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Week 40 > Contraction/conduction and cardiac glycosides > Flashcards

Contraction/conduction and cardiac glycosides Flashcards

1
Q

Contractility

A
  • Force of contraction
  • Increase preload=Increase contractility
  • Decrease afterload=Increase contractility
  • Contractility is independent of loading
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2
Q

SV factors

A
  • Contractility
  • Preload
  • Afterload
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3
Q

Fast AP

A
  • aka muscle/Long AP
  • Ventricular Myocyte
  • His-Purkinje System, Atrial and ventricular muscle
  • Mediated by Na+ influx
  • Resting membrane potential is lower than nodal
    • prevents hyperexcitabilty
    • wont spontaneously fire
    • wait for signal from nodal tissue
  • Phase 0,1,2=QRS
  • Phase 3=T wave
  • Phase:
    • Phase 0=depolariation
      • Na+ Channel opens, Na+ influx
      • Upstroke; Increase permeability of Na+
    • Phase 1: partial repolarization
      • Na+ Channel closes, K+ channel opens
      • K+ eflux
    • Phase 2: Plateau phase=K+-mediated
      • Ca2+ Channel opens, (Fast K+ Channel close)
      • Ca2+ Influx (K+ efflux)
    • Phase 3: Ca2+ Channel close, Slow K+ channel open
      • K+ efflux
    • Phase 4: Resting potential
      • stable potential; K+ eflux
  • Class I and III antiarrhythmics
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4
Q

Fast AP:Absolute refractory period

A
  • aka effective refractory period
  • Under no circumstance will heart fire/depolarize
  • phase 0-2 of Fast AP
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5
Q

Fast AP: Relative Refractory Period:

A
  • Mostly refractory but if you come in w/a strong enough stimulus=you can trigger a resopnse
  • PHASE 3
  • Problem: Long QT Syndromes
    • arrival of T wave is delayed (repolarization delayed)
    • common source for dangerous arrhythmias
    • occurs due to dysfunctional K+ channels
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6
Q

Cardiac Glycosides: Pharmocological effects:

A
  • Improves contractility
    • Increase CO
    • Increase Renal BF
    • Decrease Blood Volume and edema
    • Decrease preload
  • Sensitize the carotide sinus (Both causes Decrease HR)
    • Decrease Sympathetic tone
    • Increase Vagus tone
  • Vasodilation
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7
Q

Cardiac Glycosides: MOA:

A
  • Inhibition of Na+/K+ ATPase causes Increase in intracellular Na+
  • 2 possible mechanisms
  1. Inhibits Ca2+/Na+ exchange–>Less Ca2+ extrusion–> Increase Ca2+ intracellular
  2. Stimulates Ca2+/Na+ exchanger–> Na+ eflux, Ca2+ influx
  • Both Cause Increase of Ca2+ intracellular–>Stimulates Contractile proteins
  • Increase Force of contraction (contractility)
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8
Q

Cardiac Glycosides: Electrical effects

A
  • Inhibition of pump redistributes Na+, Ca2+, and K+
    • Depolarizes Cells
  • Increase ectopic automaticityin heart
    • due to Ca2+ Loading
  • Increase refractory period early
  • Decrease conduction velocity due to increase vagal tone
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9
Q

Effects of Digoxin on electrical properties of cardiac tissue: SA Node etc:

Therapeutic dose vs toxic doses

A
  • SA Node
    • Therapeutic: Decrease rate
    • Toxic: Decrease rate
  • Atrial Muscle
    • Therapeutic:
      • Decrease refractory period
    • Toxic:
      • Decrease refractory period
      • arrhythmias
  • AV node:
    • Therapeutic:
      • Decrease conduction velocity
      • Increase refractory period
    • Toxic:
      • Decrease refractory period
  • His-purkinje/ Ventricles:
    • Therapeutic:
      • Slight decrease refractory period
    • Toxic:
      • extrasystoles
      • tachycardia
      • Fibrillation
  • ECG:
    • Therapeutic:
      • Increase PR interval
      • Decrease QT interval
    • Toxic:
      • Tachycardia
      • Fibrillation
      • Cardiac arrest with really high doses
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10
Q

Digoxin: Pharmokinetics:

Onset, optimal serum levels, GI Absorption, Plasma half life, Daily excretion, Plasma protein, excretion

A
  • Onset of action: 10-30 mins
  • Optimal serum levels:
    • 0.5-2.5ng/mL
  • GI Absorption:
    • Tablets: 60-80%
    • Lanoxicaps: 90-100%
  • Plasma Half Life
    • 35-40 hours
      • Load dose
  • Daily excretion:
    • 30%
    • kidney disease=modify dose
  • Plasma protein Binding:
    • 20-40% excreted out
  • Excretion:
    • kidney
    • CCR=Creatine clearance level: Assess in elderly to determine if you need to modify dose
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11
Q

Digoxin: Toxicities:

A
  • High Risk of Toxicity:
    • 20-25% hospitalized patients
  • Greater risk in advanced heart disease
  • Antidote for Overdose:
    • Digoxin immune fab
  • Cardiac Toxicities:
    • Primary toxic effect is arrythmias
      • can be sinus block, AV block, AV junctional arrythmias
      • casues:
        • premature ventricular contractions (most common)
        • Tachycardia
        • Ventricular Fibrillation
  • Non-cardiac toxicities
    • Fatigue, muscles weakness
    • GI
      • Anorexia
      • Nausea-cenrally mediated
        • common early sign
    • CNS:
      • difficulty walking
      • confusion
      • halucinations
      • restlessness
      • insomnia
      • drowsiness
      • Psychoses
    • Vision:
      • blurred
      • photophobia
      • alterations in color=objects appear green or yellow
    • some make pats develop gynectomastia
      • due to androgenic effect
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12
Q

Digoxin: Factors that increase conc.

A
  • High dose (received wrong dose)
  • Reduced renal fxn
    • decreased excretion
  • Altered distribution
    • elderly-lean body mass
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13
Q

Digoxin: DDIs

A
  • Diuretics–>produce hypokalemia
    • decrease Plasma K+ and Mg2+
    • Increase serum Ca2+
    • Increase Toxicity
  • Antacids: Decrease absorption
    • Decrease K+
  • Corticosteroids:
    • decrease serum K+
    • Increase toxicity
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14
Q

What maintains Resting membrane potential in fast action potentials?

A
  • K+ Leak channels
  • Na+/K+ ATPase
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15
Q

Mechanism of Fast APs

A
  1. Nodal AP enters from adjacent cell
  2. Voltage gaded Ca2+ channels open, Ca2+ enters
  3. Ca2+ induces Ca2+ release through ryanodine receptor channels (RYR) from sarcoplasmic reticulum
  4. Local release causes Ca2+ spark
  5. Summed Ca2+ spark creates a Ca2+ signal
  6. Ca2+ ions bind to troponin to initiate contraction
  7. Relaxation occurs when Ca2+ Unbinds from Troponin
  8. Ca2+ is pumped back into sacroplasmic reticulum to storage
  9. Ca2+ is exchanged with Na+
  10. Na+ gradient is mainted by the Na+/K+ ATPase
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16
Q

How do we regulate force of contraction in the heart and steps:

A

Sympathetic stimulation (Increase Contractility and HR)

  • B-adrenergic stimulation leads to: (NE binds)
    • phosphorylationof membrane Ca2+ channels causes them to be more open–>increasing transmembrane Ca2+ influx
    • Phosphorylation of Troponin-1 inhibits Ca2+ binding to troponin-C, making it easier to remove Ca2+ from binding sites
      • Increase Ca2+ turnover into contractile proteins
    • Phosphorylation of Phospholamban, which removes inhibitiory control on sarcoplasmic reiculum ATPase, and increase Ca2+ uptake into SR
    • NET Result:
      • increased force of contraciton
      • decreased contraction time caused by increase rate of contraciton and rate of relaxation
  • Cardiac Glycosides=downside
    • inhibit Na+/K+ pump which results accumulation of Na+ intracellular is it effects all Na+/K+ ATPase pumps thorughout the body which can cause hyperkalemia
      • Na+ Intracellular Increase
      • Ca2+ intracellular increase
      • K+ Extracellular increase (hyperkalemia)
      • Increase contractility
17
Q

Control of BP

A
  • Cardiovascular system:
    • Cardiac Output:
      • Preload
      • contractility
      • Afterload
      • HR
  • Vascular
    • Vascular Resistance
      • sympathetic tone
      • Autoregulatory factors
  • Kidneys: Long term
    • fluid volume regulated by renal control
18
Q

How to figure out preload from system

A
  • Preload
    • preload=filling of the heart during diastole
      • Increase Preload=Increase Contractility
    • EDV: End Diastolic Volume
      • best indicator for how full the heart is before contraciton
      • most accurate but hard to measure=need cardiac ultrasound
    • EDP: End Diastolic pressure
      • measured by ventricular cather
      • tells us what preload is
    • CVP-Central Venous Pressure
      • most common to assess preload
      • Equilibrates with the ventricle
      • By the end of diastolic filling, the EDP=CVP
      • no catheter needed
      • Look for jugular vneous distention, bc close to inferior vena cava=reflect CVP
      • How much distention you see give you how high CVP is:
        • How high above the clavicular line you see the jugular vein OR
        • how high pulse in jugular vein
      • used to determine whether your heart is capable of moving the fluid
      • Incrrease CVP=HF
19
Q

What can make Central Venous Pressure increase?

20
Q

Contractility:Performance measures of the system

A
  • SV-need cardiac ultrasound
  • CO-need cardiac ultrasound
  • SBP-systolic Blood pressure
    • pulse amplitude (pulse pressure)=SV
    • Pulse pressure=SBP-DBP
    • Increase PP=Increase SV
  • EF: Ejection fraction
    • radiograph image or ultrasound
    • What % of starting EDV (end diastolic volume) Was ejected
    • EF= SV/EDV
    • normal: 50-60%; decreases in sick hearts
    • used most common
21
Q

Afterload of system to determine contractiility:

A
  • Afterload=Resistance
    • DBP=diastolic blood pressure
      • best indicator for resistance
      • Increase TPR=Increase Afterload
22
Q

Starling law of Heart

A

How to evaluatae contractility

  • Starling curves=loading @ constant contractilty/afterload
  • relationship b/w preload and force
    • Increased EDV (Stretch) should increase the force being produced (contractility)=Increase SV
  • Normal resting values:
    • Force: indicated by SV
      • 70mL
    • Stretch=indicated byEDV
      • 135mL
  • Increase filling(preload)–> Increase performance (Force)
  • Indices of preload (x-axis)
    • EDV
    • EDP
    • CVP
  • Indices of performance (Y-axis)
    • SV
    • LVSP
    • CO
23
Q

Diuretics:

A
  • casues body to lose water (decrease blood volume) and urinate more
  • most common for BP control:
    • Thiazide diuretics: (Thiazides)
      • ​first line
      • long term use shows decreased reactivity of vessels
    • Looop Diuretics:
      • Furosemide
      • Congestive Heart Failure
    • Potassium Sparing diuretics
      • 3rd line w/BP control
24
Q

Drugs that interrupts the RAAS

A

really effective when plasma renin activity is high

  • Angiotensin-Converting Enzyme Inhibitors
    • ACE inhibitors
  • Angiotensin Receptor BLockers (ARBs)
  • Direct Renin Inhibitor:
    • Aliskerin
  • Aldosterone Antagonist
25
Q

ACE inhibitors:

  • suffix
  • admin
  • metabolism
  • Side effects
  • DDIs
  • miscellaneous
A
  • -pril
  • inhibits ACE
  • Admin: Oral
    • except enalaprilat
    • don’t have to have food in system when you take
  • Metabolism:
    • excreted renally
  • Advise to take at night before bed to reduce risk of hypotension and maximize effictiveness
  • Side effects:
    • COUGH
      • iron supplement dampens this effect
    • Angioneurotic edema
      • more common in african americans
    • Hyperkalemia
      • applies to B-blockers, ARBS, DRIs
    • Acute renal failure in the presence of renal artery stenosis
    • Skin rash; abnormal taste sensation (iron)
    • Fetal harm due to exposre to ace inhibitors during 1st trimester
      • Never use any of the RAAS inhibitors
  • DDIs:
    • Diuretics
      • potassium sparing diuretics
    • Potassium supplements
    • Lithium
      • ACEI can raise lithium levels
    • NSAIDS
      • can inhibit antiHTN effects by retention of salt and water
  • Additional Benefits:
    • slow the progression of:
      • diabetes-induced nephropathy (proeinuria>300mg/day)
      • diabetes-induced retinopathy independent of BP lowering bc:
        • _​_Diabetes causes Increased VEGF
        • Angiotensin II interacts with VEGF=retinopathy
26
Q

Current recommendations for RAAS drug prescription

A
  • ACEIs and ARBS are the drugs of choice to prevent long-term cardiac remodeling
  • Use DRIs if side effects are not tolerated
27
Q

ARBS:

  • suffix
  • MOA
  • admin
  • metabolism
  • Side effects
  • DDIs
  • miscellaneous
A
  • -sartan/artan
  • MOA:
    • Angiotensin Type 1 antagonists (AT1 antagonists)
    • Blocks AT1 receptor
    • works similar to ACEI but:
      • ACEIs are decreasing Ang II
      • Block AT1 receptor where Ang II would bind
    • Downstream effects:
      • dilation of arterioles and veins
      • reduce excretion of K+
      • decrease release of aldosterone
      • Increase renal excreetion of Na+ and Water follows
      • Do not inhibit ACE
      • DO not increase levels of Bradykinin
  • Side effects:
    • NO COUGH-biggest advantage over ACEIs
    • same as ACEIs
  • DDIs:
    • Same as ACEIs
  • Losartan (Cozaar
28
Q

DRIs

A

Direct Renin Inhibitor=Aliskerin

  • Admin: Oral
  • MOA: Binds to the active site on renin
  • No cough
    • angioedema
  • NOT 1st line agent
  • Newer drug and more expensive
  • use if patient has side effects with angioedema from ARBs & ACEIs
29
Q

Calcium Channel Blockers (CCBs)

A
  • Aka Calcium channel antagonists
    • Slow calcium blockers
    • Calcium entry blockers
  • Calcium channels
    • critical role in the function of vascular smooth muscle and heart
  • 2 main groups
    • Nodihydropyridines: Verapamil & Diltiazem
      • acts on both VSM and heart
    • Dihydropyridines: Nifedipine
      • act on VSM only
  • MOA:
    • prevent calcium ions from entering the cell
    • greatest effect on heart and blood vessels
    • effective in low renin HTN
  • Physiologic fxns and consequences of blockade
    • VSM
      • regulate contraction= Decrease sensitivity of constriciton of vessels
      • CCBs act selectively on arterioles and arters, and arterioles of heart
        • no significant effect on veins
    • Heart:
      • Myocadrium: Ca2+ increases Contractility
        • inotropy
      • SA node: Decrease HR
      • AV node: decrease velocity of conduction
      • coupling Calcium channels to Beta1-adrenergic receptors
        • when B1 is activated, calcium influx is increased
  • Adverse effects:
    • Constipation
    • dizziness
    • facial flusing
    • headache
    • edema of ankles and feet
    • heart block-can report a heart attack on ECG
  • DDI:
    • Beta-adrenergic blocking agents
      • synergistic effect
    • Food
      • grape fruit juice (anything citrisy)
      • CYP3A4
    • Digoxin
  • Toxicity:
    • severe hypotension
    • Bradycardia and AV block
    • Ventricular tachydysrhytmias=Fatal heart syndrome
30
Q

Similarity b/w CCBs and Beta-Blockers

A

Have same effects:

  • Reduce force of contraction
  • slow HR
  • suppress conduction through AV node

DO NOT GIVE IN COMBO=SYNERGISTIC EFFECT

-can introduce new arrythmias

31
Q

Nondihydropyridines:

A
  • Type of CCB
  • Verapamil & Diltizaem
  • Admin:
    • oral or IV
  • Metabolism: Extensive 1st pass metabolism
  • MOA-act on VSM and heart
    • blacks Ca2+ channels
  • Both drugs act like one another=hemodynamic effects
    • vasodilation
    • reduced arterial pressure
    • increased coronary perfusion
  • Major therapeutic uses
    • angina pectoralis
    • essential HTN
    • cardiac dysrhythmias
32
Q

Dihydropyridines:

A

Type of CCB

  • Nifedipine/Amlodipine
    • -dipine
  • MOA: Acts on VSM
    • Blocks Ca2+ channels
  • Hemodynamic effect
    • lowers BP
    • increases HR and contractile force
  • Therapeutic use:
    • angina pectoralis
    • HTN
    • relieve migraine headache
    • suppress preterm labor
  • Adverse effects:
    • gingival hyperplasia
    • reflex tachycardia
  • DDI
    • Beta-adernergic blockers (Beta blockers)
      • often combined with beta-blocker to reduce reflex tachycardia
  • Long-acting Nifedipine reduces reflex tachycardia and is more useful in treating essential HTN than original short-acting
33
Q

Antihypertensive drugs: SNS target in CNS

A
  • Primarily target the alpha 2 receptors (Adrenergic 2) in the CNS
    • inhibit SNS
  • CNS receptors:
    • B1 (Beta 1)
      • increases SNS activity=vasoconstriction
    • alpha 2 (a2)
      • inhibits SNS activity=vasodilation
  • Outcome:
    • reduciton in postganglionic nerve activity (NE) and adrenal medulla (NE/E)
    • leads to a reduction in vascular resistance (BP
  • Positive and Negative Feedback control of NE release @ sympathetic nerve termina
    • NE binds A2 and inhibits teh SNS
      • Negative feedback
    • NE binds to Beta receptors=Increase SNS activity
      • positive feedback
35
Q

Beta-Adrenoreceptor Blockers

A

Aka Beta Blockers

  • -olol
  • Slows HR and Lowers BP
  • MOA: Block B1 adrenoreceptor (B1 receptor antagonist)
    • Heart=Reduce CO and HR
    • Kidney (B1)=reduced renin
    • CNS: inhibits SNS
    • BLood Vessels: Enhance endothelial synthesis of DGI2
  • Adverse effects:
    • Adverse lipid profile
      • can mask or induce diabetes
    • Hyperglycemia
      • can mask or induce diabetes
    • Excessive bradycardia (such as AV block), arrythmyia
      • combo with CCBs
    • Hyperkalemia
    • Fatigue, depression, insomnia, CNS effects
  • Contraindications:
    • Asthma
      • don’t use non-cardioselective B-Blcokers
      • can use cardioselective-hopefully only selects B1
    • Diabetes
    • Peripheral artery disease-challenged by Nebivolol/metoprolol
  • DDIs:
    • NSAIDs
    • K-sparing diuretics
    • CCBs–> nonodihydropyridine
      • can use with Nifediipine
    • Reasons:
      • reduced hypotensive actions=inhibits PGI2 produciton
      • Hyperkalemia
      • bradycardia
      • AV block
36
Q

Slow AP

Week 40 (2 decks)

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