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PATHO 2 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is myocarditis

A

An inflammatory disease of the myocardium (muscle layer of the heart) that can range from a mild disorder to a lethal condition.

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2
Q

What does the inflammation in myocarditis cause

A

degeneration and necrosis of cardiac myocytes.

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3
Q

what is common in myocarditits

A

conduction disruption

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4
Q

most common cause of myocarditis

A

Coxsackie viruses A and B

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5
Q

what is pericarditis

A

When the pericardium undergoes inflammation, fluid accumulates in the pericardial space.

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6
Q

fluid in pericarditis is called

A

pericardial effusion

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7
Q

What is cardiac tamponade

A

fluid accumulates to high levels of 200 mL or greater
compresses the heart
causing a condition called cardiac tamponade.

In cardiac tamponade,
heart chambers are restricted by the surrounding pericardial fluid so they cannot stretch and fill with blood

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8
Q

signs of acute pericarditis

A

Chest pain; sharp and worsens with deep breathing

Fever

Dyspnea

Pericardial friction rub: scratching sound can be heard through the stethoscope

ECG findings of ST elevations

Beck’s triad

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9
Q

Symptoms of cardiac tamponade

A

Beck triad:

hypotension
JVD
muffled heart sounds

Pulsus paradoxus occurs in 70% to 80% of patients with cardiac tamponade

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10
Q

what is pulsus paradoxus

A

Pulsus paradoxus is exhibited by a decrease in systolic blood pressure of 10 mm Hg or more with inspiration.

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11
Q

Pericarditis Tx

A 
NSAIDs
/
ASA
/
Corticosteroids (+/-) 
/
Colchicine
\+Typically for gout
\+Recently for pericarditis refractory to NSAIDs
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12
Q

Patho of Aneurysms

A

Hypertension weakens the walls of arteries, increasing development of bulges in arterial walls called aneurysms.

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13
Q

Aneurysms cause what

A

turbulent blood flow and are suceptible to rupture

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14
Q

what may be heard of aneurysms

A

Bruits

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15
Q

what are the most common areas for aneurysm

A

Aorta

Cerebral arteries

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16
Q

What are some common aneursyms

A

Abdominal aortic aneurysm
+ above or below renal artery

Thoracic aortic aneurysm

Cerebral

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17
Q

What are some variations of aneurysms

A

Dissecting aortic aneurysm

false (psudo) aneurysm

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18
Q

what is a saccular aneurysm

A

Saccular (balloon shaped)

Involves only one part of circumference

Wide neck

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19
Q

What is a fusiform aneurysm

A

Entire circumference of vessel

Gradual/progressive dilatation

Potentially extensive involvement

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20
Q

what are Berry Aneursyms

A

Subtype of saccular

Small neck

Located at bifurcation

Common Location:
Circle of Willis

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21
Q

What is a False (Psudo) aneurysm

A

Localized dissection or tear in inner artery wall

Type of hematoma

Complication of vascular interventional procedures

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22
Q

Presentation of Abdominal Aortic Aneurysm

A

Auscultation of a bruit over the abdominal aorta suggests the presence of an aneurysm.

If a pulsatile mass is evident in the abdomen during inspection or light palpation, deep palpation should not be performed until the possibility of AAA is ruled out.

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23
Q

Biggest complication of aneurysms

A

RUPTURE

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24
Q

What is a dissecting aneurysm

A

Layers of the wall of the artery are separated and blood enters the region.

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25
Q

Manifestations of Aortic Dissection

A

severe, tearing pain

Early stages
Blood pressure is elevated

Later stages
BP may be unobtainable
Syncope, hemiplegia, paralysis of lower extremities
Cardiovascular collapse -> shock -> death

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26
Q

Aortic Dissection emergency Pharm

A

beta blockers

nitrates

27
Q

What does aortic dissection need RIGHT AWAY

A

surgery - minutes count

28
Q

Printzmetal’s Variant Angina =

A

Coronary Artery Vasospasm (Supply Ischemia)

29
Q

Chronic stable angina =

A

fixed stenosis (Demand Ischemia)

30
Q

Unstable Angina =

A

Thrombus (Supply Ischemia)

31
Q

3 conditions in Acute coronary syndromee

A

unstable angina

non ST elevation MI - NSTEMI

ST Elevation MI - STEMI

32
Q

define unstable angina

A

new or changing chest pain caused by ischemia

33
Q

define NSTEMI

A

non-ST segment elevation myocardial infarction

34
Q

define STEMI

A

ST segment elevation myocardial infarction

35
Q

Cuase of Prinzmetal angina

A

Coronary artery spasm

Underlying cause??
Endothelial dysfunction

36
Q

characteristics of prinzmetal angina

A

Unique features
CAD may or may not be present

Onset timing
Rest, minimal exertion, night

Specific ECG changes
Elevated ST segment

37
Q

unstable plaque in ACS with

size of lipid core

inflammation

smooth muscle cells

A

Size of lipid core?
Large

Inflammation?
Active

Smooth muscle cells?
Proliferation into intima

38
Q

Are cardiac enzymes elveated in unstable angina?

A

NO

39
Q

Theory of Plaque Rupture

A 
Increased SNS activity
/
↑ BP, HR, & force of contraction
/
↑ force of coronary artery blood flow
/
↑ force exerted against injured endothelium
/
Plaque Rupture!
/
Platelets adhere to ruptured plaque
/
Release substances that 1) attract more platelets
and 2) contribute to vasospasm
/
Thrombus Formation
40
Q

contributing factores to SNS increase

A

psychological stress

exercise

circadian rhythms

41
Q

S/S of MI

A 
Diaphoresis
Dyspnea
Extreme anxiety
Levine’s sign (fist to chest)
Pallor
Retrosternal crushing chest pain that radiates to shoulder, arm, jaw, or back
Weak pulses
42
Q

What is acute MI

A

Ruptured plaque + thrombus
Why is there an infarction?
Blood flow disruption is prolonged

OR

Blood flow disruption is total
ECG changes? ______
Cardiac enzymes elevated? troponin levels increase with infarction but should decrease when relieved

43
Q

In Acute MI myocardial cells suffer

A

irreversible ischemic necrosis and will not function properly again

44
Q

How are MIs classified

A

STEMI
NSTEMI

by ECG findings

45
Q

Process from ischemia to infarction

A

What is ischemia?O2 deficiency
/
Importance of adenosine triphosphate (ATP)

Main energy source for cell function
Myocardial cells can not store ATP = need continuous source
/
Irreversible injury occurs within 
30 min.- 4 hr
/
Tissue necrosis begins by 4 hours
/
Necrotic tissue is cleared away by
 1-2 weeks
/
Tough fibrous scar tissue replaces necrotic tissue by 6 weeks
/ 
Infarction? Tissue death
46
Q

3 zones of Heart damage

A

Infarction = necrosis

  • mi,dead cells
  • beyond hope of revocery but can stop it from increasing

Injury

  • some recovery possible
  • can still perfuse it and restore it to become viable
  • not dead yet

Ischemia
-full recovery possible

47
Q

interventions to prevent patient to extend size of the infarction

A

Increase O2

decrease heart demand

48
Q

extent of damage of ACUTE MI is influenced by 3 factors

A

Location or level of occlusion in the coronary artery

Length of time that the coronary artery has been occluded

Heart’s availability of collateral circulation.

49
Q

what is the left anterior descending Artery

A

The LAD artery supplies the left ventricle

Most commonly involved in myocardial infarction.

50
Q

Initial Tx of Acute MI

A 
Oxygen
Morphine *
Aspirin
Nitroglycerin
Beta-blocker (if no contradictions)**

Thrombolytic agent *** if patient is eligible. Ideally, thrombolytic agents are used within 4-6 hours of the beginning of the MI.

51
Q

Immediate STEMI Pharm

A 
Oxygen
Increase 02 delivery to ischemic myocardium
/
Aspirin
Suppresses platelet aggregation
Decreases mortality 
Chew first dose
/
Morphine
Decreases pain
Reduces preload and afterload
Helps preserve ischemic tissue
/
Beta Blocker (only if not contradicted)
Reduce HR and contractility (reduce oxygen demand)
Reduces pain, infarct size, and mortality
/
Nitroglycerin
Reduces preload and afterload, limits infarct size
Does not reduce mortality
52
Q

STEMI Fibrinolytic therapy DRUG

A

Alteplase (tPA)

53
Q

Alteplase (tPA) MOA

A

Dissolves clot by converting plasminogen into plasmin

54
Q

ADV/DISAdv of Alteplase

A

Advantages?
Most effective
Disadvantages?
Works best within 30 – 70 minutes

55
Q

A/E of Alteplase

A

Bleeding

56
Q

Alteplase is always given with

A

heparin and antiplatelet therapy

57
Q

what is Nitroglycerine used for

A

Severe hypotension

Particularly with other nitrates

58
Q

Do not aminister WHAT with Nitroglycerine

A

Do not administer with sildenafil (ViagraR)

Risk of severe hypotension

59
Q

what is myocardial stunning

A

Rapid restoration of blood flow to the myocardium also contributes to injury

60
Q

what is myocardial stunning caused by

A

oxidized free radicals generated by WBCs and the cellular response to restored blood flow.

61
Q

Key info about MI

A

Acute MI is the leading cause of death in the United States and in other industrialized nations throughout the world.

Hesitation and delayed request for emergency care are major causes of death because of MI.

Survival rates for treated patients with acute MI are 90% to 95% in the United States.

Approximately 50% of individuals who suffer an MI are younger than 65 years old.

Persons with diabetes and those older than age 65 often suffer silent, asymptomatic MI.

62
Q

Key info about MI

A

Acute MI is the leading cause of death in the United States and in other industrialized nations throughout the world.

Hesitation and delayed request for emergency care are major causes of death because of MI.

Survival rates for treated patients with acute MI are 90% to 95% in the United States.

Approximately 50% of individuals who suffer an MI are younger than 65 years old.

Persons with diabetes and those older than age 65 often suffer silent, asymptomatic MI.

63
Q

Interventions for reperfusion

A

Angioplasty and atherectomy

Angioplasty and stent placement

Coronary artery bypass graft (CABG)

PATHO 2 (1 decks)

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