Heart Faliure/Dysrhythmias Flashcards

1
Q

Heart failure risk factors

A

Decreased CO that can cause accumulation in lungs (Left) or periphery (right)

  • CAD
    Obstruction in the coronary artery reduced oxygen to the myocardium

-HTN
Afterload increases resistance, causing hypertrophy and cardiac remodelling (too stiff to pump)

  • DM
    -Smoking
  • Obesity
    -High cholesterol
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2
Q

HF Causes

A

Chronic
- CAD - impaired blood flow (contractility)
- Cardiomyopathy - disease that thicken or stretch/thin (contractility)

-HTN work harder causing LEFT sided (afterload)
- Pulmonary disease like COPD causing RIGHT sided (afterload)

  • Valvular disease
    i) Valvues tight - stenotic valve so heart has to pump harder
    ii) Valves loosen - regurgitation/backflow
    (preload)

ACUTE
- Acute MI - lack of blood flow (contractility)
- Myocarditis - (contractility)

  • Hypertensive crisis - BP goes up too quick (afterload)
  • Papillary muscle rupture that closes AAV valves (preload)
  • Dysrhythmias
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3
Q

Ejection fraction

A

Percentage of end-diastolic blood volume ejected during systole

Usually 50-70%

Belor 40% = heart failure

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4
Q

HF Pathology

A

1) Systolic dynsfunction = HF WITH REDUCED EF
- Most common
- LV doesn’t contract strong enough to pump blood into the aorta
- EF usually under 40%

2) Diastolic dysfunction = HF WITH PRESERVED EF
- Inability of ventricles to relax and fill (pump still work)
- Could be due to ventricular hypertrophy or valvular disease

3) Mixed HF

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5
Q

HF Compensatory mechanism

A

1) SNS activation
- Increased HR increases contractility
= BAD as decreases time to fill, therefore less CO + more workload
- Peripheral vasoconstriction
= BAD as BP increases, increasing afterload and myocardial oxygen demand

2) Neuro-hormonal (RAAS)
- Na/water retention
= BAD - aldosterone increases blood volume/preload
- Peripheral vasoconstriction
= BAD angiotensin II increases afterload
- ADH released cause of low cerebral perfusion
= BAD as increases blood volume and preload

3) Ventricular dilation
- Enlargement of heat chambers due to increased preload/stretch
= BAD as cardiac remodelling and wont contract effectively

4) Ventricular hypertrophy
- Increased thickness and muscle mass
= BAD as contractility will be resisted, so more risk of ischemia

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6
Q

Counterregulatory mechanism

A

ANP and BNP
- Cardiac hormones that are released by the heart to promote DIURESIS (decrease preload)

Helpful but not strong enough

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7
Q

Types of HF

A

Acute vs chronic
Acute - quickly, usually with pulmonary edema
Chronic - over years of neuro-hormonal activation, usually SOB, etc (Acute can still occur)

Left vs Right
Left-sided = decreased CO or pulmonary congestion
Right-sided = increases systemic venous congestion

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8
Q

Right-sided Heart faliure

A

JVD
Peripheral edema
Anorexia, nausea, distended abdomen, splenomegaly, enlarged liver
Nocturia
Weight gain/HTN

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9
Q

Left-sided HF

A
  • Decreased CO
    Fatigue/weakness, confusion
    Tachycardia
    Oliguria
    Nocturia
    Pallor, weak peripheral pulse, cool extremities
  • Pulmonary congestion
    Cough, dyspnea
  • Orthopnea = SOB when lying down
  • Paroxysmal nocturnal dyspnea = SOB that awaken patient, relieved in upright position
  • Crackles/wheezes
  • Frothy, pink-tinged sputum
  • S24/S4 gallop
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10
Q

Cardiac cells

A

SA, AV, bundle of His, L/R bundle branches, Purkinje fibers

Properties
- Automatically - initiate own electrical impulse
- Contractility
- Conductivity - can depolarize to transmit signal
- Excitability
= ACCE of hearts

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11
Q

Electrocardiogram

A

Can detect abnormalities like ischemia, infarction, hypertrophy, electrolyte imbalance
- Note cells are normally negative and positive in depolarization

P wave = Atrial depolarization

QRS complex = Ventricular depolarization (+ atrial repolarization)

T wave = Ventricular repolarization

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12
Q

Normal Sinus Rhythm (NSR)

A

Normal rate and rhythm generate in SA node, which depolarizes faster than other cardiac cells

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13
Q

Types of ECG

A

1) 12 Leak - diagnostics
2) Telemetry = monitor

ST segments can be
i) Depression - ischemia caused by partial occlusion of coronary atery = Unstable angina & NSTEMI

ii) Segment - Complete occlusion = STEMI

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14
Q

Potassium and EKG

A

Hypokalemia
- Appearance of U wave!!!
- Predisposes to lethal rhythm called Torsade de pointe

Hyperkalemia
- Peaked T wabe
- Absent P

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15
Q

Sinus bradycardia/tachycardia

A

Bradycardia
SA nodes fires below 60 b/m
Can be athletes, medications, vagal stimulation, hypothermia, hypothyroidism, increased ICP, MI

If the patient cant tolerate it (pale, hypotensive, weak, angina, SOB) then issue

Tachycardia
SA node fires above 100 b/m
Can be stress, exercise, pain, hypotension, hypovolemia, anemia, hypoxia, hypoglycemia, MI, HF

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16
Q

Atrial fibrillation

A

Total disorganization of atrial activity
Occurs in pt with heart disease, thyrotoxicosis, alcohol intox, caffeine use, electrolyte imbalance,s tress

Atrial rate may be up to 600 bpm!!
Ventricular between 50-180
P wave is wavy

= Decrease in CO (loss of atrial kick), high risk of thrombus cause of statis

17
Q

Furosemide (Lasix)

A

MOA - acts on loop of henle to block reabsorption
Reduce work against RAAS and AGH (decrease preload)

PO/IV/IM

AE
- dry mouth, thirst, oliguria, weight loss
- hypotension, hypokalemia, tinnitus

18
Q

Hydrochlorothiazide

A

MOA - Blocks reabsorption of Na and Cl in distal convoluted tubule

Same AE as furosemide without the ototoxcity

19
Q

Spiranolactone

A

MOA - blocks aldosterone

Can also be given in liver cirrhosis

Caution with ACE and ARB as they block aldosterone and cause hyperkalemia as well!!
Other effects are impotence, ammonrhee etc

20
Q

Canaglifozin

A

Sodium-glucose co-transporter

MOA - Inhibit SGLT-2 in kidney to reduce reabsorption of glucose, causing diuresis

Used in diabetes and HF as well

AE - Yeast infection, UTI, hyponatremia, polyuria, dehydration, postural hypotension

21
Q

Sacubitril/Valsartan (Entresto)

A

ARNI (Angiotensin receptor/Neprilysin inhibitor)

MOA
I) Sacubitril - inhibit neprilysin, increasing ANP/BNP as it breaks it down
II) ARB - Block aldosterone receptor, reduce preload and vasoconstriction

AE - Hypotension, hyperkalemia, high creatinine

22
Q

Digoxin

A

Cardiac glycosides

MOA - increase myocardial activity by inhibiting enzyme Na/K ATPase, accumulating calcium
= Slows the HR BUT increases CO

Indication - HF, afib

AE
Dysrhytmias esp in hypokalemia
Bradycardia
Hypotension
GI disturbances

Potassium and digoxin
= Compete, therefore hyperkalemia causes subtherapeutic level, hypokalemia causes toxicity

23
Q

Chronic HF assessment

A

Elevates HR cause of SNS
Elevated BP
High RR w pulmonary edema, low o2
Confusion, dizzy
JVP
Crackles
Poor appetie
Oliguria if decreased renal perfusion

Acute exacerbation - 30 RR, dyspnea, wheezying, frothy pink-tinged sputum
clammy, cold, pale, cynaotic

24
Q

Hydralazine

A

Vasodilator
MOA - Acts on smooth muscle to cause dilation on arterioles
= Decrease afterload and peripheral resistance

Given for HTN and HF = potent vasodilator for arteries

AE
- Reflex tachycardia - usually taken with beta blocker to prevent this
- Hypotension

25
Q

Cardiac diagnostics

A

Transthoracic echocardiogram (Echo/TTE)
- Ultrasound of the heart
- Non-invasive

Transesophageal echocardiogram
- Invasive as inserts through esophagus

Multigated acquisition scan (MUGA)
- imaging using radioactive isotope, only in special hospital

Cardiac natriuretic peptide markers
- ANP = Atrium
- BNP - Ventricle
- NT-pro-BNP - ventricles
BNP released when diastolic BP is high (LV failure)

Electrocardiagram for dysrhythmias
Rhythm, rate, ischemia, hypertrophy
Serum electrodes can cause dysrhythmias like low mg, ca, K, or high ca, K