Heart = Pump Flashcards
(26 cards)
Amount of liters entering the right and left chambers of the heart total
5L
Pumping of the heart is a (?) phenomenon….
External factors (like the ANS) only influence the
- Intrinsic
2. Pumping rate
Propranolol
Drug that is a sympathetic antagonist
Slows heart rate
Atropine
Parasympathetic antagonist
Raises heart rate
Intrinsic heart rate is around what?
~100bpm
General signs/symptoms of heart failure
Difficulty breathing
Severe fatigue
Shortness of breathe, particularly on exertion
Tachycardia, engorged neck veins (increased right atrial pressure)
Ankle edema
Palpable tender liver
Signs of fluid in lungs
Enlargement of heart shadow on CXR
What is heart failure
Structural and functional impairment of ventricular filling or ejection of blood
Creates a condition in which the heart cannot pump sufficient O2 blood to meet metabolic demands
OR
Can only do so from an elevated filling pressure
Forward heart failure
Reduction in cardiac output due to decreased pumping action
Symptoms:
Fatigue, dizzy, confusion, asthenia
Backward heart failure
Congestive state, due to dysfunctional ventricle that does not pump out all the blood it receives
Increase ventricular filling pressure
Results:
Pulmonary edema (congestive within pulmonary vasculature)
Peripheral edema
—> fluid within other tissues like the skin, abdominal cavity
Incidence and prevalence of heart failure
5.8 million people have heart failure in the USA
38 billion annually
Most common inpatient diagnosis within this population
Incidence increases with age
—> more common in men from 45-60 years old
—> over 70, risk is equal
Blacks have 25% higher chance
Etiology of heart failure
- Most commonly from impaired myocardial contractility caused by ischemic heart disease or cardiomyopathy
MI = most common cause
- Systemic hypertension
—> cardiac valve abnormalities, pericardial diseases, or pulmonary hypertension
Stroke volume
Amount of blood ejected of the right or left per contraction
SV = EDV - ESV
Cardiac output
Amount of blood ejected out of the heart per unit of TIME
CO = SV * HR
Ejection fraction (EF)
Ratio of the volume of blood ejected from the ventricle during systole (SV) to the volume of blood present in the ventricle at the end of the diastole (EDV)
EF = SV/EDV
Factors influencing cardiac pump activity
- Contractile force of ventricular muscle
—> positive factor dependent on…
Myocardial fiber length (preload) AND
Myocardial contractility - Pressure in the aorta/pulm artery
—> negative factor known as AFTERLOAD
Preload
= ventricular load at the end of diastole, before the start of contraction
Equates to the amount of stretch on a ventricular fiber just prior to the act of contraction
Initial stretch depends on the volume of blood in the heart during diastole
Larger volume = largery stretch = increased force of the next contraction
PRELOAD = MOST IMPORTANT IN THE DETERMINING STROKE VOLUME (SV)
Length-tension (force) relationship
Diastole = lower curve…as length increases, force starts to increase slightly
Systole = upper curve…more drastic increase in force as length increases…but force decreases past optimal length
What is a substitute measure for preload, since it is hard to measure?
Right atrial pressure
Increased right atrial pressure = ?
Increased stroke volume
Thus, increased preload = increased SV
Ventricular function curve (Frank-Sterling relationship)
Relationship between preload (i.e. EDV or myocardial fiber length) and ventricular performance (i.e. SV)
SV is DIRECTLY related to EDV
Relatively linear in the normal range
= SV 60-100mL
= EDV 100-150mL
Force/tension relationship and the physical blood volume contribute to this relationship
Indices of myocardial fiber length (preload)
EDV
ED pressure
Ventricular circumference
Venous return/atrial volume
Mean atrial pressure
Indices of ventricular performance
SV
CO
Stroke work
Cardiac work
Myocardial contractility
= a property of heart muscle accounting for changes in strength of contraction
INDEPENDENT of preload and afterload!! (Intrinsic property)
It influences the relationship between SV and EDV
—> increase contractility, curve shifts upward…and vice versa
NOT THE SAME as increasing contractile force due to increased myocyte tension
Examples:
- Providing a drug that creates peak contractile force despite less than optimal conditions (such as holding cardiac myocyte fibers at 1/2 their optimal tension)
—> this change as NOTHING to do with the force-tension relationship, and exhibit intrinsic contractility - Patients with heart failure may present with reduced contractile force…despite their cardiac myocyte fibers being at optimal length
Effect of NE on contractility
Increases it…
Thereby shifting the curve up and to the left
Exhibits increased contractility = increased SV
