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Pathophysiology > Cardiovascular II > Flashcards

Cardiovascular II Flashcards

1
Q

Describe 4 risk factors for CAD

A

High lipid and LDL levels, cigarettes, hypertension, obsesity

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2
Q

Define myocardial ischemia and name one cause.

A

Imbalance of myocardial oxygen supply and demand.

Atherosclerosis is most typical

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3
Q

Describe the time line of myocardial ischemia (i.e, what happens after 10 sec, several min, how long can cardiac cells remain viable, what happens if perfusion is not restored)

A

Become ischemic within 10 seconds, reducing oxygen delivery. Anaerobic respiration occurs, lactic acid increases.
After several minutes, cells cannot contract and cardiac output decreases.
Cardiac cells are viable for up to 20 minutes. If blood flow is restored, will recover once aerobic respiration occurs.
If perfusion not restoresd, cardiac infarction occurs.

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4
Q

Describe stable angina pectoris and its cause.

A

Chest pain caused by myocardial ischemia. Caused by gradual narrowing and hardening of the arteries. Cannot dilate enough in response to increased demands through physical exercise/stress. Once demand decreases, blow flow returns to normal and no necrosis occurs.

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5
Q

Describe variant (Prinzmetal) angina and its cause.

A

Chest pains that occur unpredictably and often at rest

Caused by vasospasms of a narrowing coronary artery, may or may not have atherosclerosis.

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6
Q

Describe asymptomatic angina, what it may be due to and why it is of concern.

A

Oxygen rich blood is restricted but there is no pain/symptoms.
May be due to abnormality in pain/nerve threshold
Carries a risk for increased cardiovascular events

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7
Q

Describe the steps involved in the occurrence of an acute coronary syndrome.

A

A plaque can rupture suddently, due to apoptosis of cells at the site of lesion, release of enzymes by macrophages or shear forces of blood flow.
Once underlying tissue is exposed, thrombus can form quickly.
Thrombus may shatter quickly or may cause prolonged ischemia with infarction of the heart.

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8
Q

What are the acute coronary syndromes?

A

Any group of symptoms that attributed to the obstruction of the coronary arteries.

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9
Q

Describe the steps involved in the occurrence of unstable angina, and how it can present.

A

Occurs when surface of the plaque experiences small disruptions. Leading to small thromboses, which cause short periods of occlusion (10-20 minutes), with the return of normal circulation before significant necrosis can occur.
Can present as new-onset angina, angina that occurs at rest or angina with increase frequency/severity.

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10
Q

Why is unstable angina particularly important to recognize and what should be done immediately?

A

It predicts eventual infarction. Requires immediate hospitalization and treatment (oxygen, aspirin, morphine)

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11
Q

What is a myocardial infarction?

A

Extended period of coronary blood flow interruption, leading to necrosis.
STEMI – Clot lodges permanently in the vessel, the entire wall (epicardium to endocardium) will be involved. Intervention needs to occur immediately
Non-STEMI – Thrombus disintegrates before complete distal tissue necrosis has occurred, the myocardium inside the endocardium will be affected. Recurrent clot formation on disrupted plaque is likely.

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12
Q

Describe the sequence of events in a myocardial infarction after 8-10 sec of oxygen deprivation.

A
  1. After 8-10 sec, the myocardial oxygen reserves are used up. Anaerobic respiration occurs, but much less ATP is made, and the build-up of lactic acid changes the pH of the tissue, causing damage. Contractility of the heart is affected.
  2. Electrolyte disturbances occur, as well as hormonal release from myocardial cells (catecholamines are released, causing increased blood glucose).
  3. Ischemic conditions can be tolerated for about 20 min before irreversible damage occurs and there is apoptosis and necrosis.
  4. Enzymes are released from damaged/dead cells and these can eventually be detected in the bloodstream.
  5. Changes occur to the tissue at the infarction site, as well as heart tissue that is distant.
  6. Changes may include: decreased stroke volume, sinoatrial node malfunction, abnormal wall motion.
  7. MI causes a severe inflammatory response that ends with wound repair. The scar tissue that is formed is strong, but cannot contract and relax like healthy myocardial tissue.
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13
Q

What are 3 clinical manifestations of an MI?

A

Sudden chest pain/pressure, nausea, vomiting, clammy skin

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14
Q

How can an MI be treated?

A

Bed rest, gradual return to activity, lifestyle training

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15
Q

Define pericarditis and name one cause.

A

Acute inflammation of the pericardium

Idiopathic, surgery, infection

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16
Q

Define cardiomyopathy.

A

Diverse group of diseases primarily that affect the myocardium itself.

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17
Q

Describe two examples of cardiomyopathy, one cause for each and their effects on heart function.

A

E.g., Dilated cardiomyopathy: increased ventricular volume
Dilated: result of ischemic heart disease, diabetes, renal failure, etc.
Characterized by impaired systolic function
E.g., Hypertrophic myopathy: thickening of septum, which may obstruct outflow of left ventricle.
Hypertrophic: inherited (can obstruct outflow), or as a result of increased resistance to ventricular ejection (hypertension or aortic stenosis)

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18
Q

Why is a valvular dysfunction an endocardial disorder?

A

Because the valves are composed of endocardial tissue

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19
Q

What is one of the most common acquired causes for a valvular disfunction?

A

Rheumatic heart disease

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20
Q

Which valves in the heart are most commonly affected? Why?

A

Aortic and mitral.

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21
Q

Describe the two types of disruptions that can occur with a valvular dysfunction.

A

Stenosis: narrowing of valve opening, causing turbulent flow and enlargement of emptying chamber
Incompetent (regurgitant) valve: permits backward flow

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22
Q

What is a “heart murmur”?

A

Sounds made by abnormal flow

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23
Q

Describe an aortic stenosis and its consequences to heart function.

A

Most common valvular abnormality. Opening of aortic valve narrows, causing blood flow from left ventricle into the aorta. Increases the pressure in the left ventricle, leading to hypertrophy to compensate for the increased workload. This increases myocardial oxygen demands, may cause ischemia.

24
Q

What is a disrythmia / arrhythmia?

A

Irregular heart beat. Ranges from occasional missed or rapid beats to serious disturbances.

25
Q

What are the two general causes for disrythmias?

A

Caused by abnormal impulse generation from SA node/other pace maker, or by abnormal conduction of impulses through the hearts conduction system.

26
Q

Define brachycardia, tachycardia and inotropy.

A

Brachycardia – regular but slow heart rate, can be normal for athletes.
Tachycardia – regular rapid heart beat, can be normal (exercising, fever, stress)
Inotrophy – contractility of muscle, ventricular hypertrophy increases contractility, while myocardial infarction decreases it.

27
Q

Describe PACs, atrial flutter and atrial fibrillation. Why can these be sometimes aymptomatic?

A

PAC- Premature atrial contractions, interfere with timing of next beat
Flutter – atrial heart rate of 160-360 bpm, (AV node delays conduction). Can get several atrial depolarizations to one ventricular depolarization.
Fibrillation - >350 bpm – completely disorganized and irregular atrial rhythm accompanied by irregular ventricular rhythm. Causes pooling of blood in atria (tmt must include anticoagulants)Z

28
Q

What is meant by a partial or a total atrioventricular node abnormality?

A

Heart block occurs when conduction is excessively delayed or stopped at the AV node or bundle of His
• Partial (slower conduction) (first, second degree)
• Total (no transmission – ventricles contract on their own, but cardiac output is greatly reduced.) (second, third degree)

29
Q

Describe ventricular fibrillation and PVCs (know full name).

A

Ventricles contract independently and rapidly – ineffective in ejecting blood (death within minutes if not corrected).
PVC – Premature ventricle contractions. Additional beats of ventricles – increasing frequency can lead to ventricular fibrillation.

30
Q

What is heart failure and what are the two possible consequences?

A

When the heart is unable to generate adequate cardiac output

Inadequate perfusion of tissues, increased pulmonary capillary pressures, or both.

31
Q

What are the most important predisposing risk factors for heart failure?

A

Ischematic heart disease and hypertension

32
Q

Define preload and describe what it is determined by.

A

Volume and associated pressure in the ventricle at the end of diastole
Determined by the amount of blood entering at diastole, blood left after systole.

33
Q

What is the Frank-Starling Law of the Heart?

A

The more stretched the ventricle wall, the greater the force of the contraction (up to a maximum value)

34
Q

Define afterload and describe the characteristic that would be a good indicator of this.

A

Resistance to ejection of blood from left ventricle.

Peripheral vascular resistance is usually a good index of afterload

35
Q

What is the other name for left heart failure?

A

Congestive heart failure

36
Q

Define systolic heart failure and describe 3 causes.

A

Inability of the heart to generate an adequate cardiac output to perfuse vital tissues. Adequate output depends upon HR and stroke volume.
– Decreased contractility (due to MI, cardiomyopathy, etc.)
– Increased pre-load (stretches the muscle past the optimum) (due to decreased contractility, or significantly increased plasma volume (renal disease, IV)).
– Increased afterload (due to increased vascular resistance, caused by hypertension, for e.g.)

37
Q

Describe the “vicious circle” of systolic heart failure development.

A

– As cardiac output falls, the renin angiotensin aldosterone system (RAAS) is activated, resulting in even more increased preload (increased blood volume) and increased afterload (increased vasoconstriction).
– Baroreceptors also detect fall in BP and activate the SNS, which causes more vasoconstriction.
– The hypothalamus reacts to decreased BP and causes release of ADH, increasing blood volume.

38
Q

Describe 4 symptoms/signs of systolic heart failure, and what causes them.

A

Dyspnea, pulmonary edema, fatigue, decreased urine output. Symptoms are a result of pulmonary vascular congestion (blood is not removed from lungs efficiently) and inadequate perfusion of the systemic circulation.

39
Q

How does the restriction of salt intake and the use of diuretics act to improve systolic heart failure?

A

It concentrates on decreasing preload and afterload.

40
Q

Define diastolic heart failure and describe its cause.

A

Isolated diastolic heart failure: Pulmonary congestion despite a normal stroke volume and cardiac output.
This is caused by decreased diastolic relaxation so that there is greater ventricular pressure during relaxation. (for e.g., some forms of heart disease which cause impaired relaxation of muscle). This results in pulmonary edema, as pressure backs up into pulmonary circulation.

41
Q

Define right heart failure and name one clinical manifestation.

A

Inability of right ventricle to provide adequate blood flow into the pulmonary circulation.
Shortness of breath, fatigue, edema.

42
Q

How can left heart failure cause right heart failure?

A

Can result from left heart failure creating increased pulmonary pressure.

43
Q

What is cor pulmonale, what is its primary cause and give one example of a disease that would cause this.

A

When right failure occurs without left heart failure. Factors that increase pulmonary pressure: COPD

44
Q

Define shock.

A

The cardiovascular system fails to perfuse the tissues adequately, resulting in widespread impairment of cellular metabolism.

45
Q

Describe the basic cellular effect of shock.

A
  • If sufficient oxygen is not delivered to the cell, it switches to anaerobic respiration, which produces far less ATP.
  • Without sufficient ATP, the cell’s sodium/potassium pump operates poorly.
  • The intra/extra cellular concentrations of sodium, potassium and calcium are not maintained, interfering with functioning of nervous and muscular systems.
46
Q

Describe 3 positive feedback loops that result in ever-increasing tissue hypoxia and tissue damage.

A
  • With sodium entering cell, water follows. Interstitial fluids then pull water out of the vascular system, which results in a drop in blood pressure. Decreased volume in the vascular system intensifies the decrease in perfusion of tissues (positive feedback loop).
  • The damage to surrounding tissue activates the clotting cascade and inflammatory response, resulting in further damage to the tissues, impairing cellular metabolism (including ATP production). (positive feedback loop).
  • These acidic conditions also affect hemoglobin, decreasing its affinity with oxygen, thus decreasing the oxygen carrying capacity of the blood, which increases the tissue hypoxia (positive feedback loop).
47
Q

What is the consistent sign of shock?

A

One consistent sign is hypotension with mean arterial pressure.

48
Q

Name 4 symptoms of shock.

A

Weak, dizzy, cold, hot, increased respiratory rate

49
Q

What is the treatment for shock?

A
  • Must remove underlying cause.
  • Generally, IV fluid to expand blood volume, vasopressors (drugs that increase vasoconstriction) and supplemental oxygen.
  • Once positive feedback loops have been established, intervention is very difficult.
50
Q

Define cardiogenic shock and its cause.

A

When the heart has been damaged so much that it is unable to supply enough blood to the organs of the body. Caused by heart.
Decrease in blood pressure causes responses (increase in catecholamine release, RAAS system) that increase oxygen/nutrient demand of the heart which puts further strain on the heart, resulting in it becoming incapable of pumping an adequate volume.

51
Q

Define hypovolemic shock and its cause.

A

Not enough blood volume, caused by loss of whole blood (hemorrhage), plasma (burns) or interstitial fluid (diarrhea or diuresis) in large amounts.
Begins to develop when intravascular volume has decreased by about 15%

52
Q

What compensatory mechanisms does the body employ to counteract hypovolemic shock?

A 
Compensatory mechanisms can initially help:
–	HR and vasoconstriction increase
–	Interstitial fluid moves into blood
–	Liver and spleen add to blood volume
–	RAAS is activated, as is ADH
53
Q

Define neurogenic shock and its cause

A

Occurs after injury to the spinal cord. Result of massive vasodilation resulting from overstimulation of the parasympathetic NS and understimulation of the sympathetic NS.

54
Q

Define anaphylactic shock, its cause and its treatment.

A

A life-threatening type of allergic reaction. Basically the same as neurogenic shock: release of histamine and other compounds by mast cells as a result of a Type I hypersensitivity results in vasodilation and vascular permeability to the point of peripheral pooling and tissue edema.
Treatment involves intramuscular administration of epinephrine to cause vasoconstriction and reverse airway constriction.

55
Q

Define septic shock and its cause.

A

Septic shock is a serious condition that occurs when an overwhelming infection leads to life-threatening low blood pressure.
• Vasodilation/decreased heart contractility causing poor tissue perfusion.
• Caused by infection with micro-organism
• Release of toxins which stimulate overwhelming inflammatory response, and/or direct stimulation of overwhelming inflammatory response

Pathophysiology (10 decks)

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