Cardiovascular Disorders

what is cardiac preload?

volume of blood in the ventricles at the end of diastolic pressure

what is preload determined by?

venous return

what is venous return?

the volume of blood entering the right atrium

what is cardiac afterload?

resistance that the left ventricle must overcome to circulate blood

what increases preload?

hypervolemia, regurgitation of cardiac values, and heart failure

what affects afterload?

peripheral vascular resistance and wall tension

what increases afterload?

hypertension and vasoconstriction

what does increased afterload mean?

increased cardiac workload

is the relationship between contractility and preload positive or negative?

positive; as contractility increases, so does the preload capacity

is the relationship between contractility and afterload positive or negative?

negative; as contractility increases, afterload decreases

what happens if there is excessive afterload?

the heart muscle weakens

what is contractility?

myocardium's ability to stretch and contract in response to the filling of the heart with blood

what is stroke volume?

the amount of blood that is ejected with each contraction in the ventricle

what is left ventricular ejection fraction?

(LVEF); the percentage of blood that leaves the left ventricle each time it contracts

what is the LVEF value of a healthy individual?

60-70%

what is the LVEF value of a risk individual?

40% or lower

what does low LVEF value mean?

heart failure

what is inotropic function?

the force of contraction of the heart

what is chronotropic function?

heart rate

what do we use in medicine to alter the heart rate?

medication!

what is blood pressure?

pressure in the peripheral arterial system

what is the blood pressure equation?

BP = CO x PVR

what is cardiac output?

the volume of blood pumped/min -- ml/min

what is the equation for cardiac output?

CO = HR x SV

what is stroke volume (SV)?

the amount of blood pumped out of the heart with each contraction

what is heart rate (HR)?

beats per minute (bpm)

what is the average cardiac output of an adult?

5L/min

what is the average SV of an adult?

70ml

what is peripheral vascular resistance (PVR)?

systemic vascular resistance

how does PVR relate to diameter?

PVR is inversely related to diameter; increased diameter = decreased PVR and vice versa

*think of it as dilation vs. constriction*

what are the three ways blood pressure is regulated in the body?

1. sympathetic nervous system

2. antidiuretic hormone (ADH)

3. renin-angiotensin-aldosterone system (RAAS)

how does the sympathetic nervous system work to regulate blood pressure?

1. baroreceptor stimulation

2. activates SNS

3. uses alpha1 (vasoconstriction) and beta1 receptors (increases HR)

what happens in the SNS when alpha1 is activated to regulate BP?

vasoconstriction; this leads to increased PVR, which increases BP

what happens in the SNS when beta1 is activated to regulate BP?

increased heart rate and contractility; this increased HR leads to increased CO, which increases BP

how does ADH increase BP?

1. high osmolarity stimulates osmoreceptors to stimulate pituitary gland, which secretes ADH

2. ADH goes to the kidney and stimulates water reabsorption

3. this increases extracellular water volume, which increases blood volume, which then increases stroke volume, which then increases CO, which finally increases BP

what does ADH change to increase BP?

changes SV and CO, but not PVR

how does RAAS increase BP?

1. decreased extracellular fluid and decreased arterial BP stimulates renin secretion

2. renin becomes angiotensinogen in the liver

3. becomes angiotensin I

4. goes to the lungs and is affected by ACE (angio converting enzyme)

5. becomes angiotensin II

- in the arterioles, vasoconstriction occurs and increases PVR, which then increases BP

- in the adrenal cortex, aldosterone is created, which goes to the kidneys and stimulates water + sodium reabsorption; this increases vascular volume, which increases SV, which increases CO, which increases BP

do all three of the BP regulation systems (sympathetic nervous system, ADH, and RAAS) occur at the same time or one after another?

they all occur at the same time

what is endothelial damage caused by?

hypertension, hypercholesterolemia, smoking, and uncontrolled diabetes mellitus

what does endothelial damage cause?

endothelial dysfunction

what does endothelial dysfunction set up the development for?

atherosclerosis

what layer is the endothelium?

the innermost layer

where is the endothelium found in the majority of?

blood vessels

what are the three layers of the endothelium?

1. tunica intima = innermost

2. tunica media = middle

3. tunica externa = outermost

what kind of muscle is the endothelium?

smooth muscle

what is the first step in the formation of atherosclerosis from endothelial damage?

endothelial damage initiates inflammation, which causes WBCs to transmigrate to the site of injury

what is the second step in the formation of atherosclerosis from endothelial damage?

WBCs stick to the endothelial walls and make their way into the tunica intima, where they eat LDL and any foreign bodies

what are the 4 steps of the WBC pathway?

margination, transmigration, chemotaxis, phagocytosis

what is the third step in the formation of atherosclerosis from endothelial damage?

WBCs become foam cells due to all the LDL they have consumed; they do chemotaxis to attract more WBCs into the injury site, meaning more foam cells are created.

when there are enough foam cells, we can see them with the naked eye; these foam cells secrete growth factors, chemotaxis chemicals, and stimulates smooth muscle migration

what were cells originally before they became foam cells during atherosclerosis?

they were originally macrophages

what is the fourth step in the formation of atherosclerosis from endothelial damage?

- the atherosclerosis forms on top as a plaque; underneath, there are foam cells and macrophages

- the foam cells become a necrotic core that contains many tissue factors

- when the tissues are exposed to blood, they activate extrinsic pathway clotting cascade to keep it away from the bloodstream

why is it important for an atherosclerotic plaque to separate itself from the necrotic core of foam cells?

once the necrotic core is exposed to the bloodstream, it will activate the extrinsic clotting cascade and form a very large clot

what are the five most common areas of the body to form an atherosclerotic plaque?

in order...

1. abdominal aorta

2. coronary arteries

3. carotid arteries

4. vertebrae

5. thoracic aorta

ACCVT

All Cats Come Very Thin

(I promise I’m trying my best with these :’ ) )

what are the risks of atherosclerosis?

same as those that cause endothelial damage:

- hypertension

- hypercholesteremia

- smoking

- uncontrollable diabetes mellitus

what is peripheral arterial disease (PAD)/peripheral arterial occlusive disease (PAOD)?

they mean the same thing; this occurs when an atherosclerotic plaque obstructs blood flow to a lower extremity

what are the two types of PAD/PAOD?

acute and chronic

what are the risk factors of PPAD/PAOD?

older age, HTN, diabetes mellitus, smoking, high fat diets, sedentary lifestyle, obesity, family history, hyperlipidemia

what are the steps to peripheral arterial disease occurring?

1. occlusion of arterial blood flow

2. reduced arterial blood flow

3. tissue oxygen supply < demand

4. ischemia and anaerobic metabolism occur

5. intermittent pain; pallor, coolness, weak pulses, and paresthesia

Other Red Toppings In Ice-cream

(Never back down, never what???)

what happens when tissue oxygen supply is less than the demand of the body?

ischemic pain forms

what is one way we can check for peripheral arterial disease?

the ankle-brachial index

what is the ankle-branchial index?

comparison of the BP in the arm vs. the leg

what is the normal ankle-brachial ratio?

greater than one. the ankle pressure is greater than the brachial pressure

what is the ankle-brachial ratio of a patient with PAD?

ABI index is less than 0.5

arterial disease characteristics

- no pulse

- color is pale -> blue

- sharp pain

- paresthesia

- paralysis

venous disease characteristics

- pulse

- color is pink to red and is warm; condition is stasis dermatitis

- ache pain

- edema congestion; can't move blood back to the heart

- ulcer development

what is hypertension?

high blood pressure

what is systole?

cardiac contraction

what is diastole?

cardiac relaxation

what is deemed normal BP?

anything below 120/80 but above 90/60

how does hypertension cause atherosclerosis?

damaging force of high BP injures the endothelial lining of the arteries, which leads to atherosclerosis

how does hypertension cause heart failure?

the high resistance in HTN increases afterload, which causes cardiac hypertrophy, which causes heart failure

how does cellular adaptation during hypertension cause heart failure?

chronic increased workload leads to chronic hypertrophy, which can cause heart failure

what is an aneurysm?

a weakening in an artery wall causing localized bulging and dilation

what is a weakened artery susceptible to?

rupture; which can lead to internal hemorrhage

what do aneurysms cause?

turbulent blood flow

what are the risk factors of aneurysms?

hypertension, atherosclerosis, smoking

what are the signs and symptoms of aneurysms?

- asymptomatic until it ruptures

- bruit (indicative of turbulent blood flow)

- diminished/absent pulse

what do the signs and symptoms of aneurysms depend on?

the size, location, and integrity of the aneurysm itself

where are the most common areas for an aneurysm to form?

aorta and cerebral arteries

in three steps, how can you summarize rupture from an aneurysm?

1. vessels are weakened due to turbulent blood flow

2. rupture occurs

3. internal bleeding (hemorrhage) occurs

what is aortic dissection?

a tear in the arterial lining between tunica intima and tunica media

what happens when an aortic dissection occurs?

blood flows within the tear and forms a hematoma within the wall

what are the signs/symptoms of aortic dissection?

- pain in the chest/back

- difference between BP in left and right arm

- wide pulse pressure

what is an indication from the patient that they may be experiencing aortic dissection?

the patient describes a ripping or tearing pain in their chest

what is hypercholesteremia?

increased levels of cholesterol in the blood

what is the source of cholesterol in our body?

comes from lipoproteins in the form of HDL or LDL

what is LDL?

low-density lipoprotein; lipid>protein

what is HDL?

high-density lipoprotein; lipid

what is the "good cholesterol?"

HDL

what does LDL do?

transports cholesterol from the liver to the cells

what can happen to LDL?

it can be oxidized and deposited right on the artery wall, increasing the serum cholesterol level

what does HDL do?

transports cholesterol from the cells back to the liver, decreasing the serum cholesterol level

how does hypercholesteremia pertain to the formation of atherosclerotic plaques?

since atherosclerosis is based around the formation of foam cells that proliferate and become necrotic, they cannot form without an excess amount of cholesterol/fat in the arteries (LDL!) -- that's what causes the necrotic center, forms the plaque, and can cause the extrinsic clot pathway if it breaks and meets the bloodstream

how does smoking initiate atherosclerosis?

smoking causes endothelial damage -> atherosclerosis

nicotine is a strong vasoconstrictor of the coronary arteries (others too, but mostly coronary)

how does diabetes initiate atherosclerosis?

uncontrolled diabetes initiates atherosclerosis

where do the coronary arteries start?

distal to the aortic valve

what happens to the myocardium during diastole?

the myocardium is perfused

when does the heart actually become oxygenated?

when the valve closes

what are the three main branches of the coronary artery?

right coronary arteries, left descending artery, and left circumflex artery

what is coronary artery disease (CAD)?

heart disease from impaired blood flow