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Heart Pathophysiology > Heart Pathophys > Flashcards

Heart Pathophys Flashcards

1
Q

What happens during systole?

A

Ventricles contract forcefully –> blood to aorta –> body
Tricuspid & mitral valves shut to prevent back flow into atria
S1 = LUB

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2
Q

What happens during diastole?

A

Ventricles relax and fill with blood from the atria
Aortic and pulmonic valves shut to prevent back flow into ventricles
S2 = DUB

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3
Q

Left heart failure

A

Back up in pulmonary veins
Pulmonary edema
Pulmonary dyspnea

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4
Q

Right heart failure (due to L heart failure)

A

Increased resistance in pulmonary vasculature = pulmonary hypertension

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5
Q

Right heart failure

A 
Venous return backup
Elevated JVP (due to backup in SVC)
Backup in liver, abdomen, & rest of body due to backup in the IVC
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6
Q

Decreased forward flow

A

Dec blood flow to muscles & rest of body
Fatigue
Weakness
Shortness of breath

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7
Q

sx: orthopnea

A

SOB upon laying down
When standing blood pools to feet - when lying down blood can find its way back to the heart more easily and increases the heart’s work
A failing heart cannot handle this - blood backs up into lungs –> SOB

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8
Q

sx: paroxysmal nocturnal dyspnea

A

Same pathophys as orthopnea but
Patient wakes up in middle of the night coughing and short of breath
Classically resolves when patient gets up and goes to the window for air

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9
Q

preload

A

The pressure that fills the ventricles during diastole
The blood pressure in the L ventricle at the END of diastole, right before ventricles contract
Blood comes to the heart from the VENOUS system

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10
Q

afterload

A

Resistance that heart faces during systole
Systemic vascular resistance, the resistance to flow in the arterial tree against which the heart must work
(Afterload is created by the Arteries)

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11
Q

HF Tx: Increased forward flow by increasing cardiac output

A

Inc force of ventricular contraction
Inotropes
(Digoxin/Digitalis, Dopamine/Dobutamine, Amrinone/Milrinone

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12
Q

HF Tx: Decrease rate of contraction to increase filling time

A

Increase in filling time allows more blood to accumulate in ventricles before contraction –> inc in cardiac output
Beta Blockers
(Propranolol, Metoprolol)
Down regulate sympathetic receptors in body

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13
Q

HF Tx: Decreasing backup by decreasing the hearts work

A
  1. Decrease preload - decrease venous return
    - dilate veins = slow return of blood from veins to heart
    Tx:
    Nitrates
    Diuretics - inc urination = dec intravascular fluid volume
    ACEI , Hydralazine = arterial dilators
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14
Q

HF Tx: Decreasing backup by decreasing the hearts work

A
  1. decrease afterload
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15
Q

Kidneys in heart failure?

A

Dec perfusion pressure in kidneys
Blood volume itself NOT changed but the pressure at which volume reaches the kidneys decreases
= effective blood volume decrease
(this also occurs due to cirrhosis)

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16
Q

When the kidneys sense decreased perfusion pressure, they try to increase this pressure by doing what?

A

increasing blood volume

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17
Q

How can the kidneys increase blood volume in response to decreased perfusion pressure?

A

the renein-angiotensin-aldosterone system

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18
Q

The renin - angiotensin - aldosterone system

A
  1. Senses dec renal perfusion and releases renin
  2. Inc conversion of angiotensinigin to angiotensin I
  3. Angiotensin I conversted to angiotensin II via angiotensin converting enzyme (ACE
  4. Angiotensin II causes vasoconstriction = inc BP and stimulates aldosterone release from the adrenal gland
  5. Leads to inc Na+ absorption by kidneys, causing water to follow (osmosis)
  6. Inc vasoconstriction and inc blood volume = inc BP
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19
Q

Additionally, perceived low volume status causes release of antidiuretic hormone (ADH) from where?

A

Posterior pituitary

Inc water reabsorption in kidneys - further contributing to inc volume & inc BP

20
Q

If the heart is already having trouble handling the existing blood volume, are the kidneys and ADH helping this situation?

A

NO!

The increase in plasma volume in heart failure further aggravates the backup into the lungs & body

21
Q

What do you use to suppress the kidney and ADH?

A

ACEI
Dec conversion of angiotensin I to angiotensin II
Which leads to dec in both aldosterone release and angiotensin II -induced vasoconstriction
Inhibit further increase in blood volume & BP

22
Q

How do ARBs work?

A

Angiotensin II receptor blockers

Block angiotensin II receptor leading to dec blood volume and BP

23
Q

How do Aldosterone antagonists work?

A

Block aldosterone at its receptor

Spironolactone

24
Q

With heart disease if the musculature thickens (hypertrophy), the ventricles cannot ____?

A

relax as well

25
Q

When the ventricular musculature hypertrophies what happens?

A

The chamber size is reduced, decreasing how much blood it can receive (diastolic dysfunction)

26
Q

What happens if the ventricular musculature thins and weakens (dilation)?

A

The strength of the ventricular muscle decreases and it cannot contract forcefully (systolic dysfunction)

27
Q

What can hypertrophy of the cardiac muscle be caused by?

A 
Genetic disease (hypertrophic cardiomyopathy)
Certain pathological circumstances (think about what would make the heart work hard)
28
Q

What causes LVH? What would make the left side of the heart have to work hard?

A

The left heart has to work against the resistance of the systemic vasculature (afterload)
HTN
Aortic stenosis –> leads to LVH –> HF

29
Q

What causes RVH? What makes the R heart have to work hard?

A

Any process that increases resistance in the pulmonary vasculature (pulmonary HTN) –> RVH –> HF

30
Q

Right heart failure secondary to pulmonary cause is called?

A

cor pulmonale

31
Q

What are the consequences of cardiac hypertrophy?

A
  1. Thick wall makes it difficult to adequately perfuse
  2. Cardiac muscle outgrows blood supply –> ischemia –> angina and/or infarction
  3. The heart squeezes better but does not relax
  4. The muscle can become so thick that the chamber size becomes small –> decreased filling
  5. Decreased filling of the ventricles = decreased cardiac output
32
Q

Cardiac hypertrophy causes?

A

diastolic dysfunction - if the heart cannot relax properly, the heart cannot fill optimally thus, forward flow decreases and back up occurs

33
Q

Treatment for cardiac hypertrophy

A

Treatment should decrease HR and contractile force allowing for increased filling and cardiac output:
BB
CCB

34
Q

What is restrictive cardiomyopathy?

A

When the heart is stiff and does not relax well (diastolic dysfunction)

35
Q

Treatment for restrictive cardiomyopathy

A 
Treat the underlying cause
Treatment is the same as for HR - aim to increase forward flow and decrease backup of flow 
Inotropes
BB
Nitrates
Diuretics
ACEI/Hydralazine
36
Q

What can cause dilated cardiomyopathy?

A

Genetic diseases
Drugs, ETOH
Viral myocarditis

37
Q

What is dilated cardiomyopathy?

A

Occurs when the heart needs to handle more blood than usual (think big and floppy heart)

38
Q

What can cause L ventricular dilated cardiomyopathy?

A

Aortic regurgitation - when the left ventricle contracts, not all the blood moves out and overtime the heart dilates to accommodate for the extra blood volume
Mitral regurgitation - increases the amount of blood the left ventricle receives

39
Q

What can cause R ventricular dilated cardiomyopathy?

A

Pulmonic or Tricuspid regurgitation
Atrial Septal Defect (ASD)
Ventricular Septal Defect (VSD)

40
Q

Consequences of dilated cardiomyopathy

A

Dilated ventricle is weakened (too relaxed) and thus gives a weaker squeeze during systole (systolic dysfunction)
Leads to both diminished forward flow and backup of flow

41
Q

The closure of the AV valves correlates with what sound?

A

S1 “lub”

beginning of systole

42
Q

During systole where does the blood flow?

A

Through the aortic valve to the aorta and through the pulmonic valve to the pulmonary arteries
The AV valves are closed
Blood is filling the atria to prepare for the next cycle

43
Q

The closure of the aortic and pulmonic valves closing correlates with what sound?

A

S2 “dub”

beginning of diastole

44
Q

During diastole where does the blood flow?

A

Blood passes from the atria across the open tricuspid and mitral valves into the ventricles

45
Q

S3 is associated with that dysfunction?

A

Dilated heart/ systolic dysfunction

hint: the number 3 looks like a puffy dilated heart

46
Q

S4 is associated with that dysfunction?

A

Hypertrophied heart/ diastolic dysfunction
Sound produced when the atria squeeze against a stiff ventricle
(hint: the number 4 looks like a small chamber)

47
Q

Aortic Stenosis murmur and pathophys

A

Murmur = systolic ejection click (between S1 and S2), crescendo-descrescendo
Softer S2 (remember the valve is stiff so it does not open or close properly so sound is diminished)
Weakened and delayed carotid pulses = parvus et tardus
-this is why patients are lightheaded, dizzy
Inhibits flow –> fatigue and weakness

Heart Pathophysiology (1 decks)

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