Cardiovascular Physiology Flashcards

1
Q

What are the four chambers of the heart?

A

Right atrium (RA): Receives deoxygenated blood from the body (via vena cava)

Right ventricle (RV): Pumps blood to lungs (via pulmonary artery)

Left atrium (LA): Receives oxygenated blood from lungs (via pulmonary veins)

Left ventricle (LV): Pumps oxygenated blood to body (via aorta)

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2
Q

What are the four heart valves & their functions?

A

πŸ”΅ Atrioventricular (AV) valves (separate atria from ventricles)

Tricuspid valve: Between RA & RV
Mitral (bicuspid) valve: Between LA & LV

🟒 Semilunar valves (prevent backflow into ventricles)

Pulmonary valve: Between RV & pulmonary artery
Aortic valve: Between LV & aorta

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3
Q

Which major veins return blood to the heart?

A

Superior vena cava (SVC): Drains blood from upper body into RA

Inferior vena cava (IVC): Drains blood from lower body into RA

Pulmonary veins: Bring oxygenated blood from lungs into LA

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4
Q

Which major arteries carry blood away from the heart?

A

Pulmonary artery: Carries deoxygenated blood to lungs (only artery with deoxygenated blood)

Aorta: Carries oxygenated blood to the body

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5
Q

What is the coronary circulation?

A

The heart’s own blood supply via coronary arteries & veins

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6
Q

What are the major coronary arteries?

A

Left coronary artery (LCA) β†’ branches into:
Left anterior descending (LAD): Feeds anterior LV & septum
Circumflex artery (LCX): Feeds LA & lateral LV

Right coronary artery (RCA): Feeds RA, RV, SA & AV nodes

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7
Q

What are the major coronary veins?

A

Great cardiac vein: Runs alongside LAD

Middle cardiac vein: Drains posterior heart

Small cardiac vein: Drains RV

Coronary sinus: Main drainage, empties into RA

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8
Q

What happens when coronary arteries are blocked?

A

Myocardial infarction (MI) due to ischemia (lack of oxygen)

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9
Q

What are the key structural features of cardiac muscle?

A

Striated, short-branched cells, uninucleate, intercalated discs, larger T-tubules over Z-discs

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10
Q

What is the role of intercalated discs?

A

Allow electrical & mechanical coupling between cells for synchronous contraction

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11
Q

What makes up the intrinsic conduction system?

A

Pacemaker cells & conduction pathways coordinating atrial & ventricular contraction

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12
Q

Why do pacemaker cells have an unstable membrane potential?

A

Due to If (funny) channels, which allow slow Na+ influx & K+ efflux, leading to spontaneous depolarization

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13
Q

What are the phases of pacemaker potential?

A

1️⃣ Slow depolarization (-60mV β†’ -40mV) via If Na+ channels
2️⃣ Threshold reached (-40mV) β†’ Ca2+ influx causes depolarization
3️⃣ Repolarization β†’ K+ channels open, K+ efflux

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14
Q

ow does sympathetic stimulation affect pacemaker cells?

A

Noradrenaline & adrenaline bind to Ξ²1 receptors, increasing If channel activity, leading to faster depolarization & increased HR

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15
Q

How does parasympathetic stimulation affect pacemaker cells?

A

ACh binds to muscarinic receptors, increasing K+ permeability & decreasing Ca2+ influx, causing hyperpolarization & slower HR

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16
Q

How does the action potential of contractile myocardial cells differ from skeletal muscle?

A

Plateau phase (phase 2) in cardiac cells prevents tetanus, ensuring proper relaxation between beats

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17
Q

What are the phases of a myocardial action potential?

A

Phase 4: Resting (-90mV)
Phase 0: Rapid depolarization (Na+ influx)
Phase 1: Initial repolarization (K+ efflux)
Phase 2: Plateau (Ca2+ influx via L-type channels)
Phase 3: Repolarization (Ca2+ channels close, K+ efflux)

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18
Q

What is calcium-induced calcium release?

A

Ca2+ enters via L-type channels, triggering Ca2+ release from SR, leading to contraction

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19
Q

How does Ξ²1 receptor activation affect contraction?

A

Increases Ca2+ influx via L-type channels, enhancing SR Ca2+ release & contractility

20
Q

What are the phases of the cardiac cycle?

A

1️⃣ Rest (End Diastole): Blood fills atria & ventricles
2️⃣ Atrial Systole: Atria contract β†’ complete ventricular filling
3️⃣ Isovolumetric Contraction: AV valves close (πŸ’“ β€œlub”)
4️⃣ Ventricular Ejection: Semilunar valves open β†’ blood ejected
5️⃣ Isovolumetric Relaxation: Semilunar valves close (πŸ’“ β€œdup”)

21
Q

What causes the first and second heart sounds?

A

βœ… Lub (S1): Closure of AV valves (mitral & tricuspid)
βœ… Dup (S2): Closure of semilunar valves (aortic & pulmonary)

22
Q

What is the equation for cardiac output (CO)?

A

CO = Stroke Volume (SV) Γ— Heart Rate (HR)

23
Q

How does the autonomic nervous system regulate CO?

A

βœ… Sympathetic: ↑ HR (chronotropic), ↑ conduction speed (dromotropic), ↑ contractility (inotropic)
βœ… Parasympathetic: ↓ HR, ↓ conduction speed, ↓ contractility

24
Q

What is the Frank-Starling Law?

A

βœ… Increased preload (ventricular filling) = increased stroke volume, due to better actin-myosin overlap

25
Q

What does the Frank-Starling Law state?

A

βœ… The more the heart fills (preload), the stronger the contraction β†’ ↑ Stroke Volume (SV)

26
Q

How does increased preload affect stroke volume?

A

βœ… More blood returning to the heart (venous return) β†’ more stretch on ventricular walls

Better overlap of actin & myosin filaments
Stronger contraction β†’ ↑ SV

27
Q

What factors increase preload?

A

Increased venous return (exercise, IV fluids)
Slower HR (more filling time)

28
Q

What factors decrease preload?

A

Blood loss (hypovolemia)
Dehydration
Tachycardia (less filling time)

29
Q

How does afterload affect stroke volume?

A

Afterload = resistance the heart must overcome to eject blood

↑ Afterload (e.g., hypertension, aortic stenosis) β†’ ↓ SV
↓ Afterload (e.g., vasodilation) β†’ ↑ SV

30
Q

What is the equation for Mean Arterial Pressure (MAP)?

A

MAP = CO Γ— SVR (Systemic Vascular Resistance)

31
Q

How do baroreceptors regulate BP?

A

Located in carotid sinus & aortic arch, sense stretch, send signals to brainstem to adjust HR & vessel tone

32
Q

What hormones are involved in long-term BP control?

A

βœ… Renin-Angiotensin-Aldosterone System (RAAS):

Renin β†’ Angiotensin II: Vasoconstriction
Aldosterone: Na+ & water retention
βœ… ADH (vasopressin): Increases water retention
βœ… Atrial Natriuretic Peptide (ANP): Promotes Na+ excretion

33
Q

Where are baroreceptors located?

A

βœ… Carotid sinus (internal carotid artery) & aortic arch β†’ most sensitive to BP changes

34
Q

How do baroreceptors sense BP?

A

βœ… Stretch receptors that fire action potentials based on arterial wall stretch

34
Q

What happens when BP increases?

A

βœ… More stretch β†’ ↑ baroreceptor firing β†’ stimulates parasympathetic NS (PNS)

↓ HR (bradycardia)
↓ contractility
↓ vasoconstriction β†’ ↓ BP

35
Q

What happens when BP drops?

A

βœ… Less stretch β†’ ↓ baroreceptor firing β†’ stimulates sympathetic NS (SNS)

↑ HR (tachycardia)
↑ contractility
↑ vasoconstriction β†’ ↑ BP

36
Q

What are the two types of baroreceptors?

A

Type A: High sensitivity, rapid response
Type C: Lower sensitivity, higher threshold, better at handling high BP

37
Q

Are there other stretch receptors?

A

βœ… Yes!

Coronary artery baroreceptors β†’ More sensitive than carotid & aortic ones

Veno-atrial mechanoreceptors β†’ Detect blood volume changes (e.g., when lying down)

Unmyelinated mechanoreceptors β†’ Found in ventricles (during systole) & atria (during inspiration)

38
Q

What triggers RAAS activation?

A

Low BP (sensed by kidney baroreceptors)
Low Na+ levels
SNS activation (Ξ²1 receptors on kidneys)

38
Q

What is the function of RAAS?

A

Regulates BP & blood volume via vasoconstriction & sodium retention

39
Q

What are the steps of RAAS?

A

1️⃣ Renin release (kidneys) due to low BP
2️⃣ Renin converts angiotensinogen (liver) β†’ angiotensin I
3️⃣ ACE (lungs) converts angiotensin I β†’ angiotensin II
4️⃣ Angiotensin II effects:

Vasoconstriction β†’ ↑ BP
Aldosterone release (adrenal glands) β†’ Na+ & water retention β†’ ↑ blood volume
ADH release (posterior pituitary) β†’ ↑ water reabsorption

40
Q

How does RAAS affect long-term BP control?

A

Increases blood volume & vascular resistance, maintaining BP in hypovolemia or dehydration

41
Q

What is shock?

A

βœ… Acute failure of the CV system to perfuse tissues adequately

42
Q

What are the types of shock?

A

Hypovolemic: Blood/fluid loss (hemorrhage, burns)

Distributive: Vasodilation (sepsis, anaphylaxis)

Cardiogenic: Heart pump failure (MI, myocarditis)

Obstructive: Blockage (PE, tamponade, tension pneumothorax)

43
Q

What happens in response to blood loss?

A

βœ… Baroreceptors & chemoreceptors activate:

↑ HR, vasoconstriction, RAAS activation
Release of vasopressin, angiotensin II
Increased respiration due to hypoxia