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PATHO 2 > Cardiovascular > Flashcards

Cardiovascular Flashcards

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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
Manifestations of Aortic Dissection
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
26
Aortic Dissection emergency Pharm
beta blockers nitrates
27
What does aortic dissection need RIGHT AWAY
surgery - minutes count
28
Printzmetal's Variant Angina =
Coronary Artery Vasospasm (Supply Ischemia)
29
Chronic stable angina =
fixed stenosis (Demand Ischemia)
30
Unstable Angina =
Thrombus (Supply Ischemia)
31
3 conditions in Acute coronary syndromee
unstable angina non ST elevation MI - NSTEMI ST Elevation MI - STEMI
32
define unstable angina
new or changing chest pain caused by ischemia
33
define NSTEMI
non-ST segment elevation myocardial infarction
34
define STEMI
ST segment elevation myocardial infarction
35
Cuase of Prinzmetal angina
Coronary artery spasm Underlying cause?? Endothelial dysfunction 
36
characteristics of prinzmetal angina
Unique features CAD may or may not be present Onset timing Rest, minimal exertion, night  Specific ECG changes Elevated ST segment
37
unstable plaque in ACS with size of lipid core inflammation smooth muscle cells
Size of lipid core? Large Inflammation? Active Smooth muscle cells? Proliferation into intima
38
Are cardiac enzymes elveated in unstable angina?
NO
39
Theory of Plaque Rupture
``` 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
contributing factores to SNS increase
psychological stress exercise circadian rhythms
41
S/S of MI
``` 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
What is acute MI
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
In Acute MI myocardial cells suffer
irreversible ischemic necrosis and will not function properly again
44
How are MIs classified
STEMI NSTEMI by ECG findings
45
Process from ischemia to infarction
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
3 zones of Heart damage
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
interventions to prevent patient to extend size of the infarction
Increase O2 decrease heart demand
48
extent of damage of ACUTE MI is influenced by 3 factors
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
what is the left anterior descending Artery
The LAD artery supplies the left ventricle Most commonly involved in myocardial infarction.
50
Initial Tx of Acute MI
``` 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
Immediate STEMI Pharm
``` 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
STEMI Fibrinolytic therapy DRUG
Alteplase (tPA)
53
Alteplase (tPA) MOA
Dissolves clot by converting plasminogen into plasmin
54
ADV/DISAdv of Alteplase
Advantages? Most effective  Disadvantages? Works best within 30 – 70 minutes
55
A/E of Alteplase
Bleeding
56
Alteplase is always given with
heparin and antiplatelet therapy
57
what is Nitroglycerine used for
Severe hypotension | Particularly with other nitrates
58
Do not aminister WHAT with Nitroglycerine
Do not administer with sildenafil (ViagraR) | Risk of severe hypotension
59
what is myocardial stunning
Rapid restoration of blood flow to the myocardium also contributes to injury
60
what is myocardial stunning caused by
oxidized free radicals generated by WBCs and the cellular response to restored blood flow.
61
Key info about MI
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
Key info about MI
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
Interventions for reperfusion
Angioplasty and atherectomy Angioplasty and stent placement Coronary artery bypass graft (CABG)

PATHO 2 (1 decks)

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