Cardio Lectures Flashcards

1
Q

Define hypertension

A

A chronic elevation in blood pressure, grade 1 hypertension is classified at 140-159 Systolic and 90-99 Diastolic

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2
Q

What is the systolic and diastolic of grade 1 hypertension

A

Grade 1 = Systolic of 140-159 and Diastolic of 90-99

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3
Q

What is the systolic and diastolic of grade 2 hypertension

A

Grade 2 = Systolic of 160-179 and Diastolic of 100-109

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4
Q

What is the systolic and diastolic of grade 3 hypertension

A

Grade 3 = Systolic of >180 and Diastolic of >110

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5
Q

What are some of the consequences of hypertension

A

Left Ventricular Hypertrophy, Stroke/MI, Renal failure and Retinal damage

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6
Q

What is the short term mechanism of blood pressure regulation?

A

Short-term regulation of blood pressure is controlled by the sympathetic nervous system (SNS). Changes in blood pressure are detected by baroreceptors. These are located in the arch of the aorta and the carotid sinus. Increased arterial pressure stretches the wall of the blood vessel, triggering the baroreceptors.

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7
Q

Explain the renin-angiotensin aldosterone system

A
  1. When your blood pressure falls, your kidneys release the enzyme renin into your bloodstream.
  2. Renin splits angiotensinogen, a protein your liver makes and releases, into pieces. One piece is the hormone angiotensin I.
  3. Angiotensin I, which is inactive (doesn’t cause any effects), flows through your bloodstream and is split into pieces by angiotensin-converting enzyme (ACE) in your lungs and kidneys. One of those pieces is angiotensin II, an active hormone.
  4. Angiotensin II causes the muscular walls of small arteries (arterioles) to constrict (narrow), which increases blood pressure. Angiotensin II also triggers your adrenal glands to release aldosterone and your pituitary gland to release antidiuretic hormone (ADH, or vasopressin).
  5. Together, aldosterone and ADH cause your kidneys to retain sodium. Aldosterone also causes your kidneys to release (excrete) potassium through your urine.
    The increase in sodium in your bloodstream causes water retention.
  6. This increases blood volume and blood pressure, thus completing the renin-angiotensin-aldosterone system.
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8
Q

What is aldosterone, what does it bind to and what does it increase

A

Aldosterone is a steroid hormone that binds to the mineralocorticoid receptor and increases the transcription of ENaC and Na-K pumps in the tubule epithelia. This causes increases in Na+ reabsorption and K+ secretion

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9
Q

Define heart failure

A

Heart failure is a chronic progressive condition. Through abnormality of cardiac structure or function and systemic changes that lead to a failure of the heart to fill and/or eject blood. This then leads to a failure to deliver oxygen at a rate that is required of the metabolizing tissues

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10
Q

What are the two types of heart failure

A

Heart Failure with Preserved Ejection Fraction (HFpEF) and Heart Failure with Reduced Ejection Fraction (HFrEF)

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11
Q

In HFrEF what happens to Left Ventricular volumes and Ejection Fraction

A

When HFrEF occurs, Left Ventricular Volumes increase, and the Ejection Fraction decreases

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12
Q

What is Systolic Heart Failure and Diastolic Heart Failure

A

Systolic Heart Failure = HFrEF
Diastolic Heart Failure = HFpEF

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13
Q

What are some of the Pharmacotherapies for heart failure

A

ACE inhibitors, ARBs, Beta Blockers, Diuretics

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14
Q

What is VAD

A

VAD stands for Ventricular Assist Device

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15
Q

Define heart failure, briefly explaining and contrasting HFpEF and HFrEF

A

Heart failure is a chronic progressive condition. Through abnormality of cardiac structure or function and systemic changes that lead to a failure of the heart to fill and/or eject blood. This then leads to a failure to deliver oxygen at a rate that is required of the metabolizing tissues
HFpEF = Heart failure with preserved ejection fraction is also known as diastolic heart failure, where the wall are thickened and stiff causing the heart to struggle to fill
HFrEF = heart failure reduced ejection fraction known as systolic heart failure, where the walls are thin and dilated causing the heart to struggle to pump

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16
Q

Current end-stage therapies used to manage heart failure involve heart transplantation and ventricular assistance devices (VADs). Explain their major disadvantages (3 marks) and then elaborate on how cardiac stem cell research may allow cardiac regeneration as a future therapeutic option (2 marks).

A
  1. The current major disadvantages of VADs are, costs, longevity, bleeding, and infections
  2. Cardiac stem cells may be the future option such as the use of Neuregulin and reprogramming non-myocytes. This new research focuses on the regeneration and restoration of the function of the heart after injury.
17
Q

In an ECG what is ST segment elevation a sign of

A

an area of ischemia has developed less than an hour ago

18
Q

When is the best time to initiate hormone replacement therapy to prevent against cardiovascular disease

A

within the first 10 years

19
Q

your access to and level of healthcare and longevity is primarily related to

A

the affluence of the country you live in

20
Q

what is the measurement that is derived from tissue Doppler of the mitral annulus

A

E/A ratio

21
Q

What measures the amount of blood moving from the left atrium to the left ventricle in diastole

A

E/A ratio

22
Q

Describe the different waves of the ECG trace, link them to the changes in membrane potential of cardiac cells and the physical changes of the heart?

A

P-wave: atrial depolarisation
QRS: ventricular depolarisation
T: ventricular repolarisation

23
Q

Describe the role of cavin/caveolin/eNOS and nitric oxide in regulating cardiac stiffness

A

Cavin and caveolin proteins were reduced in old people
Cavin knockout mice have reduced caveolin activity
Cavin and caveolin proteins regulate cardiac stiffness
Caveolae (membrane mechanosensors and invaginations in membrane, when you stretch a cell, you flatten the caveolae which ejects proteins and phosphorylates caveolin 1 which inhibits NOS activity) formation and function is dependent on cavin and cavolae proteins

24
Q

Describe the history of research into the cardiovascular effects of hormone replacement therapy.
What were the initial published conclusions and how was our understanding refined over time.
What are the current recommendations?

A

Estrogen = cardioprotective
· Clinical trial prematurely ended due to ↑breast cancer risk and ↑CHD risk
· Didn’t account for the time between menopause and HRT commencement
· Findings: if HRT is started within 10 years of menopause onset = reduce risk.

25
Q

What does the T-wave of an ECG trace represent? Why is the T wave positive?

A

Ventricular repolarisation . Although repolarisation occurs in the opposite direction to depolarisation, the wave is positive. This is because the impulse is traveling from the positive to the negative end, but it is traveling away from the electrode. Therefore, two negatives make a positive.

26
Q
A
27
Q

As the blood levels the left ventricle it moves through the a number of vessel types before it reaches the right atria? Provide the correct order of the vessels blood moves through

A

Aorta-Arteries-Arterioles-Capillaries-Venules-Veins-Vena Cava- Right Atrium

28
Q

Describe the four New York Heart Association Functional Classifications of heart failure

A
  1. Asymptomatic HF: Previous MI, LV dysfunction, Asymptomatic valvular disease
  2. Symptomatic HF: known structural heart disease, shortness of breath and fatigue, reduced exercise tolerance
  3. Refractory End-Stage HF: