Exam 9 Flashcards
What are the risk factors that we are studying in the Cardiovascular continuum for this exam?
Loss of Muscle
Remodeling
Ventricular Dilation
Heart Failure
What are the 8 symptoms of Heart Failure
Shortness of Breath
Swelling of Feet and Legs (pedal edema)
Chronic lack of energy
Difficulty sleeping (orthopedic and paroxysmal nocturnal edema)
Swollen or tender abdomen with loss of appetite.
Cough with frothy sputum
Increased Urination at Night
Confusion and/impaired memory
What is Stage C Heart Failure
Structural heart disease WITH prior or current symptoms of Heart Failure
In patients with:
Known Structural Heart Disease
HF Signs and Symptoms
HFpEF
What are the Goals, Strategies, and Treatment
Goals: Improve HRQOL, control symtptoms, prevent hospital and dead
Strategies: Identify comorbidities
Treatment
Diuretics, Guidelines for Comorbidities (HTN, AF, CAD, ETC.)
Revascularization or valvular surgery as appropriate
In patients with Structural Heart Disease, HF signs and symptoms, and HFrEF, what is the goals, drugs of choice, and alternative options.
Goals: symtpoms, educate, prevent hospital, prevent death
Drugs for routine use: Diuretics (Fluid Retention), ACEI or ARB, Beta blockers, Aldosterone Antagonists
Drugs in Selected Patients: Hydralazine, Isosorbide, ACEI/ARB, Digoxin
Selected Patients: CRT, ICD, Revascularization, valvular surgery as appropriate.
In patients with Structural Heart Disease, HF signs and symptoms, and HFrEF, what is the goals, drugs of choice, and alternative options.
Goals: symtpoms, educate, prevent hospital, prevent death
Drugs for routine use: Diuretics (Fluid Retention), ACEI or ARB, Beta blockers, Aldosterone Antagonists
Drugs in Selected Patients: Hydralazine, Isosorbide, ACEI/ARB, Digoxin
Selected Patients: CRT, ICD, Revascularization, valvular surgery as appropriate.
What are the 4 Stages of ACCF/AHA Stages of HF
A - At high risk for HF but without structural heart disease or symptoms of HF
B- Structural heart disease but without signs of symtpoms of HF
C - Structural heart disease without prior or current HF Symptoms.
D - Refractory HF requiring specialized interventions.s
What are the 4 NYHA Functional Classifications related to heart failure.
I - No limit to physical activity, ordinary activity does not cause symptoms.
II - Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in symptoms of HF
III - Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes symptoms of HF.
IV - Unable to carry on any physical activity without symptoms of HF, or symptoms of HF at rest.
What does the 12-Lead EKG assess?
Heart Size
Pulmonary Congestion
Abnormality contributing to Heart Failure
What is the purpose of a 2D Echocardiogram
Assess Ventricular Function
Size
Wall Thickness
Wall motion
Valve Function
What disease state exacerbate HF
Infection
Uncontrolled HTN
Renal Failure
Fluid Overload
Thyrotoxiccosis
Anemia
Ischemia
Arrhythmias
What medications may exacerbate HF
Medication Non-Compliance
NSAIDS/Cox-2 Inhibitors
CCBs
Anti-Arrhythmics
Steroids
Saxagliptin
Piogliztazone/Rosiglatizone
In Level 3 Management of Stage B clinical HF. LVEF is <50%, which medications should not be used in these patients and why?
Thiazolidinediones (pioglitazone, rosiglitazone, trolitazone, etc.) should not be used because they increase the risk of HF, including hospitalization.
Also, nondihydropyridine CCB’s with negative inotropic effects should not be used because the effects may be harmful.
What is the FDA Black Box Warning on NSAIDS and the Risk of Heart Attack and Stroke
NSAIDS can increase the risk of heart attack or stroke in patients with or without heart disease or risk factors of heart disease.
Risk appears greater at higher doses, and is similar for all NSAIDS, and occurs within first weeks of using an NSAID.
What is the main non-Pharma recommendation for patients with risk of HF or stoke
Exercise, if you cannot exercise, rehabilitate to the point that you are able
Which three vaccinations should be HEAVILY recommended in patients with HF
Pneumonia
Flu
COVID-19
What did Munger say about pillars of HFrEF therapy in 2022.
Every patient at HFrEF gets RAASi/ARNi, B-Blocker, MRA, and SLG2i
Loop diuretics useful but depends
After initial indicated therapy for HFrEF, what percent LVEF is the threshold for either more treatment, or continued therapy and reassessment/optimazation
LVEF <40% = more therapy (scale up intensity to get above 40)
LVEF >40% = Continue and reassess often.
What are the Recommendations for Loop Diuretics (Furosemide, etc.) in HF regarding congestion and symptoms
Pts with HF who have fluid retention = diuretic
Pts with HF and congestive symptoms = thiazide addition, especially if bad response to loop diuretics.
Which loop diuretics are indicated in HF. Order from most to least
Furosemide
Bumetanide
Torsemide
When considering Furosemide vs. HCTZ, what would you with first.
When you decided, what additional therapy is necessary to ensure success
Furosemide > Thiazide
Must use with ACE/ARB/B-BLOCKER. Do not use diuretic alone as it will not improve mortality.
What are the adverse effects of Loop Diuretics in HFrEF and HFpEF?
Hypotension, Renal Deficiency, Electrolyte Depletion (K+, Mg+, predisposition to arrhythmias)
RAAS Activation = Increase risk of long term disease progression, you will see patient deteriorate instead of improve if this happens.
What medication should you switch to if patient shows no fluid retention improvement on furosemide.
Torsemide/Bumetanide.
What class of medication is primarily contraindicated in Diuretic use?
NSAIDS/COXIBS
In a patient with CKD (renal insufficiency Class I or II), what should the instructions be on the Rx when starting a diuretic
Double dose first, then BID dosing thereafter
What are counseling points for patients when starting Diuretics
- Use on prn basis initially, until pt has persistent fluid overload
- physical exam 2-3 days after diuretics
In mild to moderate HF disease, what would optimal ACEi dosage possibly do when considering diuretics?
Optimal ACEi dose would decrease diuretic requirement
If a patient has chronic history of HFrEF and has failed ARNi therapy. What would be the next line
ACEi
In a patient with HFrEF and NYHA Class II or III, what would be the best class of drug to use.
ARNi
What is the order of therapy for class of drugs excluding diuretics in HFrEF
ARNi > ACEi > ARB
Can ARNi and ACEi be used together?
If a patient failed an ARNi and you are considering ACEi what is the timing of when to start?
No ARNi +ACEi
Wait 36 hours from last dose of ARNi to start ACEi
In ACEi/ARB, what are important Contraindications regarding patient labs/comorbidities
Do not use ACEi/ARB in Patients with:
History of Angioedema
Renal Failure
Pregnant
SBP <80mmHg
SCR > 3mg/dL
K+ >5.5mmol/L
Cardiogenic Shock
How should ACEi/ARB be initiated and why?
How should dose be adjusted as patient tolerates?
What is the timeframe for improvement in symptoms.
Initiate ACEi/ARB at very low dose because of 1st dose Hypotension
Double dose weekly, titrate dose to maximum tolerated based on SBP
Improvement not seen for 1-3 months of therapy.
A patient is on K+ supplement as well as spironolactone prior to starting ACEi/ARB for HF. Doc prescribes lisinopril 2.5mg. What do you do Mr pharmacist
I tell them to stop the damn k+ supplement and the k+ sparing diuretic. That shit is contraindicated here.
What is the pro/con of sacubitril/valsartan.
Can ACE/ARBi be used in addition.
What is the dose of this therapy
Sacubitril/Valsartan is expensive but increases lifespan in HF by 1-2 years.
D/c ACE/ARB prior to therapy
Dose: start 24/26mg, 49/51mg, 97/103 BID. (Double dose every 2-4 weeks as SBP tolerates)
Are beta blockers useful in HFrEF?
What is the benefit of Beta Blockers?
Bisoprolol, Carvedilol, and Metoprolol XR are all recommended to reduce mortality and hospitalizations.
They are good because they are cheap.
B-Blockers reduce mortality by 35% and hospitalizations by 47% when taken with what?
ACEi/ARBs AND Diuretics
Which class of HF and NYHA is B-Blockers indicated in the therapy regimen?
HFrEF NYHA FC II-III (Not IV)
What are contraindications of B-Blockers and how should dosing be conducted?
Contraindications:
Bronchospastic
Bradycardia (HR<60bpm)
Heart Block
NYHA FCIV
SIGNIFICANT fluid retention (hospitalization/IV level)
IV vasodilators or Inotropes
HFrEF Hospitalization
Dosing:
Initiate at lowest dose and double dose every 2-4 weeks based on SBP tolerance.
How long does a beta blocker take to increase ejection fraction
1-6 months to reach peak/new baseline of healthy EF.
In beta blockers, titration is necessary to get patient to healthy dose and prevent toxicity.
During the titration phase, what symptoms should we specifically look for that would signify toxicity?
Hypotension (lightheaded or near syncope)
Fluid Retention or worse HF
Bradycardia/heart block (fatigue)
What are the target doses of indicated HF meds carvedilol and metoprolol
Carvedilol 25mg bid or 50mg qd
Metoprolol 100mg bid or 200mg qd
In patients with HFrEF and NYHA Class II-IV, MRA (spironolactone and eplerenone) is recommended to reduce mortality and morbidity.
What are the lab values for the patient to qualify for this therapy in addition to HFrEF dx + NYHA II-IV
EGFR >30ML/MIN/1.73M2
AND
Serum Potassium is <5.0 mEq/L
Monitor k+, renal function, risk of hyperkalemia and renal insufficiency.
A patient presents with HFrEF and NYHA class II-IV.
Labs:
EGFR: 41ml/min/1.73m2
K+: 5.9 mEq/L
BUN: 110mg/ml
SCR: 2.9mg/dL
Patient has history of hyperkalemia.
The doctor prescribes spironolactone for HF management. Is this proper therapy?
No, the patients K+ is above 5.5mEq/L.
Also, SCR must be below 2.5mg/dL.
The patients SCR and K+ need to be in correct ranges and also history of hyperkalemia are contraindicated.
MRA are contraindicated in >5.5mEq/L as it can cause life threatening hyperkalemia.
What is the correct dosing of spironolactone and eplerenone.
If the patients CrCl is 30-49ml/min/1.73m2 the dose is adjusted. What is the adjusted dose?
Spironolactone 12.5-25mg qd
Eplerenone 25mg qd
If CrCl 30-49 ml/min/1.73m2: start qod (every other day)
Important monitoring and counseling points for spironolactone
K+ supplement = d/c
Avoid high k+ foods (leafy vegetables, citrus fruits)
NSAIDS = NO
SCR and K+ labs done 2-3 days after start
What population is SGLT2i indicated.
- Chronic HFrEF
- Except Type 2 Diabetes.
What are important Adverse events in SGLT2i (dapaglifozin)
First 3 are most important
Volume Depletion
Renal AE
Diabetic Ketoacidosis
Major Hypoglycemia
UTI
Genital Infection
EGFR considered when choosing Dapagliflozin or Empagliflozin.
What are the eGFR values which indicate which to choose.
What is dosing of Dapaglifozin and Empaglifozin.
Dapagliflozin: eGFR >30mL/min
Empagliflozin: eGFR >20mL/min
Dosing for both: 10mg qd
Which pt population with HF is Hydralazine + Isosorbide Dinitrate indicated as therapy to reduce morbidity/mortality + improve Symptoms.
Hydralazine + Isosorbide Dinitrate combo therapy in African American Patients with NYHA Class III-IV and HFrEF.
Who ALSO had progressive renal dysfunction/hyperkalemia on ACEi/ARB
What is the Initiation and Maintenance dose for Hydralazine and ISDN (Isosorbide Dinitrate)
What are the Side Effects?
Can one be used without the other?
Initiation: 37.5mg Hydralazine/20mg ISDN TID
Increase Dose: 225mg H/120mg TTD daily in TID format.
Adverse Effects: Headache, dizzy, GI upset, adherence (multiple dosing)
Cannot be taken individually, must be combo therapy.
What population is Digoxin recommended in?
2 physiological systems digoxin effects?
Digoxin shown to do what in trials?
Dosing? Additional Drugs for treatment? Contraindications? Adverse Events? Lab Levels?
Symptomatic Stage C HFrEF and failed GDMT presenting +S3
Reduces activation of SNS + RAAS
Digoxin:
- NEUTRAL effect on survival. (The important one)
- reduce HF symptoms
- increase exercise tolerance
- decrease HF progression
- reduce hospitalization
Dosing: Starting dose 1.25mg qd. Digoxin is a Narrow Therapeutic Index Drug (NTID)
Use with: ACEi/ARBs, B-Blocker, SLGT2i, AND ARA agent.
Contraindicated: Advanced heart block
Adverse Event: Arrhythmias, Anorexia, N/V, Confusinon/Visual Disturbances.
Digoxin Serum Concentration Goal: 0.3-0.8ng/mL
Toxic Digoxin Serum: >2ng/mL
Which Drugs have no Benefit/Harmful Effects in HF
No Benefit:
Dihydropyridine CCBs
Vitamins, Nutritional Supplements, Hormonal Therapy.
Harmful:
NDP CCBs
10 HFrEF Commandments in little words as possible
- 2-3g Na+ diet
- Weight mgmt
- No NSAIDs
- All HF = ACEIs/ARNi, Sacubitril/Valsartan if cannot do ACEi/ARNi if can afford/cant do ACEis/ARNi
- Furosemide NYHA II-IV
- Metalazone 5-10mg prior to loop diuretic if not responding
- Spironolactone 25 in III or IV if scr >2.5mg/dl + k+ >5mEq/L
- All class II + III get metoprolol, carvedilol, or bisoprolol unless pt is decompensated (excessively dry/wet)
- Digoxin sometimes
- Everyone exercise
Which NYHA class are each class of drugs used in.
ACEi/ARB
B-Blocker
MCA’s
Diuretics
Digoxin
Hydralazine/Isosor
SGLT2i
ACEi/ARB- All classes
B-Blocker - All II and III. Sometimes use in 1 and IV
MCA’s - Always III and IV, never I, sometimes II
Diuretics- Always III + IV, sometimes II, Never I
Digoxin - Sometimes III + IV. Never I + II
Hydralazine/Isosor - Sometimes II, III, IV. Never I
SGLT2i - Rarely I, Sometimes II + III. Never IV
Which population is Ivabradine indicated in?
- NYHA Class II - III
- Stable HFrEF (LVEF <35%)
- GDMT (b-blocker included)
- Sinus Rhythym
- Resting HR = >70bpm
What is GDMT?
What drugs are involved?
Which ones are titrated?
GDMT is the management multi-drug strategy for HF.
ACEI - Titrated 2-4 weeks/increase
BB - Titrated 2-4 weeks/increase
MRA - Titrated 2-4 weeks/increase
ARNi - titrated 2/4weeks/increase
SGLT2i - not titrated
What is the treatment strategies and tiers for HFmrEF (LVEF 41% - 49%)
- Diuretics, as needed
2a. SGLT2i
2b. ACEi/ARB/ARNi
2b. MRA
2b. Beta blockers
In HFpEF (LVEF >50%) what is the treatment in tiers
- Diuretics, as needed
2a. SGLT2i
2b. ARNi
2b. MRA
2b. ARB
What is the Emporer-Preserved Outcome Trial?
Primary Composite Outcome?
EGFR Outcome?
Primary Composite Outcome: Empagliflozin lowered CV death (Composite of CV death or HF Hospitalization)
EGFR: Empagliflozin slowed the progression of CKD showing improved eGFR values in patients
In addition to optimized GDMT, a patient presents with HF with type 2 diabetes.
What drug should be added for management for hyperglycemia?
SGLT2i should be ADDED to GDMT in type 2 diabetes + HF for hyperglycemia
In patients with HF and hypertension. What is the plan for the patient who is already optimized GDMT
Optimal treatment according to HTN guidelines in patients with HF and HTN.
A patient presents with HFrEF and is on optimized GDMT. New labs show an iron deficiency, what to do?
Continue GDMT. Add IV iron replacement
Patient presents with HF and is optimized GDMT. Patient new dx of obstructive sleep apnea.
Plan?
Continue GDMT for HF. Add CPAP.
What factors contribute MOST to ADHF Hospital Readmission
Diet Noncompliance - 24%
Rx Noncompliance - 24%
Failure to Seek Care - 19%
Other - 17%
Inappropriate Rx - 16%!!!!
(That is a lot for healthcare “professionals”.)
What percent of patients will be readmitted to hospital after HF event?
Mortality % in 30 days, 1 year, and 5 years post-HF event
Hospital Readmissions:
30 Days - 20%
180 Days - 50%
Mortality
30 days - 12%
365 Days - 33%
5 Years - 50%
What is the ADHERE CART Predictors of Mortality.
What is the first factor considered in this model?
Then what is considered?
BUN = <43 is good
BUN = >43 is bad
SYS BP +-115 is next factor.
> 115 = good.
<115 = bad
<115 SYB + >43 BUN = Dead
> 115 SYB + <43 BUN = Alive.
In Acute HF, which patient evaluation factors should be considered before therapy.
- Complete Metabolic Panel (ca2+, albumin, t protein, LFTs, bilirubin, mg+, TSH)
- NT pro-BNP and tropinin I/T level
- Lactate Level:
Normal: <2mmol/L
Moderate: 2-4 mmol/L
High >4mmol/L
2D Echocardiogram unless done within last 3 months. (Assess ventricular function, size, thickness, motion, valves.)
When considering Congestion at Rest, as well as Low perfusion at rest. (The hot/cold and dry/wet stuff)
What is the worst combination.
Cold & Wet.
Makes sense, most people are dry and warm to the touch.
If you are getting Insufficient response or diuretic resistance when treating HF with loop diuretics what should you do?
Evaluate:
- Compliance, Fluid Intake
- Increase dose
- Switch to Bumetanide/torsemide
- add aldosterone antagonist
- combine loop w/metolazone
- short-term IV loop diuretics
If you are getting renal failure (rise in urea/BUN and/or SCr) with use of loop diuretics for HF, what should you do.
- Check hypovolaemia/dehydration
- d/c NSAIDS, antibiotics
- stop aldosterone antagonist
- stop thiazide if combo therapy
- reduce dose ACEi/ARB
- ultrafiltration.
If a patient is presenting with “Warm and Wet” (Congestion at Rest and No Perfusion at rest).
What is the course of action?
“Dry Out”
Diuretics
Vasodilators
-Nitroprusside
-Nitroglycerin
-Nesiritide
A 2B Recommendation, IV nitroglycerin/nitropursside or nesiritide may be used in addition to diuretic in what patient presentation
- No Hypotension
- Dyspnea
- Acute Decompensated HF
What are the effects Vasodilators have on
CO, PCWP, BP, HR, Pro-Arrhythmias, Onset (fast or slow),
CO Increase
PCWP Decrease
BP Decrease
HR Unchanged
Pro-Arrhythmia Unchanged
Rapid Onset
Nitroprusside is unique to other vasodilators in that it…
Requires high monitoring intensity, causes major hypotension, increases RAAS activity, has toxic metabolites.
If a patient presents “Cold & Dry” (Low perfusion at rest with NO congestion at rest)
What is the course of action?
“Warm Up and Dry Out”
Inotropic Drugs
Dobutamine
Milrinone
Where would short term IV inotropic support would be reasonable in which patient presentation?
- Hospitalized
- Severe SBP dysfunction
- Low BP
- Significant depressed CO
When is Inotropic support potentially harmful?
Long-term, continuous, or intermittent use
- IV parental positive inotropic agents
- No indication for inotropic
- No documented SBP dysfunction
- No low blood pressure
They need to have low bp, basically dying from heart failure to use inotropic support.
What are the three main Inotropes and their effect on CO, PCWP, BP, HR, Pro-Arrhythmias, Rapid Onset, Long Onset
Dobutamine:
- +CO, -PCWP, Neutral BP, +HR, +Pro-arrhythmia, +++Rapid onset, /longer onset
Milrinone:
++CO, - -PCWP, -BP, +HR, ++Pro-Arrhythmia, +rapid onset, ++longer onset
Levosimendan: ++CO, - -PCWP, -BP, +HR, //Pro-Arrhythmia, +Rapid Onset, +++++Longer onset.
What monitoring should you use when treating HF with vasodilators?
Continuously Monitor HR, Arrhythmias
Continuous Pulse Response, BP
Transduce CVP
Pulm Artery Catheter (pressure)
Urine output, lactate clearance, BMP, venous o2 stat
What are the indications for IABP (Intra-Aortic Balloon Counterpulsation)
Low CO state due to LVEF
Relief of Myocardial Ischemia
Hemodynamic support during and after procedures (angioplasty, angiography, cardiopulmonary bypass, etc.)
Bridge to heart transplantation and after transplantation because of cardiovascular deterioration from rejection.
What is the “natural pacemaker” of the cardiac conduction system.
Sinoatrial (SA) node. ‘Cluster of cells with high automaticity’
However…
Most conductive tissues possess some automaticity. They are typically overdriven by the SA Node.
- What are Arrhythmias?
- Cause?
- Can lead to?
- Cardiac depolarizations that are different from normal.
- Site of origin of pacemaker
Rate or regularity of pacemaker depolarization
Conduction of impulse through heart. - Can lead to bradycardias, tachycardias, and/or impaired ability of the heart to pump normally.
Which classes of drugs inhibit automaticity in relation to Arrhythmias?
B-Blockers
Ivabradine
Na+ and Ca2+ channel blockers
Adenosine and Muscarinic Agonists
K+ Channel blockers
In the Arrhythmias category, “Sinus Bradycardia, AV block”, what are drugs that cause this, and what is the mechanism which creates this arrhythmia
Drugs that Cause Sinus Bradycardia, AV Block:
Digoxin
Verapamil
Diltiazem
Why it happens:
++ Vagal Tone
Ca2+ Channel Block
Theophylline is associated with what type of Arrhythmia due to what mechanism?
Associated with ‘Multifocal Atrial Tachycardia’ due to increased intracellular Ca2+ DADs
Quinidine, Sotalol, Procainamide, Disopyramide, Dofetilide, Ibutilide, and many others are associated with what type of Arrhythmia due to what mechanism?
Polymorphic VT/Prolonged QT due to EADs.
Which condition is associated with:
- Abnormally slow HR (<60bpm)
What causes it?
Bradycardia
Causes:
- Increased Vagal Tone (e.g. well-trained athlete)
- Drug-Induced (e.g. b-blocker)
- Co-morbidities (e.g. hypothyroid, ischemia)
What is an altered impulse conduction, decreased SA node automaticity diagnosed as in practice?
Atrioventricular Heart Block
(Has multiple ‘types’ or degree’s’ of severity)
What potentially causes Atrioventricular Heart Block?
Drugs (b-blockers, non-dhp, CCBs, digoxin)
Ischemia, fibrotic tissue
Increased Vagal tone (athletic)
This class of AV block is characterized as PR interval >200 msec (1 big block)
Treatment:
- Find underlying Cause
- Not caused by permanent pacemaker
Location:
AV Node
First Degree AV Block
This class of AV block is characterized by:
- Prolonged PR interval until dropped QRS complex
Location: AV Node
Treatment:
- Find underlying cause
- not caused by permanent pacemaker
Mobitz I (Wenkebach)
Second Degree AV Block
Which class of AV block is characterized as:
No progression of PR interval with RANDOM dropped QRS
Location: Bundle of his/purkinje fibers
Treatment: find underlying cause
Likely due to permanent pacemaker
Mobitz II (Second Degree AV Block)
Which AV block is characterized by:
- Complete heart block
- P-waves march at own rate
- QRS march at own rate
- Complete Dissociation
Location: - Bundle of His/Purkinje fibers
Treatment:
Needs pacemaker
Third Degree AV Block
Which AV block is characterized by:
- Altered Impulse Conduction
- Poor conduction through part of the Bundle of His
- Right vs. Left
- Less efficient depolarization in both ventricles at same time
Treatment:
NONE
Bundle Branch Block
If a patient presents with
- Altered impulse formation or conduction
- Increased atrial myocyte automaticity
- Blocked vs. Aberrant (depending on AV note refractory or not)
What dysfunction does the patient have?
How would you treat it?
The patient has: Premature Atrial Contraction
Treatment:
- Beta-Blocker
- Non-DHP CCB
Which heart condition is called, “prelude to ventricular arrhythmias” which presents by increased ventricular myocyte automaticity?
How would you treat?
Premature Ventricular Contraction
Treatment:
- B-Blocker
- Non-DHP CCB
What are the types of Supraventricular Tachycardia?
Sinus Tachycardia
Focal Atrial Tachycardia
Atrial Flutter
Atrial Fibrillation
AVRT/AVNRT
Patient presents with:
- Abnormally fast heart rate (>100 BPM)
- Regular Rhythm
What is this called?
What are the possible causes?
What is the treatment?
Dx: Tachycardia
Cause:
Increase opening L-type voltage Ca2+ channel in SA Node which leads to faster depolarization.
Treatment: Ectopic Pacemaker
A patient presents with
HR: 220
Rhythm: Regular
P Wave: Saw Tooth Appearance
QRS (Sec): <12sec
Altered impulse conduction.
What dx for pt?
Atrial Flutter
A patient presents with
HR: 350-650bpm
Rhythm: Irregular
P-Wave: Non-existent (can’t tell)
QRS <0.12 sec
Increased Atrial Myocyte automaticity, altered impulse formation and conduction, re-entry circuits.
What dx
Atrial Fibrillation
There are 4 main types of Atrial Fibrillation. They are described respectively as:
- Terminates randomly/in 7 days
- Lasts >7 days
-Doesn’t respond to therapy in returning to normal rhythm
- Rate >110 (complications: hemodynamic instability, acute/chronic HF, ischemia)
What are these called?
Paroxysmal
- Terminates randomly/in 7 days
Persistent
- Lasts >7 days
Permanant
-Doesn’t respond to therapy in returning to normal rhythm
Rapid Ventricular Rate (RVR)
- Rate >110 (complications: hemodynamic instability, acute/chronic HF, ischemia)
Patient Presents with
Heart rate <100BPM
Rhythm: Regular
P-Wave: Absent/Unrelated.
What dx does this patient have
Ventricular Tachycardia
Patient presents with
HR: 300-600
Rhythm: Extremely irregular
P Wave: Absent
PR Interval (sec): N/A
QRS (sec): Fibrillatory Baseline
It is unstable, and you detect early afterdepolarization (r-on-t phenomenon.) Patient has history of ventricular tachycardia.
What is the patients dx?
Ventricular Fibrillation
If you are caring for a patient who is presenting either:
Pulseless Ventricular Tachycardia
Or
Ventricular Fibrillation
What would you communicate to the healthcare team?
“Code Blue Rhythm”
Shockable.
A patient presents with “Long QT Syndrome”.
What questions might you ask to help treat, why?
Is this dx something that can harm patient’s immediate health?
How would you treat?
What medications are the patient on? History of HF? Age? Bradycardia history? Female? Ischemia? Labs/Electrolyte values?
Long QT Syndrome can Cause Sudden Death
Treatment:
Avoid QT prolonging meds
B-Blockers
- Implantable cardiac defibrillator (ICD) is secondary prevention if medications/lifestyle doesn’t work.
DADs (type of afterdepolarization which cause a slow/gradual rise in QRS instead of instant) occur due to an overload of which ion?
DADs (gradual instead of instant rise) are a result of Ca2+ overload.
(E.g. Ischemia, adrenergic stress, HF)
EADs arise from phase 3 (i.e. depolarization phase) and are a result of what ion(s) dysfunctionality?
EADs arise from K+ channel block/dysfunction
Or
Increased Ca2+ or Na+ inward current. And can lead to torsades de pointes.
Which type of arrhythmia is known as the ‘circus movement’?
This type of arrhythmia causes ectopic pacemakers
It also needs to have region of fast conduction, and a region of slow/impaired conduction circulating around an island of unexcitable tissue.
This is the REENTRANT ARRHYTHMIA.
What drug therapy would be used to treat a REENTRANT ARRHYTHMIA
Treatment for REENTRANT ARRHYTHMIA:
- K+ Blocker (indirectly prolong refractory period)
- Na+ Blockers (slow conducting side circuit)
What drug therapy would be used to treat a REENTRANT ARRHYTHMIA
Treatment for REENTRANT ARRHYTHMIA:
- K+ Blocker (indirectly prolong refractory period)
- Na+ Blockers (slow conducting side circuit)
What is Enhanced Automaticity?
Enhanced cardiac automaticity refers to the accelerated generation of an action potential by either normal pacemaker tissue (enhanced normal automaticity) or by abnormal tissue within the myocardium (abnormal automaticity).
Arrhythmias caused by enhanced automaticity (e.g. sinus tachycardia, a-fib, ventricular tachycardia) are treated by what mechanisms (not drugs)
- Reduce phase 4 spontaneous depolarization
- Make threshold potention more positive (increase it)
- Make threshold more negative so it fires less (hyperpolarize)
Arrhythmias caused by re-entry/unidirectional block (e.g. a-fib, atrial flutter, AVNRT, VT/VF) are treated with?
(Mechanisms of treatment)
Decrease conduction (create bidirectional block)
Increase refractory period (prevent loop of impulse)
Suppress ectopic/premature beats that cause re-entry.
List off some causes of Arrhythmias.
There’s a lot so don’t beat yourself up.
-Hypoxia/Ischemia
-K+,Ca2+,Mg2 imbalance
-Genetic Abnormality (Wolff-Parkinson-White syndrome, long QT syndrome
-Stimulants
- Alkalosis/Acidosis
-Drugs (digoxin, quinidine, b-blockers, CCBs
- Muscle fiber stretching (preload)
- Endocrine (Thyroid, Pheochromocytoma)
Which ions are important to account for in Arrhythmias?
Na+
K+
Ca++
Which ions are important to account for in Arrhythmias?
Na+
K+
Ca++
Which Channels/Pumps do we account for in arrhythmias?
Na+/Ca++ exchange
Na+/K+ ATPase
L-Type Ca++
T-Type Ca++
Funny Na+
The SA node is responsible for being the hearts pacemaker.
Other cells contribute if they need to correct/help the SA node.
What is the “chain of command” for the different heart cells that have pacemaker capability?
- SA Node
- AV node
- His bundle
- Right/Left Bundle Branch (LBB/RBB)
- Purkinje Fibers
In a Conductive cells Action potential, what is the order of events? (Picture the P-QRS wave)
- Slow influx of Na+ (Prepotential)
- Rapid Influx of Ca2+ (Depolarization)
- Outflux of K+ (Depolarization)
In a Contractile cells Action potential, what is the order of events? (Picture the P-QRS wave)
Phase I (Rapid Depolarization)
1. Influx Na+
2. Voltage-gated ion channels open.
Phase II (plateau)
3. Na+ channel closes
4. Slow Ca2+ channel open
5. Slow Ca2+ channel close
Phase III (repolarization)
6. K+ channels close
Funny Na+ Channels,
T-Type Ca++ Channels,
And L-Type Ca++ channels
All flow which way?
What type of cardiac cells are these channels involved in?
They all flow INWARDS (not exchange channels)
Cardiac CONDUCTIVE cells.
Which ions are flowing inwards/outwards in each of these exchanges/channels?
Also, which type of cardiac cells are these involved in?
Na+, Ca++ Exchange
Na+ , K+ ATPase
Na+, Ca++ Exchange
- Na+ into cell
- Ca++ out of cell
Na+ , K+ ATPase
- Na+ out of cell
- K+ into cell.
Cardiac Contractile Cells involve which channels/junctions? Which way does it flow?
Cations through gap junctions (inwards)
Voltage-Gated Na+ channels (inwards)
Ca++ channels (inwards)
K+ channels (outwards)
What is the order of an action potential?
- P-Wave (Atrial Depolarization)
- PR Segment
- QRS Complex
- ST Segment
- T- Wave
Good to google a picture or look at slides.
____________ can be used to identify abnormal depolarization and depolarization patterns in the heart.
Electrocardiograms. can be used to identify abnormal depolarization and depolarization patterns in the heart.
Anti-Arrhythmic drugs act by altering ______ _____ _______, directly or indirectly.
Anti-Arrhythmic drugs act by altering cardiac ion fluxes, directly or indirectly.
What 4 “umbrella” determinants should be used for an appropriate drug choice for a patient’s arrhythmia?
- Precise diagnosis of the arrhythmia, including mechanism.
- Eliminating precipitating factors.
- Assessment of risk/benefit
- Minimize Risk.
