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Pathophysiology 212 > Disorders of cardiac function > Flashcards

Disorders of cardiac function Flashcards

1
Q

Pericarditis & and causes

A

inflammation of the pericardium (the membrane enclosing the heart)
Acute =

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2
Q

Pericarditis manifestations

A 
Decreased CO
Pericardial friction rub
Chest pain
Precordial
Abrupt onset, sharp, radiates
Scapula pain
increases with deep breath, cough
relief when sitting forward

ECG changes

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3
Q

Pericardial Effusion

A 
Accumulation of fluid in the pericardial cavity/space
Causes
- Inflammation of pericardium
- Infection elsewhere
- Neoplasms
- Cardiac surgery
- Trauma 
Symptoms dependent on rapidiy & amount of fluid build-up
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4
Q

Cardiac Tamponade & causes

A

Compression d/t fluid/blood
A build-up of blood or other fluid in the pericardial sac puts pressure on the heart, which may prevent it from pumping effectively.

Causes:
Trauma
Myocardial rupture post MI
Cardiac surgery
Aortic dissection
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5
Q

Tamponade: Manifestations

A

Dependent on amount and rapidity

Limits stroke volume and CO = low SBP
CNS: change in mentation
Resp: dyspnea, tachypnea
CVS: chest pain, tachycardia

  • Elevated central venous pressure & jugular venous pressure (distention)
  • Circulatory shock
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6
Q

Tamponade: Diagnosis/Treatment

A 
Muffled heart sounds- d/t to extra layer of fluid
Pulsus paradoxus
> 10 mmHg fall with respiration
ECG
- Decreased voltage
Echocardiogram
CT, MRI
Treatment: immediate pericariocentesis
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7
Q

What assists coronary artery flow?

A
  • Endothelial cells lining arteries
    -Diastolic pressure in aorta
    Time in diastole
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8
Q

What impairs coronary artery flow?

A

Atherosclerosis most common

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9
Q

Non-Modifiable Risks for CAD

A 
Sex/Gender
Post-menopausal women
Age
Ethnicity
Genetics
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10
Q

Modifiable Risks for CAD

A
  1. Hypertension
  2. Hyperlipidemia
  3. Tobacco use
  4. Diabetes
  5. Obesity
  6. Sedentary lifestyle/physical inactivity
  7. Ability to cope with stress
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11
Q

Stable Angina

A
  • Pain/pressure d/t transient ischemia
  • Precordial/substernal
  • Possible radiation
  • Possible epigastric discomfort
  • Often d/t a fixed coronary narrowing
  • Occurs with exercise/exertion/cold/emotions
  • Relieved with rest & nitroglycerine

Artery in the heart is partially blocked, so not getting enough O2.

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12
Q

Variant/Prinzmetal Angina

A

d/t spasms of coronary artery
Cause is unclear
Often @ night
Variable symptoms

Treatment is dependent on findings of investigative diagnostics

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13
Q

Silent MI

A

Silent MI’s (or atypical symptoms) are more likely in the elderly
? Less myocardium involved
? neuropathy
- hypotension, low body temp, vague complaints of discomfort, mild diaphoresis, stroke-like symptoms, dizziness, sensorium changes

Treatment is dependent on findings of investigative diagnostics

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14
Q

Acute Coronary Syndrome

A

Risk is classified based on ECG changes
Unstable Angina/Non ST-segment elevation Myocardial Infarction (non-STEMI)
ST-segment elevation MI (STEMI) - ischemia to heart muscle

All caused by an imbalance in myocardial          
oxygen supply and demand
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15
Q

Potential Causes of ACS: Primary & Secondary Causes

A

> Unstable plaque, rupturing to form a clot
- Thin fibrous cap with fatty core is most unstable
Coronary vasospasm
Atherosclerotic narrowing (progressive)
Inflammation/infection
Secondary causes
- anemia
- fever (basal metabolic rate is high)
- hypoxemia

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16
Q

Unstable Angina/Non-ST MI

A 
Typical Pattern of Manifestations
> With pre-diagnosis of “Stable Angina”
- But more severe or more often than usual
> Occurs at rest (or minimal exertion)
> Lasts > 20 minutes

If biomarkers are elevated = non-STEMI
High risk of STEMI

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17
Q

ST Elevation MI

A

Ischemic death of myocardial tissue

> Typical Pattern of Manifestations
Crushing/constricting pain; usually abrupt
- Substernal with radiation to left arm, jaw, neck

  • Epigastric distress/nausea
  • Palpitations
  • Cool, clammy skin
  • SOB
  • Anxiety

Unrelieved by rest/nitro

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18
Q

ST Elevation MI Con’t…

A

Cardiac muscle wall ischemia & necrosis

  • Subendocardial
  • Transmural = Q wave
  • “Stunned” myocardium

Cell death in 15-20 minutes

Early perfusion & revascularization can prevent necrosis.

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19
Q

Myocardial Ischemia/Necrosis result in…

A

Decreased contractile force

  • Decreased CO
  • Decreased coronary artery perfusion
  • Decreased pulmonary vasculature pressure

Interruption of conduction
- dysrhythmias

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20
Q

Diagnosis of myocardial ischemia also based on Serum Biomarkers

A

> Troponin (involved in muscle contraction)
Rises within 2-3 hrs; remains elevated for 7-10 days

> Myoglobin (functions as oxygen storage)
Rises within 1 hr, peaks at 4 hrs
Also from skeletal muscle damage

> Creatine Kinase MB (CK-MB) (levels can indicate muscular dystrophy)
Peaks at 4-6 hrs; gone in 2-3 days
Specific to cardiac muscle

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21
Q

Acute MI Treatment

A 
Oxygen
Pain relief
Reperfusion
- Fibrionolytics
- Percutaneous transluminal coronary angioplasty (PTCA)
- Stents

Coronary Artery Bypass Grafting (CABG)- taking a vein from another part of the body and using it in the heart

22
Q

Complication of an Acute MI

A
  • Arrhythmias – most common cause of sudden death
  • Reinfarction
  • Heart failure
  • Pericarditis
  • Embolic CVA or Pulmonary embolus
  • Valve deformities
  • Septal rupture
  • LV wall aneurysms/rupture
  • Cardiogenic shock
  • Dressler syndrome
23
Q

Cardiomyopathies

A 
Cardio = heart
Myo = muscle
Pathy = disorder/syndrome/bad
“Idiopathic cardiomyopathy”
Muscle disorders
Mechanical (eg: heart failure)
Electrical (eg: arrhythmias)
Primary 
Secondary
24
Q

Hypertrophic Cardiomyopathy (HCM)

A

Leading cause of sudden cardiac death in young adults

Unexplained genetic ventricular septal thickening
Poor diastolic finding
LV outflow obstruction
Left ventricular hypertrophy (LVH)
Disruption of normal conduction pathways
25
Q

Hypertrophic Cardiomyopathy (HCM) Manifestations

A 
> Variable
> Decreased stroke volume d/t impaired diastolic filling
- Dyspnea
- Chest pain
- Syncope post exertion

> Atrial fibrillation
Lethal ventricular arrhythmias

26
Q

Endocarditis & and Risk factors

A

Any infection of inner lining of heart

  • Usually staphylococcus aureus
  • Vegetative (growth)
  • Involvement of mitral & aortic valves most common
  • Acute: relatively healthy individual
  • Sub-acute/chronic: h/o valve abnormalities
Risk Factors
Infection elsewhere
Dental surgery/surgery, IV drug use/contaminants
Immunodeficiency/immunosuppression
Valve prolapse (sudden or congenital)
27
Q

Endocarditis manifestations & complications

A

> Manifestations
S&S of systemic infection
Heart sound changes
Symptoms related to embolism

> Complications
Emboli (lung, renal, brain, etc.)
Valve dysfunction
arrhythmias

28
Q

Rheumatic Heart Disease

A

> Caused by rheumatic fever
- Which occurs after streptococcal pharyngitis
- Sore throat, h/a, fever, n&v, joint pain
- One or all layers (pancarditis)
- valves
- Aschoff bodies
Immunological response but pathogenesis unclear
Acute, chronic, or recurrent

29
Q

Rheumatic Heart Disease diagnosis and treatment

A

> Acute phase = pancarditis

  • Pericardial friction rub, murmur
  • Mitral/aortic valve involvement
  • Arrhythmias

> Diagnosis

  • Evidence of GAS infection
  • Elevated WBC, ESR, CRP
  • Echocardiogram, Ultrasound

> Treatment
Antibiotics, prevention of complications

30
Q

Valvular Disorders causes

A 
Congenital
Trauma
Ischemic damage
Degenerative changes
Inflammation
31
Q

Valvular Disorders treatment

A 
Preventative
APA (antiplatelet aggregator)
Symptoms
Percutaneous valvuloplasty
Surgery
32
Q

Valvular Disorders Diagnosis

A

Auscultation
Doppler Echo
ultrasound

33
Q

When Will You Hear Murmurs?

A
  • If a valve is stenotic, you will hear a murmur of blood shooting through the narrow opening when the valve is open
  • If a valve is regurgitant, you will hear a murmur of blood leaking back through when the valve should be closed
34
Q

Mitral Valve Stenosis

A 
Fibrous, stiff tissue, often causing chordae tendineae to shorten
Incomplete opening obstructs blood flow
Causes
RF
Congenital
35
Q

Mitral Valve Stenosis manifestations & complications

A

Manifestations
-Chest pain, weakness, fatigue, palpitations

Complications

  • Arrhythmias (atrial fibrillation, atrial tachycardias)
  • Mural thrombi
36
Q

Mitral Valve Regurgitation (MVR) & causes

A

> Incomplete closing
- Some blood returns to LA during systole

> Causes

  • RDH
  • Chordae tendineae or papillary muscle rupture
  • LVH dilates orifice
  • Mitral valve prolapse
37
Q

Mitral Valve Regurgitation manifestations and complications

A

Manifestations

  • Slow process = compensation
  • Pulmonary congestion
  • Pansystolic murmur
  • LA Atrial and LV hypertrophy

Complications

  • Atrial fib
  • thrombus
38
Q

Mitral Valve Prolapse manifestations and complications

A

> Leaflets enlarge, become “floppy”
Associated with:
Marfan’s sydrome & Osteogensis imperfecta

Manifestations
“snap”
Asymptomatic
Chest pain, dyspnea, etc.
Complications
MVR, a. fib
thrombus
39
Q

Aortic Valve Stenosis causes and manifestations

A 
Narrowing causing resistance to ejection
Slow progression = compensation
Causes:
Congenital or acquired 
Male, active inflammation

Manifestations
Loud systolic ejection murmur or split S2
Chest pain, dyspnea, syncope, heart failure (LV hypertrophy)

40
Q

Aortic Valve Regurgitation & causes

A

Scarring of leaflet and/or enlarged orifice
Blood flow back into LV during diastole

Causes
RHD, ideopathic aortic dilation, congenital, endocarditis, Marfan’s, HPTN, trauma

41
Q

Chronic Aortic Regurgitation

A
  • Slow progression = compensation
  • LV enlarges but works harder

Manifestations

  • Blowing sound over valve
  • Widening pulse pressure
  • Korotkoff sounds persist to zero!
  • Tachycardia, water-hammer pulse
  • “pounding” of heart when lying down
  • Eventually orthopnea, dyspnea, paroxysmal nocturnal dyspnea
42
Q

Acute Aortic Regurgitation causes & manifestations

A

> Causes
Acute endocarditis
Trauma
Aortic dissection

> Manifestations
Too quick for compensation!
Extreme rise in LVEDP = pulmonary edema
- Decreased coronary artery perfusion
Dysrhythmias = lethal
43
Q

Patent Ductus Arteriosus

A

Persistent delay > 3 months
Normally closes @ 24-72hrs
Delay if premature

Manifestations
Dependent on size
High pressure from aorta = pulmonary hypertension

44
Q

Atrial Septal Defects

A

Non-closure of foramen ovale
Often asymptomatic until teenage

Manifestations
Increased pulmonary pressures
Atrial dilatation = dysrhythmias

45
Q

Ventricular Septal Defects cause and manifestations

A

Most common congenital heart defect (25-30% of all)
Cause:
Incomplete separation of ventricles during development invitro
1/3 close spontaneously
Manifestations dependent on size
Asymptomatic heart failure
Tachypnea, tachycardia, pulmonary congestion, failure to thrive

46
Q

Pulmonary Stenosis

A 
Obstruction of blood flow from RV
Causes
Pulmonary valve lesions
Pulmonary artery lesions
Combination

10% of all congenital cardiac disease
Often associated with other patho

47
Q

Tetralogy of Fallot

A

Most common cyanotic congenital heart defect (5-7% of all)

Pulmonic narrowing
RV hypertrophy
Ventricular septal defect
Dextroposition of aorta
Over-rides RV, attaches to septal defect
48
Q

Tetralogy of Falot manifestations and treatment

A

Manifestations
Cyanosis with increased oxygen demands
Crying, feeding, defecation
Loss of consciousness possible

Treatment
Knee-chest position
Surgery

49
Q

Transposition of the Great Arteries

A 
RV empties into aorta
LV empties into pulmonary arteries
Risk Factors
Mothers with diabetes
Boys > girls
Manifestations
Cyanosis
Survival if patent ductus arteriosus or septal defect
50
Q

Coarctation of the Aorta

A

Associated with other congenital lesions

Manifestations
BP lower in legs than in arms
Asymptomatic 
Hypertension later in life
LVH

Pathophysiology 212 (18 decks)

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