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CPR II Block 1 > Heart I > Flashcards

Heart I Flashcards

1
Q

Cardiac Dysfunction Mechanisms (6)

A 
Pump Failure
Flow Obstruction
Regurgitant Flow
Shunted Flow
Conduction Disorders
Heart/Major Vessel Rupture
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2
Q

Congestive Heart Failure

Description and Compensatory Mechanisms (3)

A

heart unable to pump blood at rate sufficient to meet metabolic demands of tissues

Frank Starling (enhanced contractility/SV) 
Hypertrophy
Neurohumoral Responses (NE, ANP, RAAS)
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3
Q

Left Sided Heart Failure

Causes (4) and Presentation (5)

A

Ischemia, HTN, Valve or Myocardial Disease

Pulmonary congestion (cough)
Paroxysmal Nocturnal Dyspnea
Atrial Fibrillation
Prerenal Azotemia
Hypoxic Encephalopathy
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4
Q

Systolic vs. Diastolic Failure

Functional and Clinical Differences

A

Systolic is decreased ejection fraction that causes poor perfusion

Diastolic is from a stiff left ventricle and causes pulmonary edema

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5
Q

Secondary Right Sided Heart Failure Cause

A

Due to left sided heart failure from pulmonary congestion

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6
Q

Primary Right Sided Heart Failure

Causes (3) and Complications (5)

A

Primary Pulmonary HTN
Parenchymal Lung Disease
Pulmonary Vasoconstriction

Nutmeg Liver
Splenomegaly
Renomegaly
Effusions
Extremity Edema
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7
Q

Atrial Septal Defects

Anatomy and Complications

A

Defect in septum secundum causing L to R shunt

Usually asymptomatic until adulthood

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8
Q

Ventricular Septal Defects

Anatomy and Complications (4)

A

In membranous interventricular septum

Symptoms present in children
Right ventricle hypertrophy
Pulmonary HTN
Cyanosis

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9
Q

Patent Ductus Arteriosus

Complications (2) and Treatment

A

Causes machinery-like murmur
Hypoxia in infants

Prostaglandin E

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10
Q

Patent Foramen Ovale

Complications (2)

A

Paradoxical embolism

Transient right sided pressure increases

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11
Q

Tetralogy of Fallot

Anatomy (5) and Symptoms (2)

A 
VSD
Subpulmonary Stenosis
Aorta Overrides VSD
Right Ventricle Hypertrophy
Boot Shaped Heart

Infant cyanosis
Squatting

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12
Q

Transposition of Great Vessels

Anatomy (3)

A

Switched systemic and pulmonary circulations

VSD and PDA often present

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13
Q

Aorta Coarctation

Associated Condition and Presentation (5)

A

Turner Syndrome

Systolic Murmur
Lower body cyanosis (if with PDA)
UE HTN, LE hypotension and LE claudication (no PDA)

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14
Q

Pulmonary Stenosis and Atresia

Complications (3)

A

Right ventricle hypertrophy
Pulmonary A. dilation
Hypoplastic right ventricle

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15
Q

Aortic Stenosis and Atresia

Complications (2)

A

Hypoplastic left heart syndrome

Williams-Beuren Syndrome

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16
Q

Ischemic Heart Disease

Main, Complications (4) and Epidemiology

A

Coronary atherosclerosis (CAD)

Myocardial Infarction
Angina
Heart failure
Sudden Cardiac Death

Leading cause of death in US

17
Q

Angina Pectoris Definition
Stable, Prinzmetal, Unstable
(Descriptions and Symptoms)

A

Paroxysmal recurrent CP without myocyte necrosis

Stable: stenotic Coronary A occlusion
Activity induced pain relieved by rest

Prinzmetal: Episodic pain spasms relieved by vasodilators

Unstable: Progressive frequency, duration and severity
Plaque rupture induced, leads to MI

18
Q

Myocardial Infarction

Pathogenesis, Necrosis Progression and Timeline

A

Most start with atheromatous Coronary A. occlusion

Necrosis distal to occlusion starts in subendocardium

Half thickness necrosis within 2-3 hours, transmural within 6

19
Q

Infarction Anatomy

LAD (3), RCA (3) and LCX (1) Areas Affected

A

LAD: Apex, Anterior LV, Anterior Septum

RCA: RV wall, Posterior LV, Posterior Septum

LCX: Lateral LV

20
Q 
Infarction Histology Features
4 hours (1), 12 hours (3), Days (3), Weeks (2)
A

4-12 hours: Coagulative necrosis starts

12-24 Hours: Nucleus pyknosis, hypereosinophilia, neutrophils infiltrate

1-3 Days: Nuclei and striations lost, neutrophils infiltrate

7-14 Days: Macrophages infiltrate, Tissue granulation

21
Q

Reperfusion

Procedures (4), Effects (2) and Injury (4)

A

Thrombolysis, Angioplasty, Stents and CABG

Salvages reversibly damaged cells
Contraction bands in irreversibly damaged cells

Reperfusion injury caused by oxidative stress, Ca2+ overload and inflammatory cells and results in hemorrhage

22
Q

MI Biomarkers

Timeline (4) and Usefulness

A

Troponin T: Rises hours 3-12 and peaks at 12-48

Troponin I: Rises 3-12 hours and peaks at 24

CK-MB: Rises 3-12 hours and peaks at 24

Troponins are the most cardiac specific and useful
Myoglobin increases first but is less specific

23
Q

MI Symptoms (4) and Complications (6)

A

CP >30 minutes
Dsypnea
Diaphoresis
N/V

Arrhythmia
Contractile Dysfunction
Fibrinous Pericarditis
Myocardial Rupture
Infarct Expansion
Ventricle Aneurysm

CPR II Block 1 (10 decks)

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