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Cardio > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What is the most common cause of right-sided heart failure?

A

Left-sided heart failure

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2
Q

What are other causes of right-sided heart failure?

A
  1. L –> R shunt

2. Chronic lung disease - cor pulmonale

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3
Q

How does inc. HR effect CO?

A

Increases then plateaus and drops off - dec. diastolic filling time

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4
Q

Impaired contractility leads to an inability to handle ________ and CVP _________.

A
  1. volume

2. increases

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5
Q

Afterload is a fx of what two things?

A
  1. Vasculature

2. Wall stress (Pxr/2wall thickness)

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6
Q

What are symptoms of heart failure?

A
  1. SOB
  2. Pitting edema
  3. Distended jugular vein
  4. S3 gallop
  5. Tachypnea
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7
Q

What does a crescendo-decrescendo murmur indicate?

A

Aortic stenosis

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8
Q

In terms of heart failure what is the PCWP to be considered “wet”

A

PCWP > 18 and RA >8

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9
Q

In terms of heart failure what is the CI to be considered “warm”

A

CI > 2.1

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10
Q

What are the 3 criteria for using an inotrope for acute heart failure?

A
  1. Advanced systolic HF + low output + hypotension
  2. Vasodilators ineffective or CI
  3. Fluid overloaded and unresponsive to diuretics or deteriorating renal fx
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11
Q

Heart failure leads to impaired ___ handling. Inotropes work to __________ calcium.

A
  1. Ca

2. Increase

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12
Q

What is a adverse effect of using an inotrope in AHF?

A

Arrhythmias

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13
Q

What are 3 typical inotropes used in AHF?

A
  1. Dobutamine
  2. Milrinone
  3. Dopamine
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14
Q

What is the MOA of Milrinone?

A

PDE inhibitor (IV infusion)
Inc. contractility and dec. afterload
** Hypotension, arrhythmia

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15
Q

What is the MOA of Dobutamine?

A

B1 agonist with weak B2
Inc. contractility with mild vasodilator
**Arrhythmia, angina, HTN, and tachycardia

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16
Q

What is the MOA of Levosimendan?

A

Troponin C to inc. its sensitivity to CA
Ca sensitizer and vasodilator
Dec afterload and LVEDP
***Not in US

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17
Q

True or False: Diuretics and Inotropes improve mortality in AHF?

A

False - dec. volume - Inc. sympathetic stimulation

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18
Q

What are 4 options for treating chest pain?

A
  1. Morphine (histamine - hypotensive)
  2. Oxygen
  3. Nitrate (hypotensive)
  4. Aspirin
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19
Q

What else is on your differential for cardiogenic shock?

A 
SIRS
Acute coronary syndrome
Aortic regurgitation
Dilated cardiomyopathy
CHF and Pulmonary edema
Mitral regurgitation 
Pericarditis and cardiac tamponade
Hypovolemic shock
Papillary muscle rupture
Acute valvular dysfunction
VSD
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20
Q

If you suspect sepsis, what must you do within 3 hours?

A
  1. Measure lactate
  2. Obtain blood cultures
  3. Broad spec antibiotics
  4. Cristalloid 30 ml/kg
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21
Q

What should you do if someone with sepsis hasn’t responded to fluids

A 
They are in Septic Shock
1. Vasopressors (target: MAP > 65)
Norepinephrine is best
Low dose vasopressin can be added
Dobutamine if inotropic support is needed
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22
Q

Automaticity

A

A cell’s ability to depolarize itself to a threshold voltage to generate a spontaneous AP

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23
Q

Cells with natural automaticity do not have a ________________.

A

Static resting voltage

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24
Q

What current is largely responsible for Phase 4 depolarization?

A

If - pacemaker current

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25
Q

If channels are activated by ____________, and mainly conduct _____.

A

Hyperpolarization (-50mV)

Na (influx)

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26
Q

Why is the upstroke much steeping in Purkinje cells than in sinus and AV nodal cells?

A

Sinus and AV nodal cells have less negative max diastolic membrane voltage so a greater number of fast Na channels are inactivated.

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27
Q

Overdrive Suppression

A

Inc. stimulation by adjacent pacemaker cells results in increased intracellular Na.

Inc. Na drives the hyperpolarizing Na/K ATPase that antagonizes the If channels preventing spontaneous depolarization

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28
Q

What is an example of altered automaticity

A

Autonomic Signaling

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29
Q

What are two ways that sympathetic stimulation increases sinus node automaticity?

A
  1. Inc. the open probability of the pacemaker channels thru which If can flow
  2. Shifts the AP threshold more negative - inc. the probability that voltage-sensitive Ca channels are capable of opening
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30
Q

What are three ways that parasympathetic stimulation decreases sinus node automaticity?

A
  1. Dec. probability that If channels are open
  2. Dec probability that Ca channels are open - inc. threshold
  3. Inc. probability that K(ACh) channels are open at rest (K efflux) - drives diastolic potential to be more neg
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31
Q

Escape rhythm

A

Impulse initiated by a latent pacemaker because the SA node rate has persistantly slowed

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32
Q

Ectopic beat

A

A latent pacemaker develops an intrinsic rate of depolarization that is faster than the sinus node

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33
Q

When do ectopic beats occur?

A

High catecholamines concentrations, hypoxemia, ischemia, electrolyte disturbances and digitalis toxicity

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34
Q

Abnormal automaticity

A

Cardiac injury leads to myocardial cells acquiring automaticity - likely due to leaky membranes and less negative resting membrane potential

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35
Q

Triggered activity

A

Early afterdepolarizations and delayed afterdepolarizations

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36
Q

Early afterdepolarization

A

Changes of membrane potential in the + direction that interrupt repolarization and are more likely to develop in conditions that prolong the AP duration

*Initiating mechanism of the polymorphic v tach Torsades de Pointes

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37
Q

EADs that occur in phase 2 are likely due to which current?

A

Inward Ca

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38
Q

EADs that occur in phase 3 are likely due to which current

A

Fast Na - more have recovered from inactive state

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39
Q

Delayed afterdepolarizations

A

May appear shortly after repolarization is complete - develop in states of high intracellular calcium - drive Na-Ca exchanger (brief inward current)

*digitalis toxicity or marked catecholamine stimulation

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40
Q

Functional heart block

A

Block occurs because an impulse encounters cardiac cells that are still refractory i.e. from drugs prolonging AP duration

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41
Q

Fixed heart block

A

Block is caused by a barrier i.e. fibrosis, scarring

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42
Q

Unidirectional block

A

AP can conduct in a retrograde direction, but prevented from doing so in the forward direction - occur w/ cellular dysfunction, different refractory periods and myocardial fibrosis

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43
Q

Most clinical cases of reentry occur within ______ regions of tissue because the conduction velocity within the reentrant loop is abnormally _____.

A

Small

Slow

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44
Q

What are the 2 critical conditions for reentry?

A
  1. Unidirectional block

2. Slowed conduction thru reentry path

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45
Q

What is he most common mechanism of ventricular tachycardia associated with areas of ventricular scar (prior MI)?

A

Monomorphic tachycardia

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46
Q

Wolff-Parkinson-White Syndrome

A

An additional connection between the atrium and ventricles (accessory pathway)

  1. Shortened PR interval
  2. Wide, slurred QRS w/ Delta wave
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47
Q

What are 3 ways of treating bradyarrhythmias?

A
  1. Anticholinergic - atropine
  2. B1-receptor agonist - isoproterenol
  3. Electronic pacemakers
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48
Q

What are two reasons bradyarrhythmias develop?

A
  1. decreased impulse formation (sinus bradycardia)

2. decreased impulse conduction (AV nodal block)

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49
Q

What are three reasons tachyarrhythmias develop?

A
  1. Inc. automaticity (SA node, latent pacemakers or abnormal myocardial sites)
  2. Triggered activity
  3. Reentry
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50
Q

What are three intrinsic factors that can suppress automaticity of SA node?

A
  1. Aging
  2. Ischemic heart disease
  3. Cardiomyopathy affecting the atrium
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51
Q

Sick Sinus Syndrome

A

SA node dysfunction - periods of inappropriate bradycardia

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52
Q

What do junctional escape rhythms (AV node/proximal bundle of His) look like on an EKG?

A

Normal, narrow QRS (40-60 bpm)
QRS not preceded by P wave
Retrograde P wave may follow QRS (inverted) in II, III and aVF

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53
Q

What do ventricular escape rhythms look like on EKG?

A

Widened QRS (30-40 bpm)

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54
Q

What does first degree AV block look like on an EKG?

A

PR interval is lengthened (> 200ms/5 sm boxes)

1:1 P : QRS

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55
Q

What causes reversible first degree AV block?

A
  1. Heightened vagal tone
  2. Transient AV nodal ischemia
  3. Drugs that depress AV nodal conduction - B blockers, Ca channel antagonists, digitalis
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56
Q

What causes irreversible first degree AV block?

A
  1. MI, chronic degenerative disease
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57
Q

How do you treat first degree AV block

A

Typically asymptomatic

58
Q

What are the two types of 2nd degree AV block?

A
  1. Mobitz type I (Wenckebach block)

2. Mobitz type II

59
Q

Mobitz type I (Wenckebach block)

A

Impaired conduction thru AV node, benign

Gradually inc. PR until QRS is blocked

60
Q

What groups of people have Mobitz type I block and how do you treat them?

A

Children, athletes, people w/ high vagal tone, sleep
Can occur in acute MI due to inc. vagal tone/ischemia
Typically not necessary, normally benign

61
Q

Mobitz type II

A

Conduction block in bundles of His or Purkinje system
Sudden, intermittent loss of QRS w/o PR interval lengthening
QRS is often widened

62
Q

What causes Mobitz type II and do you need to treat it?

A
  1. Extensive MI involving septum
  2. Degeneration of His-Purkinje system
  3. Yes. May progress to 3rd degree block w/o warning - pacemaker
63
Q

3rd degree AV block

A

Complete failure of conduction between atrial and ventricles

64
Q

What causes 3rd degree AV block?

A

MI and chronic degeneration of pathway with age

65
Q

What does 3rd degree AV block look like on EKG?

A

P wave march out

QRS: may be normal (40-60bpm) or widened at slower rates if escape rhythm comes from His-Purkinje

66
Q

How do you treat third degree AV block

A

Pacemaker

67
Q

Sinus tachycardia

A

SA discharge > 100bpm
Inc sympathetic tone/dec vagal tone
Fever, hypoxemia, hyperthyroidism, hypovolemia, anemia

68
Q

Atrial premature beats (APB) are caused by ______________ and exacerbated by _________________.

A
  1. Automaticity or reentry in an atrial focus outside SA node
  2. Sympathetic simtulation
69
Q

What do APBs look like on an EKG?

A

Early P wave with an abnormal shape

May be conducted or blocked

70
Q

How do you treat APBs?

A

Normally asymptomatic, may cause palpitations

B-blockers

71
Q

Atrial flutter

A 
Atrial activity (180-300bpm) - do not all conduct to ventricles
Caused by reentry over a large anatomically fixed circuit
72
Q

What does atrial flutter look like on an EKG

A

Sawtooth P waves

73
Q

What are predisposing factors for atrial flutter?

A
  1. Prior heart surgery
  2. Coronary disease - atrial scarring
  3. Cardiomyopathy
  4. Ablation procedures
74
Q

True or False: Atrial flutter generally occurs in patients with preexisting heart disease?

A

True

75
Q

What are people with atrial flutter at high risk for?

A

Stroke (thrombus) - anticoagulate before cardioversion

76
Q

How do you treat atrial flutter

A
  1. Beta blockers, Ca channel blockers, digoxin

2. Catheter ablation of tricuspid valve isthmus - curative 95%

77
Q

Atrial fibrillation

A

Chaotic rhythm w/ atrial rate of 350-600/min - irregularly irregular ventricular rhythm (140-160bpm)

78
Q

Rapid firing from atrial foci localized to atrial muscle extending into ______________.

A

Pulmonary veins

79
Q

What factors predispose to AF?

A

EtOH, CHF, valvular disease, HTN, coronary disease, pulmonary disease, sleep apnea, hyperthyroidism, cardiothoracic surgery – anything that inc. the size of the atria

80
Q

How can AF present clinically?

A

Dizziness, hypotension, HF

81
Q

How do you treat AF?

A
  1. Anticoagulation
  2. Rate control: AV nodal blockade (B-blockers, Ca channel blocker, digoxin)
  3. Restore sinus rhythm (cardioversion, antiarrhythmic drugs, catheter ablation)
82
Q

In AF where are clots most likely to form?

A

Left atrial appendage

83
Q

AV Nodal Reentrant Tachycardia

A

Most common form of paroxysmal SVT

Travels down slow pathway and up fast

84
Q

How does AVNRT present?

A

Young adults

Palpitation, dizziness, chest pain, dyspnea

85
Q

How do you acutely treat AVNRT

A 
IV adenosine
or 
IV verapamil/diltiazem 
or 
B-blockers
86
Q

In a person with AVNRT with frequent episodes how can ou treat them?

A
  1. Oral B-blockers, Ca channel blockers, digoxin

2. Catheter ablation of slow AV nodal pathway

87
Q

A patient with AVNRT is undergoing catheter ablation of their slow AV nodal pathway, what would happen if the fast pathway is ablated?

A

Heart block

88
Q

Atrioventricular Reentrant Tachycardias

A

Reentry using bypass tract or accessory pathway

89
Q

If the tract in AVRT only conducts retrograde it can promote _________________.

A

Supraventricular tachycardia

90
Q

If both the accessory tract and AV node conduct anterograde, what will result?

A

Ventricular Pre-excitation Syndrome (V contract sooner due to quicker signal thru accessory tract) aka Wolff-Parkinson-White

91
Q

What are patients with WPW syndrome predisposed to and why?

A

PSVTs - orthodromic AVRT
Impulse travels anterograde down AV node and retrograde up accessory tract
No delta wave, retrograde P waves

92
Q

A wide QRS with retrograde P waves indicates what on ECG?

A

Antidromic AVRT - anterograde thru accessory pathway and retrograde up AV node

93
Q

Anterograde conduction over the accessory pathway with AF or atrial flutter present can lead to what?

A

Ventricular rates up to 300 bpm
V fib
Cardiac arrest

94
Q

How do you treat someone with AVRT?

A
  1. Amiodarone or procainamide (Class I and III)
  2. If hemodynamically unstable - cardiovert
  3. Ablation of accessory pathway
95
Q

If the accessory pathway can only conduct in retrograde what can form?

A

Orthodromic AVRT - concealed accessory pathway

96
Q

Focal Atrial Tachycardia

A

Automaticity of atrial ectopic site or reentry
P-wave before each QRS (P-wave morphology is different)
Can be seen in healthy people

97
Q

AT can be caused by __________ toxicity and is also aggravated by elevated ______________ tone.

A
  1. Digitalis

2. Sympathetic

98
Q

Multifocal atrial tachycardia

A

Irregular rhythm w/ at least 3 P-wave morphologies
Average atrial rate > 100 bpm
Occurs w/ severe pulmonary disease or hypoxemia
Verapamil

99
Q

Ventricular premature beats (VPBs)

A

Ectopic ventricular focus fires an AP (can occur in healthy people)

100
Q

What does VPB look like on an EKG?

A

Widened QRS
Not related to P wave
Can be repeating or consecutive

101
Q

How do you treat VPBs?

A

Normally not necessary - observe

B-blocker for symptomatic relief

102
Q

Ventricular tachycardia is a series of 3 or more _____. Sustained VT must persist for more than ________.

A

VPBs

30 seconds

103
Q

What conditions predispose someone to VT?

A
  1. Structural heart disease
  2. MI
  3. HF
  4. Ventricular hypertrophy
  5. Primary electrical disease - long QT syndrome
  6. Valvular heart disease
  7. Congenital abnormalities
104
Q

What does monomorphic VT look like on an EKG?

A

QRS complexes are wide and identical from beat to beat w/ regular rate

105
Q

Sustained monomorphic VT usually indicates what?

A

A structural abnormality supporting a reentry circuit - MI scar or cardiomyopathy

106
Q

What does polymorphic VT look like on an EKG?

A

QRS continually changes shape and rate - Multiple foci or changing reentrant circuit

107
Q

What are the most common causes of polymorphic VT?

A
  1. Torsade de pointes

2. Acute MI

108
Q

How can you distinguish monomorphic VT from SVT?

A
  1. SVT has a narrow QRS (unless theres aberrant ventricular conduction RBBB or LBBB)
  2. Monomorphic VT has AV dissociation - no relation between P waves and QRS
109
Q

Torsades de Pointes

A

Polymorphic VT - varying amplitudes of QRS

Lightheadedness, syncope, sudden cardiac death

Cardiovert and remove stimulus

Treat symptoms with B-stimulating agents isoproterenol (shorten QT)

110
Q

What three things can lead to Torsades de Pointes?

A
  1. EAD in pt w/ long QT interval
  2. Hypokalemia or hypomagnesemia
  3. Class III drugs
  4. A few non-cardiac drugs
111
Q

What are the 3 mutations that cause Congenital Long QT Syndrome?

A

Enhance depolarizing Na current or impair depolarizing K current
LQT1: dec. outward K+
LQT2: dec. outward K+
LQT3: Inc. inward Na

112
Q

How should you acutely treat someone with VT?

A

Stable: antiarrhythmic drugs (amiodarone, lidocaine) or sedate and cardiovert

113
Q

Ventricular fibrillation

A

Immediate life-threatening arrhythmia - disordered rapid stimulation of ventricles

Often initiated by episode of VT which degenerates

114
Q

Dystrophic calcification

A

Wear and tear complicated by deposits of calcium phosphate - inc. risk with HTN, hyperlipidemia, inflammation

115
Q

Calcific aortic stenosis and mitral annular calcification are examples of what?

A

Dystrophic calcification

116
Q

Calcific aortic stenosis

A

Most common - wear and tear
Occurs in 8th-9th decade
Higher risk w/ bicuspid aortic valve (5th-6th decade)

117
Q

What are clinical effects of calcific aortic stenosis?

A

LV hypertroph
Angina, ischemia, CHF
Syncope

118
Q

How do you treat calcific aortic stenosis?

A

Valve replacement to avoid heart failure

119
Q

What is the morphology of calcific aortic stenosis?

A
  1. Calcified masses in cusps at bases
  2. Cusps not fused
  3. Free edge not involved
120
Q

Mitral Annular Calcification

A

Degenerative calcific deposits on fibrous ring at base
Women
Inc. in myxomatous valves or inc. LV pressure
Does NOT affect function
Prime site for thrombi/infection

121
Q

Myxomatous Degeneration of Mitral Valve

A 
Mitral valve prolapse (3% of adults)
One or both leaftlets enlarged, hooded, redundant, floppy
Usually no serious complications
Feature of Marfan syndrome
Deposition of mucoid material in valve
122
Q

What does a mid systolic click indicate?

A

Myxomatous Mitral valve

123
Q

What are the rare complications of myxomatous mitral valve?

A
  1. Regurgitation
  2. Infective endocarditis
  3. Mitral insufficiency
  4. Thrombi - atrial surface
  5. Arrhythmias – sudden death
124
Q

Rheumatic Fever occurs following an episode of _____________________.

A

Group A strep pyrogenes pharyngitis

125
Q

The most important complication of rheumatic fever is _______________.

A

Chronic valvular dysfunction - mitral stenosis

126
Q

What is morphology of acute rheumatic fever?

A

Pancarditis

  1. Bread and butter pericarditis - fibrin on surface
  2. Myocarditis w/ aschoff bodies
  3. Endocarditis w/ fibrinoid necrosis and verrucae - causes problems in chronic
127
Q

The classic lesion of Rheumatic Lesion is _____________.

A

Aschoff body

Anitschow cells, foci of swollen eosinophilic collagen surrounded by T lymphocytes, large macrophages, and plasma cells

128
Q

Chronic rheumatic heart disease

A
  1. Thickened valve leaflets
  2. Fusion of commissures (fishmouth/buttonhole deformities)
  3. Fusion/thickening of chordae tendinae
    MAJOR EFFECT IS MITRAL STENOSIS
129
Q

Mitral stenosis in chronic rheumatic heart disease can lead to ____________.

A 
Atrial dilatation, thrombi
Reduced CO
Pulmonary congestion 
RVH
Right-sided HF
130
Q

Hypersensitivity induced by group a strep is caused by what?

A

M protein cross react w/ glycoprotein antigens in heart, joints, etc

131
Q

How is acute rheumatic fever diagnosed?

A 
JONES CRITERIA - Major
J - Joint
O - Heart
N - SubQ Nodules 
E - Erythema marginatum
S - Sydenham chorea
132
Q

When does acute rheumatic fever occur?

A

1-4 weeks after Group A (B hemolytic) infection

Check ASO titers and antibodies to DNAase B

133
Q

When does chronic rheumatic carditis occur?

A

Years or decades after initial episode

134
Q

What is the difference between acute and subacute endocarditis?

A
  1. Acute is highly virulent, w/ normal valve and high mortality - need surgery/new valve
  2. Subacute is low virulence w/ deformed valve, responds to antibiotics
135
Q

Nonbacterial thrombotic endocarditis

A

Deposition of fibrin, platelets and other blood products on leaflets - non-destructive, noninflammatory

cancer, sepsis, hypercoaguable (pancreatic cancer)
Swan-Gatz catheter

136
Q

Libman-Sacks Endocarditis

A

SLE - Mitral and tricuspid valves
Primary antiphospholipid syndrome
Both sides of leaflet - may be on endocardium - may be verrucae
Intense inflammation

137
Q

Carcinoid Syndrome

A

Carcinoid tumors produce serotonin or vasoactive amines (bradykinin, histamine, PG)
Flushing, cramps, NVD

138
Q

Carcinoid Heart Disease

A

Plaque-like fibrosis on right side of heart (gets inactivated by MAO in lung)

SMC and collagen embed in mucopolysaccharide matrix

Tricuspid and pulmonic valves equally affected T. insufficiency and pulmonic stenosis

139
Q

GI carcinoid w/ hepatic mets

A

Mets to liver - secretion occurs directly to hepatic vein
or
Direct secretion to systemic circulation

140
Q

Artificial valve complications

A
  1. Thromboembolic complications
  2. Infective endocarditis (bio/mechanical)
  3. Structural deterioration (bioprosthesis)

Cardio (9 decks)

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