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
