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Patho > chapter 19 > Flashcards

chapter 19 Flashcards

1
Q

Disorders of Cardiac function (5)

A
  1. Coronary Artery Disease
  2. Endocardial and Valvular Disorders
  3. Disorders of the Pericardium
  4. Cardiomyopathies
  5. Heart Disease in Infants and Children
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2
Q

Coronary Artery Disease

A
  • atherosclerosis blocks coronary arteries

- ischemia causes: angina, heart attack, cardiac arrythmias, conduction deficits, heart failure, death.

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3
Q

most common cause of coronary artery disease

A

atherosclerosis

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4
Q

stable plaques

A

cause ischemia and some problems

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5
Q

unstable plaques

A

soft, mushy necrotic core that are easily broke off.

  • lead to thrombosis formation
  • can create ischemia in coronary vessels (Heart Attack, changes in conduction fo the heart, angina, death)
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6
Q

angina

A

chest pain

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7
Q

Acute Coronary Syndromes

A

things that cause reduced blood flow to muscle cells of the heart

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8
Q

how do you diagnose acute coronary syndromes?

A

ECG changes

  • T wave inversion
  • ST segment is depressed or elevated
  • Abnormal Q wave
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9
Q

ischemia disrupts which wave of an ECG the most?

A

ST wave
- disrupts the repolarization process of ST. makes a shorter action potential, less time in between depolarization and repolarization.

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10
Q

PQRST wave
P-
QRS-
T-

A

P- Atrial Depolarization
QRS- Ventricular Depolarization
T- Ventricular Repolarization

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11
Q

serum cardiac markers

A
  1. Creatine Kinase- (CK-MB) specific to cardiac muscle
  2. Troponin- TnI and TnT specific to cardiac muscle
  3. Myoglobin- not specific to cardiac muscle
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12
Q

Cardiac Panel

A

tests the serum cardiac markers (proteins)

  1. creatine kinase (CK-MB)
  2. Troponin ( TnI and TnT)
  3. Myoglobin
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13
Q

Creatine Kinase (CK-MB)

A
  • specific to only heart cardiac muscle cells
  • shows up 4-8 hours after damage
  • if specifically present in blood, can say the heart is damaged.
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14
Q

Troponin (Tnl and TnT)

A
  • can tell if troponin is coming from damaged heart cells vs damaged muscle cells. (Tnl and TnT)
  • can stay high from 3 hours-10 days
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15
Q

Myoglobin

A

found in cardiac and skeletal muscle (nonspecific marker)

  • if paired with Tnl, TnT, or CK-MB you can say its myocardial cell death
  • shows up in 1 hour
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16
Q

Unstable Aginga

A

less severe form of ischemia; no serum biomarkers

  • cardiac cells haven’t diet
  • from formation of stable plaques! not going to break off and kill you.
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17
Q

NSTEMI- non stemi myocardial infarction

A
  • non ST MI
  • result of atherosclerotic heart disease specifically formation of STABLE PLAQUE.
  • occurs at rest and lasts 20 minutes, pain is severe an d new onset.
  • TREATMENT: Nitroglycerin (vasodilator)
  • No elevation of ST- complex on ECG
  • presence of serum biomarkers
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18
Q

STEMI

A
  • ST elevation myocardial infarction
  • transmural: loss of supply to endocardium, myocardium, epicardium ( all 3 layers of heart)
  • Subendocardial: loss to inner 1/3 to 1/2 of ventricular wall. only affects part of the cardiac wall.
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19
Q

Transmural means:

A

all 3 layers of the heart have lost blood supply

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20
Q

STEMI is not relieve by ___

A

Nitroglycerin

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21
Q

STEMI symptoms:

A
  • chest pain: severe, crushing, constrictive
  • Sympathetic NS response: GI distress, Tachycardia, Anxiety, vasoconstriction, nausea, vomiting
  • Hypotension and shock- weakness in arms and legs
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22
Q

STEMI- Plan of action

A
  1. Reperfusion Therapy
  2. 12-lead ECG assessment- STEMI or NSTEMI?
  3. Pharmaceutical therapy
  4. Reestablishment of blood flow
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23
Q

Pharmaceutical therapy for STEMI

A
  • Pain management: Morphine
  • Anticoagulants and O2- Aspirin
  • Sympathetic NS antagonists (slow HR)
24
Q

the most important thing you can do when PT has a stemi

A
  • reestablish blood flow
25
Q

Complications of Acute Myocardial Infarctions

A
  • heart failure
  • thromboemboli (stroke)
  • ventricular aneurysms (^ shockable rhythm)
26
Q

Chronic Stable Anging (chest pain)

A
  • imbalance in blood supply and the heart’s O2 demands
  • Pain is similar to ACS but: occurs with exertions
    * recurrent
    * relieved with nitroglycerin
27
Q

chronic stable angina’s get worse with ___

A

anything that ^ oxygen demand

  • stress
  • exercise
  • cold
28
Q

chronic stable angina diagnosis and treatment:

A

D: pain history, risk factors, imaging/ECG, labwork

T: lifestyle modification, drugs (beta blockers, vasodilators, calcium channel blockers)

29
Q

ischemic heart disease is characterized by ____ which is associated with stable plaques.

A

stable angina

30
Q

____ is characterized by plaques with platelets stuck to them (likely to form a thrombus); they cause a range of acute coronary syndromes.

A

Unstable Angina

31
Q

__ and __ open during systole and close during diastole

A

Bi and Tricuspid Valves

32
Q

___ and __ valves open during diastole and close during systole

A

AV and PV

33
Q

Valve defects: 2

A

stenosis

regurgitation

34
Q

Stenosis

A
  • the valve won’t open all the way.
  • it’s harder to force blood through it.
  • will hear murmur of blood shooting through the narrow opening when the valve is open.
35
Q

Regurgitation

A
  • the valves won’t close all the way.
  • it leaks when “closed”
  • will hear a murmur of blood leaking back through when the valves should be closed.
36
Q

valve defects most commonly show up :

A

on the left side of the heart : mitral (bicuspid) valve

37
Q

Mitral valve disorders: 2

A
  1. Mitral valve regurgitation: goes back into left atrium
  2. Mitral valve prolapse: result of valves that become enlarged and lose some of their structural rigidity. too big and floppy so they swing back and forth instead of closing and opening properly.
38
Q

Aortic Valve Disorders (2)

A
  1. Aortic Valve Stenosis- calcification means ^ hypertrophy of left side
  2. Aortic Valve Regurgitation- valve doesn’t close properly
39
Q

when someone has an aortic valve disorder, they __-

A
  • have difficulty breathing, chest pain and discomfort

- become really aware of their heartbeat when lying down. making it hard for them to sleep.

40
Q

stenosis creates ___ pressure in aorta which means it’s not pumping enough blood to other areas of the body.

A

decreased pressure

41
Q

Lub

Dub

A

Lub- closing AV valves, called S1

Dub- closing SV valves, called S2

42
Q

Pericarditis

A

inflammation of the pericardium- release of inflammatory exudate into pericardial space

43
Q

Symptoms of pericarditis

A
  1. Sharp, radiating pain- made worse by inhaling or coughing
  2. Responsive to NSAIDS- asprin/tylenol make it go away
  3. Fever w/pericardial friction
44
Q

Most chest pain can be treated using this acronym

A 
MONA
Morphine
Oxygen
Nitroglycerin
Aspirin
45
Q

Pericarditis Diagnosis and Treatment

A

D- evaluate pain (sharp or compressed)
Auscultation- usually in neck, back, or abdomen
ECG- ST shape and distance diff than MI
Lab Testing: cardiac panel (inflam. precursors)

T- bacterial: antibiotic
viral: NSAIDS, steroid, but most often you ride it out.

46
Q

Inflammation of the pericardium may restrict the heart’s movement due to:

A
  1. Serous exudate filling the pericardial cavity (pericardial effusion)
  2. Fibrous scar tissue making the pericardium stick to the heart (constrictive pericarditis)
47
Q

Pericardial Effusion

A
  • accumulation of fluid in the pericardial cavity
  • inhibits chamber in heart filling
  • ECG shows “dampened signals
  • treatment is focused on fluid removal
48
Q

Fluid removal for Pericardial Effusion

A
  • Diuretics
  • NSAIDS
  • Pericardiocentesis- stick needle in chest, pull fluid out
49
Q

Cardiac Tompanade

A
  • pericardial effusion on steroids*
  • have so much fluid in pericardial sac that its pushing on the heart and it can’t pump.
  • signs: jugular vein distention, lowered systolic BP
  • may hear muffled heart sounds (bc of fluid) ^ HR
50
Q

Consequences of pericardial effusion

A
  1. BP and CO drop
  2. decreased BP can cause cardiogenic shock
  3. left ventricle can’t fill all the way
  4. right ventricle cant accept enough blood
51
Q

In pericardial effusion, what does the right ventricle not accepting enough blood do the body?

A

you get an increase in venous pressure and it creates jugular distension

52
Q

on inhaling, the right ventricle overfills with blood, this is called:

A

Pulsus Paradoxis

53
Q

Pulsus Paradozis

A
  • R ventricle fills too much with blood
  • L Ventricle gets squished and cant take in as much
  • decreased CO and decreased BP
  • may need Pericardiocentresis- needle into heart to suck out fluid
54
Q

Cardiomyopathies: definition

A

disease of heart muscle that makes it harder to pump blood to the rest of your body.

55
Q

Hypertophic cardiomyopathy

A
  • defects in contractile proteins that makes cells too weak
  • heart has to compensate, so intraventricular septum hypertrophies
  • the septum becomes so large it cuts off Aortic Valve
  • decreased Bp and ^ chance of fibrilation.

Patho (18 decks)

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