bio 202 cardio and raas exam

correct pathway blood flow of heart

superior vena cava - right atrium - tricuspid valve - right ventricle - pulmonary semilunar valve - pulmonary trunk - lungs - pulmonary veins - left atrium - mitral (bicuspid valve ) - left ventricle - aortic semilunar valve - aorta - systemic circulation

atria

superior chambers

ventricles

inferior chambers

right side of what is considered what

pulmonary pump - pumps blood short distance to the lungs

left side of heart is considered

systemic pump - which pumps blood to entire body

which side of the heart has thicker myocardium and why ?

left side because its pumps more force through systemic pathway

parasympathetic

rest and digest - in the medulla - vagus nerve is the main nerve

slows heart rate down

sympathetic nervous

also known as fight or flight, also in medulla

main nerves - cardiac sympathetic nerves

neurotransmitter - adrenal and epinephrine

increases heart rate and contractility

chronotropic factor

factors affecting heart rate

positive agents - sympathetic stimulation, epinephrine, thyroid hormone t3 and t4, hyperthermia

negative agents - parasympathetic, beta blockers

inotropic factor

factors affecting force of contraction (stroke volume)

positive agents - sympathetic stimulation

negative agents - beta blockers, calcium blockers

cardiac output

the total volume of blood your heart pumps out per minute

stroke volume

the amount of blood pumped out in a single beat

• amount of blood pushed out of the left ventricle in one beat

heart rate (HR)

how many times your heart beats in one minute

measured in BPM

beats per minute

stroke voume (SV) is measured in

milliliters per beat (mL/beat)

cardiac ouput is measured in

liters per minute (L/min)

what is the core formula for cardiac output

cardiac output (CO) = heart rate (HR) x Stroke volume

Everyday Example: If your resting HR is $70\text{ bpm}$ and your SV is $70\text{ mL/beat}$:

$$\text{CO} = 70 \times 70 = 4,900\text{ mL/min} \approx 5.0\text{ L/min}$$

(You pump your body's entire blood supply roughly every single minute!)

preload

how much the ventricle fills up and strethes with blood before it contracts

Think of the ventricle like a balloon:

• Small amount of air (Low Preload): The balloon barely stretches. When you let go, it releases a weak puff of air.

• Lots of air (High Preload): The balloon stretches tight. When you let go, it snaps back and snaps blood out with a powerful force.

end - diastolic volume (EDV)

the actual volume of blood in the ventrile at the end of filling (usually - 120 mL )

preload is the resulting stretch cause by EDV

more EDV causes higher preload

frank straling law of the heart

greater stretch = stronger contraction

venous return

the amount of blood retunring back to the heart through the veins

higehr venous return - higher EDV - higher preload - higher stroke volume

what changes preload

increases preload ( higher SV)

decreases preload (lower SV)

afterload

resistance or pressure the ventricles must overcome to open semilunar valves and eject blood

beggining of systole (pumping phase)

increased afterload = decreased sv

hypertension

high blood pressure

vasoconstriction

narrowing of arteriese

electrical

always happens first, mechanicl follows right after

depolarization

turn on (electrical) : sodium and calcium rush into the heart cells, flipping their electrical charge from negative to positive

what does depolarization trigger

triggers mechanical action ; systole (squeeze / contraction)

systole

the contraction phase of the heart muscle when it squeezes to pump blood out

pressure is high

diastole

relaxation/ resting

• chamber fills back up with blood

  • low pressure

normal blood pressure reading is

120/ 80

120 - systolic pressure - the peak pressure in your arteries when the left ventricle contracts

80 - diastolic pressure when the heart relaxes

repolarization

reset (electrical) - potassium leaves the heart cells, resetting their electrical charge back to negative

what does repolarization trigger

mechanical action - diastole (relaxation and filling)

plateau phase

holding the squeeze - during depolarization, calcium enters slowly to keep the cells turned on longer

• it matters because it stops the heart from cramping (tetanus) so the ventricles have time to squeeze all the blood out

what is a ECG (electrocardiogram)

a machine recording those electrical “turn on” and “reset” signals as they spread throughout the heart

What is a P wave

Its the first small upward bump seen on an ECG reading

electrical - atrial depolarization (atria turn ON)

tun on signal spreads through the top two chambers of the heart ( the atria)

what is a qrs complex

the tall sharp main spike seen on an ECG

electrical ; ventricular depolarization (ventricles turn on)

mechanical - ventricles squeeze hard (ventricular systole) shooting blood into the lungs and body

what is a t wave

its a smooth, rounded upward wave that appears right after the QRS complex on an ECG. It represents ventricular repolarization, the electrical reset signal of the ventricles as they recharge back to their resting state

reset for the next beat

what is the ST segment

its between QRS and T wave, which is the flat baseline right before the T wave represents the plateau phase of the cardiac action

coronary artery disease (CAD)

is the narrowing or blockage of the coronary arteries

primarily caused by atherosclerosis - a buildu[ of fatty plaque inside the arterial walls

non modifiable risks factors for coronary artery disease

age, sex, family history, race

modifiable risks factors for coronary artery disease

hypertension ( high blood pressure)

hyperlipidemia - bad cholesterol

smoking use

obesity

how to doctors diagnose coronary artery disease

they try and detect reduced blood flow,

they use electrocardiogram (ECG / EKG)

• st - segment depresssion or t wave inversion - indicates ischemia (lack of blood/oxygen)

Also use stress test

• evaluates how the heart performs under workload (like running on a treadmill)

treatement for coronary artery disease

it focuses on increasing oxygen supply to the heart muscle, reuding oxygen demand, and physcially clearing or bypassing blockages

• lifetysle changes

• medications

  • like ace inhibitors

  • beta blockers

ace inhibitors are ?

inhibit the RAAS pathway to lower blood pressure

what are beta blockers

block b 1 receptors to decrease heart rate and contractility

what does the cardiac cycle refer to

to one complete heartbeat, lasting roughly 0.8 seconds

it includes both contraction (systole) and relaxation (diastole) f the atria and ventricles

Blood flows from high pressure to low pressure, and valves open or close based on pressure differences.

atriventricular (AV) valves

tricuspid (right) and bicuspid mitral valve (left) - between atria and ventricles

semilunar valves

pulmonary right

aortic - left

what ar the 4 main phases of cardiac cycle

phase 1 - ventricular filling

phase 2 - isovolumetric contraction

phase 3 - ventricular ejection

phase 4 - isovolumetric relaxation

phase 1 - ventricular filliing is what

mid to late diastole

• chamber pressures - ventricular pressure is lower than atrial pressure

what is the valave status during ventricular filling

av valaves are open (blodo drains passively into ventrices)

SL valves - closed

ventricles fill passively to 70-80%, at the end of the phase atrial systole (P wave) kicks in to push the remainnig 20-30% of bood into the ventricles

phase 2 - isovolumetric contraction (early systole)

ventricles begin to contract (QRS complex), ventricular pressure rises above atrial pressure

what is the valve status during isvolumetric ontraction

av valves - snap close (prevents backflow into atria)

SL valves - closed

all 4 valves are closed at the ame time, but pressure builds rapidly

phase 3 - ventricular ejection (late systole)

ventricular pressure skyrockets and overcomes arterial pressure

what is the valve status during ventricular ejection

av valves - closed

SL valves - burst open

blood rapidly ejected out of the ventricles into the aorta and pulmonary trunk

phase 4 - isovolumetric relaxation ( early diastole)

ventricles relax and repolarize (t wave) ventricular perssure drops sharply below arterial pressure

what is the valve status during isovolumetric relaxation

av valves - closed

SL valves - snap closed ( prevents backflow from aorta)

all 4 valves are closed again,ventricles relax whiel volume stays constant until ventricular pressure dropes below atrial pressure to start phase 1 again

heart sounds - whats the first sound ( lub)

the sound Lub (sound 1) is the av valves closing at the start of ventricular systole (phase 2)

heart sounds what is the second sound (dub)

caused by SL valves closing at teh start of ventricular diastole (phase 4)

what are heart murmurs

abnormal hearth sounds casued by turbulent blood flow through damaged or leaky valves

what is congestive heart failure

occurs when the hearts pumping efficiency drops so low that blood circulation no longer meets tissue needs

blood backs up into the vessels behind the failing chamber, leading to sever fluid accumulation (congestion)

what causes left sided heart failure (LHF)

hypertension, coronary artery disease, aortic/mitral valve disorders

what does RAAS system stand for

renin - angiotensin - aldosteron system w

main trigger of RAAS system

when our blood pressure drops too low

what is low blood pressure

aka “hypotension” is a state where blood pressure drops below normal levels, normally defined as 90/60 mmHg

how do you calculate blood pressure

BP = cardiac output (CO) x total perpheral resistance (TPR)

what is total peripheral resistance (TPR)

total amount of friction or oppositino that blood encounters as it flows through all the systemtic blood vessels in our body

if your bood vessees constrict, TPR goes up, which raises blood pressure

if your blood vessels dilate (widen), TPR goes down and lowers your bp

What are steps of RAAS pathway

Blood pressure drops - triggers JG cells in kidney - kidneys release renin - renin circulates which triggers liver - liver secrets angiotensinogen - angiotensinogen turns to angiotensin 1 - ACE enzyme turns angiotensin 1 into angiotensin 2 - triggers vasoconstriction - triggers aldosterone release in kidneys- also triggers posterior pituitary gland to release ADH - which then raises bp

What does angiotensin 2 trigger

1. Vasoconstriction of blood vessels

2. Adrenal glands on kidneys release aldosterone

3. Posterior pituitary releases anti diuretic hormone

what do valve disorders do

disrupt intracradiac blood flow, placing an abnormal workload on the heart chambers

what is stenosis

is the medical term for the abnormal narrowing or structure of a passageway , duct, canal or vessel in the body

what is heart valve stenosis

valve leaflets become stiff, thickened, or fused together, preving the valve from fully opening. the upstream cardiac chamber must generate much higher pressure to force blood past the restriction (e.g., Aortic Stenosis, Mitral Stenosis).

what is spinal stenosis

The spaces within the spine narrow, putting pressure on the spinal cord and nerve roots. This causes pain, numbness, or weakness in the legs and back.

what is vascular stenosis

Blood vessels narrow due to plaque buildup (atherosclerosis) or inflammation, reducing blood supply downstream (e.g., Carotid Artery Stenosis, Renal Artery Stenosis).

what is pyloric stenosis

The opening between the stomach and small intestine thickens in infants, blocking food from entering the intestines and causing severe vomiting.

what is key causes of stenosis

1. Calcification: Calcium deposits build up on tissues over time with aging.

2. Atherosclerosis: Fatty plaque accumulation along arterial walls.

3. Inflammation & Scarring: Damage from infections (like rheumatic fever), trauma, or chronic inflammatory diseases.

4. Congenital Defects: Being born with an abnormally shaped passage or valve (such as a bicuspid aortic valve).

what are the organs used in the RAAS system

kidneys, liver, lungs, adrenal cortex and glands, hypothalamus, posterior pituitary and blood vessels

what are the enzymes used in the RAAs system

• renin

• angiotensin converting enzyme (ACE)

what are teh hormones in RAAS

angiotensinogen, angiotensin 1, angiotensin 2, aldosterone, atidiuretic hormone (ADH)

what does renin do in RAAS system

its prduced by jutaglomerular cells (JG) cells

• released when the kidneys detect low blood pressure, low sodium, or sympathetic nervous system activation

• Target Substrate: Angiotensinogen (an inactive protein circulating in the blood, made continuously by the liver).

• It selectively cleaves (cuts) the specific peptide bond between amino acids 10 and 11 on Angiotensinogen.

• Net Result: Converts the large precursor Angiotensinogen into Angiotensin I (an inactive 10-amino-acid peptide).

what does ACE do

• Produced by: Endothelial cells lining blood vessels, primarily in the capillaries of the lungs (and to a lesser extent, the kidneys).

• Target Substrate: Angiotensin I.

• Enzyme Action:

  • ACE functions as a dipeptidyl carboxypeptidase.

  • It cleaves off two amino acids from the C-terminus (end) of Angiotensin I.

  • It also breaks down bradykinin (a natural vasodilator), marking it for inactivation.

• Net Result: Converts inactive Angiotensin I into Angiotensin II (the active 8-amino-acid hormone responsible for vasoconstriction and triggering aldosterone secretion).

Hypertension

(chronically elevated blood pressure, defined as systolic $\ge 130\text{ mmHg}$ or diastolic $\ge 80\text{ mmHg}$) occurs when systemic vascular resistance, intravascular blood volume, or cardiac output remains persistently elevated.

Causes of Hypertension

90 - 95 % Of causes

Primary (Essential) Hypertension (~90–95% of cases): Has no single identifiable medical cause. It arises from a complex interaction of genetic factors and lifestyle influencers:

• Sympathetic Overactivity: Increased baseline tone causing persistent arteriolar vasoconstriction.

• Renal Handling of Sodium: Defective renal sodium excretion leading to intravascular fluid retention.

• Vascular Remodeling: Decreased arterial compliance (stiffness) and endothelial dysfunction (reduced nitric oxide production).

• Risk Factors: High sodium intake, obesity, physical inactivity, chronic stress, aging, and excessive alcohol intake.

secondary causes 5-10

Secondary Hypertension (~5–10% of cases): Directly results from an underlying, identifiable medical condition or medication:

• Renal Parenchymal & Vascular Disease: Chronic kidney disease (CKD) or Renal Artery Stenosis (which triggers excess Renin release via low renal perfusion).

• Endocrine Disorders:

  • Primary Aldosteronism (Conn's Syndrome): Excessive aldosterone causing $\text{Na}^+/\text{H}_2\text{O}$ retention and $\text{K}^+$ excretion.

  • Pheochromocytoma: Catecholamine-secreting adrenal tumor causing paroxysmal vasoconstriction.

  • Cushing's Syndrome: Cortisol excess causing mineralocorticoid effects and heightened vascular reactivity.

• Obstructive Sleep Apnea (OSA): Intermittent nocturnal hypoxia triggers massive sympathetic surges.

• Coarctation of the Aorta: Congenital narrowing of the aorta creating high pressure upstream in upper body vessels.

• Medications: NSAIDs (block vasodilatory prostaglandins), oral contraceptives, decongestants, and corticosteroids.

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what are the three main blood vessel types

• arteries

• capillaries

• veins

what are the arteries

• carry blood AWAY from the heart

• thick and stretchy

• blood pressure is very high (pulsing hard)

what are capillaries

• they trade oxygen nutrients and waste

• they are ultra thin (one cell thick)

• blood pressure is low

what are veins

• they carry blood BACK to the heart

  • thin and flexible valves

  • very low