Pathophys: Cardio Flashcards

1
Q

Definition of CHF

A

Loss of pumping action of the heart that results in congestion

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2
Q

How can you sub-divide CHF?

A

Acute/Chronic

L/R

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3
Q

What are the cardinal symptoms of LVF?

A

Dyspnea/Orthopnea/PND
Hemoptysis
Chest pain
Fatigue/Nocturia

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4
Q

What are the 4 major etiologies of CHF?

A
  1. Increased workload (PL/AL)
  2. Restricted filling (constrictive pericarditis)
  3. Myocardial dysfunction (MI)
  4. Decreased contractility (posion/infection)
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5
Q

The pathophysiology of heart failure can be explained by:

A
  1. HD changes
  2. Neurohumoral changes
  3. Cellular changes
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6
Q

HD changes in LVF can best be explained by 2 different types of dysfunction

A

Systolic dysfunction

Diastolic dysfunction

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7
Q

Etiologies of systolic dysfunction include:

A

CAD, valvular disease, HTN, aging, dilated CM

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8
Q

The 3 compensatory mechanisms employed by the body in heart failure are:

A
  1. Frank-Starling: increase preload
  2. Increased contractility (inotropes)
  3. Cardiac muscle hypertrophy
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9
Q

The neurohumoral changes experienced early in heart failure include:

A
  1. RAAS: Angio 2 vasoconstrictor
  2. ADH
  3. Cytokines and peptides: IL-1 [myocyte hypertrophy], TNF [myocyte hypertrophy, apoptosis], endothelin [myocyte hypertrophy, vasoconstriction], BNP [released when ventricle is stretched]
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10
Q

The cellular changes experienced in heart failure include:

A
  1. Inefficient Ca handling
  2. Adrenergic desensitization
  3. Myocyte hypertrophy
  4. Apoptosis
  5. Myocardial fibrosis (ventricular remodelling)
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11
Q

Cardinal signs/symptoms of RVF

A
  1. SOB: LVF, pulmonary disease, ascites/diaphragm,
  2. Pitting edema
  3. Abdominal pain: liver
  4. Increased JVP
  5. L sternal heave
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12
Q

Cor pulmonale can be caused by:

A

COPD/pulmonary hypertension, collagen vascular disease

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13
Q

Etiology of RVF

A
  1. LVF
  2. Congenital shunt
  3. Cor pulmonale
  4. RV ischemia
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14
Q

Describe the Bernheim and reverse Bernheim effects

A

Bernheim: LV deviates towards RV (aortic stenosis, HCM): no pulmonary congestion

Reverse Bernheim: Huge RV, septal deviation towards LV

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15
Q

DDX increased JVP

A

Cardiac tamponade, constrictive pericarditis, massive PE

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16
Q

S3

A

Rapid ventricular filling [physiological in children, athletes]; pathological in an already volume overloaded ventricle

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17
Q

Differentiate between a sustained and displaced apical impulse.

A

Sustained: LV hypertrophy
Displaced: Volume overloaded ventricle

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18
Q

What type of pulse pressure do you see in LVF?

A

Pulsus alternans

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19
Q

Why are LVF patients cold, pale and sweaty?

A

Sympathetic response

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20
Q

Differentiate between pulmonary edema and pleural effusion in LVF patients (based on acute/chronic).

A

Edema: acute
Effusion: chronic

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21
Q

S4

A

Filling a poorly compliant ventricle

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22
Q

Etiologies of AV block

A

Age, vagal input, muscular dystrophy, tuberous sclerosis, sarcoidosis, gout, SLE, LYME, CAD, ankylosing spondylitis

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23
Q

Palpitations generally precede tachy or brady arrhythmias

A

Tachy

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24
Q

What do you assess in an EKG?

A

Rate (300/150/100/75/60)
Rhythm
PR interval: <3 boxes

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25
The requirements for a re-entrant circuit include:
1. Slow conduction pathway 2. Unidirectional block 3. 2 pathways in a small area
26
3 etiologies of tachyarrhythmias
1. Increased automaticity 2. Spontaneous depolarization 3. Re-entrant circuit
27
2 etiologies of bradyarrhythmias
1. Decreased automaticity | 2. Decreased conduction
28
Describe the varying degrees of heart block.
1. First: prolonged PR-interval 2. Second 1: increasing PR-interval, dropped QRS 2. Second 2: stable PR- random dropped QRS 3. Third degree: AV dissociation
29
WPW Syndrome is AD/AR?
AD
30
WPW Syndrome on EKG
Short PR interval, wide QRS with delta wave | Bundle of Kent accessory pathway
31
Long QT syndrome etiology & pathogenesis
1. AD 2. Class 3 anti-arrhythmic drugs (i.e. digitalis) * Hypoxia, stress can lead to decreased function of K+ channels
32
Difference between AFib & A Flutter on EKG
AFib: oscillations | A Flutter: symmetrical F waves
33
The only electrical connection between the atria & ventricles
Bundle of His
34
Loud S1
MS, short PR, tachycardia
35
Soft S1
MR, long PR, poor systolic function, A/P regurgitation
36
Loud S2
Systemic HTN, Pulmonary HTN, ASD
37
Soft S2
AS/PS; AR/PR
38
A2-P2 normal split occurs during…
Deep inspiration
39
A2-P2 wide split occurs during…
R BBB
40
A2-P2 fixed split occurs during…
ASD
41
P2-A2 split occurs during…
L BBB
42
S3
Volume overload / increased pre-load and decreased diastolic time
43
S4
Atrial gallop normally masked by LV [poorly compliant ventricle]
44
What is a thrill?
A palpable murmur
45
Early/Mid-Systolic Murmur heard best at 2nd interspace that radiates to neck
AS
46
Early/Mid-Systolic Murmur heard best at apex/LLSB
HOCM
47
Pansystolic murmur heard best at apex that radiates to axilla/back
MR
48
Pansystolic murmur heard best at LLSB
VSD
49
Pansystolic murmur heard best at LLSB that radiates to neck
Tricuspid regurgitation
50
Late systolic murmur heard best at apex/LLSB
MVP
51
Continuous systolic-diastolic murmur heard best at LLSB
PDA
52
Early diastolic decreshendo murmur heard best at 3rd interspace
AR
53
Mid-diastolic low pitched murmur heard best at apex
MS, short PR, tachycardia
54
Mid-diastolic low pitched murmur heard best at LLSB
Tricuspid stenosis
55
Does S4 disappear in Afib?
Yes
56
Differentiate between concentric and eccentric ventricular hypertrophy.
Concentric: LVH/sustained; Eccentric: Volume/laterally displaced
57
Partial development of the Aorticopulmonary septum
Truncus arteriosus occurs because partial development of the aorticopulmonary septum. There is a unique vessel rising from the heart. Most of the patients are going to have symptoms of congestive heart failure in the first week of life.
58
Anterior-Superior displacement of aorticopulmonary septum
Tetralogy of Fallot TOF occurs when there is an anterosuperior displacement of the aorticopulmonary septum. It has 4 typical findings: The aorta is displaced to the right, overriding the ventricular septum, so the pulmonary outlet is going to be smaller, causing overload of the right ventricle and hypertrophy.
59
Failure of the aorticopulmonary septum to rotate in a spiral
Transposition of the great arteries occurs when the pulmonary artery rises from the left side and the aorta rises from the right side in this condition. Patients only survive if there is a communication between left and right sides as a patent ductus arteriosus, ventricular septal defect, or atrial septal defect.
60
________________________ accounts for the greatest percentage of total blood volume.
Post-capillary blood volume
61
Causes of dilated cardiomyopathy.
``` Viral (Coxsackie B) Peripartum CM ETOH Chronic SVT Cardiotoxic drugs Thiamine deficiency ```
62
T/F The foramen ovale is patent in 20-30% of normal adults.
True
63
The most common underlying etiology of native valve bacterial endocarditis?
Mitral valve prolapse
64
The most common congenital malformation affecting the heart in Turner's syndrome.
Bicuspid aortic valve