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Cardio Flashcards

1
Q

torsades de pointes

  • what is it
  • caused by
  • what drugs induce it
  • ECG findings
  • tx
A
  • part of ventricle not repolarizing correctly -> re entrance loop created -> V fib -> SCD
  • decrease in K, Mg, Ca
  • anti-arrythmics (I Na/potassium blockers , III k blockers), antibiotics (macrolide), antipsychotics (haloperidol), antidepressants (TCA). antiemetics (ondansetron)
  • magnesium sulfate
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2
Q

congenital QT syndrome

  • what is it
  • types and what makes them different
A
  • inherited ion channel defects

- romano ward (only cardiac) and Lange-Nielsen (cardic + sensorineuro deafness)

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3
Q

brugada syndrome

  • what is it?
  • genetics
  • epi
  • ECG findings
  • tx
A
  • defect in Na channel causing abnormal repolarization
  • auto dom
  • asian male
  • psuedo right BBB and ST elevation V1-3
  • ICD
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4
Q

Wolff Parkinson White syndrome

  • what is it
  • ECG findings
  • sequalae
  • TX
A
  • accessory conduction pathway ( bundle of kent), bypassing the slowing of speed through the AV node, causing ventricles to depolarize earlier
  • scoop between P wave and QRS (dela wave), shorter PR interval, longer QRS complex
  • re-entrant loop -> ventricular tachycardia
  • Ablation of bundle of kent
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5
Q

A-fib

  • what is it
  • ECG findings
  • risk
  • types
  • sequalae
  • tx
A
  • irritated atrial pace maker cells begin to undergo structural and electrical changes -> some begin to out pace SA node and cause part of atria to beat faster -> atria begins to fibrillate -> only some of the waves can get through to AV node to cause ventricles to depolarize
  • no p wave, irregularly spaced QRS
  • heart dx (HTN, CAD), binge drinking
  • stroke, from blood stagnating in atria
  • antithrombotic, rate/rhythm control, ablation
  • paroxysmal (< 1 wk), persistent (1 wk - 1 yr), long standing (> 1 yr), permanent (not going to tx)
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6
Q

A flutter

  • what is it?
  • what does it do to ventricles?
  • ECG findings
  • types
  • TX
A
  • identical, back to back atrial depolarization, very fast
  • AV node has long repolarization so only picks up on some of the atrial depolarizations -> use ratio
  • saw tooth p wave, use ratio and count how many p waves to QRS complex
  • 1: around tri-cuspid valve (the pathway is slower here, so is able to form re-entrant loop); 2: unknown origin
  • ablation
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7
Q

V fib

  • what is it?
  • TX
A
  • ventricles are damage by heart dx -> undergo changes -> different parts of ventricular pace maker cells depolarize faster than SA node -> ventricles begins to fibrillate-> can’t pump blood
  • CPR, defib to get to reg rhythm and ICD
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8
Q

1st degree AV block

  • what is it
  • sxs
  • tx
A
  • PR interval prolonged, greater than 5 little boxes
  • asymptomatic
  • find out what is causing and remove, but other than that nothing else
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9
Q

2nd degree AV block, Mobitz I/ Weinkebock

  • what is it
  • sxs
  • tx
A
  • PR interval progressively gets longer until ventricular beat drops
  • aymptomatic
  • none
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10
Q

2nd degree AV block, Mobitz II

  • what is it
  • sxs
  • TXX
A
  • ventricular beat is randomly dropped, there is not a progressively longer PR interval
  • fatigue, syncope, dizziness
  • pacemaker
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11
Q

3rd degree AV block

  • what is it
  • sxs
  • tx
A
  • atria and ventricles beat completely separatley, atria beat faster than ventricles, ventricles are paced by bundle of HIS or purkinje fibers and so have 30-40 BPM
  • dizziness, syncope, death
  • pacemaker
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12
Q

Bundle branch block

  • cause
  • right
  • left
  • ECG findings
  • leads
  • tx
A
  • fibrosis/scarring in one of the bundle branches preventing the conduction of the signal
  • the right ventricle will beat after the left ventricle
  • the left ventricle will beat after the right ventricle
  • Long QRS
  • 1 and 6; left: WilliaM, right: MarroW
  • only if accompanied by HF, need pacemaker
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13
Q

ANP

  • what is it
  • effects in kidney
  • effects on vessels
A
  • release from atrial myocytes in response to high blood vol and atrial pressure
  • decreases Na reabsorption -> decrease fluid reabsorption -> decrease blood vol
  • dilate them -> decrease atrial pressure
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14
Q

BNP

  • what is it
  • effects in kidney and vessel
  • used for
A
  • released from ventricular myoctes in response to increase in tension
  • same as ANP, but lasts longer
  • DX of HF
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15
Q

Baroreceptors

  • role when BP low
  • carotid massage
A
  • increase sympathetic response -> vasoconstrict, increase HR, increase contraction -> increase BP
  • increase pressure on carotid sinus, increases afferent firing -> increase AV node refractory period -> decrease HR
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16
Q

Chemoreceptors

  • peripheral, location and what they use to detect
  • central, location and what they use to detect
A
  • carotid and aortic bodies stimulated by increase in pCO2 and decrease in pH of blood and pO2
  • stumulated by changes in bloof pH and and pCO2 of interstital fluid in brain, do NOT respond to O2 levels
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17
Q

Right to Left shunts

  • sxs
  • 5T’s
A
  • cyanosis when born, blue babies

- Truncus arteriosus, Transposition, Tricupsid atresia, Tetrology of Fallot, TAPVR

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18
Q

Truncus arteriosus

  • what is it
  • caused by
  • tx
A
  • truncus arteriosus fails to split into aorta and pulm. A
  • aorticopulmonary septum does not form
  • surgery
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19
Q

Transposition of Great vessels

  • what is it
  • caused by
  • need
  • tx
A
  • RV goes to aorta and LV goes into pulm a
  • failure of aorticpulmonary septum
  • Atrial or ventricular septal defect; so that blood can mix
  • surgery
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20
Q

Tricupsid Atresia

  • what is it
  • need
A
  • tricuspid valve does not form

- both atrial and ventricular septal defect

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21
Q

Tetrology of Fallot

  • what is it?
  • seriousness
  • associated with
A
    1. entrance into pulmonary artery is very small -> 2. right ventricle hypertrophies; 3. ventricular septal defect -> hypertrophied right heart pushes into left ventricle
  • depends on how small the opening to PA is and how much RV hypertrophies; less obstruction -> allows for left to right movement of blood through the ventricular septal defect , but more obstruction causes pressure on right side of heart to overcome pressure on left side of heart and deoxy blood sent from right to left ventricle and out into systemic circulation
  • chrom 22 deletions and digeorge syndrome
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22
Q

Ebstein anomaly

  • what is it
  • caused by
  • sequlae
A
  • tricuspid valve is lower in ventricle, making the right atrium big and right ventricle really small
  • lithium exposure in utero
  • tricuspid regurg -> right HF
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23
Q

Left to Right heart shunt

  • sxs
  • VAPE
A
  • cyanosis appears at later age

- VSD, ASD, PDA, eisenmenger syndrome

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24
Q

Ventricular Septal Defect

  • frequency
  • what is it
  • sequlae
  • tx
A
  • most common
  • hole in septum between ventricles and since left has higher pressure it will shunt blood to right side
  • left hypertrophy -> left HF
  • most resolve on own,
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25
Q

Atrial Septal Defect

  • what is it
  • difference from patent foramen ovale
  • sequlae
  • incidence
A
  • septum between atria does not form correctly, left atria has higher pressure and so blood is shunted into right atrium; usually bc of ostium secundum
  • ASD is because septum don’t form correctly, while PFO is because the tissue does not fuse
  • Left HF and paradoxical emboli
  • high in pts with downs
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26
Q

Patent Ductus Arteriosus

  • what is it
  • sounds like
  • how to shut
  • how to keep open
A
  • shunt between PA and aorta, in fetus allos blood to bypass lungs, when born the pressure in aorta increases and blood is then sent from aorta into pulm artery
  • continuous, machine like murmur
  • Endomethacin -> ENDS PDA
  • Prostaglandins ->
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27
Q

Eisenmenger syndrome

  • cause by
  • why
A
  • uncorrected left to right shunt
  • blood being shunted from left to right causes the right side of heart to have more blood -> increase in pressure -> over time it hypertrophies -> when it becomes stronger it will switch to right to left shunt
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28
Q

Coarctation of the aorta

  • what is it
  • sxs
  • compensation
A
  • narrowing of aorta where PDA was located
  • HTN in UE and slow pulse in LE
  • uses intercostal arteries to help supply thoracic area and circumven the narrowing -> causes those vessels to become enlarged -> arteries erode ribs -> cause indentations seen on xray
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29
Q 
What heart defect do the following exposures/circumstances cause
- EtOH
- Congenital Rubella
- Downs
- DMII mother
- Marfans
Lithium exposure
- Turners
- Williams
22q11
A
  • Etoh: VSD, ASD, PDA, TOF
  • Rubella: PDA
  • Downs: VSD, ASD
  • DMII: Transposition of great vessels, VSD
  • Marfans: thoracic aortic aneursym
  • Lithium: ebstein
  • Turner: bicuspid aortic, and coarctation of aorta
  • Williams: Aortic stenosis
  • 22q11: TOR, transposition
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30
Q

Hypertension

  • definition
  • risk
  • urgency
  • emergency
A
  • BP greater than 130/80
  • age, obesity, DMII, CAD, high salt
  • > 180/120; w/o end organ damage
  • > 180/120 w/ organ damage (strpke, retinal hemm, MI, kidney injury, ecclampsia)
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31
Q

Hyperlipidemia

  • what is it
  • sequlae
  • signs
A
  • high LDL in blood; from eating too much fat or carbs
  • atherosclerosis -> CAD
  • xanthomas (on skin or on tendons), corneal arcus
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32
Q

Arteriosclerosis

  • definition
  • hyaline
  • hyperplastic
  • Monckeberg sclerosis
A
  • hardening of arteries -> wall thickened and decrease in elasticity
  • thickening of vessel in HTN or DMII
  • onion skin appearance with sever HTN
  • affects the media of medium arteries and harden arteries without blocking blood flow
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33
Q

Atherosclerosis

  • definition
  • location
  • risk
  • pathogenesis
A
  • form of arteriosclerosis caused by build up of cholesterol plaques
  • aorta> coronary > popliteal > carotid
  • dyslpidemia, smoking, HTN, DMII, age, men
  • endo dysfunction -> macrophage and LDL accumulate -> foamy macrophage -> fatty streak -> smooth muscle proliferation and migration -> fibrous plaque -> atheroma -> pieces can break off causing blockage of arteries
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34
Q

Atherosclerosis

  • definition
  • location
  • risk
  • pathogenesis
A
  • form of arteriosclerosis caused by build up of cholesterol plaques
  • aorta> coronary > popliteal > carotid
  • dyslpidemia, smoking, HTN, DMII, age, men
  • endo dysfunction -> macrophage and LDL accumulate -> foamy macrophage -> fatty streak -> smooth muscle proliferation and migration -> fibrous plaque -> atheroma -> pieces can break off causing blockage of arteries
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35
Q

Aortic Aneursym

  • definition
  • AAA: why? presentation?
  • Thoracic aortic aneursym: cause
A
  • pathologic dilation of the aorta
  • atherosclerosis of abdominal aorta, pulsatile/throbbing mass
  • caused by marfans, tertiary syphilis, HTN
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36
Q

Aortic dissection

  • definition
  • sxs
  • type A
  • Type B
A
  • longitudinal intimal tear forming a false lumen
  • tearing, sudden CP, unequal BP in arms
  • involves ascending aorta -> tx with surgery
  • involves descending aorta only -> tx with beta blocker and vasodilator
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37
Q

Stable Angina

  • arteries are
  • when does it occur
  • tx
A
  • more than 70% occlusion of vessels
  • exertional CP
  • nitro and rest
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38
Q

Vasospastic Angina

  • what is it
  • ECG
  • Triggers
  • Risks
  • TX
A
  • pain at rest due to coronary A spasm
  • causes ST elevation
  • triggered by cocaine, EtOH, and triptans
  • Smoking
  • Ca channel blocker, nitrate, smoking cessation
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39
Q

Unstable Angina

  • what is it
  • ECG/labs
  • when
A
  • usually occurs when part of plaque ruptures causing blood clot to form on top of plaque, making hole even smaller
  • ST depression or T wave inversion; w/o increase in troponin
  • at rest
40
Q

Coronary steal syndrome

A
  • coronary vessels distal to stenosis are dilated at max, when vasodlator is given it allows for blood normally going to heart to go to systemic circukation, since coronary vessels are already max dilated they can’t deliver any more blood to area -> decrease in blood to heart tissue
41
Q

MI

  • caused by
  • STEMI
  • NSTEMI
A
  • rupture of atherosclerotic plaques -> blocks rest of artery
  • increase in troponin and ECG changes
  • ST elevation -> transmural infarct (full thickness of myocardium was effected)
  • Non- ST elevation -> not full thickness, usually just subendocardial (least amount of blood delivered to this area normally, first to be deprived with blockage)
42
Q

Embyronic structure….gives rise to

  • bulbus cordis
  • endocardial cushion
  • left horn of sinus venosus
  • posterior, sub and supracardinal veins
  • primitive atrium
  • primitive pulmonary vein
  • primitive ventricle
  • right common cardinal vein and right anterior cardinal vein
  • right horn of sinus venosus
  • truncus arteriosus
A
  • BC: smooth parts of ventricles
  • EC: atrial and ventricular septums
  • L Horn: Coronary sinus
  • Post, sub, and supra: IVC
  • Prim atrium: Trabeculated part of both atria
  • Prim pulm V: smooth part of left atrium
  • Primitive ventricle: Trabeculated part of both ventricles
  • Right common and ant cardinal v: SVC
  • Right horn: smooth part right atrium
  • TA: ascending aorta and pulm trunk
43
Q

Septation of the atria

Steps

A
  • septum primum grows towards endo cushions
  • septum primum is split and make foramen secundum
  • septum secundum begins to grow until it covers foramen secundum creating the foramen ovale
44
Q

Fetal circulation

A
  • umbilical vein -> 1 to hepativc vein to liver, other through ductus venosus to bypass liver and go straight to IVC -> right atrium -> 1 to right ventricle other through foramen ovale to left atrium -> from right ventricle will go to pulm trunk and some will pass through ductus arteriosus straight into aorta and rest go to lungs -> blood in left atria go to left ventricle and then out through aorta to rest of system -> back to umbilical arteries
45
Q

Layers of pericardium

- innervated by

A
  • fibrous layer
  • parietal layer of serous pericardium
  • visceral layer of serous pericardium
  • phrenic nerve
46
Q

Coronary blood upply

  • RCA branches
  • LCA branches
  • Heart dominance
A
  • marginal and PDA
  • LAD, circumflex
  • which branch the PDA comes off
47
Q

Artery and part of heart it supplies

  • LAD
  • circumflex
  • RCA
  • PDA
A
  • anterior left ventricle, ant 2/3 of septum
  • left atrium, posterior left side
  • SA node, Ant right side of heart
  • Posterior heart and posterior 1/3 septum
48
Q

Stroke volume

A

EDV- ESV

49
Q

EF

A

EDV- ESV / EDV

50
Q

CO

A

SV x HR

51
Q

Pulse Pressure

A

SBP - DBP

52
Q

Starling curve

- what does it mean

A
  • the greater the EDV -> the greater the stretch of the muscle -> more myosin and actin overlap
  • if it gets over stretched then actin and myosin cant touch and lose contractility ability
53
Q

Pre load

  • what is it
  • importance
A
  • amnt of blood pushed into ventricle

- greater the pre-load -> the more contractility

54
Q

Afterload

  • what is it
  • importance
A
  • the amount of pressure in the aorta that the ventricle has to push against in order to get the aortic valve to open
  • bigger the afterload the less the contractility force
55
Q

Systolic mumurs

- list

A
  • aortic stenosis
  • mitral/tricuspid regurg
  • mitral valve prolapse
  • ventricular septal defect
56
Q

aortic stenosis

- type of murmur

A
  • crescendo-decrescendo
57
Q

mitral/tricuspid regurg

A
  • holosystolic, high pitched, blowing murmur
58
Q

aortic stenosis

  • type of murmur
  • where to listen
A
  • crescendo-decrescendo

- heart base that radiates towards coronary arteries

59
Q

mitral/tricuspid regurg

- type of murmur

A
  • holosystolic, high pitched, blowing murmur
60
Q

mitral valve prolapse

  • type of murmur
  • where and when to listen
A
  • late systolic crescendo murmur with mid systolic click bc of cordae tendonae tensing
  • at apex right before S2
61
Q

ventricular septal defect

  • type of mumur
  • listen to at
A
  • holosystolic, harsh sounding

- tricuspid

62
Q

aortic regurg

- type of mumur

A
  • high pitched blowing, early diastolic, decresecendo murmur
63
Q

Mumurs based on location

  • Aortic
  • Pulmonic
  • Tricuspid
  • Mitral
  • Atrial septal defect
  • Ventricular septal defect
A
  • A stenosis: systolic murmur, Aortic regurg: diastolic murmur
  • Pulmonic stenosis: systolic ejection murmur, pulm regurg: diastolic murmur
  • T regurg: holosystolic murmur , T stenosis: diastolic murmur
  • Mitral regurg: holohsystolic , mitral valve prolapse: systolic, mitral stenosis: diastolic
  • Systolic ejection murmur
  • Holosystolic murmur
64
Q

mitral stenosis

type of murmur

A

mid to late diastolic opening snap and then rumbling murmur

65
Q

Splitting

  • normal: what is it
  • wide
  • fixed
  • paradoxical
A
  • inspiration -> increases intrathoracic pressure -> increase venous return -> increase RV filling -> increase RV stroke vol -> increase RV ejection time -> delayed closure of pulmonic valve
  • when there is delay in RV emptying and pulmonic valve closes late then there will be exaggerated delay during inspiration
  • occurs with atrial septal defect, ASD -> left to right shunt -> increase RA and RV vol -> increase flow through right ventricle regardless of inspiration
  • when there is conditions that delay aortic valve closure; so on inspiration when pulmonic valve is usually delayed, the aortic and pulmonic will close at same time since they’re both delayed
66
Q

PDA

-mumur

A

continuous and machine like

67
Q

change to pressure volume loop
- aortic stenosis
- mitral regurg
-

A
  • increase in pressure of LV during systole and increase in ESV, so long skinny square
  • decrease in ESV bc blood is going into both aorta and LV, increase in EDV because more blood is being pushed in from left atrium, but there is not an isovolumetric contraction in the left ventricle because of regurg -> short, fat curve
68
Q

change to pressure volume loop; what is happening, what does the loop look like compared to normal, what does it do to stroke vol?

  • aortic stenosis
  • mitral regurg
  • aortic regurg
  • mitral stenosis
A
  • increase in pressure of LV during systole and increase in ESV, so long skinny square, decrease in stroke volume
  • decrease in ESV bc blood is going into both aorta and LV, increase in EDV because more blood is being pushed in from left atrium, but there is not an isovolumetric contraction in the left ventricle because of regurg -> short, fat curve, increase in stroke vol
  • increase in EDV because blood comes back into ventricle from aorta -> loop is same height but wider bc of increase in EDV, increase in stroke volume
  • decrease in EDV bc cant push as much blood from left atria to left ventricle, decrease in ESV because not as much blood is pumped in and it is able to push majority of it out –> loop is same height but skinnier, decrease in stroke volume
69
Q

Myocardial action potential

  • phase 0
  • phase 1
  • phase 2
  • phase 3
  • phase 4
A
  • 0: Na in, rapid depolarization
  • 1: Na close, K open, slight dip down
  • 2: Ca open and K stay open, plateau phase
  • 3: Ca close, K still open, rapid repolarization
  • 4: If it hyperpolarized then Na/K ATPase will even everything back out to resting membrane potential
70
Q

Pacemaker action potential

  • phase 4
  • phase 0
  • phase 3
A
  • funny channel: Na gradually coming in
  • 0: Ca channel open, slow depolarization
  • 3: Ca channels close, K open, repolarize slowly
71
Q

ECG normal

  • P wave
  • Q
  • R
  • S
  • T wave
  • QRS complex
  • U wave
A
  • atrial depolarization during diastole, SA to AV
  • negative dip bc the AV is sending to bundle of HIS and there is a lot of tissue
  • biggest positive dip because the anterior portions of the ventricles are being depolarized
  • big drop because the lateral portions of the ventricles are depolarizing which is away from the leads
  • Ventricles repolarizing, goes opposite the leads but since it is getting more negative it shows up as a positive wave.
  • ventricular depolarization, no more than 3 little boxes, 120 ms
  • another wave after the T wave before the p wave, seen in hypokalemia
72
Q

Evolution of MI (gross, light)

  • 24 hrs
  • 1-3 days
  • 3-14 days
  • 2 wks to several months
A
  • 24: G- occluded artery and dark mottling; L- early necrosis, edema, hemmorrhage,
  • 1-3: G- hyperemia; L- extensive necrosis, PMNs come in
  • 3-14: G- hyperemic border with soft yellow softening; L- macrophages come in with granulation at margins
  • 2 wks: G- recanclized artery w/ grey/white scar; L- contracted scar complete
73
Q

DX of MI

  • 1st 6 hrs
  • after 4 hours
  • reinfarction
A
  • ECG, ST elevation (STEMI) or ST depression (NSTEMI)
  • ECG and troponin
  • CK-MB
74
Q

Localization of STEMI

  • anteroseptal
  • anteroapical
  • antero lat
  • lateral
  • inferior
  • PDA
A
  • v1, v2
  • v3, v4
  • v5, v6
  • I, AVL
  • II, III, AVF
  • ST depression in V1-3 with tall R waves
75
Q

Treatment for MI

  • NSTEMI
  • STEMI
A
  • anticoagulation, antiplatelet, beta blocker, ACE inhibitor, statin, clopidogrel, nitro/morphine
  • above meds + reperfusion therapy (cardiac cath with stent placement)
76
Q

MI complications ( what is it, when will it occur?)

  • cardiac arrythmia
  • fibrinous pericarditis
  • pap muscle rupture
  • Inter ventricular septal rupture
  • ventricular pseudoaneursym formation
  • ventricular free wall rupture
  • true ventricular aneursym
  • dressler syndrome
  • LV failure and pulm edema
A
  • arrythmia: irregular beat, that can lead to v-fib and then death; make sure to monitor 24 hrs after MI
  • pericarditis: friction rub, 1-3 days after
  • pap rupture: posterior wall, especially with PDA MI -> can cause mitral regurg, 2-7 days after MI
  • septal rupture: caused by clean up of necrotic tissue by macrophages resulting in septal opening, 3-5 days
  • psuedoaneurysm:
  • free wall: one of the walls has too much necrosis and when cleaned up it ruptures -> cardiac tamponade; 5-14 days
  • aneursym: bulge of myocardium with contraction, 2 weeks to several months
  • dressler: auto immune reaction resulting in pericarditis, several weeks
  • LV fail: secondary to LV infarction
77
Q

Dilated Cardiomyopathy

  • what is it
  • categorization
  • incidence
  • causes
  • findings
  • murmur
  • tx
A
  • eccentric hypertrophy, allchambers grow larger but thin out–> less pumping ability
  • systolic heart failure because heart can’t effectively pump
  • most common
  • alcohol abuse, beri beri, coxsackie, cocaine, chagas, doxorubicin
  • HF, S3, mitral regurg
  • bigger ventricle -> mitral valve gets pulled away from eachother, can’t make good seal -> mitral regurg -> holosysytolic murmur
  • Na restriction, ACE inhibitors, B-blocker, diuretics
78
Q

Hypertrophic Cardiomyopathy

  • what is it
  • categorization
  • where
  • murmur
  • cause for primary
  • histo
  • tx
A
  • concentric hypertrophy, ventricles thicken and space inside becomes smaller
  • diastolic heart failure because heart cannot fill
  • septal wall of left ventricle
  • thickened septal wall -> small hole for blood to be squeezed through -> creascendo-decrescendo murmur
  • autosomal dominant mutation, to sarcomere or troponin t
  • myocyte dissarray
  • beta blocker, NO digoxin
79
Q

Restrictive Cardiomyopathy

  • what is it
  • categorization
  • causes
  • tx
A
  • cardiac muscles are restricted and can’t stretch, same size and thickness
  • can’t stretch -> doesn’t fill as well -> diastolic heart failure
  • amyloidosis (TTR), sarcoidois (granulomas in heart tissue), endocardial fibroelastosis
  • tx underlying cause
80
Q

ECG changes with hypertrophy

  • right atria
  • left artria
  • right ventricle
  • left ventricle
A
  • larger P wave (taller) in V1, V2, II, III, AVF
  • longer P wave with 2 peaks in lead II
  • tall R wave in lead 1
  • very tall R wave in leads 5 and 6
81
Q

Heart failure

  • what is it
  • systolic vs diastolic dysfunction
  • cor pulmonale
  • TX
  • sxs of left heart failure
  • sxs of right heart failure
A
  • heart unable to effectively pump and body is not being perfused correctly
  • dyspnea, orthopnea, JVD rales -> fluid is backing up into lungs
  • systolic is when heart cant pump -> increase EDV -> EF decreases; diastolic is when heart cant fill -> decrease in EDV and ESV -> EF persevered
  • only right sided heart failire, due to increase in pulmonary pressure
  • ACE inhibitors (decrease renin), Beta blocker (decrease stress on heart) and spironolactone (decrease fluid reasborption)
  • orthopnea, parox nocturnal dyspnea, pulmonary edema
  • hepatomegaly, JVD, peripheral edema
82
Q

Shock

- what is it

A

inadequate organ perfusion and delivery of nutrients for normal tissue and cellular function

83
Q

Hypovolemic Shock

  • caused by
  • skin
  • preload
  • CO
  • afterload
  • TX
A
  • hemmorhage, dehydration, burn
  • cold, clammy
  • decreased
  • decreased
  • increased -> everything vasoconstricts to prevent loss of blood and keep it moving
  • IV fluids
84
Q

Cardiogenic Shock

  • caused by
  • skin
  • preload
  • CO
  • afterload
  • TX
A
  • MI, HF, arrythmia
  • cold, clammy
  • varies
  • decreased
  • increased
  • ionotropes (help contract more)
85
Q

Obstructive Shock

  • caused by
  • skin
  • preload
  • CO
  • afterload
  • TX
A
  • PE, cardiac tamponade, tension pneumo
  • cold, clammy
  • varies
  • decreased
  • increased
  • relieve obstruction
86
Q

Distributive Shock

  • caused by
  • skin
  • preload
  • CO
  • afterload
  • TX
A
  • sepsis, anaphylaxis, CNS injury
  • warm, dry
  • decreased
  • varies
  • decreased
  • IF, pressors, epi
87
Q

Bacterial Endocarditis

  • acute: caused by, vegetations
  • chronic: caused by, vegetations
  • sxs
A
  • staph aureus, large on normal valves
  • strep viridans, small on diseased valves
  • Fever, Roth spots (round white spot on retina), Osler nodes (tender raised lesions on pads of fingers/toes), Murmur, Janeway lesion,
    Anemia (small/painless lesion on palm or sole) , nail bed hemmorrhage, emboli
88
Q

Rheumatic fever

  • what is it?
  • what causes it?
  • SXS
A
  • antibodies towards strep M protein cross react with self antigens in heart -> cause damage to valves (mitral)
  • Strep pyo infection
  • JONES
89
Q

Pericarditis

  • what is it
  • sxs
  • auscultation
  • causes
  • TX
A
  • inflammation of the pericaridum
  • sharp pain aggravated by inspiration and relieved y sitting up and forward
  • friction rub
  • coxsackie B, AI (SLE, RA), STEMI
  • NSAID, steroids
90
Q

Myocarditis

  • what is it
  • causes
A
  • inflammation of myocardium -> enlargement of all chambers
  • bacterial (lyme dx, mycoplasma pneumo); viral (adeno, coxsackie B); parasitic (t cruzi, t gondii); toxin (black widow venom); drug (cocaine, doxorubicin), AI (kawasaki)
91
Q

Cardiac tamponade

  • what is it
  • sxs
  • ECG
A
  • compression of heart by fluid in pericardial space -> decrease in CO
  • hypotension, distended neck veins, distant heart sounds; high HR
  • low voltage QRS
92
Q

Syphilis heart dx

  • what happens
  • sequlae
A
  • attacks vasa vasorum on aorta w/ atrophy of wall and dilation of aorta
  • aneursym of ascending aorta
93
Q

Giant cell arteritis

  • category
  • epi
  • sxs
  • patho
  • tx
A
  • large vessel vasculitis
  • old women
  • unilateral headache, temporal A tenderness, blindness bc of opthalmic a occlusion
  • focal granulomas in the carotid a
  • high dose steroids
94
Q

Takayasu arteritis

  • category
  • epi
  • sxs
  • patho
  • tx
A
  • large vessel vasculitis
  • asian women, older than 40
  • weak upper extremity pulses, fever, night sweats, joint painm
  • granulomas and thickening/narrowing of aortic arches and proximal great vessels
  • steroids
95
Q

Buerger disease

  • category
  • epi
  • sxs
  • patho
  • tx
A
  • medium vessel vasculitis
  • heavy smoker, male greater than 40
  • intermittent claudication -> gangrene
  • segmental thrombosing vasculitis with vein and nerve involvement
  • smoking cessation
96
Q

Kawasaki disease

  • category
  • epi
  • sxs
  • sequlae
  • tx
A
  • medium vessel vasculitis
  • asian children older than 4
  • conjunctival injection, rash, cervical adenopathy, strawberry tongue, fever
  • may develop coronary artery aneurysms
  • IV Ig and aspirin
97
Q

Poly arteritis nodosa

  • category
  • epi
  • sxs
  • patho
  • tx
A
  • medium vessel vasculitis
  • ## middle aged men

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