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organ systems > First aid Cardiology > Flashcards

First aid Cardiology Flashcards

1
Q

coronary blood flows peaks in

A

early diastole

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2
Q

coronary artery occlusion most common

A

LAD

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3
Q

most posterior part of the heart is:

A

Left atrium
enlargement:
compress the esophagus –dysphagia
compress the left recurrent laryngeal nerve, branch of the vagus and cause hoarseness

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4
Q

Fick principle cardiac output

A

CO= rate of O2 consumption/arteriol O2 content-venous oxygen content

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5
Q

MAP

A 
MAP = CO x TPR
MAP = 2/3 diastolic pressure + 1/3 the systolic pressure
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6
Q

SV

A

SV = EDV - ESV

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7
Q

During exercise

A

increased SV and HR to keep CO, but as SV plateaus later in exercise only HR increases to maintain CO

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8
Q

What can cause an increased pulse pressure?

A 
hyperthyroidism
aortic regurg
arteriosclerosis
obstructive sleep apnea (increased sympathetic tone)
exercise
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9
Q

decrease in pulse pressure

A

aortic stenosis
cardiogenic shock
cardiac tamponade
advanced heart failure

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10
Q

myocardial oxygen demand

A 
Increases:
increased after load (arterial pressure)
Increased contractility
Increased HR
Increased ventricular diameter (increased wall tension)
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11
Q

hydralazine

A

arterial vasodilator, decrease afterload

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12
Q

Viscosity

A

increase:
polycythemia, hyperproeteinemic states (MM) abd hereditary spherocytosis

decrease:
anemia

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13
Q

Resistance

A

R = delta P/ flow Q

= 8(viscosity)(length)/pi r^4

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14
Q

S3

A

in early diastole during rapid ventricle filling phase. Associated with increase filling pressures (mitral regurg, CHF) and more common in dilated ventricles, slosh slosh (but normal in children and pregnant females)

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15
Q

S4

A

atrial kick!
in late diastole . high atrial pressure, associated with ventricular hypertrophy. Left atrium must push against a stiff LV wall

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16
Q

a wave JVP

A

atrial contraction

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17
Q

C wave JVP

A

RV contraction (closed tricuspid valve bulges into RA)

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18
Q

x descent JVP

A

atrial relaxation and downward displacement of TV during ventricular contraction, absent in tricuspid regurgitation

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19
Q

v wave JVP

A

increase RA pressure due to filling against a closed tricuspid valve

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20
Q

y descent

A

blood flow from RA to RV

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21
Q

Normal splitting

A

S1, A2P2 inspiration leads to a drop in intrathoracic P, increases venous return, increased RV sv and RV ejection time, delayed closing of pulmonc valve

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22
Q

wide splitting

A

S1 A2 P2
seen in conditions that delay RV emptying (pulmonary stenosis, right bundle branch block).
Delay in RV emptying causes delayed pulmonic sound (regardless of breath). An exaggerated of normal splitting

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23
Q

fixed splitting

A

S1 A2 P2
ASD left to right shunt
increase RA and RV volumes, increase flow through pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed

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24
Q

paradoxical splitting

A

S1 P2 A2
Seen in conditions that delay LV emptying (aortic stenosis, LBBB)
normal in order of valve closure is reversed so that the P2 sound occurs before a delayed A2 sound. Therefore on inspiration, P2 closes later and moves closer to A2 thereby paradoxically ELIMINATING the split

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25
Q

ASD murmur

A

best heard in the pulmonic area

commonly presents as a pulmonary flow murmur (increased flow through the pulmonary valve) and a diastolic murmur (increased flow across the tricuspid)
NO murmur from blood flow ACROSS the actual ASD because there is no increased pressure gradient
the murmur will later progress to a louder diastolic murmur of pulmonary regurgitation from dilation of the pulmonary artery

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26
Q

hand grip (increases the systemic vascular resistance)

A

increase intensist:
-MR, AR, VSD

Decrease intensity:
AS, hypertrophic cardiomyopathy murmurs

MVP: increase in intensity, but a later onset of click/murmer

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27
Q

Valsalva (phase 2), standing (decrease venous return)

A 
decrease intensity:
most murmurs including AS
Increase:
hypertrophic cardiomyapthy murmur
MVP: decrease intensity, have an earlier onset of click/murmer
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28
Q

rapid squatting (increased venous return increases preload ) after prolongued squatting increase after load

A

decrease intensity of:
hypertrophic cardiomyopathy murmer

increase intensity of:
AS

MVP: increase intensity and later onset click/murmer

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29
Q

systolic sounds

A

Aortic/pulmonic stenosis, mitral/tricuspid regurg, VSD

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30
Q

Diastolic heart sounds

A

aortic/pulmon regurg and mitral/tricuspid stenosis

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31
Q

Mitral regurg

A

holosystolic, high pitched blowing murmur
loudest at apex, radiates to axilla, enhanced by maneuvers that in TPR (squatting and hand grip)
MR is often due to ischemic heart disease, MVP or LV dilation

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32
Q

Tricuspid regurg

A

loudest at tricuspid area
holosystolic, high pitched blowing murmur
radiates to right sternal border
enhanced by maneurmers that increase RA return (inspiration)
TR commonly caused by RV dilation.
Rheumatic fever and infective endocardidtis can cause either MR or TR

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33
Q

Aortic stenosis

A

Crscendo-decrescendo systolic ejection murmur.
LV» aortic pressure during systole
loudest at heart base, radiates to carotids
pulses parvus et tardus - pulses are weak with a delayed peak.
can lead to syncope, angina and dyspnea on exertion
often due to age related calcific stenosis or bicuspid aortic valve

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34
Q

VSD

A

holosytolic, harsh sounding murmer, loudest in the tricuspid area, accentuated with hand grip maneurver due to afterload

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35
Q

mitral valve prolapse MVP

A

laste systolic crescendo murmer with midsystolic click (MC; due to sudden tensing of chordae tendineae
best heard over apex
loudest just before S2
usually benign
can predispose to infective endocarditis
can be caused by myxomatous degeneration, RF, or chordae rupture
occurs earlier with maneurvers that decrease venous return (valsalva or standing)

This is because those maneuvers which decrease the volume of the left ventricle (Valsalva, standing) will cause the prolapse to occur sooner and more severely, while those that increase venous return and diastolic filling (squatting) and thereby enhance the ventricular volume, help to maintain tension along the chordae and to keep the valve shut

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36
Q

AR

A

high pitched blowing early diastolic decresendo murmur.
wide pulse pressure when chronic
can present with bounding pupses and head bobbing
often due to aortic root dilatio, biscuspid aortic valve, endocarditis or RF. the murmer inscreases with hand trap, vasodilators decrease the intensist of the murmur

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37
Q

Mitral stenosis

A

follows opening snap (due to abrupt halt in leaflet motion in diastole after rapid oepning due to fusion at leaflet tips).
delayed rumbling late diastolic murmur
decrease interval between S2 and opening snap correlates with increased severity. LA»LV pressure
often occurs secondary to RF
Chronic MS can result in LA dilation.
enhanced by maneurvers that increase LA return (expiration)

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38
Q

respiration and Left heart

A

During inspiration, expansion of the lungs and pulmonary tissues causes pulmonary blood volume to increase, which transiently decreases the flow of blood from the lungs to the left atrium. Therefore, left ventricular filling actually decreases during inspiration. In contrast, during expiration, lung deflation causes flow to increase from the lungs to the left atrium, which increases left ventricular filling. The net effect of increased rate and depth of respiration, however, is an increase in left ventricular stroke volume and cardiac output.

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39
Q

PDA

A

Continuous machine like murmur across systole and diastole
loudest at S2
often due to congenital rubella or prematurity
best hear at the left infraclavicular area (pulmonic valve region)

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40
Q

1 big box

A

0.2 s or 200 ms

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41
Q

1 small box

A

40 ms

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42
Q

box heart rate

A 
1 300
2 150
3 100
4 45
5 60
6 50
7 43
8 37
9 33 beats/min
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43
Q

1 full stip is 10 seconds

A

so counts the complexes and multiply by 6 to bet bpm

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44
Q

P wave

A

atrial depolarization, atrial repolarization is masked by the QRS

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45
Q

PR interval

A

-conduction delay through the AV node (normally less than 200 ms) (less than a big box)

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46
Q

QRS

A

ventricular depolarization (less that 120 ms)

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47
Q

T wave

A

ventricular depolarization

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48
Q

ST segment

A

isoelectric, ventricles depolarized

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49
Q

QT

A

mechanical contraction of the ventricles

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50
Q

u wave

A

caused by hypokalemia, bradycardia

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51
Q

speed of conduction -

A

purkinje> atria> ventricles> Av node PAVA

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52
Q

pacemakers

A

SA> AV> bundle of his> purkinje/ventricles

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53
Q

conduction pathway

A

SA, atria, AV done then to common bundle, then bundle branches then purkinje fibers and finally ventricles

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54
Q

Torsades de pointes

A

-polymorphic ventricular tach
-characterized by shifting sinusoidal waveforms on ECG
-can progress to V fibb
-Long QT interval predisposes to torsades de pointes
-caused by drugs that decrease K and Mg
Treat with MgSO4

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55
Q

Drugs that prolong QT

A 
Some Risky Meds Can Prolong QT:
Sotalol
Risperidone
Macrolides
Chloroquine
Protease inhibitors (-navir)
Quinidine (Class 1a)
Thiazides
56
Q

Romano-ward syndrome

A

congenital long QT syndrome
inherited disorder of myocardial repolarization, typically due to ion channel defects, increases risk of suddencardiac death due to torsades de points

Autosomal DOMINANT
pure cadiac phenotypes

57
Q

Jervell and Lange-Nielsen syndrome

A

congenital long QT syndrome
inherited disorder of myocardial repolarization, typically due to ion channel defects, increases risk of suddencardiac death due to torsades de points

Autosomal RECESSIVE
sensorineural deafness!

58
Q

wolff-parkinson white syndrom

A

abnormal fast accessory conduction pathway from atria to ventricle via the bundle of kent, bypasses the rate slowing AV node

  • as a result ventricles begin to partially depolarize earlier, giving rise to characteristic delta wave and shortened PR interval
  • may result in supraventricular tach
59
Q

afibb

A

irregular irregular
no discrete P
irregularily spaced QRS

60
Q

atrial flutter

A

back to back atrial depolarization waves
sawtooth appearense
use 1a, 1C or III.

61
Q

v fibb

A

a completely erratic rhythm with no identifiable waves. fatal arrhythmia without immediate CPR and defibrillation

62
Q

AV block 1st degree

A

PR interval is prolonged > 200 ms

63
Q

AV block 2nd degree mobitz type 1 (wenckebach)

A

progressive legnthing of PR interval until a beat is DROPPED, usually asymptomatic

64
Q

AV block 2nd degree mobitz type II

A

dropped beats that are NOT processed by a change in length of PR.
often found in 2:1 block, where there are 2 or more P waves to 1 QRS response
often treated with pacemaker

65
Q

AV 3rd degree block

A

atria and ventricles beat independantly of each other, both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes. The atrial rate is faster than the ventricular rate.
Lyme disease can result in 3rd degree heart block

66
Q

Lyme disease

A

3rd degree heart block

67
Q

atrial naturetic peptide

A
  • released from atrial mycoses with stretch
  • vasodilation
  • decreased Na reabsorption at renal CT
  • contricts efferent, dilates afferent renal via cGMP –> diuresis contributing to the aldosterone escape
68
Q

B-type (brain) natriuretic peptide

A

released from ventricular myocytes in response to increased tension
-longer half life, similiar to ANP
good test for HF, good NPV
-available in recombinant form Nesiritide for treatment of heart failure

69
Q

Aortic arch receptors

A

transmit via vagus nerve to solitary nucleus of medulla

70
Q

Carotid sinus (dilated region at carotid bifurcation)

A

transmits via glossopharyngeal nerve to solitary nucleus to medulla

71
Q

Baroreceptors in hypotension

A
  • decreased in Atrial P, decreased stretch, decreased afferent baroreceptor firing (vagus to solitary nucleus of medulla) , increased efferent firing sympathetic firing (post ganglionic, via spine etc) and decreased efferent parasymp stimulation (vagus).
    leads to vasoconstriction, increased HR, increased contractility, increased BP
72
Q

Carotid massage

A

increased P on carotid sinus, increases stretch, increased baroreceptor firing, increased AV node refractory period, decreased HR.

Carotid sinus massage: increase pressure on carotid artery –> increase stretch –> increase afferent CN IX firing –> signal thru nucleus tractus solitarus in medulla–> increase parasympathetic outflow to heart via CN X firing—> decrease heart

73
Q

Cushing reaction

A

increased intracranial pressure constricts arterioles, this leads to cerebral ischemia and reflex increase in sympathetic tone in perufusion pressure HTN. Increase stretch and reflex baroreceptors induced bradycardia (parasympathetic vagus)

HTN, bradycardia and respiratory depression

note increase vagus –> acid, ulcers

74
Q

Peripheral carotid and aortic bodies are stimulated

A

-decrease in PO2 ( hyperventilation

75
Q

Central chemoreceptors are stimulated by

A

changes in pH and PCO2 of brain interstitial fluid

76
Q

Edema

A

excess fluid outflow into interstitium commonly caused by:

  1. increased hydrostatic capilliary pressure (Pc in heart failure)
  2. decreased plasma proteins, decreased plasma onctoc (Pi c , nephrotic syndome, liver failure)
  3. increased permiability factor (K) caused by toxins, infections, burns
  4. Increased interstitial fluid colloid osmotic pressure (interstitial oncotic pressure, like a lymphatic blockage
77
Q

R to L shunsts
early cyanosis, often diagnosed prenatally or become evident immediately after birth. usually require urgent surgical repair and or maintenance of PDA

A 
Truncus arteriousus (1 vessel)
Transposition (2 sitched vessels)
Tricuspid atresia
Tetrology of Fallot
Total anomalous pulmonary venous return
78
Q

Total anomalous pulmonary venous return

A

pulmonary veins drain right into right heart circulation (SVC, coronary sinus etc) associated with an ASD and sometimes PDA to allow R to Left shunt

79
Q

tricuspid atresia

A

no tricuspid, requires both an ASD and VSD for viability

80
Q

terology of fallot

A

caused by anterosuperior displacement of the infundibular septum. most common cause of early childhood cyanosis

  1. Pulmonary infundibular stenossis
  2. RVH - boot shaped heart
  3. Overring aorta
  4. VSD (right to left due to pulmonary stenosis)

Squatting increases SVR which would decrease the R to L shunt and improves cyanosis

81
Q

ASD

A

distinct from PFO in that septa are missing tissue (septum secundum) rather than unfused
-loud S1 and fixed split S2 (more filling of RA and RV, delated closing of pulmonic valve).

82
Q

Eisenmenger syndrome

A

uncorrected L to R shunt (VSD, ASD, PDA) eventually increased pulmonary blood flow and pathologica remodeling of vasculature leading to pulmonary arteriolar HTN. RVH to compensate the shunt becomes R to L this will cause late cyanosis, clubbing and polycythemia

83
Q

Coarcatation of aorta:

infantile type

A

associated with bisupid aortic valve and other heart defects:
aortic narrowing is proximal to insertion of ductus arteriousus (pre ductal). Associated with Turner syndrome
can present with close ductus arterioles

84
Q

Coarcatation of aorta:

A

associated with bisupid aortic valve and other heart defects:
aorta narrowing is distal to ligamentum arteriosusm (post ductal). assoc with notching of ribs due to collateral circulation, HTN in upper extremities and weak, delayed pulses in lower extremities

85
Q

xanthoma

A

lipid laden histiocyte in the skin

86
Q

corneal arcus

A

lipid in cornea , appears early in life with hypercholesterolemia. commonly in elderly

87
Q

arteriolosclerosis

A

arterioles:
hyaline (thickening of small arteues in essential HTN or DM)
hyperplastic onion skinning as seen in severe HTN

88
Q

aortic aneurism

A

localized pathologic dilation of the aorta, may cause pain, which is a sign of leaking, dissection, or imminent rupture

89
Q

AAA

A

HTN male, >50 years, assoc. atherosclerosis

90
Q

Thoracic AA

A

associated with cystic medial degenration due to HTN (older) or Marfan (younger)
assoc. 3 syphyilis (obliterative endarteritis of the vasa vasorum)

91
Q

Aortic dissection

A

longitudinal intraluminal tear forming a false lumer. assoct with HTN, bicuspid aortic valve and inhere tied connective tissue disorders like Marfan
tearing chest pain, sudden onset, radiating to back

92
Q

stable angina

A

secondary to atherosclerosis, resolves at rest

93
Q

variant angina (pinzmetal)

A

occurs at rest! secondary to coroanry arter spasm, known triggers at tobacco, cocaine, triptans but trigger is often unknown
treat with calcium channel blockers, nitrates and smoking cessation

94
Q

MI 4-12 hours

A

Gross changes: Dark discoloration
Microscopic Changes: early coagulative necrosis, release of necrotic cell contents into blood, edema, hemmorrhage and wavy fibers
Complications:
arrhythmia, HF, cardiogenic shock, death

95
Q

MI 1-3 days

A

Gross changes: hyperemia, yellow pallor
Microscopic Changes: tissue surrounding infarct shows accute inflammation with neutrophils, extensive coagulative necrosis
Complications:
fibrinous pericarditis presents with chest pain and friction rub

96
Q

MI 3-14 days

A

Gross changes: hyperemic border, central yellow brown softening-maximally yellow and soft for ten days
Microscopic Changes: macrophages then granulation tissue at margins
Complications:
free wall rupture: tamponade; papillary muscle rupture –> mitral regurg; intraventricular spetal rupture due to macrophages mediated structural degradation
LV pseudoaneurism (mural thrombus plugs hole in myocardium time bomb)

97
Q

MI 1-3 weeks

A

Gross changes: red border emmerges as granulation tissue enters from edge of infarct
Microscopic Changes: granulation tissue with plum fibroblasts, collagen and blood vessel
Complications:

98
Q

MI 2 weeks to months

A

Gross changes:white scar
Microscopic Changes: fibrosis and contracted scar complete
Complications:
aneurism, mural thrombosis and dressler syndrome (resulting in fibrinous pericarditis from autoimmune phenomena , several weeks post MI)

99
Q

MI 12-24 hours

A

Gross changes:
Microscopic Changes: neutrophil migration starts
reperfusion injury may cause contraction bands due to free radical damage
Complications:arrhythmia, HF, cardiogenic shock, death

100
Q

CK-MB

A

useful in diagnosing reinfarction following acute MI because levels return to normal in 48 hours

101
Q

troponin 1

A

rises after 4 hours, remains elevated for 7-10 days

102
Q

ST elevation

A

STEMI acute transmural infarction

103
Q

ST depression

A

subendocardial infarct (subendo is especially vulnerable to ischemia)

104
Q

MI Anterior wall (LAD)

A

V1-V4

105
Q

MI Anteriospetal (LAD)

A

V1-V4

106
Q

Anteriolateral (LAD or LCX)

A

V4-V6

107
Q

Lateral Wall (LCX)

A

I avL

108
Q

Inferior wall (RCA)

A

II, III, aVF

109
Q

Dilated cardiomyopathy

A 
systolic dysfuction ensures. Eccentric hypertrophy (sarcomeres added in series)
Idiopathic or congenital
-Wet beriberi
Coxsackie B
Chagas
Cocaine use
Doxorubicin
hemochromatosis
peripartum cardiomyopathy

HF, S3, dilated

110
Q

Hypertrophic cardiomyopathy

A

60-70% familial, autosomal dominant
commonly the b-myosin heavy chain mutation
rarely assoc. Friedrich ataxia
cause of sudden death in young athlets

findings: S4, systolic murmer

diastolic dysfuction ensues
marked ventricular hypertrophy, often septal predominance

hypertropied septum to close to anterior mitral leaflet can cause an outflow obsturction leading to dyspnea and possible syncope

111
Q

Restrictive/infiltraive cardiomyopathy

A

diastolic dysnfuction ensues
major causes:
sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastos (thick fibroelastic tissue in endocardium of young children, loffler syndrome, hemachromatosis

112
Q

loffler syndrome

A

endomyocardial fibrosis with prominent eosinophillic infiltrate

113
Q

systolic dysfunction

A

low EF, poor contractility, often secondary to ischemia heart disease or dilated cardiomyopathy

114
Q

diastolic dysfunction

A

normal EF and contractility, impaired relaxation, decreased compliance

115
Q

CHF reducing mortality

A

ACE inhibitors, B blockers (except in actue decompensated HF), ARB, spirinolactone.

116
Q

hemosiderin-laden macrophages

A

heart failure cells in the lungs

117
Q

Bacterial endocarditis Acute

A

s.aureus

118
Q

Bacterial endocarditis Subacute

A

viridans step, smaller vegetations on congenitally abnormal or diseased valves

119
Q

Bacterial endocarditis culture negative

A

coxiella bunetti, bartonella spp

120
Q

Bacterial endocarditis prosthetic valves

A

s. epidermidis

121
Q

Bacterial endocarditis nonbacterial secondary to:

A

malignancy (colon cancer s bovis), hypercoagulable state, lupus (mantic/thrombotic endocarditis)

122
Q

Bacterial endocarditis, which valves?

A

Mitral valve!

Tricuspid valve in IV drug abuse (s. aureus, pseudomonas, candida)

123
Q

Bacterial endocarditis clinical findings

A
  1. Fever
    2 Roth spots (round white spots on retina surrounded by hemorrhage)
  2. Osler nodes (tender raised lesions on fingers or toe pads)
  3. Janeway lesions (small painless eythematous lesions on palm or sole)
  4. Murmer
  5. Anemia
  6. splinter hemmorages on nail bed
124
Q

RF which valves?

A

Mitral>aortic»tricuspid

early lesion is MR late is MS

125
Q

RF histo and titers

A 
ASO titers
Aschoff bodies (granuloma with giant cells and anitschkow cells (enlarged macrophages with ovoid, wavy, rod-like nucleus.

Type II hypersensitivity: antibodies to M protein cross react with self antigens.

126
Q

RF clinical

A 
fever
erythema marginatum
valvular damage
increased ESR
red hot joints
subcutanoues nodules
St. Vitus dance syndenham chorea
127
Q

Acute pericarditis

A

sharp pain, aggravated by inspiration, and relieved by sitting up and leaning foward. Presents with friction rub, ECG WIDESPREAD St-segmant elevation and/or PR depression

128
Q

fibrinous pericarditis

A 
Caused by:
dressler syndrome (AI, 7 weeks ish post MI)
uremia
radiation
 loud friction rub!
129
Q

serous pericarditis

A

viral pericarditis: resolve spont.

noninfectious inflammatory disease: RA, SLE

130
Q

Suppurative/purulent pericarditis

A

pneumococcus, streptococcus

131
Q

pulses paradoxus

A 
decrease in systolic blood pressure by >/ 10 mmHg during inspiration
cardiac tamponade
asthma
obstructive sleep apnea
pericarditis
croup
132
Q

cardiac tamponade

A

compression of heart by fluid, leading to decreased CO
equilibration of diastolic pressures in all 4 chambers

findings:
Beck triad (hypotension, distended neck veins, distant heart sounds).
increased HR
pulsus peridoxus
kussmual sign
ECG shows low voltage QRS and eletrical alternates

133
Q

Kussmaul sign

A

(paradoxical rise in jugular venous pressure (JVP) on inspiration) during cardiac tamponade

134
Q

Cardiac most common tumor

A

metastasis (melanoma, lymphoma)

135
Q

Myxoma

A

most common primary cardiac tumor in adults
90% in atria, LA
ball valve obstruction

136
Q

rhadomyomas

A

most frequent primary in kids

assoc. tuberous sclerosis

organ systems (25 decks)

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