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ICM II > Cardiology > Flashcards

Cardiology Flashcards

1
Q

ECG

A
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2
Q

Which leads point in the downward direction?

A
  • aVF (straight down, 90 degrees)
  • II (60 degrees)
  • III (120 degrees)
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3
Q

Which lead is at 0 degrees?

A

I

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4
Q

What is a normal range for mean axis of depolarization?

A

-30 to 110

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5
Q

What is a quick way to know that the axis of depolarization is in the normal range?

A

“Thumbs up sign”

If pt is positive in lead I and positive in aVF, they are in normal range (0-90)

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6
Q

What part of electrical conduction of the heart does the P wave represent?

A

Atrial depolarization

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7
Q

What part of electrical conduction of the heart does the QRS complex represent?

A

Ventricular depolarization

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8
Q

What part of electrical conduction of the heart does the T wave represent?

A

Ventricular repolarization

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9
Q

If lead I is isoelectric, which lead do you look at to determine direction of the axis of depolarization?

A

aVF

  • If (+), axis is +90
  • If (-), axis is -90
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10
Q

If lead II is isoelectric, which lead do you look at to determine direction of the axis of depolarization?

A

aVL

  • If (+), it is -30
  • If (-), it is +150
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11
Q

If lead aVF is isoelectric, which lead do you look at to determine direction of the axis of depolarization?

A

Lead I

  • If (+), it is 0
  • If (-), it is +180
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12
Q

What does a long QT interval indicate?

A

Problems with repolarizing the ventricles

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13
Q

How is heart rate calculated?

A

Find an R wave which peaks on a heavy line – the next heavy black line is 300, followed by 150, 100, 75, 60 and 50

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14
Q

In normal sinus rhythms, the P wave is upright in which leads?

A

Leads I and II

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15
Q

What does the PR interval indicate?

A

Time it takes for stimulus to travel from the SA node to the ventricles

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16
Q

What does an inverted T wave represent?

A

Ischemia

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17
Q

How is the QT interval affected by LV hypertrophy?

A

Lengthened

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18
Q

How is the QT interval affected by digitalis?

A

Shortened

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19
Q

How is the QT interval affected by hypokalemia?

A

Lengthened

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20
Q

How is the QT interval affected by MI?

A

Lengthened

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21
Q

How is the QT interval affected by Hypercalcemia?

A

Shortened

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22
Q

How is the QT interval affected by myocarditis?

A

Lengthened

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23
Q

How is the QT interval affected by thyrocosis?

A

Shortened

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24
Q

How is the QRS complex affected by AV node escape rhythm?

A

Narrowed

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25
Q

How is the QRS complex affected by ventricular escape rhythm?

A

Widened

depolarization wave spreads slowly via abnormal pathway in the ventricular myocardium and not via the His bundle and bundle branches

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26
Q

What is the inherent HR of the following?

  • Atria
  • AV node
  • Ventricles
A
  • Atria: 75/min
  • AV node: 60/min
  • Ventricles: 30-40/min
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27
Q

What do you look for on an ECG to determine whether the patient has heart block?

A

Whether every P wave is followed by QRS

Yes => No heart block

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28
Q

What do you look for on an ECG to determine whether the patient has ischemia?

A

Inverted T wave

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29
Q

Diagnose:

A

Sinus bradycardia

  • Sinus rhythm
  • HR = 45
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30
Q

What are the characteristics of 1st degree heart block?

A
  • P is followed by QRS
  • PR interval is more than a box away (>250ms)
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31
Q

What are the characteristics of 2nd degree heart block type I?

A

PR prolongation but just drops a beat out of no where

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32
Q

What are the characteristics of 2nd degree heart block type II?

A

PR interval is the same before and after the block

(block is below the His-purkinje system)

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33
Q

What are the characteristics of 3rd degree heart block?

A
  • QRS complexes are going at their own rate
  • don’t always see a p wave at end b/c it is superimposed on QRS
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34
Q

What are the characteristics of a 2:1 AV block?

A

Pattern: P, QRS, P, (skip), P, QRS, P, (skip)

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35
Q

What are the characteristics of atrial fibrillation?

A
  • Ventricular rate is irregularly irregular, no discernable P waves
  • upper chambers are just quivering
  • see slide 88
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36
Q

What are the characteristics of atrial flutter?

A
  • Fast, but it is a circuit in the atrium going about 300 bpm
  • See a saw-tooth pattern
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37
Q

Determining L from R bundle branch block

A
  • Bundle branch block
    • Widened QRS
  • L or R?
    • Look at lead V1
    • Look at last part of QRS
    • If most energy is above the isoelectric line => Right
    • If most energy is below the line => Left
    • ***Think of a turn signal
    • Reference: ekg.academy
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38
Q

What are the characteristics of acute ischemia? How can you tell if it affects the anterior heart or the inferior heart?

A
  • Acute ischemia:
    • ST elevation
  • Anterior heart
    • Leads V2, V3
  • Inferior heart
    • Leads II, III, aVF
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39
Q

What are the characteristics of an old infarct?

A

Significant Q wave

  • wider than 1 mm or
  • length 1/3 QRS amplitude
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40
Q

What are the characteristics of ischemia?

A
  • T wave inversion
  • ST interval depression
  • See slide 103
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41
Q

What are the characteristics of pericarditis?

A
  • Diffuse ST elevation (everywhere)
  • PR depression
  • They will have a rub that is worse when they lean forward
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42
Q

Intro to CHF

A
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43
Q

Decreased perfusion to the kidney activates what system? What is the result?

A
  • Activates Renin - Angiotensin - Aldosterone system
  • Result:
    • Na and water retention
    • Vasoconstriction
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44
Q

What is abnormal about the beta receptors in CHF?

A
  • Downregulate themselves
    • not as affected by NE (doesn’t permit vasodilation for example)
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45
Q

What is the effect of the SNS in CHF?

A
  • Increases afterload
  • Increases HR
  • Impairs contractility
  • Increases O2 demand of the heart
    • provokes ischemia
  • Triggers arrhythmia
  • Ca overload and apoptosis
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46
Q

What electrical abnormalities can be present in CHF?

A
  • A-V dysynchrony
  • Abnormal impulse propagation in the ventricules
  • Atrial or ventricular arrhythmias
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47
Q

What can cause high-output CHF?

A
  • Thyrotoxicosis
  • Beri beri
  • A-V fistula
48
Q

What are the physical signs of Right sided CHF?

A
  1. JVD
  2. Tricuspid regurg
  3. Peripheral edema
  4. S3 gallop
  5. Hepatojugular reflex
    • pushing on liver makes jugular distention increase
49
Q

What are the physical signs of Left sided CHF?

A
  • Rales (crackles)
  • Mitral regurg
  • Pulmonary congestion
  • S3 gallop
    • early diastolic sound
  • Abnormal apical impulse
50
Q

What are the symptoms of CHF?

A
  • Dyspnea
    • Orthopnea
    • Parosysmal nocturnal dyspnea
  • Cheyne-stokes respiration
    • breathing pattern with apnea and hyperventilation
  • Nocturia
51
Q

What is most important for diagnosis of CHF?

A

Thorough H&P

52
Q

What are some causes of CHF?

A
  • CAD (Most common)
  • Valvular disease
  • Congenital disease
  • Tachycardia
  • Chagas
  • Toxins:
    • ETOH
    • Cocaine
    • Adriamycin
53
Q

What toxins can result in CHF?

A
  • EtOH
  • Cocaine
  • Adriamycin
54
Q

Should CHF patients be on ACE inhibitors?

A

Yes

55
Q

What is the MOA of Beta-blockers in CHF?

A
  • Improve relaxation
  • Protect myocardium from catecholamines
  • Negative chronotrope
    • Decrease O2 demand
  • Increase beta-receptor density
56
Q

What response do natriuretic peptides cause in the body?

A

Na and H2O diuresis

(counter the RAAS system)

57
Q

Shock

A
58
Q

Patient has mild hypotension, tachycardia, and tachypnea. There is also an increase in the anion gap. In what stage of shock is the patient? How effective is treatment?

A
  • Stage I
    • Compensated
  • Treatment is most effective in this stage
59
Q

Patient appears cool, cyanotic, and diaphoretic. He has hypotension, tachycardia, and tachypnea. He also has a decrease in urine output. In what stage of shock is the patient? How effective is treatment?

A
  • Stage II
    • Compesatory mechanisms begin to break down
  • Aggressive therapy can reverse changes
60
Q

Patient is found to have hypotension, tachycardia, and tachypnea. There are also signs of end organ damage and DIC. In what stage of shock is the patient? How effective is treatment?

A
  • Stage III
    • Irreversible
  • Therapy is not effective
61
Q

What is the cause of acidosis in shock? What problems result? What are the corrective measures?

A
  • Cause:
    • anaerobic metabolism
    • Toxins
  • Result:
    • alters oxy-hemoglobin dissociation
    • Hypoxia worsens
  • Corrective measures:
    • Add buffer (NaHCO3)
    • Correct respiratory component
62
Q

What type of shock is characterized by a low CO and a high SVR? What is the cause?

A
  • Cardiogenic shock
    • Cause: cardiomyopathy
    • Volume replacement makes worse
  • Hypovolemia
    • hemorrhage
    • dehydration
    • fluid loss due to injury or burns
    • Volume replacement makes better
63
Q

What type of shock is characterized by a decreased SVR and a CO that may be normal, high, or low?

A

Septic Shock

64
Q

Patient has a low CO and a high SVR. Volume replacement worsens the problem. Which type of shock is this?

A

Cardiogenic shock

65
Q

Patient has alow CO and a high SVR. Volume replacement fixes the problem. Which type of shock is this?

A

Hypovolemia

66
Q

When can pressor support be used in the treatment of shock?

A

Only once hypovolemia is corrected

67
Q

Pulmonary Hypertension

A
68
Q

What is the effect of an increase in length of the vessel on vascular resistance?

A

Resistance will increase proportionately

69
Q

What is the effect of an increase in viscosity of blood on vascular resistance?

A

Resistance will increase proportionately

70
Q

What is the effect of an increase in radius of the vessel on vascular resistance?

A

The resistance will decrease (by a power of 4)

Ex: radius increases by a factor of 2, resistance will decrease by a factor of 16

71
Q

In pulmonary HTN, how is the intima and media changed?

A
  • Intima:
    • hyperplasia
  • Media
    • Hypertrophy
  • Also interstitial fibrosis occurs
72
Q

What is Eisenmenger’s Syndrome? What is the result?

A
  • Eisenmenger Syndrome
    • A previously L => R shunt changes to a R => L shunt
      • often due to increased pulm pressure from overload and damage
  • Result
    • Fatal (lack of oxygenation)
73
Q

What is the result of Cor Pulmonale?

A

RV failure

74
Q

In pulmonary HTN, how is JVP affected?

A
  • Large a wave
  • Prominent v-wave
75
Q

What murmurs are common with Pulm HTN?

A
  • Closely split S2 with loud P2
  • PA click and murmur
  • RV S3 gallop
76
Q

What changes in the carotid occur with Pulm HTN?

A

Low volume

(blood stuck in veins)

77
Q

What laboratory abnormalities can be found in Pulm HTN?

A
  • Polycythemia
    • response to hypoxia
  • Increased liver function tests
    • response to congestion of liver
78
Q

What ECG findings occur in Pulm HTN?

A
  • Right axis deviation
  • R atrial abnormalities
  • LV hypertrophy
79
Q

How is primary Pulmonary Hypertension diagnosed? What population is most affected? What are the symptoms?

A
  • Diagnosis
    • exclusion of other possibilities
  • Population
    • young women
  • Symptoms
    • Chest pain
    • Loud P2
    • Dyspnea on exertion
80
Q

What is the best treatment for Cor Pulmonale?

A

O2

81
Q

Cardiomyopathy

A
82
Q

Dilated cardiomyopathy results in dysfunction of what cardiac mechanism?

A

Contraction

(systole)

83
Q

What causes dilated cardiomyopathy?

A
  • EtOH
  • Cobalt
  • Uremia
  • Hypocalcemia
  • Hypophosphatemia
84
Q

Hypertrophic cardiomyopathy results in dysfunction of what cardiac mechanism?

A

Filling

(diastole)

85
Q

What causes hypertrophic cardiomyopathy?

A
  1. Genetics
  2. Abnormal sympathetic stimulation
  3. Ischemia (coronary artery disease)
  4. Collagen abnormality
86
Q

What are the clinical manifestations of hypertrophic cardiomyopathy?

A
  • Dyspnea
  • Angina pectoris
  • Fatigue
  • Syncope
  • Palpitations
87
Q

What murmurs can be present with hypertrophic cardiomyopathy?

A
  • S3 gallop
  • S4 gallop
  • Systolic crescendo - decrescendo murmur
  • Systolic thrill
  • Mitral regurg (if systolic anterior motion is present)

***Best heard at apex

88
Q

Treatment of HCM is focused on trying to change what cardiac characteristics?

A
  • Decrease contractility
  • Increase ventricular compliance
  • Increase ventricular volume
  • Increase systemic arterial pressure
  • Increase dimensions of outflow tract
89
Q

What pathophysiological signs are present in restrictive cardiomyopathy? What forms of cardiac dysfunction result?

A
  • Myocardial fibrosis
  • Hypertrophy
  • Infiltration

This causes:

  • Excessively rigid ventricular walls
  • Abnormal diastolic function
    • impeded ventricular filling
  • Abnormal systolic function
90
Q

What are the clinical manifestations of restrictive cardiomyopathy?

A
  • Weakness and fatigue
  • Increased central venous pressure
    • JVD
  • Peripheral edema
    • Ascites
    • Anascara
  • Inspiratory increase in venous pressure
    • aka Kussmaul’s sign
91
Q

What is Kussmaul’s sign?

A

An inspiratory increase in venous pressure

(present in Restrictive Cardiomyopathy)

92
Q

What causes restrictive cardiomyopathy?

A
  • Amyloidosis
  • Sarcoidosis
  • Inherited infiltrative diseases
  • Endomyocardial disease
93
Q

What are the causes of myocarditis?

A
  • Infectious
    • most common is Coxsackie A and B
  • Toxic
  • Chemical
  • Drugs
  • Physical Agents

Not more specific than that in ppt

94
Q

A patient has a history of prodromal “flu”. Which type of pericarditis is most likely? How can this be confirmed?

A
  • Viral pericarditis
    • Cocksackie A or B
    • Echovirus
    • EBV (mono)
  • Confirmation
    • Viral titers
95
Q

Patient with pericarditis has been on dialysis. What is the most likely cause of the pericarditis? What complication can result?

A
  • Cause:
    • Uremia
  • Complication
    • Hemodynamic instability
96
Q

What type of MI is most likely to cause pericarditis? How long post-MI is it most likely to occur?

A
  • Type:
    • Transmural MI
  • Time frame
    • 2-3 days post-MI
  • May have atrial arrhythmias
97
Q

Which cancers are most likely to cause pericarditis?

A
  • Bronchogenic
  • Breast
  • Lymphoma
  • Leukemia
  • Melanoma
98
Q

What symptoms commonly occur with pericarditis?

A
  • Chest pain
    • Pleuritic
  • Dyspnea
  • Fever
99
Q

What findings on physical exam indicate acute pericarditis?

A
  • Friction rub
  • Tachycardia
  • Increased JVP
  • Pulsus paradoxus
    • large decrease in systolic BP on inspiration
100
Q

What is the differential diagnosis for the signs and symptoms of Acute Pericarditis?

A
  • Acute MI
  • Pneumonia with Pleuritis
  • Acute pulmonary embolism
  • Chest trauma causing Pneumothorax
  • GI disturbance
101
Q

What are the clinical manifestations of Cardiac Tamponade?

A
  • Physical exam:
    • Beck’s Triad:
      • Hypotension
      • Elevated venous pressure
      • Small, quiet heart
    • Pulsus paradoxus
    • Tachycardia
    • Tachypnea
  • History:
    • Chest pain
    • Dyspnea
102
Q

What is found on ECG for a patient with cardiac tamponade?

A
  • ST elevation (pericarditis)
  • Electrical alternans
    • alternation of QRS complex amplitude oraxis between beats and a possible wandering base-line
  • Low voltage
103
Q

Which part of the heart cycle is affected by constrictive pericarditis?

A

Diastole

(Restricted filling of the heart)

104
Q

What are some causes of constrictive pericarditis?

A
  • TB
  • Uremia
  • Irradiation
  • Surgery
  • Connective tissue disorders
  • Cancer
105
Q

What are the clinical features of Constrictive Pericarditis?

A
  • Diastolic pericardial knock
  • Elevated venous pressure
    • Edema
    • Hepatomegaly
    • Ascites
    • Elevated jugular venous pressue (Kussmaul’s sign)
  • Elevated left heart pressure
    • Dyspnea
    • Cough
    • Orthopnea
  • Low cardiac output
    • Fatigue
106
Q

What are the differences in signs and symptoms between cardiac tamponade and constrictive pericarditis?

A
107
Q

Congenital Heart Disease

A
108
Q

Atrial septal defect

  • Type of shunt
  • Cyanotic?
  • Complications
  • Murmur
  • ECG findings
  • Method of diagnosis
A
  • Type of shunt
    • L => R
  • Cyanotic?
    • No
  • Complications
    • Asymptomatic thru mid adult life
    • A-fib
  • Murmur
    • Systolic ejection murmur: upper LSB
    • Persisten split of S2
  • ECG findings
    • RV conduction delay
  • Method of diagnosis
    • Echo
109
Q

Ventricular Septal Defect

  • Type of shunt
  • Cyanotic?
  • Complications
  • Murmur
  • ECG findings
  • Method of diagnosis
A
  • Type of shunt
    • L => R
  • Cyanotic?
    • No
  • Complications
    • Infective endocarditis
    • Heart Failure
  • Murmur
    • holosystolic murmur at lower LSB and apex
  • ECG findings
    • LV enlargement
  • Method of diagnosis
    • Echo and Doppler
110
Q

Patent Ductus Arteriosus

  • Type of shunt
  • Cyanotic?
  • Complications
  • Murmur
A
  • Type of shunt
    • L => R
  • Cyanotic?
    • No
  • Complications
    • Infective endocarditis
    • LV failure
  • Murmur
    • Machine murmur
    • Bounding pulse
    • Wide pulse pressure
      *
111
Q

Eisenmenger Syndrome

  • Type of shunt
  • Cyanotic?
A
  • Type of shunt
    • R => L
    • previously L => R, but reversed due to pulm HTN
  • Cyanotic?
    • Yes
112
Q

Coarctation of the Aorta

  • Definition
  • Presentation
  • Consequences
A
  • Definition
    • stenosis of aorta
    • No shunt or cyanosis
  • Presentation
    • Upper body HTN
  • Consequences
    • Aortic rupture or dissection
    • Heart Failure
    • Infective endocarditis
    • Cerebral hemorrhage
113
Q

Tetrology of Fallot

  • Definition
  • Presentation
A
  • Definition
    • Pulmonary stenosis
    • VSD
    • Transposed aorta
    • RV hypertrophy
  • Presentation
    • Cyanotic
    • Dyspnea
    • Squatting
      • increases systemic bp to force more blood into pulm circulation
114
Q

Ebstein’s Anomaly

  • Definition
  • Consequences
A
  • Definition
    • Abnormal tricuspid valve (displaced into RV)
    • Pulm or aortic valve stenosis
  • Consequences
    • May be asymptomatic until adulthood
    • (doesn’t describe consequences specifically)
115
Q

Transposition of the Great Vessels

  • Consequence
A

Cyanosis

Must have other defect to serve as a shunt between the sides of the heart

ICM II (12 decks)

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