Week 2 - Intro to Cardiac Disease Flashcards

1
Q

What are the two categories of heart disease?

A

Congenital

Acquired (most cases)

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2
Q

List 5 primary causes of acquired heart disease?

A

Chronic degenerative valve disease
Cardiomyopathy
Endocardial infection
Pericardial disease
Rate/rhythm abnormalities

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3
Q

What is the hearts main goal?

A

To maintain blood pressure and perfusion by:
1. Normal systemic arteriole pressure
2. Cardiac output (HV x SV)
3. Venous pressure remain equal

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4
Q

What is blood pressure impacted by?

A

Vascular resistance - force exerted on the blood by the vasculature

Cardiac output

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5
Q

What are the three things that affect stroke volume?

A

Preload - the volume of blood/hydrostatic pressure within the ventricles at the end of diastole (when finished filling)

Afterload - pressure the heart works against to open the aorta in systole (main factor = arteriole blood pressure)

Contractility

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6
Q

Heart failure can be acute or chronic, which is the most common?

A

Chronic - usually degenerative conditions

Acute is rare

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7
Q

In simple terms, what is the first thing that happens in heart failure?

A

Cardiac output falls

Detected as a fall in blood pressure

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8
Q

How do the following conditions affect cardiac output?

CDVD, DCM, HCM, Congenital

What does this mean for clinical signs?

A

CDVD – regurgitation means fall in FORWARD flow and CO

DCM – systolic failure – ventricles cannot contract properly - fall in stroke volume and therefore CO

HCM/RCM, ventricle cannot FILL – fall in CO

Congenital disease – if develop failure because CO fall

CLINICAL SIGNS ALL THE SAME WHATEVER THE CAUSE

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9
Q

What are the mechanisms that the heart uses to restore blood pressure?

A

BODY THINKS DROP IN CO IS DUE TO TRAUMATIC BLOOD LOSS RATHER THAN HEART DISESE -> COMPENSATORY MECHANISMS DO MORE HARM!

Sympathetic NS activation

R.A.A.S

Cardiac enlargement (last consequence)

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10
Q

What does the sympathetic nervous system do to try and restore blood pressure?

A

Increase HR (problem in heart disease)

Vasoconstriction -> increase presser (problem if not enough blood or if heart sick and needs to cope with higher pressure)

Kidney release renin

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11
Q

What is the consequences of R.A.A.S activation?

A
  1. Systemic vasoconstriction (increase BP with heart cannot cope with)
  2. Increase blood volume (increasing the fluid the body has to deal with)
  3. Renal sodium and fluid retention (to increase blood volume)
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12
Q

What are the effects of the compensatory mechanisms?

A

Heart rate goes up
Vasoconstriction
Contractility goes up
Salt and water retained
(Cardiac enlargement)

CO DECREASE -> COMPENSATORY MECHANISMS -> SICK HEART HAS TO COPE, NO RISE IN CO -> REPEAT CYCLE

CLINICAL SIGNS START WHEN HEART STRUGGLES AND GO INTO FAILURE

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13
Q

What is the problem of the compensatory mechanisms?

A

CO DECREASE -> COMPENSATORY MECHANISMS -> SICK HEART HAS TO COPE, NO RISE IN CO -> REPEAT CYCLE

CLINICAL SIGNS START WHEN HEART STRUGGLES AND GO INTO FAILURE

Ideal in the short terms
- sudden blood loss (e.g. trauma)

Inappropriate in long term
- worsens heart function
- treatment is to pause compensatory mechanisms (e.g. preventing the kidneys from retaining fluid)

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14
Q

How does an increase in heart rate and contractility affect a sick hear?

A

HEART RATE GOES UP
-SICK HEART WORKING HARDER
-OXYGEN NEEDS GO UP

CONTRACTILITY GOES UP
-SICK HEART WORKING HARDER
-OXYGEN NEEDS GO UP

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15
Q

How does vasoconstriction of arteries affect a sick heart?

A

Increase afterload (increase aortic pressure) = CO Falls more

Blood will take the path of least resistance -> regurgitate through valves

Increase afterload – valves leak more (fluid accumulation)

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16
Q

How does vasoconstriction of veins affect a sick heart?

A

Increase voluming returning to heart

Increase atrial pressures

Increase likelihood of oedema

17
Q

How does salt and water retention affect a sick heart?

A

Volume returned to heart increases

Volume of fluid in vessels increases

Increase pressure in capillaries

Oedema develops

18
Q

How does cardiac enlargement affect a sick heart?

A

AV valves leak more (stretches atrium)

Oxygen needs go up

Oxygen supply goes down

Cells die (stretched from increase pressure and lack of O2) – not replaced, scar tissue forms

CONTRACTILITY FALLS FURTHER

19
Q

Why do most patients present with pulmonary oedema?

A

Pulmonary oedema - fluid in alveoli

Due to left-sided disease

Oedema is a consequence of the compensatory mechanisms
- Fluid backs up into pulmonary vein
- Backs up towards leg
- Fluid leak into capillaries
- Capillaries leak into lung

20
Q

What is the medical management to help prevent the cpmpensaorty mechanisms?

What must you be careful of?

A

Reduce fluid build up – diuretics

Antagonise RAAS – ACE inhibitors +/- aldosterone antagonists

Vasodilate - pimobendan (reduce blood pressure and stabilise cardiac muscle)

Mechanisms are there to maintain BP so don’t overdose!

And cannot bock SNS -> just the compensatory mechanism!