CV DIT notes

7/28/2019 CV DIT notes

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Principle #12

In order to maintain the harmony of the stakeholders, the leveraging and deleveraging of stakeholders of human life

requires an agreed upon system of fairness and forgiveness that honors all stakeholders. The heart is at the core

of that system

Principle #16

Every stakeholder of human life has primary sources of energy and matter which ultimately were derived fromanother stakeholder. Heart is the source of energy and matter for all the cells of the body, which came from other

stakeholders.

Overview & Ventricle Development

Heart Embryolog - mesoderm

EMBRYONIC STRUCTURE GIVES RISE TO

Truncus arteriosus (TA) Ascending aorta and pulmonary trunk

Bulbus cordis Smooth outflow tracts of both ventricles

Primitive ventricle Trabeculated left and right ventriclesPrimitive atria TrabecuIated left and right atria

Left horn of sinus venosus ( SV) Coronary sinus

Right horn of SV Smooth part of the right atria

R common & anterior cardinal vein SVC

Truncus Arteriosus - aka spiral septum/aorticopulmonary septum came from Neural crest cell

6 Truncoconical Spiral Septum Defects

Fenestrae

Ventral Septal Defect

Tetralogy of Fallot *

Persistent Truncus Arteriosus *

Transposition of great vessels * (RV aorta LV PA)

Dextrocardia

Embryologic Development of the heart


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Heart tube Atria of 4-chambered heart

- Tube grows, elongates and folds into S Shape

- Atrial chamber lays posteriorly in S and ventricular chamber lays anterior in S

- Atrial chamber grows and incorporates superior vena cava and pulmonary vein

- septum primum forms

- septum secundum forms incompletely (leaving foramen ovale)- cell death in septum primum forms osmium secundum

What divides the R & L atria?

Septum Primum & Septum Secundum

How is blood shunted from R atrium to the L atrium in an embryo?

Through the foramen oval and osmium secundum

Ventricles & Outflow Tract Separation

- Ventricle chamber lays anteriorly in S shaped heart tube

- Muscular ventricular septum forms which begins to divide the ventricles

- Truncoconial swellings (ridges) of truncus arterioles meet, fuse, and zip (both superiorly and inferiorly) in a 180

turn to form spiral septum

- Inferior portion of spiral septum meets with muscular ventricular septum to divide the ventricles and form aorta

and pulmonary arteries


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Ventricular remodeling to for AV valves

Myocardium erodes

- Ventricles enlarge as a result

- Residual mesodermal tissue becomes fibrous and forms chord tendinae

- Forms papillary muscles & AV valves

Fetal Circulation- Umbilical vein brings O2 blood from the placenta to the Liver

- Blood mixes O2 blood from umbilical vein with deO2 blood from LE in the Ductus Venosus

- Then it enters the Inferior Vena Cava and enters into the R atrium

- The blood can go to the L atrium through the Foramen Ovale or to the R ventricle and into the Pulmonary Artery

- In pulmonary artery can go to the lungs or the ductus arterioles into the left sided circulation into the aorta

- If it enters the lungs it will return to the left atrium and meet with some of the DeO2 blood from the R atrium via

Foramen Ovale

- Then it goes into the Left ventricle and aorta it will meet with with the other blood from the ductus arterioles and

will circulate to the rest of the body- The blood will then recirculate to the umbilical arteries back to the placenta to get more nutrients


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Transition into adult circulation

- infant takes it first breath closes fetal circulation & opens adult circulation

- with breath in intrathoracic pressure and resistance in pulmonary vasculature

- sucks blood from R side of heart into lungs and pulling blood from inferior and superior vena cava L atrial

pressure > R atrial pressure

- Foramen Ovale closes. L sided circulation pressure gets high and pushes out through aorta

- Left sided pressure is higher than the R side pressure, the ductus arteriosus will close

- if you want to keep ductus arteriosus open, you would give PGE

- if it remains opens tin machine like systolic and diastolic murmur with a patent ductus arterioles then


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administer anti-PGE like NSAID (endomethacin). Murmurs within first 24 hours of life are not usually pathological

Aortic Arch Derivatives

1st arch - maxillary artery

2nd arch - Stapedial artery and hyoid artery

3rd arch - Common Carotid artery & proximal internal carotid artery

4th arch - on L aortic arch on R proximal part of R subclavian6th arch - Proximal part of pulmonary arteries and on L, ductus arteriosus

1st arch is Maximal

Second = Stapedial

C is the 3rd letter of the alphabet

4th arch (4 limbs) = systemic

6th = pulm & pulm-to-systemic shunt (ductus arteriosus)

ADS Causes

- Ostium secundum gets too big and overlaps the foramen oval

- Absence of the sputum secundum

- Neither the septum secundum nor the septum primum develop

Structures that grow close to the opening/canal btwn the atrial chamber & ventricular chamber into 2 small

openings?

- Superior and Inferior Endocardial Cushions

Genetic Abnormality commonly associated with endocardial cushion defects***

Down Syndrome (trisomy 21)

Ductus Arteriosus Closure

- Increase in O2, Decreased Prostaglandins

- Indomethacin


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Foramen Ovale Closure

- Decrease in pulmonary vascular resistance, Increase in left atrial pressure

Right to Left Shunts

Congenital Heart Disease "Blue Babies" - early cyanosis

- bypassing pulmonary circulation and not oxygenating enough blood

5 T's RL Shunts

- Tetralogy of Fallot (MCC of early cyanosis)

- Transposition of great vessels

- Trancus Arteriosus - Failure of TA to divide into pulmonary trunk and aorta; + VSD

- Tricuspid Atresia - characterized by absence if Tricuspid valve and hypoplastic RV; requires ASD + VSD

- Total anomalous pulmonary venous return (TAPVR) - pulmonary veins drain into R heart circulation; associated with

ASD and PDA to allow for LR shunting to maintain CO

Tetralogy of Fallot

- defect in infundibular septum

1. Pulmonary Stenosis

2. RVH

3. Overriding Aorta

4. VSD

- infants have cyanotic spells and learn how to squat to after load and prevent excessive RL shunting

- Cyanosis & Boot Shaped Heart

Transposition of great Vessels

- The spiral did not take place of the spiral septum

- Aorta leaves RV and Pulmonary artery leaves LV

- separate of systemic and pulmonic circulations

- need VSD, PDA or Patent FO to allow mixing of blood (give PGE)


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Offspring of Diabetic moms

- Transposition of great vessels

- Hypoglycemia

- Large gestational age

- Clavicle Fractures, shoulder dystocia, Erb-Duchenne palsy, failure to progress

Eisenmenger Syndrome

- Uncorrected LR Shunt overloading pulmonary vasculature

- hypertrophy of right ventricle change to RL shunt

- less oxygenation

Left to Right Shunts and other anomalies

D-Defects: pDa, vsD, asD, avsD

VSD

- MC congenital cardiac anomaly

- 40% close in first 6 months

- Loud holosystolic murmur = small defect

ASD

- loud S1 + wide fixed split S2


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CO = SV X HR

Fick's Principle :

CO = rate of O2 consumption

art O2 - venous O2

Mean arterial pressure (MAP) = CO x TPR = Q*R

MAP = diastolic pressure + systolic pressure

- MAP is important for dosing esp cardiovascular drugsPulse pressure = systolic pressure - diastolic pressure

- pressure involved in the pulse and proportional to SV

Pulse pressure : stroke volume

SV = CO/HR = EDV - ESV

- Early stages of exercise CO is due to SV and then during sustained exercise due to HR

- If HR is too high then incomplete diastolic filling CO

Cardiac Output Variables****

- More contractility more pushing out blood SV- Afterload - lots of back pressure from aorta harder to push out blood SV

- Preload - pushing more blood into your heart push more blood out SV

Cardiac Drugs: Sites of Action

Contractility:

Cathecolamines (1 rc)

Ca pump in sarcoplasmic reticulum IC Ca EC Na

Digitalis

Contracility:

1 blockade

Heart failure - less muscle

Acidosis, hypoxia, hypercapnea

Non-dihydropyridine Calcium Channel Blockers (Verapamil)

- SV with Anxiety due to catecholamines or exercise or pregnancy ( preload)

- Myocardial Oxygen demand by afterload then heart needs to pump harder and needs more O2 heart size,

hypertrophic myopathy

- MI - must dec the amount of O2 the heart needs, e.g. ACE inhibitors, decrease contractility, e.g. metropolol,

Preload & Afterload

- Preload = EDV - comes from Atrial volume, pressure in atrium or central venous pressure

- preload: exercise blood volume

- prEload: vEnodilators (nitroglycerin) - pool blood into the veins

- Afterload = MAP - proportional to peripheral resistance

- Afterload: vasodilators (hydrAlAzine) - expand arteries and dec pressure on aorta

- Preload & Afterload: ACE Inhibitors & ARBs


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Cardiac Drugs & Sites of Action

- Na-CA counter-transporter - if you block Na and Ca will stay in cell more Contractility

- IC Na or EC Na Na gradient will affect Ca concentration

- Na-K ATPase pump - if you block this pump, you will have less EC Na and then less activity on the ion exchange

Ca

Digitalis - inhibits Na-K ATPase pump ultimately IC Ca levels contractility

Charting Cardiac Output

Starling Curve

- Exercise the curve goes up to the left

- for each preload you push more blood out due to contractility

- Heart failure shifts the curve to the right

- for any preload there is low CO

- Fix contractility by giving digoxin/digitalis


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Ejection Fraction

EF = SV/EDV = (EDV-ESV)/EDV

EV = what your heart pumps out / what your heart can hold = the amount of blood your heart ejects

EF = Contractility

Normal 55% < 55% = Heart failure

Resistance Pressure Flow

P = Q x R Ohm's law V = IR

R = P / Q = 8nL / r^4 n = viscosity

Viscosity R

Polycythemia, Hyperproteinemic States, Herditary spherocytosis

Viscosity in anemia

Cardiac & Vascular Function Curves

-Inotropy = Contractililty

- Inotropy = Heart failure, narcotic overdose

- Inotropy = Exercise

- Add TPR = Afterload

- for a given preload you will have less CO as you increase afterload

- Shift curve to right - Inotropy or afterload

- Shift curve to left - Inotropy or afterload

Heart Failure Pathophysiology

Normal Pressures

- PCWP = measures the pressure in the LA 12

- measured by the Swan-Ganz catheter - placed in the internal jugular vein or subclavian vein into the superior

vena cava into right atrium to the right ventricle; inflate the balloon and it enters the heart into the R pulmonary

artery until it can't go any father at the branching point (wedge)

- measures approximation of the left ventricle diastolic pressure 10


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- Mitral stenosis - PCWP > LV Mitral valve is stenosed while the RA is contracting and pressure rises which

PCWP

CHF

-pump failure - pressure forward will drop and pressure rises in the fluid entering the heart- syndrome due to acquired or inherited abnormality of cardiac structure or function

- contractility pump failure due to MI or Chronic HTN

- LV Contractility CO BP body wants to compensate for CO Sympathetic ACT & RAA

- Carotid sinus detects CO sympathetic LV contractility CO + Peripheral edema

- RAA - retain Na & H2O preload CO + peripheral edema

- LV contractility also pulmonary venous congestion RV output pulmonary edema + peripheral edema

- Dyspnea on Exertion - fluid backs up on the pulmonary vasculature

- Cardiac Dilation - greater Ventricular EDV

Left Heart Failure (pulm symptoms)

- Pulmonary Edema - Paroxysmal Nocturnal Dyspnea

- Orthopnea - SOB lying down and better sitting up

Right Heart Failure (peripheral symptoms)

- Peripheral pitting edema

- JVD - central venous pressure


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- Hepatic congestion - hepatomegaly (nutmeg) liver

Renin-Angiotensin-Aldosterone System

- Renin is produced in the kidneys, stimulated by 1 Receptors of the sympathetic nervous system or by the macula

dense cells can sense reduced Na in filtrate or JG apparatus which senses the bp drop

- Renin cleaves Angiotensinogen AGI in liver

- AG Converting enzyme in lungs and kidneys turn AGI AGII

- Angiotensin II tenses angios (vasoconstrictor) acts on AGII Rc on vascular SM BP

- AGII stimulates Aldo release from the Adrenal Cortex (zone glomerulosa)

- Aldo creates a favorable Na gradient for Na & Water to be reabsorbed in the kidney

Heart Failure Medications

CHF Medications

Improve Survival: ACE Inhibitors, ARBs, Aldosterone Antagonist, blockers

Symptomatic: Loop Diuretics, Thiazides, Nitrates, Digoxin

- Chronic Treatment

- Contractility CO Digoxin Contractility (Inotroph) CO

- RAA ACE Inhibitors/ARBS Angiotensin

- Aldosterone Aldosterone Antagonist (Spironolactone or Apleranone)

- Na & Water Retention

Loop Diuretics (heavy duty) or Thiazide- Sympathetic Activity blockers metoprolol or carvedilol

- blocker will help chronically help the effects of the excess sympathetic activity cardiac remodeling

- Contraindicated in acute CHF because they depress myocardial contractility

**Which 2 beta blockers are indicated for the treatment of chronic heart failure?

Carvedilol and Metoprolol (long acting)

- Acute Treatment

- ER pt with heart failure 4+ pitting edema foaming at the mouth, acute exacerbation + long standing vhf


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- LMNOP

- Lasix (loop diuretic)

- Morphine (for air hunger/relaxation)

- Nitrates (dilate peripheral vasculature)

- Oxygen (as needed)

- Positioning and Pressors (pool blood into legs & inotropic drugs)

- stop blocker- start adrenergic agonists - dobutamine or phosphodiesterase inhibitor

**Which beta blocker is indicated for acute decompedsated CHF?

Contraindicated in acute CHF because they depress myocardial contractility

-Nesiritide (BNP)

- Recombinant B(brain)-type natriuetic peptide causes in cGMP & vasodilation

- Na & water excretion (diuretic)

- BNPs are secreted by myocytes when left ventricle is failure and the EDV and heart is stretching, used as adiagnostic test for CHF 100 (vs COPD exacerbation)

- Used for acute decompensated heart failure

- can cause hypotension, does not improve mortality

Cardiac Glycosides (Digoxin)

- Myocardial contractility

- aka Digitalis, foxglove plant

- treat chronic CHF, reduces symptoms

- helps control heart rate in Afib, by conduction at the AV node (only resting heart rate)

- Lots of side effects and low therapeutic index

- cholinergic effects - Blurry yellow vision

- ECG - ST scooping, bradycardia**

- Antidote is Atropine - will raise the heart rate and reverse the bradycardia,

correct hypokalemia (give Mg+), temporary pacemaker, tachycardia (treat with lidocaine), anti-digoxin Fab

fragments

- Worsened by renal failure, hypokalemia, quinidine


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- Ca necessary to stimulate the actin and myosin to contract

- more CA more contractility

- If you block ion exchange, less Ca leaves the cell, and more contraction

- Na-K ATPase maintains the Na gradient by EC Ca

- Digoxin blocks the Na-K ATPase

Capillaries & Edema

Capillary Fluid Exchange- Blood goes into capillaries out to interstitium back to capillaries + lymphatics

- Excess fluid in interstitium = edema

PC = capillary pressure - hydrostatic pressure - pushes fluid out of capillary

Pi = interstitial fluid pressure - hydrostatic pressure - pushes fluid into capillary

Arterial end - capillary pressure exceeds the interstitial pressure

Venous end - pressures evens out

c = plasma colloid osmotic pressure - pulls fluid into capillary

i = interstitial fluid colloid osmotic pressure - pulls fluid out of capillary

net filtration process = Pnet = [(Pc - Pi) - (c - i)]Kf = filtration constant Jv = net fluid flow = Kf Pnet

capillary failure - Pc (heart failure), venous pressure

plasma proteins - c (nephrotic syndrome), liver failure, malnutrition

capillary permeability - Kf (toxins, infections, burns), histamine, bradykinin

interstitial fluid colloid osmotic pressure - i (lymphatic blockage)

Pitting Edema - excess fluid in absence of additional colloid, watery edema, gravity dependent phenomenon, like

water balloon

Non-pitting edema - no indentation, colloid in interstitial fluid like jello

Transudate - capillary pressure plasma proteins water, protein poor

Exudate - protein capillary permeability protein richNa & Water retention - renal disease or RAA

Capillaries & Shock

Shock

- cardiac failure or vascular failure

- Hypovolemic - Blood loss (trauma), Burns (insensible fluid loss)

- Cardiogenic Shock - MI, PE, CHF, Arrhythmia, Cardiac Tamponade, Tension PTX, Cardiac Contusion


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Hypovolemic/cardiogenic Septic

Low-output failure High-output failure

TPR TPR

CO Dilated Arteriorles, venous return

Cold, clammy pt (vasoconstriction) Hot pt (vasodilation)

SVR CO Hypervolemia IV fluid, blood

Heart Failure LMNOP

Sepsis/Anaphylaxsis Antibiotics, IV Fluids, NE

Neurogenic IV Fluids, steroids

Central Lines

- Femoral- easiest site with least risk; most uncomfortable, max 5-7 days

- Subclavian- easy to find, 3-4 weeks, more comfortable, risk of pneumothorax, CI COPD or lung tumors

- Internal Jugular- good landmarks, 3-4 weeks, uncomfortable, risk of carotid puncture or pneumothorax orperforating the L SC vein (where IF and L SC meet)

- Swan-Ganz Catheter- right IJ > left SC > right SC > left IJ

Femoral Region

Lateral Medial NAVEL

Nerve, Artery, Vein, Empty Space, Lymphaticsx

"dirty" STDs lymphatics closest to genitalia

Palpate for artery then insert need 1-2 cm medially next to pulse


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- contractility pressures SV

- preload vol in atria vol in ventricle

Pressure/Time: Aorta, LV, LA


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Dicrotic Notch - pressure goes back up into aorta after aortic valve closes due to elasticity which aortic pressure

Coronary pressure takes place after aortic valve closes during diastole which allows perfusion of the arteries of the

heart

Diseases that affect elasticity of aorta: Marfan syndrome and Syphillis "tree barking of the aorta"

Heart Sounds & Jugular WavesCardiac Cycle

Heart sounds

- turbulence after valve closes

S1 - after Mitral Valve closes

S2 - after Aortic Valve closes

S3 - early diastole, rapid ventricular filling, associated with filling pressures (preload) in dilated ventricles, children,

pregnant women

Dilated ventricles - dilated CM, CHF, Mitral Regurge, LR shuntsS4 - right before S1, atrial kick, late diastole, atrial pressure associated with ventricular hypertrophy, pushes against

a stiff ventricular wall

Stiff LV - Hypertrophic CM, aortic stenosis, chronic HTN, after MI

Jugular Pulse

- Different waves of JVP

At Carter's X, Vehicle's Yield

- a wave - atrial contraction, before mitral valve closure, maximizing filling of ventricles before systole

- c wave - right ventricular contraction with tricuspid bulging from ventricle into atrium

- x descent - ventricles are empty, the bulging relaxes into ventricles

- v wave - atrial pressure, filling against a closed tricuspid valve

- y descent - blood flows from atria to ventricles, during diastole

ECG

- QRS - mitral valve closure, ventricular contraction, into systole

Splitting

- Splitting of S2 can be normal esp in younger individuals esp in athletically trained ppl

- Normal splitting happens with inspiration

- Aortic valve is closing before pulmonic valve

- intrathoracic pressure and blood goes more into R atrium

- more preload in R ventricle and takes a bit longer to close the pulmonic valve during systole

- .interventricular septum gets pushed to the left slightly due to volume vol of L ventricle

- Wide splitting of S2 - associated with pulmonic stenosis or RBBB not only with inspiration


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- Split S2 on expiration always pathological

- Fixed splitting associated with ASD

- high pressure on L side of heart, and L atrium is filling the R side of heart

- preload from L atrium and more goes into R ventricle

- Pulmonic valve takes longer

- Paradoxical splitting

- aortic stenosis or LBBB

- more volume in L ventricle and delaying the Aortic valve in comparison to pulmonic valve

Systolic Murmurs

- read clinical scenario, systolic vs diastolic, where is it best heart

- listen to diff parts of chest

- watch if its louder on inspiration/expiration or splitting

Auscultation of the Heart

- A - right 2nd IC space

- P - left 2nd IC space

- T - left 4th IC space

- M - left 5th IC space @ midclavicular line (apex of heart)

Benign heart sounds

Split S1

Split S2 on inspiration

S3 in pt < 40 y/o

Early quiet systolic murmur


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Heart murmurs

- Diastole - filling ventricles, mitral valve & tricuspid are open, aortic and pulmonic are closed

murmurs - M or T stenosis, A or P regurgitation

- Systole - ventricles are contracting, A & P are open, M & T are closed

murmurs - A or P stenosis, M or T regurgitation

- Isovolumetric contraction and isovolumetric relaxationContrxn - M & T valves are closed, S1 is complete, contract ventricles, A & P closed, no systolic murmur or

aortic stenosis

Relaxation - ventricles relaxed, all valves closed

Bedside Maneuvers

Inspiration - neg IT pressure, preload, tricuspid mumur

Expiration - mitral murmur due to L atrium filling

Hand grip - afterload (SVR), mitral regurg

Valsalva maneuver - IT pressure, opposite of inspiration, preload & after load, most murmurs, mitral prolapse, hypertrophic cardiomyopathy murmur

Squatting - compresses the veins, and lowers the heart venous return, compresses arteries PVR after load,

mitral prolapse Hypertrophic CM murmur

Systolic Murmurs

- Aortic stenosis

- no murmur during first part of systole, heart is contracting and the V pr not > aortic pressure so aortic valve

is still closed (isometric contrxn)

- ejection click , stiff valves opening due to calcifications

- systolic murmur, radiates up to carotids, weak pulses (pulsus parvus et tardus), syncope

- 5 causes of aortic stenosis: Bicuspid aortic valve (> 40), Senile/degenerative calcs (> 60), chronic rheumatic

valve disease, congenital unicuspid valve, syphilis (tree barking of aorta)


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- Mitral regurgitation

- murmur begins immediately following S1

- holosystolic murmur -- high pitched blowing murmur

- radiate to axilla, lying in L lateral decubitis position

- enhanced with after load TPR, hand grip or squatting

- causes: ischemic heart disease, LV dilation, endocarditis, rheumatic fever- can be associated mitral valve prolapse

Left Lateral Decubitis Murmurs

- Mitral regurgitation

- Mitral Stenosis

- Left sided S3 or S4 heart sounds

- Mitral Prolapse

- very common usually not problematic

- floppy mitral valve, opens back into the atrium mid systolic click

- enhanced by valsalva venous return

- mitral valve prolapse can predispose to endocarditis only if you have mitral regurgitation

- does not cause turbulent blood flow or valve damage


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- Tricuspid regurgitation

- holosystolic murmur loudest at tricuspid

- enhanced by maneuvers that atrial return like inspiration

- cause: endocarditis and rheumatic fever, IV Drug Users

- VSD murmur- defect in interventricular septum

- looks like mitral or tricuspid regurgitation

- holosystolic murmur best heard at tricuspid

- louder during inspiration, clinical scenario very impt to diff btwn T regurge murmur

Diastolic Murmurs

Heart murmurs

- Aortic regurgitation

- Diastole - Mitral & tricuspid valves are open, A & P are closed

- Regurgitation will produce a diastolic murmur begins after S2

- Ventricles are relaxed,you can't hear the mitral valve stenosis until mitral valve opens

- heart is contracted and emptied into the aorta and starts to relax

- blood is flowing back normal systolic blood pressure, systemic diastolic will be low wide pulse pressure

- causes: aortic root dilation, syphilis, marfan syndrome, bicuspid valve, rheumatic fever

- Murmurs associated with Rheumatic Fever


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- Mitral regurge or mitral stenosis, aortic regurge or aortic stenosis, tricuspid regurge

- Mitral stenosis

- not present immediately after S2 because of isometric relaxation

- mitral valve opens and is stenotic and snaps open

- expiration will enhance the murmur

- diff between split S2 sound: diastolic murmur not just snap- S2 split will be more prominent in inspiration

- can result in L atrial dilation, rheumatic disease

- Patent Ductus Arteriosus

- continuous machine like murmur

- always blood flowing through PDA

- keep it open with PGE

- close it with endomethacin (NSAIDs)

Action Potentials

Cardiac Myocyte Physiology

- EC Ca enters the muscle during the plateau state of the AP Ca stimulates more release from SR

- Cardiac muscle APs have a plateau due to a Ca influx.

- Cardiac nodal cells spontaneously depolarize during diastole automaticity due to If channel (constant influx of

Na)


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- Cardiac myocytes are electrically coupled to each other by gap junctions

Ventricular Action Potential

- 4 phases

- resting membrane potential is determined by what it is freely permeable to

- normal resting potential -75 (K) +55 (Na) +20 (Ca)

- Phase 0 - starts at -75 then voltage gated Na channels open drives up towards +55- Phase 1 - Initial repolarization, some Na closes, Voltage gated K channels open up too

- Phase 2 - Plateau, voltage gated Ca channels open and drives potential up towards +20 triggers more CA to be

released myocyte contraction

- Phase 3 - Rapid repolarization, more permeability to K, lose Ca channels

- Phase 4 - resting potential, high K permeability steady state around -75

Effective refractory period - phase 0 - phase 3 - can't elicit a phase 0 depolarization;

- if you ERP then you will have to wait longer to depolarize again, slow heart rate

How to change slope of phase 0 - Na permeability

- if you prolong phase 1 by using Na channel blockers

How to prolong phase 3 - K permeability

- if you prolong it by using K channel blockers

Pacemaker Action Potential


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- SA & AV nodal cells

- No phase 1 or phase 2

- Phase 4 - resting membrane potential around -60 (freely permeable to K)

- gradual increase, Na channels are spontaneously opened till it reaches the threshold

- Phase 0 - voltage gated Ca channels opens at threshold

- No plateau at all

What will inhibit phase 0

- CCB

What will affect the slope of phase 4

- blockers, will decrease the slope prolonging phase 4

Antiarrhythmics

No Bad Boy Keeps Clean

Na+ channel blockers

- Phase 0 Na channels open up

- Na channels blockers work on phase 0 and elongating ERP

Class IA (slows phase 0, prolongs phase 3) - Quinidine, Procainamide, Disopyramide

- Procainamide - Wolfs Parkinson White, cause reversible SLE syndrome (SHIPP)

- Quinidine - cinchonism, thrombocytopenia, torsades de points ( QT)

Double Quarter Pounder

Class IB (shortens phase 3) - Lidocaine, Mexiletine, Tocainide, Phenytoin

Lettuce Tomato Mayo Pickles

- Lidocaine - acute ventricular tachyarrhythmias and slow HR down, digitalis or MI

Class IC (markedly slows phase 0) - Flecainide, Propafenone

Fries Please

-blockers

- cAMP and CA currents slope of phase 4 in nodal cells

Class II (suppresses phase 4 depolarization rate) - Esomolol

- Supraventricuar Tachycardia, afib and atrial flutter

- can mask hypoglycemia * : Glucagon


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K+ channel blockers

- slows release of K and elongates the ERP

Class III (prolongs phase 3) - Sotalol, Amiodarone

- Afib

- Amiodarone - WPW, pulmonary fibrosis, hepatotoxicity and hypo/hyperthyroidism

check PFTs, LFTs, and TFTs - 40% Iodine by weight

has class I, II, III, IV effects

Calcium Channel Blockers

- dihydropyridine (nifedapine works on blood vessels) and non-dihydropyridine (work at the heart)

- slope of phase 0 in nodal cells, and elongating ERP since Ca causes depolarizations

Class IV (slows the action potential) - Verapamil, Diltiazem

- constipation, flushing, edema and heart block

- do not combine with blockers

Other antiarrhythmics

- Adenosine - K leaving the cell hyperpolarizing cell

- permeability to Ca cannot depolarize (flatline stop heart)

- used to diagnose SVT

- blocked by theophylline (COPD) & caffeine

- K+ - depresses ectopic pacemakers in hypokalemia and digoxin toxicity; should be above 4

- Mg2+ - effective in torsades and digoxin toxicity; should be above 2


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**pt who codes for > 5 minutes - acidosis is associated with hyperkalemia (H+-K+ pump) give Ca and bicarb

Atria to AV conduction

Electrocardiogram

Axis

- 12 lead EKG: I, II, III, aVL, aVR, aVF, v1, v2, v3, v4, v5, v6

- Axis of deviation of the electrical conductance of the heart.

- Measures the signal of your heart in a certain direction

- Net signal of heart is down and to the left

- aVR - measures from center to right, it will have a negative deflection of QRS complex (below the line)

- aVL - positive deflection of EKG since vector is in line with axis

- Bipolar leads

I - R to L

II - R arm to L foot

III - L arm to L foot


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- The net electrical signal (cardiac axis) will fall within the shaded region in normal cardiac pathology

Left axis deviation: Right axis deviation:

inferior wall MI RV hypertrophy

L anterior fascicular block Acute R heart strain (PE)

L ventricular hypertrophy L posterior fascicular block

LBBB RBBB

High Diaphragm Dextrocardia

- Look at Limb lead I and II; If they're positive then it's usually normal


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- Look at aVR; if positive, there is pathology, completely opposite direction

ECG tracings

- tiny box - 0.04 seconds

- big box 0.2 seconds

- PR interval - through AV node normal < 0.2 sec (1 big box)(1st degree HB)

- QRS - ventricular depolarization, equal on both sides < 0.12 sec (3 small boxes) (V arrhythmia)

- T wave - ventricular repolarization, inversion (recent MI), peaked T wave ( K), flat T wave ( K)

- U wave - associated with K and hypokalemia, another bump after T wave

- SA > AV > Bundle of His

- Afib

irregularly irregular, no discrete P waves

SA node not in sync (Atrial enlargement)

No coordinated Atrial contraction no P

Pooling of blood in atria clot

predispose to SVT

: time is critical < 48 synchronized cardiovert,

> 48 anticoagulation (heparin) then coumadin

rate control - just fix rate, stay on anticoagulation therapy

Digoxin, blockers, CCB

rhythm control - back to sinus rhythm

K+ channel blockers: Sodolol and Amiodalone


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- A flutter

- sd

Problems with the AV conduction

- AV block

1 heart block

prolonged PR interval > 0.2 secs

usually benign, asymptomatic

Lyme disease can cause AV nodal block

- Mobitz type I (wenckebach)

2 heart block

progressive lengthening of PR until beat is dropped (W=warning)

mostly benign

- Mobitz type II

2 heart block

no lengthening of the PR interval, just a dropped beat

greater tendency to turn into a 3 heart block

: pacemaker


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- Third Degree

atria and ventricles beat independently of each other

P & QRS are present but are not coordinated

P > QRS, Narrowing of the QRS (from AV node)

Lyme disease

: pacemaker

Wolf-Parkinson White Syndrome

Ventricular pre-excitation syndrome

accessory conduction pathway that bypasses the AV node

Bundle of Kent

blurred ventricular contraction that is called wave

can result in a reentry circuit SVT ( : Adenosine)

: Procainamide (Na channel blocker), Amniodarone (K channel blocker)

Ventricular Arrhythmias

Ventricular premature contractions

beats ka PVCs

early occurring widened QRS complexes

microrentry of the purkinje fibers

usually benign


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Ventricular Bigeminy

PVC follows each sinus beat

Normal, big one, normal big one

Trigeminy - 2 normal 1 PVC

Ventricular Escape Complex (rhythm)

failure of the sinus & AV node to generate an impulse widened QRS

usually after a pause (larger than a normal RR interval)

rate is slow

Ventricular Tachycardia

3 or more successive ventricular complexes

non-sustained Vtach - during < 30 seconds

sustained > 30 sec leads to hemodynamic collapse

usually ~100 bpm

rhythm is usually regular

wider QRS interval

Torsades de pointes

Type of Ventricular Tachycardia

shifting sinusoidal waveforms on the EKG

Ventricular Fibrillation

uncontrolled rhythm, on identifiable waves

can lead to hemodynamic collapse

emergency defibrillation needed


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Physiology of BP regulation

Maintenance of MAP

Body must keep BP in order to perfuse and O2 the organs

If BP drops, the body uses the SNS and the RAA (chronic)

Renin Angiotensin Aldosterone System

Kidney sense low BP at JG apparatus and secretes renin

Renin converts Ag AGI

ACE in the lungs converts AG I AG II

Aldosterone has kidney reabsorb Na & water

Baroreceptors & chemoreceptors

Medullary vasomotor center (solitary nucleus) sends a vasoconstricting signal to HR

Baroreceptors

Baroreceptor on aortic arch via vagus ( BP)

Baroreceptor on carotid sinus via glossalpharyngeal nerve (/ BP)

Sense stretch signal efferent sympathetic firing + Vagus inhibition of heart Adrenergic 1 receptors

responsible for vasoconstriction

Sense stretch vagus signal to heart to slow heart and BPUse for SVT carotid massage heart rate or Adenosine

Chemoreceptors

peripheral chemoreceptors in carotid and aortic bodies - respond to low PaO2, PaCO2, pH

central chemoreceptors - pH and PCO2 in the brain, do not directly respond to O2

Cushing rxn - cranial pressure constrict arterioles in brain cerebral ischemia CO2 Hypertension

Bradycardia + Respiratory Depression Intracranial lesion with Intracranial pressure (e.g. hemorrhage)

Physiology of vasoconstriction

Smooth Muscle Contraction


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- Adrenal gland - z. glomerulosa - aldosterone

- adrenal gland - z. fasciculata - cortisol

- adrenal gland - medullary chromatin cells - Epi & NE

- Liver - Angiotensinogen

- JGA of kidneys - Renin

- Lungs - ACE

- Glomerulus - GFR- Tubules - AG II, ADH, Aldosterone

- Local tissue effectors - NO, PG, 5HT, Histamine, Bradykinin, Adenosine, Acidosis, Lactate, O2, CO2, K+

Hypertension

Circulation through organs

Liver - largest part of the systemic output, lots of metabolic functions

Kidneys - eliminate harmful waste & maintain fluid & electrolyte balance & pH; receives highest blood flow per gram

of tissue

Heart - big btwn arterial O2 and venous O2 since heart can extract about 100% of O2 it receives; O2 demands aremet by coronary blood flow

Autoregulation

Organ Factors determining autoregulation

Heart Local metabolites-O2, adenosine, NO

Nitrates**** - (Create NO causes decrease in preload, systemic venous dilation O2

demand)

Brain Local metabolites-C02 (pH)

Kidneys Myogenic and tubuloglomerular feedback

Lungs Hypoxia causes vasoconstriction

Skeletal muscle Local metabolites-lactate, adenosine, K+

Skin Sympathetic stimulation most important mechanism-temperature control

Note: the pulmonary vasculature is unique in that hypoxia causes vasoconstriction so that only well-ventilated areas

are perfused. In other organs, hypoxia causes vasodilation.

Hypertension

High blood pressure 140/90, 90% is essential

CO or TPR afterload

Kidney disease - renal failure or renal artery stenosis

Other causes: Drugs (cocaine, amphetamines), Medications (OCPs, steroids, NSAIDs, antidepressants),

Obstructive sleep apnea, coarctation of the aorta, endocrine (hyperthyroidism, pheochromocytoma,

hyperaldosteronism, cushing syndrome)

Prehypertension - 120-139/80-8


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Left-sided hypertrophy

early form of end organ damage due to HTN

myocytes get bigger and the wall gets concentrically bigger thickening of the LV wall

myocardial O2 demand, LV - stiff and less compliant S4

No in heart diameter, less filling,

Precursor left-sided heart failure

RF for MI

Aortic Dissection

tear in the intima of the aorta which allows blood to dissect into the walls of the aorta forming a false lumen

heart will pump into both lumens

2 main causes: hypertension and certain diseases (cystic medial necrosis or mar fans)

MC in ascending aorta

Tearing chest pain that radiates through to the back

Widening of mediastinum on Xray

High mortality2 types:

Type A - acending aorta, aortic arch; surgical management

Type B - descending aorta; medical management

: blocker to lower BP in aortic dissection, reduce arterial pressure and slope of rise of BP

Antihypertensive Agents

ACE inhibitors

Captopril, Enalopril, Lisinopril -pril

ACE prevents AGI AGII, also inhibits breakdown of bradykinin (vasodilator) Reduces after load & preload

Rise of Renin levels due to loss of inhibition

Help prevent remodeling of the heart and also mortality

Used also in diabetic kidney disease to reduce the rate of proteinuria and diabetic nephropathy

SE: C - cough (elevated levels of bradykinin) A - angioedema P - proteinuria (prevent)

T - taste changes (dysgeusia) O - hypOtension P - pregnancy problems (teratogenic)

R - rash I - Inc Renin L - lowering AGII, Hyperkalemia, reduce GFR and creatinine

ARBs

Losartan - sartan

block AG II receptors, stop stimulation and aldosterone secretion

SE: similar SE like angioedema, except no cough


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Aliskiren

Renin inhibitor only for HTNcan still caused hyperkalemia and renal insufficiency

contraindicated in pregnancy

Hydralazine

Vasodilator - cGMP act myosin phosphatase

dilates arterioles > veins, reduces afterload

Hypertensive crisis, HTN, HTN in pregnancy

SE: reflex tachycardia (often given with blocker), fluid retention, drug-induced lupus

Drug Induced Lupus "SHIP"

Sulfasalazine

Hydralazine

Isoniazid

Procainamide

Safe HTN Meds in Pregnancy

Hydralazine

Methyldopa

Labetalol

Nifedipine

Minoxidil

Opens K channels & hyper polarizes SM (Ca channels stay closed)contraction relaxation

used for severe HTN or for hair loss (hypertrichosis)

SE: hypertrichosis, hypotension, reflex tachy, fluid retention/edema


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CCBs

Dihydropyridine CCB: nifedipine, amlodipine, felodipine, incardipine, nisoldipine -pine

act on vascular SM to cause vasodilation (mostly arteries)

HTN, angina, vasospasm, esophageal spasm, migraine prophylaxis

SE: peripheral edema, flushing, dizziness, constipation, reflex tachy

Non-dihydropyridine CCB: verapamil, diltiazem @ block Ca channels at pacemaker cells

HTN, angina, arrhythmias

SE: cardiac depression, AV-block, flushing, dizziness, constipation

Nitroglycerin, Isosorbide dinitrate

cause vasodilation by releasing NO in SM cGMP relaxation

work on veins > arteries preload

can be in combo with Nitrate and hydrazine to reduce both after load & preload

pools blood peripherally (use for pulmonary edema)SE: reflex tachy, hypotension, flushing, headache

Antihypertensive Therapy

Essential HTN, no comorbidities - Thiazide Diuretic

ALLHAT - showed thiazide reduced risk of stroke

can add ACE/ARB -blocker, CCB

HTN + CHF - Loop Diuretic (Furosemide)

blocker, ACE inhibitors, ARBs, and K sparring diuretics (aldo antagonist - spironolactone)

can combo

no blockers with cardiogenic shock , no CCB

HTN + Diabetes - ACE/ARB

kidney protective; reduce proteinuria

Thiazides are ok

blockers can mask hypoglycemia

Post-MI/CAD - Thiazide, blocker, ACE/ARB

dec mortality

use CCB and Nitrates for angina

Afib - Diltiazem/verapamil (rate control)

Bradycardia - avoid diltiazem/verapamil, blockers

slow heart down

Renal insufficiency - ACE/ARB

dec proteinuria, but can also worsen creatinine hyperkalemia

avoid K sparring diuretics

Renal artery stenosis

avoid ACE/ARB renal insufficiency


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BPH - blocker (lower BP and help urinary retention)

Hyperthyroidism - Propranolol (manage hyperthyroid symptoms)

Hyperparathyroidism - Loop Diuretic (facilitate urinary excretion of Ca)

avoid thiazide (retain Ca)

Osteoporosis - Thiazide (retain Ca)

Gout - avoid Thiazide can cause hyperuricemia

Pregnancy - Hydralazine, Methyldopa, Labetalol, Dihydropyridine CCBavoid ACE/ARB

Migraines - CCB, blocker

Essential Tremor - Propranolol

Malignant Hypertension treatment

Severe hypertension that is rapidly progressive end-organ damage

Nitroprusside - cGMP via direct release of NO, can dilate both arteries and veins

short acting, but can cause cyanide toxicity

Diaxozide - opens K in cells in pancreas and shuts insulin secretionalso opens K channels in vascular SM vasodilation (like Minoxidil)

Atherosclerosis & Coronary Artery Disease

Arteriosclerosis

- Sclerosis/scarring/hardening of the arteries

- Monckeberg's arteriosclerosis - calc in the media of the arteries benign pipestem arteries, does not

obstruct blood flow, does not involve intima

- Arteriolosclerosis - hyaline thickening of small arteries and arterioles, e.g. diabetes or HTN

- Atherosclerosis - fibrous plaques and atheromas that form in the intima of the arteries

Atherosclerosis

- disease of elastic arteries, involving the intima, in medium sized or muscular arteries

- Summary: Start with endothelial cell dysfunction accumulation of M and LDL foam cell formation

fatty streaks smooth cell migration (platelet derived growth factor) TGF fibrous plaques atheroma

- Location of plaques are important: Abdominal Aorta, Coronary Arteries, Popliteal Artery, Carotid

Artery

Pathogenesis of Atherosclerosis

- Endothelial injury leads to vascular permeability, leukocyte adhesion, and thrombosis

- Accumulation of lipoproteins: occurs in the vessel wall and is mostly LDL

- Monocyte adhesion to the endothelium: subsequent migration of monocytes into intima and transformation

into M and foam cels

- Platelet adhesion

- Factors release: ACT platelets, M, vascular wall cells, induce SM recruitment

- SM cell proliferation and ECM production

- Lipid accumulation: occurs extracellularly and within M and SM cells


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Complications of Atherosclerosis based on location

- smaller vessels can become occluded and then compromise distal tissue perfusion

- ruptured plaque can embolize atherosclerotic debris and cause distal vessel obstruction or can lead to acute

vascular thrombosis (stroke)

- destruction of the underlying vessel wall can lead to aneurysm formation with secondary rupture &

thrombosis

Abdominal Aortic Aneurysm- atherosclerotic plaque compressing the underlying media

- Nutrient and waste diffusion is compromised

- Media degenerates and necroses, leading to arterial wall weakness

- MC in men over 50 and in smokers

- Presents as a pulsating mass in the abdomen

- consequences include: rupture leading to fatal hemorrhage, embolism from atheroma, obstruction of a

branch vessel and impingement on an adjacent structure (ureter)

- monitor by US but if > 5 cm must treat with surgery

Coronary Arteries


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- RCA Marginal Artery Posterior Descending (Interventricular) artery (80%)

-LCA Circumflex LAD PD (20%)

- SA and AV nodes - supplied by RCA Arrhythmia

- RCA (80)% supplies inferior portion of left ventricle via PDA (right dominant heart)

- Coronary Artery occlusion MC occurs: in left anterior descending (supplies anterior interventricular septum)

Anterior Wall MI

- Coronary arteries fill during diastole

- Posterior part of the heart is the left atrium which can cause dysphagia (esophagus) or hoarseness (recurrent

laryngeal nerve)

Ischemic Heart Disease

Angina

- narrowing of 75% of the CAD

- Stable - predictable, 2 atherosclerosis; ST segment depression on EKG, retrosternal chest pain

- Unstable - unpredictable, worsening, ST Depression

- Prinzmetal's angina - 2 coronary artery spasm, ST elevation (more ischemia) then reversal

dihydropyradine CCB - nifedapine

- Coronary steal syndrome - vasodilator may aggravate ischemia by shunting blood from area of critical

stenosis to high perfusion

- MI - Most often due to acute thrombosis results in myocyte necrosis or sudden cardiac death

- Sudden cardiac death - death within one hour usually due to ventricular arrhythmia

- Chronic ischemic heart disease - progressive CHF over many years due to chronic ischemic myocardial

damage


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5 Deathly Causes of Chest Pain

- Aortic Dissection (or dissecting aortic aneurysm)- tearing pain, radiating to back

- Unstable angina

- MI

- Tension Pneumothorax - collapsed lung and one way valvular disruption of lung, air gets into pleural cavity

- PE

Most likely causes of chest pain

Prinzmetal's angina - ST segment elevation only during brief episodes of chest pain

MSK chest pain - pt is able to point to localize the chest pain with one finger

Costochondritis/MSK - chest wall tenderness on palpation

Aortic Dissection - rapid onset sharp chest pain that radiates to the scapula

Spontaneous Pneumothorax - rapid onset sharp pain in a 20 year old associated with dyspnea

GERD, esophageal spasm - occurs after heavy meals and improved by antacids

Pericarditis - sharp pain lasting hours-days and is relieved by sitting forward

MSK pain - pain made worse by deep breathing and/or motion, pleuritic chest painShingles/Herpes Zoster - chest pain in a dermatomal distribution, pain precede rash

GERD, MSK pain - MCC of non-cardiac chest pain

Costochondritis

- inflammation of cartilage where the ribs connect to the sternum

- painful when moving chest wall and pressing on it

- - NSAIDs

Antianginal Therapy

MVO2 by decreasing

EDV BP Contractility HR Ejection Time

Nitrates (reflex) (reflex)

blockers

Combo

Combo therapy lowers the MVO2 more than Nitrates & blockers alone

ACE Inhibitor ( afterload) also used

Lipid Lowering Agents

HMG CoA reductase inhibitors (-statins) - LDL HDL TG

- prevents conversion of HMG-CoA to cholesterol precursor

- Hepatotoxicity (LFTs), Rhabdomyolysis

Niacin B3 - LDL HDL TG

- inhibits lipolysis in adipose tissue and reduced hepatic VLDL secretion

- Red flushing, hyperglycemia (acanthosis nigricans) hyperuricemia (gout)


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Bile Acid Resins (cholestyramine, colestipol, colesevelam) - LDL slightly HDL slightly TG

- Prevents intestinal reabsorption of bile acids

- tastes bad, go discomfort, absorption of Fat soluble vitamin, cholesterol gallstones

Cholesterol Absorption Blockers (ezetimibe) - LDL

- Prevents cholesterol reabsorption at SI brush border

- LFTs, diarrhea

Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate) LDL HDL TG- Upregulates LDL TG clearance

- Myositis, hepatotoxcity ( LFTs) cholesterol gallstones

Omega 3 FA - fish oil & flaxseed oil - TG

- reduce severity of RA and arrhythmias

Elevtaed TGs

- can lead to pancreatitis, must be 600-700's can get as high as up to 2000

- Fibrates are first line + Omega 3 FA

MI Pathophysiology

LAD - MC artery occluded in MI; anterior wallRCA - 2nd most common Circumflex - 3rd most common

Adrenergic Sx: Diaphoresis, Tachycardia, Retrosternal pain, Left Arm and Jaw, Dyspnea, Fatigue

blockers mask the symptoms, but reduce mortality

Older women or diabetics- do not have classic presentation

Reversible injury - 30-40 minutes

Evolution of an MI

0-4 hours

gross: None


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micro: None

risks: Arrhythmias

4-24 hours

gross: Dark mottling

micro: Contraction bands (early coag necrosis), Neutrophil emigration, CKMB, Troponin I, CPK

risks: Arrhythmia

1-3 daysgross: Dark mottling

micro: Coag necrosis, loss of nuclei, Striations, Neutrophils

risks: Arrhythmias

3-4 days

gross: Hyperemia

micro: Neutrophils

risks: Arrhythmias

5-10 days

gross: Hyperemic border, yellow tan softeningmicro: Margin Granulation tissue

risks: Wall rupture tamponade, Papillary muscle rupture, interventricular muscle rupture

10 days - 8 weeks

gross: Gray, white scar

micro: collagen cellularity

risks: Dressler syndrome - fibrous pericarditis

> 2 months

gross: complete scar

micro: dense collagen scar

risks: ventricular aneurysm

Diagnosis & Treatment of MI

ECG diagnosis of MI****


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Gold Standard

ST elevation of at least 1mm in 2 contiguous leadsT wave inversion

New LBBB

New Q waves (at least 1 block wide or height of total QRS complex)

Left anterior Descending Anterior Wall V1-V3 (V4-V5) ST elevation

Left circumflex Lateral Wall aVL V5 V6

Right Coronary Inferior Wall II, III, aVF

Right Coronary Posterior Wall R precordial EKG: V4

Serum diagnosis of an MI

CPK - elevated with any type of muscle damage

Cardiac troponin I - most specific, rise after 4 hours, elevated 7-10 days, used of Diagnosis

CK-MB - elevated to heart muscle, but other muscle can show, used to diagnosis re-infarction

Myoglobin - rises quickly before 4 hours for damaged heart muscle

ECG - ST elevation (transmural MI), ST depression (subendocardial infarct/ischemia), pathologic Q wave

(transmural/old infarct)

Types of infarcts

Endocardium - superficial layer that lines the chambers, can get infected (endocarditis); most vulnerable since the

heart is perfused from the coronary arteries from the outside in

Myocardium - muscular layer

Pericardium - outside layer of heart that can get inflamed (pericarditis)

Transmural Infarcts Subendocardial Infarcts

necrosis due to ischemic necrosis of < 50% of ventricular wall

Affects entire wall subendocardium esp vulnerable to ischemia


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ST elevation on ECG, Q waves ST depression on ECG

MI complications

1. Cardiac Arrhythmias - MCC of death and first few days during healing

Ventricular fibrillation - MC lethal arrhythmia

2. Left Ventricular Failure & Pulmonary Edema - S4 heart sound

3. Cardiogenic Shock4. Ventricular free wall rupture cardiac tamponade

papillary muscle rupture severe mitral regurge

interventricular septum rupture VSD + murmur

5. Ventricular aneurysm formation - scar tissue embolism from mural thrombus (anticoagulate)

6. Fibrinous Pericarditis - postinfartion, friction rub, lean forward for relief

7. Dressler's Syndrome - AI phenomenon resulting in fibrinous pericarditis 5-7 weeks post mi

MI Treatment

"MONA"Morphine - pain/stress

Oxygen - get more O2 to heart and body

Nitrates - preload, sublingual or topical paste or iv

Aspirin - acutely or colpitagril (if allergic to aspirin)

blockers - O2 demand, infarct size, mortality, risk risk of acute cardiogenic shock if LV dysfunction

ACE - after load, O2 demand, cardiac remodeling, risk of HF and death

Statins - stabilize atherosclerotic plaques, inflammation and LDL

Mg & K - PRN - MG > 2 and K > 4 prevent arrhythmias

Cardiomyopathies & Endocarditis

Cardiomyopathies

Muscle pathology of the myocardium

Dilated CM - most common

heart gets bigger and adds sarcomeres in series

systolic dysfunction, abnormal contraction

S3 sound, laterally displaced PMI

causes: Alcohol abuse, wet Ber1Ber1, Coxsackie b virus myocarditis, Cocaine use, Chagas' disease

(+megacolon/esophagus), Doxorubicin/Donorubicin toxicity, hematochromatosis, peripartum cardiomyopathy,

myocardial ischemia

Hypertrophic Obstructive CM - HY

aka idiopathic hypertrophic subaortic stenosis

concentric hypertrophy - sarcomeres in parallel (disorderly)

mostly a hereditary disease (AD) vs LVH is mostly due to HTN

lots of hypertrophy of the IV septa, and too close to mitral valve leaflets outflow obstruction


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normal sized heart + S4 (stiffen ventricle) apical impulse is enlarged/diffuse

systolic murmur (similar to aortic stenosis) valsalva will make it larger (diff vs aortic stenosis)

MCC of sudden death in healthy young athletes

blocker or non-dihydropyridine CCB (verapamil) slow down the heart and diastolic filling

Restrictive obliterative CM

depositing stuff onto the myocardium disrupting diastolic functionmuscle becomes thickened and becomes restrictive

sarcoidosis (granulomas), amlyoidosis, post radiation fibrosis, endocardio fibroelastosis (congenital), Loffler's

syndrome (eosinophils will endomyocardial fibrosis) hemochromatosis

Myocarditis

can cause dilated CM

Generalized inflammation of the myocardium (not from ischemia)

MCC in US: Coxsackievirus (echovirus & influenza virus)

Histo diffuse interstitial infiltrate of lymphocytes with myocyte necrosis

Bacterial Endocarditis

characterized by lesions or vegetation (mass of platelets, fibrin, mass of organisms and inflammatory cells) that

sit on valve leaflets

subacute bacterial endocarditis - can have vegetations with granulomatous tissue in the center

Dx: multiple blood cultures, echocardiogram (TEE) to look for vegetations

S&S of endocarditis

fever, chills weakness, anorexia, anemia

new regurge heart murmur* or heart failure

mitral valve is mc; tricuspid mc in IVDU septic pulmonary infarcts

splinter hemorrhages in fingernails

Osler's nodes (painful red nodules on finger and toe pads)

Janeway lesions (erythematous macules on palms and soles)

roth spots (retinal hemorrhage with clear central areas) - rare

signs of embolism: brain infarct focal neuro defects, renal infarct hematuria, splenic infarct abdo or

shoulder pain

systemic immune reaction: glomerulonephritis, arthritis

Organisms 75% are from:

s. aureus (high virulence acute endocarditis) - large vegetations on previously normal valves, rapid

viridans streptococci - subacute (low virulence) smaller vegetations on already abnormal valve

dental procedures or previous rheumatic fever

enterococci (fecalis) - vancomycin resistant endocarditis

coagulase (-) staph - staph epidermitis

IVDU: Pseudomonas or Candida or Staph epidermitis

s. bovis - might also have colon cancer


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negative cultures: HACEK organisms: Haemophilus, Actinobacilus, Cardiobacterium, Eikenella, Kingella

Complications: Rupture to the chord ten, glomerulonephritis, suppurative pericarditis, embolism, valvular damage

Libman-Sacks endocarditis

non-infective endocarditis

sterile wart-like vegetations on both sides of the valve

associated w SLE

Other Cardiac Pathology

Rheumatic Heart Disease

Autoimmune phenomenon 2 to a bacterial infection - Type II HSR

Pharyngitis Group A hemolytic Strep Pyogenes (Scarlet fever)

Autoantibodies from the disease that attack the heart

MC MItral valve but also can be the aortic valve

Mitral valve relapse as an early lesion mitral stenosis

Aschoff bodies, areas of fibrinoid necrosis + mononuclear multinucleate giant cells (granulomas)Anitchkow's cells and elevated ASO titers

Diagnostic criteria (Jones) for rheumatic fever

Evidence of group A strep (ASO titer)

2 Major + 1 Minor

Major: JONES

joints (migratory polyarthritis)

(pancarditis)

Nodules (subcutaneous

Erythema Marginatum (serpiginous skin rash/annular lesion)

Sydenham chorea (chorea of the face, tongue, upper-limb)/St. Vitus dance

Minor: arthralgia, fever, ESR or CRP, prolonged PR

Pericarditis

Pleuritic chest pain, sharp with inspiration, better sitting up and leaning forward

distant heart sounds + friction rub

diffuse ST segment elevation in most leads or PR depression

Fibrinous: Dressler's syndrome, uremia, radiation


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Serous: noninfectious inflammatory diseases (lupus), viral pericarditis

Suppurative/purulent - usually bacterial infection (pneumococcus, streptococcus)

Hemorrhagic - TB or melanoma

Can resolve completely or become a restrictive pericarditis

Kussmaul's Sign - JVD with inspiration - (pathological)

Cardiac Tamponade

Compression of the heart by fluid, blood or pericardial effusion

leads to CO and equilibration of diastolic pressures in all 4 chambers

hypotension JV, distant heart sound, pulses paradoxes, HR

Pulsus Paradoxus

Exaggerated response in amplitude of systolic blood pressure during inspiration 10 mmHg

take a deep breath and inspire IT pressure blood will rush into R heart

pushes on IV septum to the left smaller in inspiration than expiration

if left ventricle vol is smaller CO systolic BP is lower in inspiration (normal)

sign of cardiac tamponade

Causes with exaggerated inspiration: cardiac tamponade, asthma, chronic sleep apnea, pericarditis

EKG: Electrical Alternans*** - specific, but sensitive - alternating electrical impulses

Alternating QRS amplitude

Kussmaul's Sign vs Pulsus Paradoxus

Kussmaul's sign Pulsus Paradoxus


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JVD w inspiration SBP 10 mmHg w inspiration

capacity of RV capacity of LV

Constrictive pericarditis >> tamponade Cardiac Tamponade >> Pericarditis

Syphilitic Heart disease

Tertiary Syphilus disrupts the vasa vasora, BV that supply aorta

Dilation of Aorta and valvular ring aorta regurge or stenosisAortic aneurysms or stenosis tree bark appearance

Cardiac tumors

Myxomas - MC primary cardiac tumors in adults

occur in LA, LA myxoma

look like a ball of tissue in the atrium

obstruct mitral valve syncope

can go into the LV tumor plop

Rhabdomyomas - MC in childrenAssociated with tuber sclerosis, astrocytoma and angiomyolipoma (renal)

Metastasis - MC cardiac tumor

melanoma, lymphoma

kussmal's sign - R side of heart can't fill properly JVD with inspiration

Varicose Veins

tortuous dilation of the superficial veins due to venous pressure

one way valves in veins are worn out - venous insufficiency

leads to poor wound healing and ulcers on skin

Raynaud Phenomenon

Arterial vasospasm poor blood flow to skin and fingers/toes

brought on by cold temperatures or emotional stress

causes pallor or cyanosis reperfused becomes red

can be part of mixed CT disease or Beurger's disease or lupus or crest scleroderma

dihydropyradine CCB - vasodilator or low dose aspirin

Vascular tumors

Sturge-Weber disease

congenital d/o that affects capillaries causing intracranial AV malformation

leptomeningial hemeangioma affect brain & eye

port-wine stain in the opthalmic region of the trigeminal nerve vascular malformation

seizures, early onset glaucoma seizures, hemiplegia


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Strawberry Hemangioma

benign capillary hemangioma of infancy that resolve spontaneously

Cherry Hemangioma

benign capillary HA of the elderly, looks like mole

Pyogenic GranulomaPolypoid capillary hemangioma, ulcerate and bleed

trauma and pregnancy

Cystic Hygroma

cavernous lymphangioma of neck, turner syndrome

Glomus tumor

benign painful, red-blue tumor under fingernails

Bacillary angiomatosis

due to Bartonella Henselae infections, benign papules in AIDS pts

Kaposi's Sarcoma

indolent variant - associated with older men of mediterranean descent

endemic variant - in Subsuherent africa

Infectious - with HIV or HHV-8

causes proliferation of vessels & lymphatics of the skin and also sometimes internal organs

Angiosarcoma

liver lesion associated with vinyl chloride, arsenic, and ThO2

Lymphangiosarcoma

lymphatic malignancy with persistent lymphedema

Small-vessel vasculitis

Microscopic polyangiitis

affects kidneys pauci-immune glomerulonephritis pANCA + myeloperoxidase (MPO) ANCA

Wegener's granulomatosis (Granulomatosis with polyangiitis)****

focal necrotizing vasculitis, necrotizing granulomas in the lung & upper airway, and cANCA necrotizing

glomerulonephritis


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(Wegener's and Good pastures - only dz that affect both lung and kidneys, diff Wegener's also affect UA and

lungs + granulomas)

S&S: UA disease, dyspnea, hemoptysis, hematuria

: cyclophosphamide and corticosteroids

Churg-Strauss syndrome

Granulomatous vasculitis with eosinophilia with asthma, sinusitis, peripheral neuropathy

Differential Diagnosis for Eosinophilia:

NAACPNeoplasm

Allergy/Atopy

Asthma

Addison's disease

Collagen vascular diseases

Parasites

Henoch-Scholein Purpura

cause a rash on the buttocks and legs in children, palpable purportarthralgia in knees + abdo pain (intestinal hemorrhage/melena)

esp after an URI + IgA immune complexes/nephropathy

self-limiting temporary disease

Medium Vessel Vasculitis

Polyarteritis Nodosa

Kawasaki Disease


55/55

Buerger Disease

Large-Vessel Vasculitis

Temporal Arteritis

Takayasu Arteritis

CV DIT notes

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