Heart Faliure/Dysrhythmias Flashcards
Heart failure risk factors
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
HF Causes
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
Ejection fraction
Percentage of end-diastolic blood volume ejected during systole
Usually 50-70%
Belor 40% = heart failure
HF Pathology
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
HF Compensatory mechanism
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
Counterregulatory mechanism
ANP and BNP
- Cardiac hormones that are released by the heart to promote DIURESIS (decrease preload)
Helpful but not strong enough
Types of HF
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
Right-sided Heart faliure
JVD
Peripheral edema
Anorexia, nausea, distended abdomen, splenomegaly, enlarged liver
Nocturia
Weight gain/HTN
Left-sided HF
- 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
Cardiac cells
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
Electrocardiogram
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
Normal Sinus Rhythm (NSR)
Normal rate and rhythm generate in SA node, which depolarizes faster than other cardiac cells
Types of ECG
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
Potassium and EKG
Hypokalemia
- Appearance of U wave!!!
- Predisposes to lethal rhythm called Torsade de pointe
Hyperkalemia
- Peaked T wabe
- Absent P
Sinus bradycardia/tachycardia
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
Atrial fibrillation
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
Furosemide (Lasix)
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
Hydrochlorothiazide
MOA - Blocks reabsorption of Na and Cl in distal convoluted tubule
Same AE as furosemide without the ototoxcity
Spiranolactone
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
Canaglifozin
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
Sacubitril/Valsartan (Entresto)
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
Digoxin
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
Chronic HF assessment
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
Hydralazine
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
Cardiac diagnostics
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
