Cardiovascular Physiology Flashcards by Nader Farhead

What are the four chambers of the heart?

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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What are the four heart valves & their functions?

🔵 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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Which major veins return blood to the heart?

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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Which major arteries carry blood away from the heart?

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

Aorta: Carries oxygenated blood to the body

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What is the coronary circulation?

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

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What are the major coronary arteries?

Left coronary artery (LCA) → 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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What are the major coronary veins?

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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What happens when coronary arteries are blocked?

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

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What are the key structural features of cardiac muscle?

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

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What is the role of intercalated discs?

Allow electrical & mechanical coupling between cells for synchronous contraction

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What makes up the intrinsic conduction system?

Pacemaker cells & conduction pathways coordinating atrial & ventricular contraction

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Why do pacemaker cells have an unstable membrane potential?

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

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What are the phases of pacemaker potential?

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

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ow does sympathetic stimulation affect pacemaker cells?

Noradrenaline & adrenaline bind to β1 receptors, increasing If channel activity, leading to faster depolarization & increased HR

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How does parasympathetic stimulation affect pacemaker cells?

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

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

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

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What are the phases of a myocardial action potential?

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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What is calcium-induced calcium release?

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

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How does β1 receptor activation affect contraction?

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

What are the phases of the cardiac cycle?

1️⃣ Rest (End Diastole): Blood fills atria & ventricles
2️⃣ Atrial Systole: Atria contract → complete ventricular filling
3️⃣ Isovolumetric Contraction: AV valves close (💓 “lub”)
4️⃣ Ventricular Ejection: Semilunar valves open → blood ejected
5️⃣ Isovolumetric Relaxation: Semilunar valves close (💓 “dup”)

What causes the first and second heart sounds?

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

What is the equation for cardiac output (CO)?

CO = Stroke Volume (SV) × Heart Rate (HR)

How does the autonomic nervous system regulate CO?

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

What is the Frank-Starling Law?

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

What does the Frank-Starling Law state?

✅ The more the heart fills (preload), the stronger the contraction → ↑ Stroke Volume (SV)

How does increased preload affect stroke volume?

✅ More blood returning to the heart (venous return) → more stretch on ventricular walls Better overlap of actin & myosin filaments Stronger contraction → ↑ SV

What factors increase preload?

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

What factors decrease preload?

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

How does afterload affect stroke volume?

Afterload = resistance the heart must overcome to eject blood ↑ Afterload (e.g., hypertension, aortic stenosis) → ↓ SV ↓ Afterload (e.g., vasodilation) → ↑ SV

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

MAP = CO × SVR (Systemic Vascular Resistance)

How do baroreceptors regulate BP?

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

What hormones are involved in long-term BP control?

✅ Renin-Angiotensin-Aldosterone System (RAAS): Renin → Angiotensin II: Vasoconstriction Aldosterone: Na+ & water retention ✅ ADH (vasopressin): Increases water retention ✅ Atrial Natriuretic Peptide (ANP): Promotes Na+ excretion

Where are baroreceptors located?

✅ Carotid sinus (internal carotid artery) & aortic arch → most sensitive to BP changes

How do baroreceptors sense BP?

✅ Stretch receptors that fire action potentials based on arterial wall stretch

What happens when BP increases?

✅ More stretch → ↑ baroreceptor firing → stimulates parasympathetic NS (PNS) ↓ HR (bradycardia) ↓ contractility ↓ vasoconstriction → ↓ BP

What happens when BP drops?

✅ Less stretch → ↓ baroreceptor firing → stimulates sympathetic NS (SNS) ↑ HR (tachycardia) ↑ contractility ↑ vasoconstriction → ↑ BP

What are the two types of baroreceptors?

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

Are there other stretch receptors?

✅ Yes! Coronary artery baroreceptors → More sensitive than carotid & aortic ones Veno-atrial mechanoreceptors → Detect blood volume changes (e.g., when lying down) Unmyelinated mechanoreceptors → Found in ventricles (during systole) & atria (during inspiration)

What triggers RAAS activation?

Low BP (sensed by kidney baroreceptors) Low Na+ levels SNS activation (β1 receptors on kidneys)

What is the function of RAAS?

Regulates BP & blood volume via vasoconstriction & sodium retention

What are the steps of RAAS?

1️⃣ Renin release (kidneys) due to low BP 2️⃣ Renin converts angiotensinogen (liver) → angiotensin I 3️⃣ ACE (lungs) converts angiotensin I → angiotensin II 4️⃣ Angiotensin II effects: Vasoconstriction → ↑ BP Aldosterone release (adrenal glands) → Na+ & water retention → ↑ blood volume ADH release (posterior pituitary) → ↑ water reabsorption

How does RAAS affect long-term BP control?

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

What is shock?

✅ Acute failure of the CV system to perfuse tissues adequately

What are the types of shock?

Hypovolemic: Blood/fluid loss (hemorrhage, burns) Distributive: Vasodilation (sepsis, anaphylaxis) Cardiogenic: Heart pump failure (MI, myocarditis) Obstructive: Blockage (PE, tamponade, tension pneumothorax)

What happens in response to blood loss?

✅ Baroreceptors & chemoreceptors activate: ↑ HR, vasoconstriction, RAAS activation Release of vasopressin, angiotensin II Increased respiration due to hypoxia