6.3: heart failure & dysrythmias

What is heart failure? 

• ___

• Leading to fluid volume overload bc ____

TYPES OF HEART FAILURE

• Left ventricular failure: most common

→aka ____

→causes backup in ____

• Right ventricular failure: often a result of ___

→associated with ____

→aka ____

• Systolic failure (HFrEF): problem with ___

• Diastolic failure (HFpEF): problem with ____

What is heart failure? 

• Heart becomes weak and fails to pump blood forward, so it backs up

• Leading to fluid volume overload bc blood and fluids start to back up against the circulatory pathway

TYPES OF HEART FAILURE

• Left ventricular failure: most common

→aka congestive HF

→causes backup in lungs first: Fluid hanging out in lungs instead of being moved to rest of the body

• Right ventricular failure: often a result of left ventricular failure

→associated with having untreated congestive heart failure

→Cor pulmonale

• Systolic failure (HFrEF): problem with contraction and ejection

• Diastolic failure (HFpEF): problem with relaxing and filling

Right	Left
Right side is supposed to pump blood to the lungs, then oxygenate in the lungs, then return to systemic. If it doesn’t happen, ____ signs/ symptoms: ____	Congestive & fluid overload, think of someone who’s drowning bc lungs are filled with fluid. Blood backing up into lungs. signs/ symptoms: ___

Right

Left

Right side is supposed to pump blood to the lungs, then oxygenate in the lungs, then return to systemic. If it doesn’t happen, blood will back up into spaces like the rest of the body: edema/ swelling Swelling of legs & hands Weight gain Edema Large neck veins (JVD) Lethargy/ fatigue Irregular HR Nocturia Girth (ascites/ abnormal buildup of excess fluid inside peritoneal cavity: weight gain should never surpass 2-3lb per day bc will worsen bodily function)

Congestive & fluid overload, think of someone who’s drowning bc lungs are filled with fluid. Blood backing up into lungs. Dyspnea Rales (crackles = wet lungs) Weakness/fatigue Orthopenia (shortness of breath from lying down → standing up) Nocturnal paroxysmal dyspnea (waking up feeling like drowning bc of fluid-filled lungs) Increased HR Nagging COUGH Gaining weight (2-3lb/day)

SYSTOLIC HF VS. DIASTOLIC HF

Both asides aren’t pushing as much as its supposed to 

Systolic	Diastolic
• Decreased ____ Force of contraction weak → ___ • Low output→ ___ • SNS: ____ • Workload increases → contractility decreases • Increased end diastolic blood volume → ventricular dilation	• What happens? ___ • ____ • Less blood in ventricles and decrease ___ • Low cardiac output increases ___

• Inotropy = ____

• Negative remodeling of heart: ___ of heart

• When not perfusing well, kidneys get involved: _____ 

  • More ___: holds more volume → fluid retention

SYSTOLIC HF VS. DIASTOLIC HF

Both asides aren’t pushing as much as its supposed to 

Systolic

Diastolic

• Decreased ventricular output Force of contraction weak → heart cannot effectively squeeze out blood • Low output→ baroreceptors stimulate SNS (attempt to raise HR to get fluid out of heart) • SNS: increase HR and contractility • Workload increases → contractility decreases • Increased end diastolic blood volume (amount of blood in ventricle right before it contracts (preload)) → ventricular dilation

• Cardiac cells die and become fibrotic (bc not enough oxygen) • Stiff ventricle resists filling (like new balloon) • Less blood in ventricles and decrease cardiac output • Low cardiac output increases work of heart

• Inotropy = the force or strength of myocardial (heart muscle) contraction

• Negative remodeling of heart: hypertrophy of heart

• When not perfusing well, kidneys get involved: RAAS system may release renin, convert angiotensin I → angiotensin II, aldosterone holds onto fluid  → more fibrosis to heart bc 

  • More antidiuretic hormone: holds more volume → fluid retention

• failing heart cannot pump enough blood to meet body's demands, causing the kidneys to mistakenly "think" the body is severely dehydrated or experiencing blood loss

DIAGNOSING HEART FAILURE

• History and physical assessment

→Comorbidities, ROS (review of systems, like urinary or liver function) and exam findings

• Echocardiogram – measures ____ (ejection fraction, should be greater than ___, can help classify how bad HR is by seeing how much it decreases over time), ventricle sizes

• Chest x-ray (see ___ activity & see ____)

• EKG (analyze heart rhythm abnormalities and dysrhythmias)

• Labs – cardiac enzymes (like troponin), BNP (brain natriuretic peptide: measures how severe HF is)

• Stress test: putting someone on a treadmill and analyzing their CO2 & O2, EKG, increase amount of energy expended to analyze changes in their heart rhythm

• Cardiac cath: insert percutaneously that goes into the heart and measures its activity

echocardiogram: ejection fraction, should be >50%

chest xray: see heart activity + how much fluid is in lungs

CLINICAL MANIFESTATIONS OF: CONGESTION

Left to lungs: (respiratory related)	Right sided symptom: R to rest of body
• Dyspnea, orthopnea, paroxysmal nocturnal dyspnea • Cough • Crackles not clearing with cough • ___ • Dependent edema • Abdominal bloating	• __ • ___ distention • Sleep ___ • Fatigue

CLINICAL MANIFESTATIONS OF: POOR PERFUSION AND LOW CARDIAC OUTPUT

• Decreased exercise tolerance

• Muscle wasting

• Weakness

• Anorexia or nausea (if intestines aren’t getting adequate perfusion, food will stay in digestive tract for longer and no longer feel hungry)

• Weight loss

• Lightheadedness/dizziness (brain lacks perfusion)

• Confusion, AMS 

• Tachycardia at rest (sitting up from a chair is exhausting bc lack of perfusion)

• ____

• Cool/vasoconstricted extremities

• Pallor, cyanosis (blue tinge in skin)

HEART FAILURE TREATMENT: The “Big Five”

• ACE inhibitor/ARB

• Aldactone (diuretics)

• Digoxin

• Lasix (release fluid from body)

• Beta blocker (decrease HR while increase strength of contractions)

CLINICAL MANIFESTATIONS OF: CONGESTION

Left to lungs: (respiratory related)	Right sided symptom: R to rest of body
• Dyspnea, orthopnea, paroxysmal nocturnal dyspnea • Cough • Crackles not clearing with cough • Rapid weight gain • Dependent edema • Abdominal bloating	• Ascites • Jugular venous distention • Sleep disturbances • Fatigue

CLINICAL MANIFESTATIONS OF: POOR PERFUSION AND LOW CARDIAC OUTPUT

• Decreased exercise tolerance

• Muscle wasting

• Weakness

• Anorexia or nausea (if intestines aren’t getting adequate perfusion, food will stay in digestive tract for longer and no longer feel hungry)

• Weight loss

• Lightheadedness/dizziness (brain lacks perfusion)

• Confusion, AMS 

• Tachycardia at rest (sitting up from a chair is exhausting bc lack of perfusion)

• Oliguria with recumbent nocturia (during the day, when they’re trying to perfuse blood to brain, kidney doesn’t work as effectively so low urine output. Night: body is at rest and kidney works to release more urine)

• Cool/vasoconstricted extremities

• Pallor, cyanosis (blue tinge in skin)

HEART FAILURE TREATMENT: The “Big Five”

• ACE inhibitor/ARB

• Aldactone (diuretics)

• Digoxin

• Lasix (release fluid from body)

• Beta blocker (decrease HR while  increase strength of contractions)

Cardiac glycosides: Digoxin 

Digoxin is only one in US

• Troublesome drug (tricky med bc ____)

• Decreases morbidity (decreases SE) but not mortality/ make someone live longer

• May cause increased mortality in women

• Narrow therapeutic range: 0.5-2 ng/mL

MOA	-locks the membrane of ___ & impacts ____ -by blocking it, ___ Ionotropic, dromotropic, chromatropic effects: _____
Therapeutic Uses	____ • Heart Failure • Atrial fibrillation, Atrial flutter • Cardiogenic Shock
Adverse effects	___ • ___ • If in doubt, hold digoxin ____ ____ Monitor ____ • N/V, anorexia, vision changes (_____)
Interactions	Causes of Toxicity • ___ (<3.5 mEq/L) →Loop diuretics • ___ (<1.5 mEq/L) • ___ (>10.2 mg/dL) • Elderly: decreased renal and liver function (inability to clear digoxin)
Responsibilities	Administration: • _____  → hold if less than ____ Distribution: ____  Elimination: ____ • Must check renal function
Pearls	• S/S of toxicity • Drug levels and electrolyte draws • _____

Cardiac glycosides: Digoxin 

D for “dysrythmia SE”

Digoxin is only one in US

• Troublesome drug (tricky med bc narrow therapeutic range)

• Decreases morbidity (decreases SE) but not mortality/ make someone live longer

• May cause increased mortality in women

• Narrow therapeutic range: 0.5-2 ng/mL

MOA	-locks the membrane of Na + K & impacts how forceful heart is pumping -by blocking it, changes how fast heart beats & changes conduction/ SA node  • Positive Inotropic Effect = heart squeezes harder (by inhibiting Na/K pump) (“in the tropics, in the tropic: citrus fruit, squeeze lemon/ orange to get juice”) • Inhibits Na-K ATPase and calcium accumulates in myocytes • Competes with K+ for binding sites • Negative Dromotropic effects: slows impulses AV node (“dromotropic: drive: how fast u push on the petal & how fast eh impulse is”) • Negative Chronotropic effects: beats slower (“chrono: think chronological time, slower, changes beat”)
Therapeutic Uses	Help pump more efficiently • Heart Failure • Atrial fibrillation, Atrial flutter • Cardiogenic Shock
Adverse effects	Dysrhythmias • May mimic ANY dysrhythmia • If in doubt, hold digoxin Bradycardia Monitor K+ (if no K+ binding site from blockage due to drug, excess K+ may stay outside of cell- hyperkalemia (K+ in relation to plasma)) Monitor dig levels for toxicity • N/V, anorexia, vision changes (yellow/green halos)
Interactions	Causes of Toxicity • Hypokalaemia (<3.5 mEq/L) →Loop diuretics = POTASSIUM WASTING • Hypomagnesemia (<1.5 mEq/L) “hippos like mango and kale” • Hypercalcemia (>10.2 mg/dL) • Elderly: decreased renal and liver function (inability to clear digoxin)
Responsibilities	Administration: • Listen to apical pulse one FULL minute  → < 60BPM , hold Distribution: 23% of digoxin is bound to albumin. Proteins help to bind to digoxin and distributes throughout the body → if someone has  Elimination: renal • Must check renal function
Pearls	• S/S of toxicity • Drug levels and electrolyte draws • Measure pulse BEFORE taking and when to call MD

DYSRHYTHMIAS

Etiology/ causes	• Electrolyte imbalances (like K+ which has 3 different moments in the heart contraction steps) alter action potential  • Medications (stimulation of SNS or blocking beta cells or prolonging QT interval) • ___  • Aging, structural damage
Manifestation	• ECG, ↓ Cardiac Output

Impulse Formation	Slowed Conduction
– Ectopy: ___ – Atrial rhythms (Supraventricular) – Junctional rhythms – Ventricular rhythms – Types • Fibrillation • Flutter • Tachy • Brady	– __ blocks – ___ Blocks

Types of dysrhythmias 

“Sinus arrhythmias"	Ectopy (early contraction)
• Tachycardia (>100bpm) • Bradycardia (<60bpm) description: ____	• Premature Atrial Contraction (PAC) • Premature Ventricular Contraction (PVC) description:____

DYSRHYTHMIAS

Etiology/ causes	• Electrolyte imbalances (like K+ which has 3 different moments in the heat contraction steps) alter action potential  • Medications (stimulation of SNS or blocking beta cells or prolonging QT interval) • Hypoxia  • Aging, structural damage
Manifestation	• ECG, ↓ Cardiac Output

Impulse Formation	Slowed Conduction
– Ectopy (extra beat) – Atrial rhythms (Supraventricular) – Junctional rhythms – Ventricular rhythms – Types • Fibrillation • Flutter • Tachy • Brady	– AV blocks – Bundle Branch Blocks

Types of dysrhythmias 

“Sinus arrhythmias"	Ectopy (early contraction)
• Tachycardia (>100bpm) • Bradycardia (<60bpm) Working together but faster or slower than normal	• Premature Atrial Contraction (PAC) • Premature Ventricular Contraction (PVC) Normal heart beats & rates but then one that looks abnormal

Atrial flutter	Atrial fibrillation
-Atria activity looks like ___  -speed of heart beats: ____ -what is inmeasurable in the graph of atrial flutter? ___	-description: ___

Ventricular rhythms	Ventricular fibrillation
→____ wave of ventricular rhythm looks like: ___	-description: ____

Atrial flutter	Atrial fibrillation
-Atria activity looks like a saw: sharp pointy tip, predictable fast rhythm  -Normal or slightly faster than normal -Can’t measure PR interval bc theres too many	-Unpredictable & uncoordinated (irregular R-R intervals)

Ventricular rhythms	Ventricular fibrillation
→Ventricular tachycardia (important to know bc if they have a pulse, it won’t be for long and lead to death) (irregular, coarse wave forms of diff shapes, ventricles are quivering) -look like tombstones	(rapid, disorganized pattern of electrical activity in ventricle in which electrical impulses arise from many different foci)

ANTIDYSRHYTHMIC CLASSIFICATIONS

• Class I: Sodium Channel Blockers (no need to learn in this course)

• Class II: Beta blockers

• Class III: Potassium Channel Blockers

• Class IV: Calcium Channel Blockers

• Non classed drugs

.

CLASS II: Beta Blockers: propranolol 

Why	• ___ • ____
Patho	• Block ___ • Causes ___ • Decrease ___ • Slow ____
SE	• CNS: hypotension, bradycardia, AV block • Resp: bronchospasm, dyspnea (bc propranolol is beta blocker) • GI: NV • Loss of libido, decreased exercise tolerance
Caution	• Thyroid dysfunction, hepatic, diabetes

CLASS II: Beta Blockers: propranolol 

“vents (ventricular issues) propel (propranolol) from air”

Why	• Supraventricular Tachycardia (SVT): really fast HR in ventricles but not in atria • Premature Ventricular Contractions (PVC’s): heart skipping a beat
Patho	• Block beta adrenergic receptors • Causes depression of phase 4 of action potential • Decrease HR, cardiac excitability, and cardiac output • Slow conduction through AV node and prolong AV node repolarization
SE	• CNS: hypotension, bradycardia, AV block • Resp: bronchospasm, dyspnea (bc propranolol is beta blocker) • GI: NV • Loss of libido, decreased exercise tolerance
Caution	• Thyroid dysfunction, hepatic, diabetes

CLASS III: Potassium Channel Blockers: Aminodarone (PO, IV)

Why	• ___ • Results in ___
Patho	• Block ___
AE	↓HR, ___, visual impairment

CLASS III: Potassium Channel Blockers: Aminodarone (PO, IV)

“Kale (K+) is Very Fibrous”

Why	• First line for V-fib maintenance • Results in prolonged electrical impulses in all heart cells
Patho	• Block potassium channels and slow outward movement of K during phase 3 of the action potential prolonged
AE	↓HR, lung damage (tends to build up & linger in various body tissues over time, including lung tissue), visual impairment

CLASS IV: Calcium Channel Blockers 

Only non-dihidopyridines	• Examples: Verapamil & diltiazem • Slow____ • Delay ___ • Reduction of ____ • Block ___, depression generation of action potentials
AE	•↓HR, AV block, Heart failure, hypotension, constipation

CLASS IV: Calcium Channel Blockers 

Only non-dihidopyridines	• Examples: Verapamil & diltiazem • Slow SA node automaticity • Delay AV conduction • Reduction of myocardial contractility (by blocking Ca+ ions) • Block calcium ions across the cell membrane, depression generation of action potentials
AE	•↓HR, AV block, Heart failure, hypotension, constipation

Other antidysrhythmics

Adenosine (usually emergent option)

• Short ___, termination of ___

• Convert ___

• Tell them to ____

Other antidysrhythmics

Adenosine (usually emergent option)

• Short half life (works quickly & leaves from body early), termination of paroxysmal SVT

• Convert SVT to Sinus rhythm when vagal maneuvers are ineffective

• Tell them to hold their breath & bear down to get themselves out of that phase