plateau - Ca++ channels join the K+ channels and let Ca++ flow in (prolonging repolarization)
- Phase 3: Rapid repol - Ca++ channels close, starting rapid repol
- Phase 4: sodium channels recover and return to the resting state. Some cells here allow an ion leak so they have automaticity
What is the difference between effective and relative refractory period
- effective - the amount of time before any AP can be conducted again
- relative - after the ERP, how long before you can get an AP with the steepest slope for phase 0 (i.e. without a reduced conduction velocity)
label the following on an ECG: PR interval, PR segment, QT interval, ST interval, ST segment
Describe the autonomic innervation of the heart. What effect does SNS and PSNS have? Where are they heavily innervating?
- SNS - increases automaticity and cond. velocity, decreases refractoriness
- PSNS - opposite
- Innervation: lots of both in the nodes
- -nodes more sensitive to PSNS
- -everything else is WAY more sensitive to SNS
What to Class Ia, b, and c do? What effect does this have on the action potentials?
- They all bind to the sodium channels
- Class 1a (quinidine): slows phase 0 upstroke, prolongs AP duration
- class Ib (lidocaine): shortens duration of AP, no effect on phase0 slope
- Class Ic: only slows upstroke, with no effect on refractory period
What do class III and IV antiarrhythmics do?
- Class III: increase AP duration (by messing with K channels), no effect on slope 0
- Class IV: CCB's, lengthen AP at nodal tissue by slowing the influx of Ca
What are the three criteria for re-entry?
- 1) 2 roughly parallel pathways
- 2) one with a longer refractory period
- 3) pathway with shorter refractory period conducts more slowly.
list examples for increased automaticity (2), re-entry (3), triggered activity (2)
- increase auto- sinus tachycardia, multifocal atrial tachy
- re-entry: scar-related VT, atrial flutter, AVRT, AVNRT
- triggered activity: TdP, digitalis toxicity
On an ECG, what would you see that suggest true (ectopic) atrial tachy? premature atrial contractions?
TAT: weird looking P-waves, wobbly rhythms
premature atrial cont: junctional p waves before, in, or after QRS
What is on the DDX for PSVT (4)
- orthodromic AVRT
- True (ectopic) atrial tachy
- 1:1 atrial flutter
Describe how AVNRT works. How would you terminate it?
It is basically a re-entry tachycardia in the AV node. terminate it with vagal maneuvers (bear down, ice on face, carotid massage)
What would you expect to see on the ECG for ventricular pre-excitation
- -delta wave (early excitation down ABT)
- -short PR (because of the lack of delay in AVN)
- -wideish QRS because the ventricles are being depolarized in two places
When can you diagnose Wolf-Parkinson-White syndrome?
when there is pre-excitation on the ECG AND there is documented SVT or symptoms of SVT
How can you differentiate ventricular tachy from antidromic AVRT?
Look for a delta wave on a previous ECG
What are the ECG characteristics of atrial fibrillation (4)
- -irregularly irregular rhythm
- -undulating baseline
- -no clearly discernible p-waves
- -any QRS morphology
What are the goals of AF management (to goals with details)
- 1) Decrease stroke, CHF, and mortality
- - HR control
- -rate control vs rhythm control
- 2) Decrease symptoms (palps, SOB, chest pain, syncope, etc)
- -HR (rate and rhythm) control
Describe how the CHADS2 scoring system for a fib works?
- CHF - 1 point
- HTN - 1 point
- Age>75 - 1 point
- Diabetes - 1 point
- Stroke/transient ischemic attack - 2 points
- 0 points: just use ASA
- 1: either ASA or anticoagulate (patient dependent)
- 2+: always anticoagulate
List three major findings in VT in order of prevalence.
any cardiac rhythm originating below the bundle of His, rate >120 BPM, and is not V fib or V flutter
What is the DDx for wide-complex tachy (4)?
- SVT with aberrancy
- -bundle branch aberrancy + SVT
- -old BBB + SVT
- -Pre-excitation + SVT
- Rapid ventricular paced rhythm
What are the three major things you are looking for to differentiate VT from SVT with aberrancy? (these favour VT)
- 1) AV dissociation (beat frequency b/n V and A)
- -capture beats
- -fusion beats
- 2) NW axis
- 3) all precordial leads look roughly the same
Definition of aortic aneurysm?
dilation > 50%
Difference between true and false aneurysm
- True: involves all three layers
- false: only involves 1-2 layers
In the following pericardial diseases describe if it is constrictive pericarditis or cardiac tamponade that causes:
a) kussmaul's sign (paraxoical increase in JVP on inspiration)
b) pulsus paradoxus (>10 mm FALL in BP on inspiration)
c) pericardial "knock"
- a) Kussmaul's sign: constrictive (Right heart cannot fill because of restriction, left heart also has problems but not as much)
- b) pulsus paradoxus: tamponade (LV is having problems filling (low pressure filling, exaggerating the normal physiological fall in sBP with inspiration)
- c) knock: constrictive
How does carotid sinus massage/vagal maneuvers treat SVT?
It stimulates the vagal nerve, increasing the parasympatheric tone of the heart. getting it to chill the f*&@ out!
What produces TdP? Why is it dangerous? How would you treat?
Looks like a twisted ribbon on ECG. Caused by a prolonged QT and weird T wave.
It can degenrate into V. flutter/fib
fix the cause: low K+/Mg++, bradycardia, QT prolonging drugs (mostly class III, some class I). can shorten the QT with lidocaine in acute situations.
What is sudden cardiac death?
cardiac arrest in the setting of heart disease. Called this regardless of if you get the heart going again or not.
define heart failure (2 definitions)
- 1) syndrome of impaired ability of the ventricle to fill and or eject blood. It is a clinical diagnosis
- 2) inability of the heart to meet the demand of the body, with or without congestion
What are the most common predisposing factors for CHF in order of prevalence (top 5)
- CAD (by far!!!)
- cardiomyopathy (includes idiopathic)
- valvular heart disease
What neuro-hormonal activity would you expect to see in CHF?
- increased SNS (increased norepi, bad)
- Increased RAAS (bad)
- Increased ANP and BNP (good thing, vasodilate and diuresis)
- Increased ADH (vasopressin, bad)
What is a really bad sign in CHF? Explain the mechanism.
hyponatremia (<138), it is because you are hypervolemic and this is diluting the Na+. In HF there is low BP, so the pituitary is pumping out ADH like a mad man. This causes water retention, but sodium is still excreted.
What is Paroxysmal Nocturnal Dyspnea? Why is it so important?
PND is during the day the edema is in your legs, when you lay down at night it goes to your lungs.
VERY specific for CHF
What are the two pulses you expect to see in CHF?
- pulsus alternaans - alternating strong and weak pulse
- dicrotic pulse - accentuated closure of aorrtic valve
Describe the NYHA classes for heart failure.
- Class 1: no symptoms with everyday activity
- Class 2: symptoms with ordinary exertion
- Class 3: symptoms with minimal exertion
- Class 4: symptoms at rest, cant do any physical activity
- Remember that these can be adjusted with treatment
What do you expect to see on CXR in a patient with CHF (5)?
- Heart Enlargement (>50% of thorax)
- pleural Effusions
- Re-distribution (pulmonary edema)
- kerly B lines
- Bronhiolar-alveolar cuffing
What are the AHA stages of heart failure
- A - high risk but no structural HD or symptoms
- B - SHD, but no symptoms
- C - SHD and prior/current symptoms
- D - refractory HF
How would you treat stage A and B heart failure
- Stage A: treat risk factors
- Stage B: same as A, plus ACEi's and beta blockers if decreased EF or prior MI. Prevent symptomatic HF
What are the 5 goals of therapy in HF?
- 1) improve Sx
- 2) reduce mortality
- 3) slow or reverse heart failure
- 4) identify and Tx the underlying cause of precipitant
- 5) reduce embolotic events
What levels of salt restriction should you have in a patient with mild CHF? severe CHF?
- mild (NHYA I-II): <3g per day
- severe (NHYA III-IV): <2g per day
Describe the phamacological therapy for CHF stage C. Which of these has a mortality benefit?
- 1) diuretics
- 2) lower the RAAS
- -aldosterone antagonists (spironolactone)
- 3) beta blockers
- 4) Digoxin
2 and 3 have mortality benefits
Which two drugs have NO INDICATION in asymptomatic HF patients?
digoxin and diuretics
Which murmurs tend to radiate more. left or right?
A holosystolic murmur best heard at the tricuspid listening post. What 2 things could it be?
- 1) ventricular septal defect
- 2) tricuspid regurg
If you hear a loud, machinery, type murmur through diastole and systole what is it likely to be?
patent ductus arteriosus
What are the three things you need to do extra maneuvers for (e.g. valsalva and standing to squatting) in order to change loading conditions (preload, afterload, contractility)? explain
HOCM (Hypertrophic Obstructive cardiomyopathy): valsalva increases intrathoracic pressure and decreases venous return, transiently reducing LV size (makes murmur worse)
Aortic stenosis: valsalva transiently decreases flow through aorta and the murmur decreases
Mitral valve prolapse (MVP): valsalva decreases blood to LV (altering the geometry), causing the click and murmur to occur earlier.
Which people are most likely to have AVNRT?
Young Healthy females
What drugs do you use to treat SVTs involving the AV node?
NOT nifedipine (better for peripheral CCB'ing?)
What is the CCS functional classification of angina?
- Class I: angina only with strenuous/prolonged exercise
- Class II: angina brought on by moderate exercise (walking more than 2 blocks, climbing more than a flight of stairs)
- Class III: marked limitation in exercise, cant even do the class 2 activites
- Class IV: cant carry out any activity without angina, +/- angina at rest.
What is the DDX of chest pain (7, besides ACS)
- aortic dissection
- pulmonary embolism
- esophageal spasm
- acute cholecystitis
Describe the anatomic site, leads involved, and artery involved for the ECG.
- Inferior - II, III, aVF - RCA
- Anteroseptal - V1, V2 - LAD
- Anteroapical - V3, V4 - distal LAD
- Anterolateral - V5, V6, aVL, I - CFX
- Posterior - V1, V2 (tall R wave, not Q wave) - RCA
Ideally, how long do you have to get someone with a STEMI reperfused
1 hour (the golden hour) from MI
What are the only drugs that have been proven to lower your risk of CAD
Describe the TIMI score for STEMI (not details on how to score, but what it is for)
- basically identifies patients that are more likely to have:
- -intracoronary thrombus
- -impaiired flow
- -increased burden of artherosclerosis
In STEMI what is the only drug that has been shown to improve cardiac function long term?
beta blockers (decrease oxygen demand of the heart)
Describe the adjunct therapy that can be used after a STEMI (10)
- morphine - treat pain
- glycoprotein IIb/IIIa inhibitors
What is the definition of unstable angina
- Classic angina:
- -poorly localized chest/arm pain
- -brought on by exertion or stress
- -relieved by nitroglycerin or rest
- Then ADD any one or more of these 3:
- -occuring at rest and lasting>20 mins
- -severe or new onset
- -crescendo pattern
Describe what you need to get a TIMI score for UA/NSTEMI. What does it mean?
- -Age>=65 - 1 point
- ->= 3 cardiac risk factors - 1 point
- -known CAD (stenosis of >50%) - 1 point
- -ASA in last 7 days - 1 point
- -recent (<24hr) angina - 1 point
- -ST deviation - 1 point
- -increased cardiac markers - 1point
if the score is 3+ consider early LMWH and angiography
Describe what you would do for high, intermediate, or low risk UA/NSTEMI
- high risk: early cardiac cath and medical management
- intermediate risk: Medical management and semi-early cath
- low risk: ASA and outpatient tests
What are the 3 antiplatelet drugs used in ACS? Common names
- Plavix (clopidogrel) - P2Y12 (ADP) receptor blocker
- GPIIbIIIa blocker - abxicimab (reopro)
- ASA - aspirin
Describe the anti-ischemic therapy for ACS (with drug names)
- 1. beta blockers (metroprolol)
- 2. nitrates (nitro)
- 3. CCB's : nefedipine, amlodipine
Name 2 anticoagulants used in ACS. Who should get it?
- 1) heparins (enoxaprin - LMWH)
- 2) Direct thrombin inhibitors (bivalirudin)
All patients should get this
What drugs should all patients with ACS get? What interventions?
- ASA - 81 mg
- P2Y12 blocker (Plavix)
All except lowest risk should get a stent
What are the three etiologies of aortic stenosis? When do these become symptomatic?
- Congenital: bicuspid, unicuspid (50-60 years)
- Rheumatic (20-50 years)
- Degenerative (calcific) (70-80 years)
What Sx do you expect to hear on Hx for aortic stenosis. Findings on PE? Findings on auscultation?
- Sx: angina, syncope, CHF
- PE: pulsus tardus et parvus, sustained apical impulse (not displaced), carotid-radial delay
- Ausc: crescendo-decresendo systolic murmur transmitted to the right clavicle and carotid
When giving an echo for aortic stenosis what is a normal max flow, what is abnormal?
normal is 1 m/s, anything more than 4m/s is severe aortic stenosis
What are the three common situations you would be looking for acute aortic regurg?
- known aortic valve IE
- aortic dissection
- blunt chest trauma with pulm congestion
What do you expect to see on PE for acute aortic regurg?
heart has not had a chance to compensate yet
- low BP (less CO)
- pulse pressure is narrow and low
- quiet, early diastolic murmur
What would you do if you see acute aortic regurg?
THIS IS A SURGICAL EMERGENCY, there can be severe hypotension here. Valve replacement usually
6 most common causes of aortic regurg in order of prevalence
- CT disorders with dilation of aortic root
- Rheumatic fever
- calcification of aortic valve
Why do you get exertional angina in chronic aortic regurg? Why is it worse at night?
increased LVEDP prevents proper perfusion of the myocardium. Worse at night because that is when we have the lowest diastolic pressure
What findings do you expect on chronic aortic regurg?
- The signs of a volume overloaded heart
- - wide pulse pressure (big diff between systolic and diastolic) - waterhammer pulse
- - pistol shot sounds over the femoral arteries (Traube's)
What is a good way to differentiate aortic and pulmonary murmurs?
Which location are they the loudest at? Left 2nd IC is pulm, right 2nd IC is the aorta
The pulmonary murmurs get louder on ispiration because of increased venous return.
What extra maneuvers can you get the patient to do in order to hear aortic regurg better?
get them to sit, lean forward, and exhale (heard best after expiration)
When you hear a rumble, what should you automatically be thinking?
Do you want to listen for S3 and S4 with the bell or the diaphragm?
what are 5 etiologies of dilated cardiomyopathy?
- tachycardia induced
what is the most common cause of death in young athletes?
Top 3 treatment options for HCM
- minimize LVOT obstruction
- treat arrhythmia
- restrict competitive sports
4 indications for heart transplant
- advanced intractable heart failure
- intractable arrhythmia
- intyractable congenital heart condition
- intractable angina that cant be treated
Contraindications to heart transplant
- severe irreversable pulm HTN
- other organs are shitty
3 things that should come up on an angina pain Hx
- heavy, tight, retrosternal pain
- worsened by exertion
- relieved by rest and nitrates
What is on the differential for central cyanosis in a newborn (5)?
- Tetralogy of Fallot
- Transposition of the great arteries
- Tricuspid atresia
- Truncus Arteriosus
- Total anomalous pumonary venous drainage/return
What is the tetralogy of fallot?
- pulmonary stenosis
- right ventricular hypertrophy
- overriding aorta
While waiting for surgery, what should you give babies to help them survive
prostaglandins (keeps the ducts open)
What causes acute and subacute IE
- acute: S. aureus
- sub-acute: veridans strep, enterococci, CoNS, GNB
what are 4 processes in IE that contribute to clinical manifestations
- 1) local destructive effects of valves
- 2) emboli
- 3) seeding of remote sites
- 4) tissue injury from circulating immune complexes
What is the difference between a true and false anerysm?
true involves all three arterial wall layers
What are the top 4 risk factors for aneurysm?
- family Hx
- old age
What us usually the etiology of aortic dissection?
What is the classic triad of a ruptured AAA
- pulsatile mass
Difference in seriousness of an ascending aortic dissection and a descending aortic dissection
Ascending is a surgical emergency because it can dissect to the heart
descending is still an emergency, but can often be treated medically (decrease HTN)
three main surgical indications for AAA
- 1) size: males-5.5 cm and larger; females: 5 cm and larger
- 2) rate of enlargement (>1cm/year)
- 3) symptoms
5 major risk factors for peripheral artery occlusive disease
name three peripheral arterial occlusive disease. Which of these are limb-threatening?
- 1) claudication: pain on exertion
- 2) ischemic rest pain: pain at rest
- 3) ischemic tissue loss: necrosis (50% mortality at 5 years)
2 and 3 are limb threatining
Describe the three parts of diabetic feet
- 1) neuropathy: A-V shunts, pressure points
- 2) arteropathy: atherosclerosis
- 3) compromised tissue immunity and healing: high glucose levels fuck with immune system
Where do emboli tend to lodge?
What are the 5 things you should look for in acute arterial occlusion?
- 1) pulselessness (late)
- 2) pain
- 3) pallor
- 4) paresthesia (numbness)
- 5) paralysis
Describe the Stanford and DeBakey classification of aortic dissection. How do you treat according to the stanford class.?
- -type A - ascending arch is involved (surgery)
- -type B - ONLY the descending arch and lower is involved (usually managed by lowering BP and contractility)
- -type I - ascending and descening
- -type II - ascending only
- -type IIIa - descending thoracic only
- -type IIIb - thoracic and abdominal
What supplies both the SA node and the AV node.
What is the duke treadmilltest score?
score = #of minutes exercising - 5(max ST depression) - 4(chest pain)
- 4 or higher is low risk
- 4- -11 is intermediate risk
- -11 get them to the cath lab
How does one grade murmurs (1-6)
- I: barely audible
- II: faint, but immediately audible
- III: easily heard
- IV: III with thrill
- V: Very loud, heard with stethoscope lightly on chest
- VI: don't need stethoscope on chest
What is the normal range for:
QT (corrected, and rule of thumb)
- PR = 0.12 to 0.2
- QRS < 0.12
- QT: rule of thumb is less than half of RR, corrected = QT/sqrt(RR)
Describe first, second and third degree heart blocks
- 1st: prolonged PR
- -type (mobitz) I: gradual prolonging of PR until a ventricular beat is dropped
- -type (mobitz) II: PR is constant but all the sudden a vent beat is dropped
- 3rd: no p wave makes it to the ventricles
What are the RF's for Afib?
- PIRATE mnemonic
- Pulm disease
- Rheum valve disease
- Electrolyte abnormalities/Endocarditis
- Sick sinus syndromes/Stimulants
What is the treatment for A fib
- CCB's, Cardioversion
list 4 systolic murmurs and 2 diastolic
systolic: AS, mitral regurg, mitral valve prolapse
diastolic: aortic regurg, mitral stenosis
What has been shown to have a survival benefit in in CHF? Which ones are only for Sx relief?
ACEi and Beta blocker in combination
diuretics and digoxin are only for Sx relief
Difference between orthodromic AVRT, antidromic AVRT, and AVNRT
- AVRT: pre-excitation via an accessory bundle
- -ortho: straight down the AV node
- -anti: goes backwards up the AV node
- AVNRT: is basically AVRT within the AV node.
How to figure out HR on the ECG (2 ways)
300 divided by the number of squares between adjacent beats
six times the number of beats at the bottom for irregular beats
What do you see on ECG in ischemia? MI?
ischemia: ST depression, T wave inversion in V1-V6
infarction: ST elevation (3-5 hours), T wave inversion (weeks to months), deep Q waves (>6 months)
How do you treat acute exacerbations of CHF?
- Lasix (furosemide)
- Position (upright)
With regards to calcium, which diuretics spare it, which ones lose it?
loops lose it, thiazides take it in
Describe what S3 and S4 mean
- S3 means that it is floppy dilated heart
- S4 means that stiff and concentrically hypertrophic
5 most common causes of CHF?
- 1) CAD
- 2) HTN
- 3) idiopathic (dilated cardiomyopathy)
- 4) Valvular
- 5) alcohol
What is the most common cause of sudden death in young, healthy athletes?
Hypertrophic Obstructive Cardiomyopathy
Describe what the problem is in the three types of cardiomyopathy. Major etiology for each.
- dilated: impaired contractility, ischemia and long standing HTN
- Hypertrophic: impaired relaxation, genetic usually
- restrictive: impaired filling, non dilated and preserved systolic function, infiltrative diseases like amyloidosis, sarcoidosis, and hemochromatosis
What are the major risk factors for CAD? (9)
- increased LDL
- decreased HDL
- family Hx
- peripheral artery disease
Are the cardiac enzymes elevated in unstable angina?
U Aint got enzymes in Unstable Angina
How to treat someone coming in with an MI
Definition of dyslipidemia
- LDL > 130 mg/dL
- HDL < 40 mg/dL
Target BP's in normal people. People with diabetes or renal disease.
- Normal: <140/90
- diabetes and renal disease: <130/80
TMT for HTN
ABCD again (not to be confused with the ABCD for a fib)
Complications of MI
- CRASH PAD
- Cardiac Rupture
- HTN/Heart Failure
Acute pericarditis triad
chest pain, friction rub, ECG changes
quartet for cardiac tamponade
- -increased JVP
- -pulsus paradoxus
What does a diastolic rumble mean?
When you hear a mid-systolic click, what should you be thinking?
mitral valve prolapse (MVP)
When you hear a holosystolic murmer that radiates to the axilla, what should you be thinking
describe the anitarrhythmic drug classification
- Some Block Potassium Channels
- I - Sodium channels
- II - beta-Blocker
- III - Potassium Channel Blocker
- IV - CCB
What would you like to do?
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