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Pathophysiology > Patho: Cardiovascular > Flashcards

Patho: Cardiovascular Flashcards

1
Q

What is Coronary Artery Disease?

A

A condition that includes “Angina Petoris” and “myocardial Infarction”

These result from decreased O2 to the heart

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2
Q

How does the coronary circulation work?

A

It is the circulation around the heart muscle (myocardium)

It is Intermittent and Pulsating.

Blood flow is ineffective during ventricular contraction b/c of the compression by the contracting myocardium to pump out blood.

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3
Q

What is Anastomoses?

A

-They are Networks of fusing arteries in the coronary circulation.
This helps explain why, if the cornary ateries are bocked, how the heart can still manage to get nutrients.
-Regular aerobic (w/ O2) exercise contributes to cardiovascular fitness by stiulating the development of collateral channels.

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4
Q

What are collateral channels?

A

Secondary channels for blood flow.

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5
Q

What is ARTeriosclerosis?

A

A term used referring to conditions that cause arterial changes.

  • Degenerative changes to the arteries and arterioles >50yrs olds.
  • Leads to ischemia and necrosis in various tissues

Common in the Kidney: Renal failire, brain:Stroke, and heart: MI.

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6
Q

Patho of ARTeriosclerosis

A
  • Aging makes the vessel walls lose elasticity.
  • Narrowed lumens are caused by the vessel walls hardening and thickening.
  • Ischemia can result from complete obstruction of the vessles
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7
Q

What is ATHEROsclerosis

A

A condition which involves the presence of “Atheromas” which blocks the circulation and weakens the arteries.

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8
Q

What are Atheromas?

A
  • Deposits of lipids, cells, fibrin, and cellular debris.
  • Often have attached clots.
  • Form inside the vessel walls, primarily in the large arteries, the coronary arteries, carotid arteries.
  • They occlude blood flow.
  • They initially start off as fatty streaks, then becomes larger and begins to project into the lumen of the vessel.
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9
Q

Patho of ATHEROsclerosis

A

1) The formation of atheromas beings with endothelial injury to the arteries (young age)
2) injury causes inflammation, leading to the accumulation of WBC’s and lipids at the surface of the lining and inside the layer of smooth muscle.
3) Smooth muscle will proiliferate in resonse to this, and will lead to the formation of plaque.
4) Lipids and fibrous tissue (to replace damaged tissue) then gather and accumulate, increasing the size of the plaque.
5) As plaque increases in size, inflammation continues and the cyles of inflammation and deposit continues.

(Formation of Atheromas from injury–> inflammation and accumulation of WBC and lipids –> Proliferation as a response creating plaque –> accumulation of lipids and fibrous tissues –> plaque increases)

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10
Q

More patho of ATHEROsclerosis

A
  • Blood flow progressively decreases b/c the lumen narrows and pressure increases (which could create an embolism)
  • Plaque may rupture resulting in the formation of a clot and total obstruction of the vessel.
  • Atheroma weakens the arterial wall reducing its elasticity.
  • Loss in eleasticity forms a weak point in the wall of the vessel, making it susceptible to an aneuryam or hemorrhage of the vessel.
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11
Q

Inherent risk factors for ATHEROsclerosis

A

Genetics
-Cholesterol Balance

> 40yrs.

Gender: males when young, females when older (post menopause b/c no longer using cholesterol to make hormones)

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12
Q

Modifiable risk factors of ATHEROsclerosis

A

Diet: high in fatsLifestyle: Exercise (form anastmoses), vevous return

Obesity: best to lose weight.

Smoking: decr. HDL (bring cholesterol back to the liver), Incr. LDL (bad cholesterol that’s kept in the peripheral artieries), encourages clot formation, vasocontrictor.

Uncrontrolled BP: HTN –>damanes vessel walls.

Diabetes: Sugars and fats (Hyerlipidemia)

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13
Q

What is Angina Pectoris?

A

“Temporary myocardial ischemia”It is chest pain

-Results from an enlarged artheroma that causes a paritial obstruction to the coronary arteries.

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14
Q

Cause of Angina

A

Partial obstruction of coronary arteries leading to lack of oxygen to the cardiac muscle.

Due to:

  • Impaired blood flow
  • Cardiac demand for oxygen has increasd.
  • Or a combo of the two.
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15
Q

Etiology of Angina

A
  • Atherosclerosis
  • Arteriosclerosis
  • vasospam
  • Myocardial hypertrophy (enlarged heart muscle which needs more oxygen which increased O2 demand and delivery)
  • Severe anemia
  • Respiratory disease
  • Onset often requires exertion.
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16
Q

Patho of Angina

A

Blocked arteries causing decreased blood flow to the heart.
Partial lack of oxygen to the heart.
-The heart has some level of autoregulation to control vasodilation of the coronary arteries to try maintain blood flow.
-During rest if there is a demand for oxygen, any need for increased CO can lead to a deficit of oxygen delivery and damage to the myocardium.
-Angina pain can vary and may or may not continue to be an MI.
-Most acute cases don’t cause permanent damage
-If chronic, frequent O2 demans can cause damage to the myocardium.
Severity varies on person to person

17
Q

S/s of Angina.

A

Tightness/pressure in chest
May radiate down left arm/up neck
Pallor
Excessive sweating: “fight or flight” responseNausea

18
Q

Tx of Angina

A

Rest

Vasodilators: (act to reduce systemic resistance and relieve some of the work needed to be done by the heart)
-Nitroglycerin

19
Q

What is Myocardial Infarction?

A

Occurs when a coronary artery is completely obstructed.Leads to prolonged ischemia and cell death of the myocardium. Most common cause is “Atherosclerosis”

20
Q

Risk factors of MI

A

Stress b/c it can cause many different was of leading to an MI or cardiac death

Ex: Stress-> Incr. BP + HR -> Incr. Deman for O2 -> Ischemia -> MIand more. Slide 25

21
Q

Patho of MI

A
  • Heart tissues becomes necrotic, developing an area of injury leading to inflammation, leading to ischemia.
  • Myocardial contractility and conduction are quicly lost.
  • Without proper tx, the area of infarction may increase resulting in an increased loss of function.
  • collateral circulation may reduce the size of the infaction area, but depnds on the area thats blocked and location of anastomoses (network of arteries)
22
Q

Three possible causes of an MI

A

Can develop in one of 3 ways:

1) Thombus builds to block artery.
2) vasospasm occurs in the presence of a partial occlusion, leading to total obstruction.
3) Emboli occurs and lodges in a smaller branch of a coronary artery.

23
Q

S/s of and MI

A
  • Pressure/burning and heaviness in the chest (less intense pain in women than men)
  • SOB, sweating, weakness, fatigue
  • Nausea, indigestion
  • Anxiety and fear-Low grade fever
  • Enzymes released from dying myocardial cells can be used for Dx ( Troponin)
24
Q

Prognosis of an MI

A

Depends on size of the infarct, presence of collateral circulation, and amount of time before Tx.

Irreversible damage may be prevented if blood flow is restored within 20-30min with thrombolytic therapysome function of the heart can resume starting 48hrs after the MI an inflammation decreases.

The heart cannot regenerate. Area of the heart that has been damaged is replaced by fibroud and non-functional tissue. One MI increases the risk for other MI’s, CHF, or stroke.

25
Q

What is Congestive Heart Failure?

A

Failure of the heart to pump sufficiently

26
Q

Etiology of CHF

A

The heart cannot pump well enough blood to meet metabolic needs of the body.
Is usually a complication of another conditon.Is chronic in most cases.
May be d/t structural defects (inafarction, valve defect) or increased demands of the heart (HTN, lung disease)usually involves failure of one side of the heart, then the other.

27
Q

Homeostatic Compensations of CHF

A

Decrease in systemic blood flow –> increase in renin and aldosterone secretion –> increase in afterload and increase in preload.

1) Sympathetic nervous system:Decreased CO will stimulate:
- Increased HR
- Increased peripheral resistance.

2) Cardiomegaly:
- Chambers dilate and heart muscle hypertophies d/t increased need for contractility.
- ventricle wall thickens, therefore the myocardium needs more O2.
- As the body cannot maintain adequate O2 delivery to the myocardial cells, it leads to myocardial cell death and increased areas of fibrosis (non-functional tissue)

28
Q

Patho of CHF

A

Two problems occur b/c the heart cannot pump properly:

1) CO decreased
2) Backup congestion develops
- Circulation behind the affected ventricle slows
- leads to output from the ventricles being less than the amount of blood coming into the ventricles.

29
Q

What effects does decreased Cardiac Output have on the body?

A
  • Results in less blood reaching the varioud organs and tissues
  • Leads to decreased cell function creating fatigue/lethargy
  • mild acidosis occures compensating for increased respiration that’s trying to get O2 around the body.
  • Ventricle cannot pump its load adequately, therefore the blood return to that side of the heart is impaired.
30
Q

What effects does Backup Congestion have on the body?

A

This occurs d/t pumping problems in the affected ventrivcle.

  • The circulation behind the affected ventricles gets slowed and backs up causing either pulmonary problems or systemic problems.
  • Ventricle output is less than ventricle input.
31
Q

What is Left-Sided CHF?

A

Failure of the Left side of the heart to pump properly.-If the left side cannot pump properly against the systemic pressure –> Left ventricle stays full –> blood cannot return to the Left side of the heart from the pulmonary circulation –> congestion in the pulmonary circulation –> increased capillary pressure and pulmonary edema. And b/c there’s no blood flow to the systemic system, there is decreased renal blood flow.

32
Q

What is Right-Sided CHF?

A

Failure of the Right side of the heart to pump properly.

-Decreased RV output–>less blood flows to the left side of the heart or into the systemic system –>congestion backsup into the systemic system –>blood backsups into systemic circulation –> Congestion in legs,feet, portal circulation, neck veins.Decreased blood flow in systemic circulation = no blood to renal system.

33
Q

Etiology of CHF

A

Infarction affects the pumping ability of the heart, valvular changes or congenital heart defect may cause failure of the affected side.CAD is the leading cause of CHF
Increased systemic hypertension b/c the blood is harder to pushPulmonary disease b/c of back flow into the lungs causeing an increased pressure. And the right side of the heart will fail b/c its pushing against a higher pressure from the lungs.

34
Q

S/s of CHF

A

S/s get worse as the disease progresses

Forward effects: (L to R)

  • Decreased blood supply to tissues
  • General hypoxia
  • Fatigue
  • Weakness
  • dyspnea
  • SOB with exerction
  • Exercise intolerance b/c of lack of O2 and incr. oxygen deman
  • Cold intolerance
  • Dizziness(All occur b/c of decr. CO)
  • Pleural effusion (from backup into heart leaking into pleural space)
  • Ascites b/c of systemic congestion leaking into peritoneal cavity.

Compensation mechanisms:-tachycardio, pallor, daytime oliguria.

35
Q

S/s of Left Sided CHF

A

1) Difficulty Breathing when lying down b/c fluid accumulates in lungs when prone.
2) Cough d/t fluid in the lungs
3) Acute pulmonary edema during sleep. Sleep can be disrupted b/c the pt will wake in a panic, coughing blood tinged soutum, can develop pulmonary infection.

36
Q

S/s of Right Sided CHF

A

1) Edema: feets, legs, buttocks
2) Hepatomegaly and splenomegaly, digestive disturbances b/c of lack of blood
3) Ascites that may impair respiration (b/c its pushing on diaphragm)
4) Must tx acute Right Sided falure quickly b/c it can lead to incr. ICP, as evidenced by headache, visual disturbances and flushed face.

37
Q

Tx of CHF

A

Anymeasure that can reduce the workload of the heart

  • Diuretics (to help decreased fluid amount so there isn’t pulmonary congestion or systemic edema)
  • Decrease HR (Digoxin)
  • Rest (decr Oxygen demand from heart)
  • Heart transplant (to cure)

Pathophysiology (7 decks)

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