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Pathophysiology > Class 2 chapter 19 > Flashcards

Class 2 chapter 19 Flashcards

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1
Q

Pericarditis

A

Inflammation of pericardium (outside of heart)

Acute =

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2
Q

Pericarditis manifestations

A 
Decreased CO
Pericardial friction rub
Chest pain (precordial - right where heart is, 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

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4
Q

Cardiac tamponade

A

Compression d/t fluid or blood

Emergency situation

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5
Q

Cardiac tamponade causes

A

Trauma (MVA)
Myocardial rupture post MI
Cardiac surgery
Aortic dissection

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6
Q

Cardiac tamponade manifestations

A

Dependent on amount and rapidity
Limits stroke volume (amount that leaves with every heartbeat) and CO = low SBP (CNS = change in mentation, resps = dyspnea and tachypnea, CVS = chest pain and tachycardia)
Elevated central venous pressure (pressure in R atrium) and jugular venous pressure
Circulatory shock (not getting blood pumped properly to organs)

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7
Q

Cardiac tamponade diagnosis

A

Muffled heart sounds (extra sac of fluid around heart so won’t be able to hear lub dub as easily)
Pulsus paradoxus (>10 mmHg fall with respirations, abnormally large decrease in SBP during inspiration)
ECG (decreased voltage)
Echocardiogram (can see if fluid is around heart)
CT, MRI

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8
Q

Coronary artery disease = coronary heart disease

A

Heart disease caused by impaired flow to coronary arteries

Chronic or acute

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9
Q

Non-modifiable risks for coronary artery disease

A

Sex/gender (men> women, post-menopausal women)
Age
Ethnicity
Genetics

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10
Q

Variant/prinzmetal angina

A 
D/t spasms of coronary artery
Cause is unclear
Often at night
Variable symptoms
Treatment is dependent on findings of investigative diagnostics
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11
Q

Acute coronary syndrome

A

Looking at ST segment elevation (ischemia to heart muscle)
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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12
Q

Acute coronary syndrome causes

A

Unstable plaque, rupturing to form a clot (thin fibrous cap with fatty core is most unstable)
Coronary vasospasm (spasms of artery)
Atherosclerotic narrowing (progressive)
Inflammation/infection
Secondary causes (anemia - during surgery, fever - makes heart muscle pump harder, hypoxemia)

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13
Q

ST elevation MI

A

Ischemic death of myocardial tissue
Cardiac muscle wall schema and necrosis (subendocardial, transmural = Q wave - big, “stunned” myocardium)
Cell death in 15-20 minutes
Early perfusion and revascularization can prevent necrosis

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14
Q

ST elevation MI manifestations

A 
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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15
Q

Myocardial ischemia/necrosis results in

A

Decreased contractile force (decreased CO, coronary artery perfusion, pulmonary vasculature pressure - pressure in system backs up to lungs)
Interruption of conduction (dysrhythmias)

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16
Q

MI diagnosis

A

Based on serum biomarkers
Troponin (rises within 2-3 hours, remains 7-10 days, serial = multiple so you know where they are in heart attack)
Myoglobin (rises within 1 hour, peaks at 4 hours, also from skeletal muscle damage)
Creatine Kinase MB (peaks at 4-6 hours, gone in 2-3 days, specific to cardiac muscle)

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17
Q

Acute MI treatment

A

Oxygen
Pain relief
Reperfusion (fibrionolytics - break up clots, percutaneous transluminal coronary angioplasty PCTA - put balloon in artery and expands to open up artery, stents)
Coronary Artery Bypass Grafting CABG (vein from another part of body and transplant it into heart)

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18
Q

Acute MI complications

A

Arrhythmias – most common cause of sudden death
Reinfarction
Heart failure
Pericarditis
Embolic CVA or Pulmonary embolus
Valve deformities (have to work properly for blood flow)
Septal rupture (separates ventricles)
LV wall aneurysms/rupture
Cardiogenic shock (heart unable to deliver oxygenated blood to brain)
Dressler syndrome

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19
Q

Idiopathic cardiomyopathy

A

Muscle disorders (mechanical - heart failure, electrical - arrhythmias)
Primary
Secondary

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20
Q

HCM manifestations

A

Variable
Decreased stroke volume d/t impaired diastolic filling (dyspnea, chest pain, syncope (passing out) post exertion)
Atrial fibrillation
Lethal ventricular arrhythmias

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21
Q

Endocarditis

A

Any infection of inner lining of heart (usually staphylococcus aureus, vegetative - things starting to grow, involvement of mitral and aortic valves most common)
Acute - relatively healthy individual
Sub-acute/chronic - h/o valve abnormalities

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22
Q

Rheumatic heart disease

A

Caused by rheumatic fever (which occurs after streptococcal pharyngitis, sore throat, fever, NV, joint pain, headache, one or all layers - pancarditis, valves, aschoff bodies - see on heart under microscope)
Immunological response but pathogenesis unclear
Acute, chronic or recurrent
Acute phase = pancarditis (pericardial friction rub, murmur, mitral/aortic valve involvement, arrhythmias)

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23
Q

Rheumatic heart disease diagnosis

A

Evidence of GAS (group A) infection
Elevated WBC, ESR, CRP
Echocardiogram
Ultrasound (can see valve moving and how much blood is going through)

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24
Q

Rheumatic heart disease treatment

A

Antibiotics

Prevention of complications

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25
Valvular disorders causes
``` Congenital (from childhood) Trauma Ischemic damage Degenerative changes (vegetation growing over time) Inflammation ```
26
Valvular disorders diagnosis
Auscultation Doppler Echo Ultrasound
27
Valvular disorders treatment
``` Preventative APA (antiplatelet aggregator) Symptoms Percutaneous valvuloplasty (fixing valve) Surgery ```
28
Mitral valve stenosis
Fibrous, stiff tissue, often causing chordae tendineae to shorten Incomplete opening obstructs blood flow
29
Mitral valve stenosis causes
RF | Congenital
30
Mitral valve regurgitation causes
RHD (rheumatic heart disease) Chordae tendineae or papillary muscle rupture LVH dilates orifice (opening) Mitral valve prolapse (flops back when shouldn't)
31
Aortic valve stenosis
Narrowing causing resistance to ejection | Slow progression = compensation
32
Aortic valve stenosis causes
Congenital or acquired | Male, active inflammation
33
Aortic valve regurgitation causes
RHD, ideopathic aortic dilation, congenital, endocarditis, Marfans, HPTN, trauma
34
Chronic aortic regurgitation
Slow progression = compensation | LV enlarges but works harder
35
Acute aortic regurgitation causes
Acute endocarditis Trauma Aortic dissection
36
Heart disease in infants and children
``` Patent ductus arteriosus Atrial septal defects Ventricular septal defects Pulmonary stenosis Tetralogy of fallout Transposition of the great arteries Coarctation of the aorta ```
37
Heart disease in infants and children
``` Patent ductus arteriosus Atrial septal defects Ventricular septal defects Pulmonary stenosis Tetralogy of fallout Transposition of the great arteries Coarctation of the aorta ```
38
Patent ductus arteriosus
Persistent delay >3 months Normally closes at 24-72hrs Delay if premature
39
Patent ductus arteriosus manifestations
Dependent on size | High pressure from aorta = pulmonary hypertension
40
Ventricular septal defects
Most common congenital heart defect (25-30% of all)
41
Ventricular septal defects causes
Incomplete separation of ventricles during development invitro 1/3 close spontaneously
42
Ventricular septal defects manifestations
Dependent on size Asymptomatic = heart failure Tachypnea, tachycardia, pulmonary congestion, failure to thrive
43
Pulmonary stenosis
Obstruction of blood flow from RV
44
Pulmonary stenosis causes
Pulmonary valve lesions Pulmonary artery lesions Combination
45
Tetralogy of fallot
Most common cyanotic congenital heart defect (5-7% of all) 1. Pulmonic narrowing 2. RV hypertrophy 3. Ventricular septal defect 4. Dextroposition of aorta (over-rides RV, attaches to septal defect)
46
Tetralogy of fallot manifestations
Cyanosis with increased oxygen demands (crying, feeding, defecation) Loss of consciousness possible
47
Tetralogy of fallot treatment
Knee-chest position | Surgery
48
Transposition of the great arteries
RV empties into aorta | LV empties into pulmonary arteries
49
Transposition of the great arteries risk factors
Mothers with diabetes | Boys > girls
50
Transposition of the great arteries manifestations
Cyanosis | Survival if patent ductus arteriosus or septal defect
51
Coarctation of the aorta
Associated with other congenital lesions
52
Coarctation of the aorta manifestations
BP lower in legs than in arms Asymptomatic Hypertension later in life LVH
53
Pericarditis causes
``` Viral Bacterial Uremia (kidneys – a lot of toxins in blood) Neoplastic (cancer) Radiation Trauma Drug toxicity ```
54
Pericarditis complications
Pericardial Effusion Cardiac Tamponade Dressler Syndrome (post heart attack)
55
Pericardial effusion causes
``` Inflammation of pericardium Infection elsewhere Neoplasms (tumours) Cardiac surgery Trauma ```
56
Cardiac tamponade treatment
Immediate pericardiocentesis (removal of fluid in pericardium)
57
Dresslers syndrome
Pericarditis that happens after heart attack Usually 4-6 weeks Self-limiting (rarely leads to tamponade)
58
Dresslers syndrome manifestations
Low grade fever Pleuritic pain Pericardial friction rub and/or effusion
59
What assists coronary artery flow?
Endothelial cells lining arteries Diastolic pressure in aorta (able to fill arteries) Time in diastole (the faster your heart goes, the less time to fill arteries)
60
What impairs coronary artery flow?
Atherosclerosis
61
Modifiable risks for CAD
``` Hypertension Hyperlipidemia Tobacco use Diabetes Obesity Sedentary lifestyle/physical inactivity Ability to cope with stress ```
62
Stable angina
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 and nitroglycerine (helps to open up arteries in heart and increase flow)
63
Silent MI
More likely in the elderly (less myocardium involved, neuropathy - neurological issues because of another disease processes. hypotension, low body temp, vague complaints of discomfort, mild diaphoresis, stroke-like symptoms, dizziness, sensorium changes)
64
Unstable angina/non ST MI 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 (blood values) are elevated = non-STEMI High risk of STEMI
65
Cardiomyopathies
``` Cardio = heart Myo = muscle Pathy = disorder/syndrome/bad stuff ```
66
Hypertrophic cardiomyopathy (HCM)
Leading cause of sudden cardiac death in young adults Unexplained genetic ventricular septal thickening Poor diastolic filling LV outflow obstruction Left ventricular hypertrophy (LVH) Disruption of normal conduction pathways
67
Endocarditis risk factors
Infection elsewhere Dental surgery/surgery, IV drug use/contaminants Immunodeficiency/immunosuppression Valve prolapse (sudden or congenital)
68
Endocarditis manifestations
Signs and symptoms of systemic infection Heart sound changes (lub dub sounds different) Symptoms related to embolism
69
Endocarditis complications
Emboli (lung, renal, brain) Valve dysfunction Arrhythmias
70
When will you hear a murmur?
If a valve is stenotic (stiff), you will hear a murmur of blood shooting through the narrow opening when the valve is open If a valve is regurgitant (going backwards), you will hear a murmur of blood leaking back through when the valve should be closed
71
Mitral valve stenosis manifestations
Chest pain, weakness, fatigue, palpitations
72
Mitral valve stenosis complications
Arrythmias (atrial fibrillation, atrial tachycardias) | Mural thrombi
73
Mitral valve regurgitation
Incomplete closing | Some blood returns to LA during systole
74
Mitral valve regurgitation manifestations
Slow process = compensation Pulmonary congestion Pansystolic murmur L Atrial and LV hypertrophy
75
Mitral valve regurgitation complications
Atrial fibrillation | Thrombus
76
Mitral valve prolapse
Leaflets enlarge, become “floppy” | Associated with connective tissue disorders (mar fan’s syndrome, osteogensis imperfecta)
77
Mitral valve prolapse manifestations
“Snap” Asymptomatic Chest pain, dyspnea
78
Mitral valve prolapse complications
Mital valve regurgitation Atrial fibrillation Thrombus
79
Aortic valve stenosis manifestations
Chest pain, dyspnea, syncope, heart failure (LV hypertrophy)
80
Aortic valve regurgitation
Scarring of leaflet and/or enlarged orifice | Blood flow back into LV during diastole
81
Chronic aortic regurgitation manifestations
Blowing sound over valve Widening pulse pressure (difference between systolic and diastolic) Korotkoff sounds persist to zero! Tachycardia or water hammer pulse (heart pumps really hard and strength of pulse is very exaggerated) “Pounding” of heart when lying down Eventually orthopnea, dyspnea, paroxysmal nocturnal dyspnea
82
Acute aortic regurgitation manifestations
Too quick for compensation Extreme rise in LVEDP (left ventricular end diastolic pressure) = pulmonary edema (decreased coronary artery perfusion) Dysrhythmias = lethal

Pathophysiology (13 decks)

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