Clinical Pathophysiology Made Ridiculously Easy: Cardiovascular System Flashcards

1
Q

Which valve lies between right atrium and right ventricle?

A

Tricuspid valve

*tRIcuspid is on the RIght

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2
Q

Which valve lies between right ventricle and it’s outflow vessel?

A

Pulmonic valve

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3
Q

Which valve lies between left atrium and left ventricle?

A

Mitral valve

*mitraL is on the Left

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4
Q

Which valve lies between left ventricle and its outflow vessel?

A

Aortic valve

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5
Q

Which valves snap shut during systole, preventing back flow?

A

The tricuspid and mitral valves

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6
Q

Which valves snap shut during diastole, preventing back flow?

A

The pulmonary and aortic valves

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7
Q

Where would you hear abnormal lungs sounds on a pt with left heart failure?

A

You may hear crackles in the bases of the lungs as a result of excess fluid. The worse the failure the more fluid in the lungs, the higher up in the lung fields these cracks will be heard.

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8
Q

In the absence of other illnesses, what kind of fluid do you find in the lungs during Left Heart Failure: transudative or exudative?

A

Transudative fluid, which is from increased intralumenal pressure from fluid backed up from the left ventricle.

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9
Q

What is the effect on the body of Left Heart Failure? What signs and symptoms would you find?

A

You would have decreased flow from the left heart to the body, which would cause blood to back up in the pulmonary vasculature. This would cause increased pressure in the pulmonary veins, which causes transudation of fluid into the lungs. You would then have pulmonary edema which causes dyspnea, and possibly crackles in the lung bases.

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10
Q

What is the cause of Right Heart Failure? Why?

A

Left Heart Failure. Because backup of flow in left heart can increase pressure in the pulmonary vasculature, left heart failure can cause pulmonary HTN and subsequent right heart failure.

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11
Q

Which ventricle is “stronger” and why?

A

Left ventricle is stronger. Right ventricle is not as strong since it pumps blood into the lower pressure pulmonary system, compared to the higher-resistance (higher pressure) system of the peripheral vasculature that the left ventricle pumps into.

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12
Q

Which ventricle has thicker walls? Why?

A

Left ventricle has thicker walls than the right because the left ventricle pumps into the higher-resistance, higher pressure system of the peripheral vasculature. Right ventricle, with thinner walls, pumps into the low pressure pulmonary system.

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13
Q

Where does the blood back up in right heart failure? What would you notice on physical exam?

A

The blood in the right ventricle comes from the body, or the venous return via the superior and inferior venae cavae. On PE you would see elevated jugular venous pressure (JVP). the jugular veins in the neck are a straight shot to the superior vena cava. You would also possibly see ascites, hepatic congestion, peripheral edema, etc.

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14
Q

What is preload? What creates it?

A

The pressure that fills the ventricles during diastole. More specifically, preload is the blood pressure in the left ventricle at the end of diastole, right before the ventricles contract. It is created by blood coming from the venous system.

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15
Q

What is afterload?

A

The resistance that the heart faces during systole. It is the systemic vascular resistance or the resistance to flow in the arterial tree against which the heart must work. (AFTERLOAD is created by ARTERIES)

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16
Q

What are the goals of tx for heart failure? How is this accomplished?

A

Increase forward flow, decrease backup of flow. You increase forward flow by increasing cardiac output. To decrease backup, you must decrease workload on the heart. So you increase the heart’s ability to pump, and decrease how much it has to pump against.

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17
Q

What two mechanisms do you use to increase forward flow (increasing cardiac output)?

A
  1. Increase the force of ventricular contraction (inotropes, e.g., digoxin/digitalis, dopamine/dobutamine, amrinone/milrinone).
  2. Decrease rate of contraction to increase filling time (beta-blockers, e.g., propranolol, metoprolol). The increased filling time increases amount of blood pumped at a time, increasing cardiac output.
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18
Q

What’s the strategy to decreasing fluid backup by decreasing heart’s work?

A

To decrease work, you should try to decrease both the preload and the afterload (since heart’s job is to pump the preload against the afterload). You can decrease preload by decreasing venous return which you can do by dilating the veins, slowing the return of blood to the heart, (nitrates dilate veins). You can also use diuretics, which decrease intravascular fluid volume.

To decrease afterload, you can use arterial dilators (e.g., ACE inhibitors, hydralazine)

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19
Q

What is the MOA of digoxin in CHF?

A

It increases contractility of the heart, which helps increase cardiac output, which helps with forward flow.

20
Q

What is the MOA of beta-blockers? (propranolol, metoprolol, etc)

A

*

21
Q

What is the MOA of ACE inhibitors? What are examples?

A

*

22
Q

What is the MOA of hydralazine?

A

*

23
Q

How do the kidneys get involved in CHF?

A

During CHF there is decreased cardiac output, and as a result the perfusion pressure in the kidneys decreases, (this is called decreased effective blood volume, the volume is the same but the amount that reaches the kidneys decreases). When the kidneys sense a decrease in perfusion pressure activates the renin-angiotensin-aldosterone system to increase perfusion pressure.

24
Q

What is the MOA of the Renin-Angiotensin-Aldosterone system?

A
  • Kidneys sense a decrease in perfusion pressure and releases Renin.
  • Renin increases the conversion of angiotensinogen to angiotensin I.
  • Angiotensin I gets converted to angiotensin II by the angiotensin converting enzyme (ACE).
  • Angiotensin II causes vasoconstriction, which raises blood pressure.
  • Angiotensin II also stimulates aldosterone release from the adrenal glands.
  • Aldosterone causes sodium resorption by the kidneys, which causes water to follow it, which increases intravascular volume.
  • Increased vasoconstriction and increased blood volume raises blood pressure.
  • Also, Antidiuretic Hormone (ADH) gets released from the posterior pituitary gland when there is perceived low volume status in the blood vessels and in the kidney.
  • ADH causes water reabsorption in the kidneys which also increases volume and increases blood pressure.
25
Q

What medications are used to prevent increased blood pressure through the renin-angiotensin-aldosterone system (RAA)?

A
  • ACE inhibitors – inhibit conversion of angiotensin I to angiotensin II (which decreases aldosterone release and angiotensin II-induced vasoconstriction).
  • ARBs (angiotensin II receptor blocker) – block the angiotensin II receptor which also decreases aldosterone release and angiotensin II-induced vasoconstriction.
  • Aldosterone Antagonists – an example would be Spironolactone. This blocks aldosterone at it’s receptor , which decreases sodium reabsorption (along with water)
26
Q

What are the four components of the heart that help it to pump blood?

A
  • Muscle
  • Valves
  • Electrical conduction system
  • Heart’s own blood supply
27
Q

What are the signs/symptoms of decreased forward flow?

A
  • Fatigue
  • Weakness
  • Shortness of breath

(Because organs and tissues not getting enough blood flow.)

28
Q

What are the signs/symptoms of backup of

A
  • SOB
  • paroxysmal nocturnal dyspnea
  • orthopnea
  • edema
  • elevated JVP
29
Q

Ventricle hypertrophy causes what kind of contraction dysfunction?

A

Diastolic dysfunction, because the heart isn’t able to relax as well to fill appropriately with blood, the ventricular chamber also gets smaller because of the greater wall thickness.

30
Q

Ventricular dilatation, or thinning of ventricular wall, causes what kind of contraction dysfunction?

A

Systolic dysfunction, because it cannot contract as forcefully.

31
Q

What causes Left Ventricular Hypertrophy?

A
  • HTN, increased blood pressure in the arteries (increased resistance)
  • Aortic stenosis
32
Q

What causes Right Ventricular Hypertrophy?

A

Anything that causes increased resistance in pulmonary vasculature (left heart failure, pulmonic valve stenosis, pulmonary causes)

33
Q

Right heart filature secondary to pulmonary causes

A

Corpulmonale

34
Q

What are the consequences of cardiac hypertrophy? Why?

A
  • Causes diastolic dysfunction because the thickened heart wall causes the ventricle to relax very well during diastole. Also, a thickened wall eventually diminishes the space in the ventricle so it doesn’t fill with as much blood. Combination of inability to relax or fill with blood (which are both diastolic issues) cause diastolic dysfunction.
  • A hypertrophied heart also needs more blood supply, and eventually can outgrow its blood supply, putting it at risk for ischemia.
35
Q

Treatment for cardiac hypertrophy

A
  • You are treating an hypertrophied heart that has a smaller heart chamber size and does not fill optimally, so you need to decrease heart rate to promote optimal filling of chamber, and to increase contractile force (increase filling and cardiac output)
  • Beta blockers and Ca channel blockers achieve this?
36
Q

Which is the infiltrative cardiomyopathy?

A

Restrictive cardiomyopathy

37
Q

Causes of restrictive cardiomyopathy?

A

Accumulation of substances in heart muscle including: amyloid (amyloidosis, multiple myeloma), iron (hemochromatosis), carload (rare), Pompe’s disease (rare)

38
Q

Treatment for restrictive cardiomyopathy?

A

Same as for heart failure: increase forward flow and decrease back up of flow

39
Q

What can cause dilated cardiomyopathy?

A
  • Genetic dz, drugs (like cocaine and amphetamines), alcohol, viral myocarditis
  • Dilation of left ventricle: Aortic regurgitation, mitral regurgitation
  • Dilation of right ventricle: Pulmonic regurgitation, tricuspid regurgitation, atrial septal defect (ASD), ventricular septal defect (VSD)
40
Q

Consequences of cardiac dilation?

A
  • Systolic dysfunction, heart is able to relax just fine, but has weaker squeeze during systole.
  • Leads to diminished forward flow and increased backup of flow.
41
Q

What can cause systolic dysfunction?

A
  • Dilated cardiomyopathy

* Weakening of heart muscle secondary to ischemia

42
Q

Difference between systolic and diastolic dysfunction

A
  • Systolic dysfunction is caused by cardiac dilatation because the heart wall is weakened and thinner and is able to relax, but has a weakened “squeeze” during systole. This is caused by: genetic dz, drugs (cocaine, amphetamines), alcohol, viral myocarditis, right heart dilation (aortic regurgitation, mitral regurgitation), left heart dilatation (pulmonic regurgitation, tricuspid regurgitation, atrial septal defect, ventricular septal defect). Eventually causes decreased forward flow, and increased backup of flow.
  • Diastolic dysfunction is caused by cardiac hypertrophy because the heart wall is thickened, it causes a smaller heart chamber, and is unable to relax as well and fill with blood during diastole. This is caused by increased vascular resistance in either the peripheral vasculature (left ventricular hypertrophy), or increased resistance in pulmonary vasculature (right ventricular hypertrophy). Eventually causes decreased forward flow and increased backup of flow.
43
Q

Treatment of cardiac dilatation

A

Same as for heart failure: increase forward flow (inotropes) and decrease backup of flow (nitrates [dilate veins], diuretics [decreases intravascular volume], ace inhibitors and hydralazine [dilates arteries])

44
Q

S1

A

Sound of mitral and tricuspid valves snapping shut just before systole

45
Q

S2

A

Sound of aortic and pulmonic valves snapping shut just before diastole

46
Q

S3

A

Is associated with heart failure, specifically dilated heart/systolic dysfunction

47
Q

S4

A

Associated with heart failure, specifically hypertrophied heart/diastolic dysfunction