Cardiovascualr Flashcards

Question

**Sinus Rhythm**

Answer 1

- Normal heartbeat triggered by **SA node** - Resting adult rate: **70–80 bpm** (vagal tone slows it from intrinsic 80–100 bpm) - Indicates healthy conduction from SA node down through heart

Answer 2

- Abnormal site of spontaneous depolarization -> aka outside of SA node - *AV node*: 40–50 bpm → called **nodal rhythm** - *Other sites*: 20–40 bpm → too slow to sustain life

Answer 3

- Begins around **–60 mV**, maintained by **Na⁺/K⁺ ATPase** (3 Na⁺ out, 2 K⁺ in) - Membrane **slowly depolarizes** as **Na⁺ leaks in through “funny” (If) channels** - This gradual influx creates the **pacemaker potential** (prepotential) **1. Pacemaker potential (prepotential)** - Begins at –60 mV - Na⁺ leak channels (If) cause slow depolarization - Gradually reaches threshold (~–40 mV) **2. Depolarization** - At threshold, **voltage-gated Ca²⁺ channels open** (L-type) - **Ca²⁺ rushes in** → sharp depolarization to ~0 mV **3. Repolarization** - **K⁺ channels open**, K⁺ exits → returns membrane to ~–60 mV - **Ca²⁺ channels close** (voltage-dependent) - **Ca²⁺ is removed** by: - Na⁺/Ca²⁺ exchanger (NCX) → main mechanism (3 Na⁺ in / 1 Ca²⁺ out) - Ca²⁺ ATPase (PMCA) → minor role - SERCA → sequesters Ca²⁺ into SR (not out of cell) - Cycle restarts immediately (no flat phase) **Cycle duration** - SA node fires ~every 0.8 sec → 75 bpm - AV node and other pacemakers are slower, only take over if SA node fails **Key contrast with contractile cells**: - No stable resting potential - AP upstroke is driven by **Ca²⁺**, not Na⁺ - Lacks a plateau phase (no sustained contraction)

Answer 4

- Resting potential ~–90 mV, maintained by Na⁺/K⁺ ATPase - Myocytes have sarcomeres and stable membrane potential 1. **Depolarization** → Stimulus opens voltage-gated Na⁺ channels → Na⁺ enters → rapid depolarization to +30 mV → Na⁺ channels close quickly 2. **Plateau phase (~200–250 ms)** → Depolarization spreads along the **sarcolemma** and down into **T-tubules** (which are invaginations of the sarcolemma and filled with extracellular fluid) → This opens L-type voltage-gated Ca²⁺ channels (dihydropyridine receptors) located in the T-tubule membrane → **Ca²⁺ enters from the extracellular fluid inside the T-tubules into the sarcoplasm** → Because this Ca²⁺ crosses the sarcolemma, it directly contributes to the membrane potential and prolongs depolarization → That Ca²⁺ then binds to Ca²⁺-gated channels on the sarcoplasmic reticulum (ryanodine receptors) → SR releases additional Ca²⁺ into the sarcoplasm (this intracellular release does not affect membrane potential) → Sustained Ca²⁺ influx balances partial K⁺ efflux, maintaining the plateau near 0 mV 3. **Repolarization** → Ca²⁺ channels close, K⁺ channels open fully → K⁺ exits rapidly → returns membrane to resting potential (–90 mV) 4. **Absolute refractory period (~250 ms)** → Prevents wave summation and tetanus → ensures rhythmic contraction → Caused by **inactivation of voltage-gated Na⁺ channels** - After opening (m-gate), Na⁺ channels enter an inactivated state (h-gate closes) - Channels cannot reopen until membrane repolarizes and resets their gates - This inactivation is time- and voltage-dependent

Answer 5

- **sarcolemma**: Muscle cell plasma membrane - **sarcoplasm**: Muscle cell cytoplasm - **sarcoplasmic reticulum**: specialized smooth endoplasmic reticulum. Stores calcium and regulates calcium release. Sarcoplasmic reticulum surrounds each myofibril. - **terminal cisterna**: Enlarged areas of the SR with large amounts of calcium. Are on either side of t-tubules. Release of calcium from cisternae triggers muscle contractions. - **T-tubules**: invaginations of the sarcolemma which penetrate into the interior of the muscle fiber surrounding each sarcoplasmic reticulum. Transmit action potential through the cell allowing simultaneous contraction of entire cell. are filled with extracellular fluid, essentially - **Triad**: Two terminal cisterna surrounding a t-tubule. - **myofibril**: Contractile component, composed of bundles of myofilaments. There are thin and thick filaments. - **mitochondria**: energy producers. - **multiple nuclei**

Answer 6

*Action Potential Duration* - **Skeletal**: ~2 ms - **Cardiac**: ~200–300 ms *Depolarization* - **Skeletal**: Fast Na⁺ influx - **Cardiac**: Fast Na⁺ influx followed by prolonged Ca²⁺ influx (plateau) *Refractory Period* - **Skeletal**: Short → allows tetanus - **Cardiac**: Long → prevents summation and tetanus *Excitation-Contraction Coupling* - **Skeletal**: Direct voltage-gated Ca²⁺ channel–SR coupling; little extracellular Ca²⁺ required - **Cardiac**: Requires extracellular Ca²⁺ → triggers SR Ca²⁺ release (CICR) *Contraction Overlap with AP* - **Skeletal**: AP ends before contraction begins - **Cardiac**: AP and contraction overlap → 1:1 beat-to-contraction match

Answer 7

*Location* - **Autorhythmic**: SA node, AV node, conduction system - **Contractile**: Atrial and ventricular myocardium *Resting Potential* - **Autorhythmic**: Unstable (~–60 mV), no true rest - **Contractile**: Stable (~–90 mV) *Trigger to Fire* - **Autorhythmic**: Spontaneous Na⁺ influx (funny channels) → Ca²⁺ upstroke - **Contractile**: Stimulated by adjacent cell → Na⁺ upstroke *Depolarization Ion* - **Autorhythmic**: Ca²⁺ (T-type then L-type) - **Contractile**: Na⁺ (fast voltage-gated) *Plateau Phase* - **Autorhythmic**: None - **Contractile**: Present → due to slow Ca²⁺ influx *Function* - **Autorhythmic**: Set heart rate and rhythm - **Contractile**: Generate force to pump blood

Answer 8

- **P wave**: SA node fires → **atria depolarize** → Followed by **atrial systole** (contraction) ~100 ms later → Ends as atria enter **diastole** during QRS - **PR segment**: Time between end of P wave and start of QRS → Reflects **signal delay at AV node** → Allows atria to fully contract before ventricles depolarize - **PR interval**: Time for signal to travel from SA node through AV node → Includes **P wave + PR segment** → Ensures complete **ventricular filling** before systole **QRS Complex (Q, R, S) – Electrical & Mechanical Events** *Q wave* - First small negative deflection - Represents **initial septal depolarization** (interventricular septum) *R wave* - Large upward deflection - Represents **main ventricular depolarization**, especially **left ventricle** *S wave* - Small negative deflection after R - Represents **final depolarization of ventricular base** *Atria* - **Repolarize** during QRS complex - Repolarization is **masked** by strong ventricular signals - **Atrial diastole** begins - **QT interval**: Full period of **ventricular depolarization to repolarization** → Duration of **ventricular systole** - **ST segment**: Ventricles remain depolarized → corresponds to **plateau phase of AP** → Still in **ventricular systole** - **T wave**: **Ventricular repolarization** → Followed by **ventricular diastole (relaxation)** and passive filling - **Clinical note**: **ST elevation or depression** may indicate myocardial infarction (MI)

Answer 9

- Resting heart rate > 100 bpm - Atrial tachycardia: rapid firing in the atria, ventricles follow → heart rate can reach ~180 bpm - Ventricular tachycardia (V-tach): fast rhythm from the ventricles, often due to repeated premature contractions → Can reduce cardiac output and be life-threatening - Causes include stress, anxiety, stimulants, fever, or heart disease - May occur briefly during exercise (training), but if it persists at rest, it can increase the risk of stroke

Answer 10

Uncoordinated Electrical Activity **Atrial fibrillation**: impulses ~500 bpm → quivering atria, not true contraction → Ventricles may still beat ~180 bpm due to irregular conduction through the AV node → Reduced ventricular filling (atria don't contract effectively) → Can increase stroke risk due to blood pooling → Not immediately fatal, but increases long-term risk of stroke and heart failure **Ventricular fibrillation**: chaotic stimulation among ventricular cells → No coordinated contraction → no cardiac output → **cardiac arrest** → Fatal within minutes without emergency defibrillation → Hallmark of myocardial infarction (MI)

Answer 11

- Delivers a **powerful electrical shock** to the chest - Goal: **depolarize the entire myocardium simultaneously** - Purpose: → Stop chaotic fibrillation (esp. **ventricular fibrillation**) → Allow **SA node** to regain control and **reset sinus rhythm** - Used during **cardiac arrest** or life-threatening arrhythmias → Gives ventricles a chance to respond to normal electrical pacing

Answer 12

1. **Quiescent Period (Late Ventricular Diastole)** - All chambers relaxed - **AV valves open**, blood flows passively into ventricles - Ventricles ~70–80% full - **SA node fires** near end → triggers next phase 2. **Ventricular Filling (Phase 1)** a. **Rapid filling**: AV valves fully open → blood rushes in (occurs durring quiescent period) b. **Diastasis**: Slower passive filling as atria and ventricles equalize pressure (occurs durring quiescent period) c. **Atrial systole**: Atria contract (P wave) → push final blood into ventricles → End-Diastolic Volume (EDV) ~130 mL 3. **Isovolumetric Contraction (Phase 2)** - Ventricles depolarize (QRS complex) → begin contraction - **AV valves close** (first heart sound S₁) - All valves shut → no volume change yet - Ventricular pressure rising rapidly 4. **Ventricular Ejection (Phase 3)** - Pressure exceeds aortic/pulmonary pressure → **semilunar valves open** - Blood ejected → **stroke volume ~70 mL** - Remaining ~60 mL = End-Systolic Volume (ESV) - Occurs during **ST segment and T wave** 5. **Isovolumetric Relaxation (Phase 4)** - Ventricles repolarize (T wave) → relax - **Semilunar valves close** (second heart sound S₂) - All valves shut → volume constant - Ventricular pressure drops rapidly → Cycle restarts as **AV valves reopen** once pressure in ventricles < atria

Answer 13

**Cardiodynamics: Volumes and Stroke Output** - **End-Diastolic Volume (EDV)** → Volume in ventricle **after diastole**, before contraction → ~130 mL (passive filling + atrial systole) → Represents **maximum filling** - **End-Systolic Volume (ESV)** → Volume in ventricle **after systole**, after contraction → ~60 mL → Blood that remains **after ejection** - **Stroke Volume (SV)** → Volume of blood **ejected per beat** → SV = EDV – ESV = **130 mL – 60 mL = 70 mL** - **Clinical Note** → Left and right ventricles must eject **equal volumes** → Even a 1% mismatch could cause complete imbalance of blood in minutes

Answer 14

**Left Ventricular Failure** - Cause: Left ventricle pumps **less blood** than right → blood backs up into lungs - Result: Increased **pulmonary pressure** → fluid leaks into alveolar tissue - Pathophysiology: → Right heart continues pumping to lungs → Left heart can’t keep up → pulmonary congestion → Fluid fills alveoli → **gas exchange impaired** - Symptoms: → **Shortness of breath**, sense of **suffocation**, crackles on auscultation - Clinical note: → Fluid barrier prevents **oxygen diffusion** across alveolar membrane

Answer 15

**Right Ventricular Failure** - Cause: Right ventricle pumps less blood than the left → Blood backs up into systemic veins - Result: Increased venous pressure → fluid leaks into tissues → Leads to **generalized/systemic edema** - Clinical Signs: → **Hepatomegaly** (enlarged liver) → **Ascites** (fluid in abdominal cavity) → **Jugular vein distension (JVD)** → Swelling of **fingers, ankles, and feet** - Progression: → Can lead to **total heart failure** if untreated

Answer 16

**Sympathetic Nervous System (SNS)** - *Origin*: Cardioacceleratory center (medulla) - *Neurotransmitter*: **Norepinephrine** → binds **β-adrenergic receptors** - *Targets*: SA node, AV node, myocardium, coronary vessels - *Effects*: - ↑ Heart rate: norepinephrine increases cAMP → directly bind **If (funny current)**, and increase PKA phosphorylation and activation of **Ca²⁺ channels** → Cells reach threshold faster → fire more often - ↑ Ca²⁺ influx in contractile cells via **L-type Ca²⁺ channels** → More Ca²⁺ → stronger contraction → more cross-bridge formation - Widespread innervation - Max HR limited by SA node refractory period (~230 bpm) **Parasympathetic Nervous System (PNS)** - *Origin*: Cardioinhibitory center (medulla via **vagus nerve**) - *Neurotransmitter*: **Acetylcholine (ACh)** → binds **muscarinic receptors** - *Targets*: SA node, AV node - *Effects*: - Opens **K⁺ channels** → K⁺ efflux → hyperpolarization - ↓ Heart rate (cells fire less often) - Minimal effect on contractility - Localized innervation **Resting Tone** - *Parasympathetic tone* predominates at rest - *Sympathetic tone* dominates during stress, exercise, or danger

Answer 17

- *Definition*: Amount of blood ejected by each ventricle in **1 minute** - *Formula*: **CO = Heart Rate × Stroke Volume** - *Typical Values*: - **Resting CO**: 4–6 L/min - **Exercise**: - Fit individuals → up to 21 L/min - Elite athletes → up to 40 L/min - **Peak HR**: ~160–180 bpm - RBCs complete one full circuit in ~1 minute **Cardiac Reserve** - *Definition*: Difference between **maximum** and **resting** CO - *Increases* with fitness - *Decreases* with heart disease

Answer 18

- *Higher Brain Centers* (cerebral cortex, limbic system, hypothalamus) → Modulate HR via emotion/thought (e.g. fear, love) → Relay signals to medullary cardiac centers - *Proprioceptors* (in muscles/joints) → Detect movement/activity → Signal increase in HR before metabolic demand → Stimulates **sympathetic output** - *Baroreceptors* (aortic arch, carotid sinus) - Detect stretch/pressure changes - Signal sent to **cardioinhibitory** (PNS) or **cardioacceleratory** (SNS) centers in medulla → **↑ BP** → ↑ baroreceptor firing → **parasympathetic** activation → ↓ HR → **↓ BP** → ↓ baroreceptor firing → **sympathetic** activation → ↑ HR - *Integration*: Cardiac centers in medulla oblongata coordinate **PNS (vagus)** and **SNS (cardiac nerves)** output to adjust heart rate appropriately

Answer 19

- *Cause*: Sudden, severe **emotional or physical stress** (e.g. grief, fear) - *Mechanism*: Temporary **weakening of left ventricular wall** → Impairs contraction → Heart assumes **balloon-like shape**, resembling a *takotsubo* (Japanese octopus trap) - *Symptoms*: Mimic heart attack (chest pain, shortness of breath) → No coronary blockage - *Outcome*: Usually **reversible** with supportive care

Answer 20

- *Cardiac center*: Located in **medulla oblongata**, regulates **heart rate and strength of contraction** → Integrates input from brain, baroreceptors, and chemoreceptors → Modulates **parasympathetic (vagus)** and **sympathetic (cardiac nerves)** output **Chemoreceptor Input** - Found in: **aortic arch**, **carotid arteries**, and **medulla** - Respond to changes in: - **CO₂** (hypercapnia) - **pH** (acidosis if pH < 7.35) - **O₂** levels (less influential) - *Function*: Primarily adjust **respiration**, but can **increase heart rate** via SNS → Helps **eliminate CO₂**, restore **pH homeostasis** **Negative Feedback Loops** - *Baroreflex*: Responds to **pressure** - *Chemoreflex*: Responds to **blood chemistry** - Both loops influence cardiac center to adjust **HR and vessel tone**

Answer 21

*Chronotropic = any substance that alters **heart rate** (positive ↑HR or negative ↓HR)* **Neurotransmitters** - **Epinephrine & norepinephrine (catecholamines)**: powerful **positive chronotropes**. cAMP increases activity of L-type Ca2+ chanels and Na+ funny if channels [although glucagon increases cAMP contractile cells do not have may glucogon receptors **Drugs** - **Caffeine**: inhibits **cAMP breakdown** → prolongs sympathetic stimulation → ↑HR - **Nicotine**: stimulates **catecholamine release** → ↑HR **Hormones** - **Thyroid hormone (TH)**: increases number of **adrenergic receptors** on heart → increases sensitivity to sympathetic input → ↑HR **Electrolytes** *Potassium (K⁺)* L-type Ca²⁺ channels (which mediate the upstroke) require a sufficiently negative membrane potential to "reset" (de-inactivate). Without repolarization, many stay inactivated → slower or failed depolarization T-type Ca²⁺ channels also require a negative potential to recover from inactivation If (HCN) Na⁺ channels are less affected—they activate during hyperpolarization, but if the membrane is already near threshold, their activation window is reduced, so less inward current contributes to depolarization 2. **Hypokalemia** (↓ extracellular K⁺) -> **HARD TO REACH THRESHOLD** → ↑ K⁺ gradient → **more K⁺ efflux** → RMP becomes **more negative** (hyperpolarized) → **Harder to reach threshold** → ↓ excitability → May **prolong repolarization** → risk of early afterdepolarizations and arrhythmias *Calcium (Ca²⁺)* *Ca²⁺ has very low resting permeability, so changing extracellular Ca²⁺ does not significantly change RMP.* 1. **Hypercalcemia** → May **slow HR** (negative chronotropy) → high extracellular Ca²⁺ binds to and stabilizes the outer surface of L-type Ca²⁺ channels, making them require a more positive voltage to open. → raises threshold for depolarization 2. **Hypocalcemia** ↓ extracellular Ca²⁺ → less Ca²⁺ binds near L-type Ca²⁺ channels -> Channels activate more easily (at more negative voltages) → **Threshold is lower** → SA node reaches threshold sooner → **↑ firing rate** ↑ heart rate (positive chronotropy)

Answer 22

- Governed by: **preload**, **contractility**, **afterload** - *↑ Preload or contractility* → ↑ stroke volume - *↑ Afterload* → ↓ stroke volume

Answer 23

- = *Tension in ventricle before contraction* (linked to **EDV**) - **Preload** refers to the **initial stretch of ventricular muscle fibers** at the end of diastole - *↑ Venous return → ↑ EDV (end-diastolic volume) → ↑ stretch of myocardium* → More stretch increases **passive tension** in the ventricle → Leads to **greater force of contraction** during systole due to increased myofilament overlap / more cross bridges - **Frank-Starling Law**: - Stroke volume ∝ end-diastolic volume (EDV) - More stretch = more optimal cross-bridge formation between actin and myosin = stronger contraction - If sarcomeres are too short or overstretched → ↓ overlap → weaker contraction - So: **More EDV = more preload = more tension = stronger contraction**

Answer 24

- = *Force of contraction at given preload* - *Mechanism*: ↑ intracellular **Ca²⁺** → ↑ actin-myosin cross-bridges → stronger contraction **positive inotropes** 1. **Catecholamines** (e.g. epinephrine, norepinephrine) → Bind β₁-adrenergic receptors on cardiomyocytes → activates Gs protein → ↑ cAMP→ enhanced **Ca²⁺ influx** and **SR Ca²⁺ cycling** → ↑ Ca²⁺ release from SR during each beat → more cross-bridge formation → stronger contraction 2. **Glucagon** → Also activates Gs protein → ↑ cAMP→ enhanced **Ca²⁺ influx** and **SR Ca²⁺ cycling** → Increases force of contraction via more available Ca²⁺ for cross-bridges 3. **Digitalis (digoxin)** → Inhibits **Na⁺/K⁺ ATPase** → ↑ intracellular Na⁺ → Reduces gradient for **Na⁺/Ca²⁺ exchanger** → less Ca²⁺ removed from cell → ↑ intracellular Ca²⁺ stored in SR → more released during each beat 4. **Hypercalcemia** ↑ extracellular Ca²⁺ → more enters via **L-type Ca²⁺ channels** during phase → Triggers greater **Ca²⁺-induced Ca²⁺ release** from SR → ↑ intracellular Ca²⁺ → more **actin-myosin cross-bridges** **↑ contractility** (positive inotropy) *Note*: High Ca²⁺ also stabilizes fast Na⁺ channels → raises threshold → ↓ excitability, but this affects AP initiation, not contraction strength **negative inotropes** 1. **Hypocalcemia** → ↓ extracellular Ca²⁺ → less Ca²⁺ enters via **L-type Ca²⁺ channels** during depolarization → ↓ Ca²⁺-induced Ca²⁺ release from sarcoplasmic reticulum (SR) → ↓ intracellular Ca²⁺ → fewer actin-myosin cross-bridges → weaker contraction 2. **Hyperkalemia** → ↑ extracellular K⁺ → resting membrane potential becomes less negative (depolarized) → Inactivates **voltage-gated Na⁺ channels** (Na⁺ chanels need a negative membrane potential to reset)→ slows depolarization → ↓ action potential amplitude → ↓ Ca²⁺ entry → less Ca²⁺ release from SR → ↓ intracellular Ca²⁺ → reduced contractility 3. **Vagal stimulation (parasympathetic, via ACh)** → Activates **M₂ muscarinic receptors** → ↓ cAMP in contractile myocytes → Minimal direct effect on ventricular myocytes (they have fewer M₂ receptors)

Answer 25

- = *Resistance to ejection from ventricle* - Mainly **arterial pressure** (aorta or pulmonary trunk) - ↑ Afterload → harder to open semilunar valves → ↓ stroke volume - **Increased by**: - **Hypertension** - **Pulmonary disease** (e.g. COPD) - **Cor pulmonale** = RV failure from pulmonary resistance

Answer 26

systole - ↑ chamber pressure (ventricles contract) - blood ejected into arteries - ↑ arterial pressure (peak = **systolic BP**) diastole - ↓ chamber pressure (ventricles relax) - blood fills atria and ventricles - ↓ arterial pressure (low point = **diastolic BP**) chamber pressure - atria: always low (~5 mmHg), slight rise during contraction - ventricles: - low during diastole (filling) - rises sharply during systole (up to 120 mmHg in left, 25 mmHg in right) tip: arterial pressure reflects ventricular systole, not atrial activity

Cardiovascualr Flashcards

(50 cards)