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Patho test 1 > Chap 19 Disorders of Cardiac Function > Flashcards

Chap 19 Disorders of Cardiac Function Flashcards

1
Q

Pericarditis
acute = ?

Causes:

A

Acute =

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2
Q

Pericarditis manifestations:

A
  1. Decreased CO
    Pericardial friction rub- during auscultation from inflamed pericardial surfaces: tissue on tissue
  2. Chest pain
    Precordial- (space between parietal and visceral pericardium. Right by heart ). Start here and radiate to neck, back ,abd or side.
    –Abrupt onset, sharp, radiates
    –Scapula pain
    –Increases with deep breath or cough
    –Relief when leaning forward- takes the pressure of your chest off it. Feels much better
  3. ECG changes
  4. Tx: depend on cause: antibiotics, antiinflams
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3
Q

What is Dressler Syndrome?

A

Post heart attack. Pericarditis a week or two after.

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4
Q

Pericardial Effusion:

A
  • Accumulation of fluid in the pericardial cavity/space— compresses heart chambers.
  • Higher fluid=higher compression.
  • Small amount of fluid and may be symptomatic
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5
Q

Pericardial Effusion

Causes:

A

Causes:

  • Inflammation of -pericardium
  • Infection elsewhere, can end up in pericardium
  • Neoplasms
  • Cardiac surgery
  • Trauma
  • *Symptoms depend on how fast and amount of fluid build-up
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6
Q

cardiac tamponade:

A
  • -Compression d/t fluid or blood in pericardial sac. EMERGEMCY.
  • -Build up of blood of other fluid in pericardial sac puts pressure in the heart, which may prevent it from pumping effectively.
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7
Q

Cardiac Tamponade

Causes:

A 
Causes:
>Trauma
>Myocardial rupture post MI
>Cardiac surgery
>Aortic dissection: inner wall of the aorta, the large blood vessel branching off the heart, tears. Blood surges through the tear, causing the inner and middle layers of the aorta to separate (dissect).
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8
Q

Cardiac Manifestations:

A

Dependent on amount and rapidity

  1. Limits stroke volume and CO = low SBP
    >CNS: change in mentation
    >Resp: dyspnea, tachypnea
    >CVS: chest pain (from coronary arteries not filling), tachycardia
  2. Elevated central venous pressure & jugular venous pressure
  3. Circulatory shock- not getting enough blood to organs
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9
Q

Tamponade Diagnosis:

A
  1. Muffled heart sounds
  2. Pulsus paradoxus- ***
    - ->10 mmHg systolic fall with respiration
    - -exaggeration of normal variation in systolic BP
  3. ECG- see decreased voltage (electrocardiogram) reviles nonspecific T wave changes and low QRS voltage. Hearts electrical activity
  4. Echocardiogram- ultrasound of heart. Provides pictures of the structures.
  5. /6. CT, MRI
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10
Q

Tamponade Treatment:

A

depends on progression.
-In large: Pericardiocentesis (removal of fluid) tx of choice. With needle to draw fluid away from heart (release the pressure)

-in sml effusion- NSAIDS, colchicine or corticosteroids to min fluid accumulation.

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11
Q

Coronary Artery Disease =

A

Heart Disease.

Heart disease caused by impaired flow to coronary arteries

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12
Q

What assists coronary artery flow?

A
  • -Endothelial cells lining arteries
  • -Diastolic pressure in aorta
  • -Time is diastole to fill coronary arteries
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13
Q

What impairs coronary artery flow?

A

Atherosclerosis

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14
Q

Non-Modifiable Risks for CAD

A 
>Sex/Gender
--Post-menopausal women
>Age
>Ethnicity
>Genetics
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15
Q

Modifiable Risks for CAD

A
  • -Diet
  • -Exercise
  • -Smoking
  • -HTN
  • -Hyperlipidemia
  • -DM
  • -obesity
  • -Stress
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16
Q

Stable Angina

A
  1. Pain/pressure d/t transient ischemia
  2. Precordial/substernal
    - -Possible radiation
    - -Possible epigastric discomfort
  3. Often a FIXED coronary narrowing
  4. Occurs with exercise/exertion/cold/emotions
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17
Q

Stable Angina relieved with?

A

rest & nitroglycerine**

  • -relax (widen) bld vessels. Allows bld to flow more easily, reducing workload and amnt of O2 needed by heart. Dilate coronary arteries
  • -You can have ASCD/CAD without angina!!!
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18
Q

Variant/Prinzmetal Angina

A

> d/t spasms of coronary artery
Cause is unclear
Often @ night when person is at rest. Midnight-early morn
Variable symptoms

Treatment is dependent on findings of investigative diagnostics

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19
Q

Silent MI:

A

atypical symptoms and more likely in the elderly.

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20
Q

Silent MI diagnosis:

causes:

Manifestations:

A

ECG -show the changes that happened to the heart during the silent MI

cause: often unsure.
>? Less myocardium involved
>? Neuropathy

Manifest:
Hypotension, low body temp, vague complications of discomfort, mild diaphoresis, stroke-like symp, dizzy, sensorium changes

Treatment is dependent on findings of investigative diagnostics

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21
Q

Acute Coronary Syndrome

two types:

A

-classified based on presence or absence of ST-segment.

> Risk is classified based on ECG changes

  1. Unstable Angina/Non ST-segment elevation Myocardial Infarction (non-STEMI)
  2. ST-segment elevation MI (STEMI)All caused by an imbalance in myocardial
    oxygen supply and demand
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22
Q

Potential Causes of ACS

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
  • -Hypoxemia
  • -Surgery!!!!!
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23
Q

Unstable Angina/Non-ST MI

Typical pattern of Manifestations:

A

Typical Pattern of Manifestations

> With pre-diagnosis of “Stable Angina”
More severe or more often than usual

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24
Q

Unstable Angina/Non-ST M

Course of pain has 3 features:

A
  1. Occurs at rest (or minimal exertion) and Lasts more than 20 minutes
  2. Severe and described as flank pain and new onset
  3. More severe, prolonged and frequent than any prior experience

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

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25
Q

Serum biomarkers for ACS are:

A

> Cardiac specific troponin I and troponin T, myoglobin and creatine kinase.

> As the myocardial cells become necrotic, their intracellular contents begin to diffuse into the surrounding interstitium and then into the blood

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26
Q

ST Elevation MI

Typical pattern of Manifestations:

A

Heart attack
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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27
Q

ST Elevation MI

Cardiac muscle wall ischemia & necrosis

A

> Subendocardial

> Transmural (across entire wall or organ or vessel). Full thickness of the vent wall and common when there is obstruction of a single artery = Q wave

> “Stunned” myocardium- some myocardium can recover when blood flow is re-established but critical abnormalities in biochemical function may persist. Person might have areas of dysfunctional myocardium.

Cell death in 15-20 minutes
Early perfusion and revascularization can prevent necrosis!!!

28
Q

Myocardial Ischemia/Necrosis result in

A
  1. Decreased contractile force
    - -Decreased CO
    - -Decreased coronary artery perfusion
    - -Increased pulmonary vasculature pressure
  2. Interruption of conduction
    - -Dysrhythmia
29
Q

Diagnosis also based on Serum Biomarkers

A
  1. Troponin-
    - Rise within 2-3 hrs; remains 7-10 days

2.Myoglobin-
Rises within 1 hr, peaks at 4 hrs Also from skeletal muscle damage

  1. Creatine Kinase MB (CK-MB)-
    - -Peaks at 4-6 hrs; gone in 2-3 days
    - -Specific to cardiac muscle
30
Q

Acute MI Treatment

A
  1. Oxygen
  2. Pain relief
  3. Reperfusion
    >Fibrionolytics- clot busting drugs. If given in time, lessen the damage
    >Percutaneous transluminal coronary angioplasty (PTCA)- through femoral/inguinal artery to open blocked artery d/t atherosclerosis. Blow up balloon and put a stent
    >Stents
  4. Coronary Artery Bypass Grafting (CABG)
31
Q

Complication of an Acute MI

A

> Arrhythmias – most common cause of sudden death
Reinfarction- repeat infarction after initial infarct
Heart failure
Pericarditis
Embolic CVA or Pulmonary embolus
Valve deformities
Septal rupture
LV wall aneurysms/rupture
Cardiogenic shock- cell death from O2 and nutrient starvation
Dressler syndrome- post MI, consists of fever, pleuritic pain, pericarditis and/or a pericardial effusion

32
Q

Cardiomyopathies

Cardio = heart
Myo = muscle
Pathy = disorder/syndrome
A

“Idiopathic cardiomyopathy”- cause unknown

> Muscle disorders

  • -Mechanical (HF)
  • -Electrical (arrhythmias)

> Primary- genetic or acquired

> Secondary- presence of multisystem disorder. Other myocardial disorder. Drugs, DM, muscular dystrophy, autoimmune disorders.

33
Q

Hypertrophic Cardiomyopathy (HCM)

A

*Leading cause of sudden cardiac death in young adults

> Unexplained genetic ventricular septal thickening

  • -Poor diastolic filling
  • -LV outflow obstruction
  • -Left ventricular hypertrophy LVF
  • -Disruption of normal conduction pathways
34
Q

HCM Manifestations

A

> Variable- may progress to end stage heart failure
Decreased stroke volume d/t impaired diastolic filling
–Dyspnea,
–chest pain,
–syncope
Atrial fibrillation
Lethal ventricular arrhythmias

35
Q

Endocarditis

A

Any infection of inner lining of heart

> Usually staphylococcus aureus
Vegetative (grows like a veg) leisions form on heart valves
Involvement of mitral & aortic valves most common
Acute: relatively healthy individual
Sub-acute/chronic: h/o valve abnormalities

36
Q

Endocarditis Risk Factors:

A
  • Infection elsewhere
  • IV drug abuse, dental surgery
  • family hx
  • Valve prolapse (sudden or congenital)
37
Q

Endocarditis
Manifestations:

Complications:

A

Manifestations – effects aortic and mitral valves

  • -S&S of systemic infection, fever-chills
  • -Heart sounds changes
  • -Symptoms related to emboli

Complications

  • -Emboli (lung, brain, renal)
  • -Valve dysfunction
  • -Arrhythmias
38
Q

Rheumatic Heart Disease

A
  1. Caused by rheumatic fever
    - -Which occurs after streptococcal pharyngitis
    - -One or all layers
    - -Aschoff bodies- inflam lesions within the connective tissue elements of the heart, bld vessels, joints and SC tissue
  2. Immunological response but pathogenesis unclear
  3. Acute, chronic, or recurrent
39
Q

Rheumatic Heart Disease
Acute phase:

Diagnosis:

Treatment:

A

Acute phase = pancarditis. Involves all 3 layers of heart (endo, myo, pericardium)

Diagnosis:

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

Treatment:
Antibiotics, prevention of complications

40
Q

Valvular Disorders

causes:

A
  • -Congenital
  • -Trauma
  • -Ischemic damage
  • -Degenerative changes
  • -Inflammation
41
Q

Valvular Disorders

Diagnosis:

A
  • -Auscultation
  • -Doppler Echo
  • -Ultrasound
42
Q

Valvular Disorders

Treatment:

A
  • -Preventative
  • -APA
  • -Symptoms
  • -Percutaneous valvuloplasty
  • -Surgery- repair or replacement
43
Q

If an aortic valve is regurgitant, you will hear a murmur of blood leaking back through to left vent when

A

during diastole

this will cause a heart murmur

44
Q

When Will You Hear Murmurs?

A

If a valve is stenotic, you will hear a murmur of blood shooting through the incomplete opening of the hardened valve

45
Q

Mitral Valve Stenosis

A

> Fibrous, stiff tissue, often causing chordae tendinae to shorten

> Incomplete opening of mitral valve obstructs blood flow- left atrium distension and impaired filling of left vent

46
Q

Mitral Valve Stenosis

Causes:

A

> RF- rheumatic fever (fever from inflam and pain in joints)

>Congenital

47
Q

Mitral Valve Stenosis

Manifestations:

A

Depends on severity of obstruction and related to elevation in left atrial pressure and pulm congestinon, decreased CO, impaired L vent filling, L atrial enlargement, atrial arrhythmias and mural thrombi

48
Q

Mitral Valve Stenosis

Complications:

A

Pulm congestion, paroxysmal dyspnea and orthopenea,

Palpations, chest pain, weakness, fatigue

49
Q

Mitral Valve Regurgitation (MVR)

and causes:

A

> Incomplete closing
Some blood returns to LA during systole_

Causes:

  • -RHD (rheumatic heart disease)
  • -Chordae tendineae or papillary muscle rupture
  • -LVH dilates orifice
  • -Mitral valve prolapse (floppy mitral valve syndrome)
50
Q

Mitral Valve Regurgitation

Manifestations:

A

> Slow process = compensation
Pulmonary congestion
Pansystolic heart murmur
L Atrial and LV hypertrophy

51
Q

Mitral Valve Regurgitation

complications:

A
  • -can be well tolerated, symptoms 6-10 yrs after diagnosis
  • -left vent becomes impaired
  • -forward stroke vol decresses
  • -left atrial pressure increases
  • -develop pulm congestion
52
Q

Mitral Valve Prolapse
associated with:

Manifestations:

Complications:

A

> Leaflets enlarge, become floppy

Associated with:
Marfan’s sydrome & Osteogensis imperfecta

Manifestations:
Often asymptomatic
Minority have chest pain-mimic angina, dyspnea, fatigue, anxiety, palpations, and light-headedness

Complications:

    • mainly asymptomatic
    • some ppl have chest pain mimicking angina
  • -dyspnea, fatigue, anxiety, palpitations, and light-headness
53
Q

Aortic Valve Stenosis

A

Narrowing causing resistance to ejection from vent into aorta. L vent wall becomes thicker
Slow progression = compensation

54
Q

Aortic Valve Stenosis

causes:

A

Congenital or acquired

Male, active inflammation

55
Q

Aortic Valve Stenosis

Manifestations:

A
  • -From auscultate- loud systolic ejection murmur or single paradoxically split second heart sound.
  • -Then angina, syncope, HF develop
56
Q

Aortic Valve Regurgitation

Causes:

A

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

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

57
Q

Chronic Aortic Regurgitation

Manifestations:

A

Slow progression = compensation
LV enlarges but works harder

Manifestations:
>high-pitched or blowing sound over valve
>Intra-aterial pulse pressure
>Korotkoff sounds persist to zero!
>Tachycardia or palpations, head pounding, premature vent contractions.
>Eventually orthopnea, dyspnea, paroxysmal nocturnal dyspnea

58
Q

Acute Aortic Regurgitation
Causes:

Manifestations:

A

Causes:
>Acute endocarditis
>Trauma
>Aortic dissection

Manifestations:
>Too quick for compensation!
>Extreme rise in volume to left vent.

Dysrhythmias = lethal

59
Q

Patent Ductus Arteriosus

Manifestations:

A

Persistent delay > 3 months

  • -Normally closes @ 24-72hrs
  • -Delay if premature

Manifestations:
Dependent on size
–continuous runoff from the of aortic blood to pulm artery.
– a large PD, runoff continuous resulting in increased pulm blood flow, pulm congestion and increased resistance against which the right side of the heart must pump

60
Q

Atrial Septal Defects

A

> Non-closure of foramen ovale
Often asymptomatic until teenage

Manifestations:
Increased pulmonary pressures

61
Q

Ventricular Septal Defects

A

Most common congenital heart defect
Cause:
Incomplete separation of ventricles during development invitro
1/3 close spontaneously

Manifestations dependent on size

62
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

63
Q

Tetralogy of Fallot

A

Most common cyanotic congenital heart defect

  1. Pulmonic outflow channel narrowing (valve)
  2. RV hypertrophy
  3. Ventricular septal defect- opening between L and R septum
  4. Displacement of aorta over vent septal defect
64
Q

Tetralogy of Falot
Manifestations:

Treatment:

A

Manifestations:
Cyanosis with increased oxygen demands

Treatment:
Knee-chest position
Surgery

65
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 most common

66
Q

Coarctation of the Aorta

A

Associated with other congenital lesions

Manifestations:
–disparity in pulsations and BPs in arms and legs

Patho test 1 (4 decks)

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