Cardiac Output Flashcards
Cardiac Output function
VITAL to homeostasis
Controls amount of blood flow to the tissues. Prevents undue stress on the heart.
Depends on venous return, which, in turn, depends on the rate of flow to the tissues.
Rate of flow to tissues depends on tissue needs (i.e. it depends on Total Peripheral Resistance). Therefore, cardiac output is proportional to the energy requirements of the tissues.
HR factors
Primarily varied by altering balance of parasympathetic and sympathetic influence on SA node.
Sympathetic stimulation speeds it up
Parasympathetic stimulation slows heart rate.
Average End Diastolic, Stroke Volume, End Systolic Volume, and Ejection Factions
- EDV - 120-130ml
- SV output - 70 ml
- ESV - 50-60ml
- Ejection Fraction - 60 % [70/120]
The volume of blood pumped each minute
CO = SV x HR
COis cardiac output expressed in L/min (normal ~5 L/min) Note difference between CO & CI.
SV - is stroke volume per beat.
HR- is the number of beats per minute.
Stroke Volume
The volume of blood pumped out by each ventricle per each contraction.
Determined by extent of venous return and by sympathetic activity.
Intrinsic control of Cardiac output
Heart muscle operates short of its optimal sarcomere length.
Stretch it by bringing more blood back to the heart
Increase in stroke volume, increases contractility.
Extrinsic control of Cardiac output
NE from sym. + Epi. from adrenal medulla →↑ opening of Ca++ channels → more Ca++ inside → ↑ force of contraction
Factors that increase Cardiac Output
- SNS - (Epi, Nor Epi)
- T3 + T4 (metabolic increase)
- Increase in Body Temp
- Increase in Calcium.
- decrease in PO2 - (hypoxia)
- Increase in CO2
- decrease in pH
Factors that decrease Cardiac Output
- PSNS - (Ach)
- Decrease in Calcium
- Increase in Potassium
Factors that increase Preload
- Increase in EDV - Venous return
a)muscular activity
b) respiratory pump
(deep inspiration - increase in abdominal pressure; decrease in thoracic pressure)
c) SNS - Nor Epi on smooth muscle
venomotor tone / constriction - Filling time -
Increased HR - decreases filling time.
How MI’s affect preload
The heart muscle has scar tissue and will not stretch as much, decreasing preload.
Frank Sterling’s Law
Greater the stretch, the greater the force of contraction.
[more stretch allows for more cross-bridging which increases preload and SV]
Ejection Fraction (EF)
- % of the EDV that is pumped by the ventricle (important clinical parameter) the EF should be about 55-60%
[ SV/EDV ]
Increases during exercise.
SV determinants
- Preload - The amount of myocardial stretch (EDV)
- Contractility - intrinsic strength of cardiac muscle.
- Afterload - amount of of resistance the ventricles need to overcome to send blood to the aorta and pulm. trunk. [arterial pressure, valvular pressure]
Contractility determinants
- SNS - Epi, Nor Epi act on ß1 adrenergic receptors - which increases Ca2+ levels, increases contractility and increases SV.
- Hormones - T3 and T4 stimulates genes in cardiac cells and proteins which increase ß1 receptors and increases cont. and SV.
- Increase in Glucagon.
- Drugs - ( Digitalis, epi, atropene)
Afterload determinants
[Increase in afterload, decreases SV]
- Stenotic valves
- vessel occlusion
- HTN
- plaque buildup
Increases back pressure in arterioles; increases BP
Heart Rate
Heart rate is directly proportional to cardiac output
Adult HR is normally 80-100 beats per minute (bpm.)
Heart rate is modified by autonomic, immune, and local factors.
An increase in parasympathetic activity via M2 cholinergic receptors in the heart will decrease the heart rate.
An increase in sympathetic activity via B1 and B2 adrenergic receptors throughout the heart will increase the heart rate
Cardiac Reserve
the difference between resting and maximal CO.
CO limits
Normal CO – 5 L/min
Plateau – 13 L/min
Hyper-effective heart plateau – 20 L/min
Hypo-effective heart plateau – 5 L/min
Hyper-effective heart conditions
- Nervous excitation
- Cardiac Hypertrophy
- Exercise – Marathon runners may get 30 to 40 L/min
- Aortic Valve Stenosis
Valvular disease
Increased output pressure
Congenital heart disease
Myocarditis
Cardiac anoxia
Toxicity
The result of Cardiac muscle fiber stretch
Cardiac fibers contract MORE FORCEFULLY when stretched thus ejecting MORE
BLOOD (increased SV)
If SV is increased, then ESV is decreased!!
Slow heartbeat and exercise
Slow heartbeat and exercise increase venous return (VR) to the heart, increasing SV.
VR changes in response to blood volume, skeletal muscle activity, alterations in cardiac output
⬆️VR , ⬆️EDV, ⬆️ SV
and vice versa. (Proportional relationship)
Blood loss and extremely rapid heartbeat decrease SV
Venous Return’s affect on CO
- Within physiological limits the heart pumps all the blood that returns to it from the veins
- Venous return increases when there is an increase in the blood flow through peripheral organs
- Peripheral blood flow is a major determinant of CO.
Factors that decrease contractility
- Acidosis
- Increased extracellular K+
- Calcium channel blockers
Effects of Autonomic Activity on Contractility
I. Sympathetic stimulation
Release norepinephrine from symp. postganglionic fiber
Also, EP and NE from adrenal medulla.
Have positive ionotropic effect (stronger heart muscle contractions)
Ventricles contract more forcefully, increasing SV, increasing ejection fraction and decreasing ESV.
II. Parasympathetic stimulation via Vagus Nerve
Releases ACh
Has a negative inotropic effect
Hyperpolarization and inhibition
Force of contractions is reduced, ejection fraction decreased.
Sympathetic effects on CO
- Can increase heart rate 70 to 180-200 BPM
- Can double force of contraction
- Sympathetic nerves release norepinephrine.
Believed to increase permeability of Ca2+ and Na+.
Parasympathetic effects on CO
Parasympathetic (vagal) decreases cardiac output
Can decrease heart rate to 20-40 BPM
Can decrease force of contraction by 20-30%
Parasympathetic nerves release acetylcholine
Increases permeability to K+
Compensation for Increased Blood Volume
- Increased CO increases capillary pressure, sending more fluid to tissues.
- Vein volume increases
- Pooling of blood in the liver and spleen
- Increased peripheral resistance reduces cardiac output.
SNS effect on over volume in veins
- Increases contractility of the heart.
- Decreases volume by contracting the veins.
- Increases filling pressure
- Increases resistance
Disease States Lowering Total Peripheral Resistance
- Beriberi: insufficient thiamine – tissues starve because they cannot use nutrients.
- AV fistula: e.g. for dialysis.
- Hyperthyroidism: Reduced resistance caused by increased metabolism
- Anemia (lack of RBCs): effects viscosity and transport of O2 to the tissues
Disease States Lowering Cardiac Output
1.Heart attack, valvular disease, myocarditis, cardiac tamponade, shock
- Decreased venous return caused by:
a) Reduced blood volume
b) Venous dilatation (increased circulatory volume)
c) Venous obstruction
Chemical Regulation of the Heart
- The hormones epinephrine and thyroxine (T4) increase heart rate
- Renin, ADH, and aldosterone regulate BP.
- Intra- & extracellular ion concentrations must be maintained for normal heart function.
Hypocalcemia
Reduced ionic calcium depresses the heart
Hypercalcemia
Dramatically increases heart irritability and leads to spastic contractions
Hypernatremia
Blocks heart contraction by inhibiting ionic calcium transport
Hyperkalemia
Leads to heart block and cardiac arrest
IV calcium gluconate given to stabilize cardiac membrane.
Baroreceptor effect on the heart
- stimulated by increase in arterial pressure (stretch)
- Effect: negative chronotropic and inotropic
- regulates the heart when BP increases or drops -
involved in short term regulation of BP
Chemoreceptor effect on the heart
stimulated by decrease in oxygen, decrease in pH, or increase in CO2
overall effect: positive chronotropic and inotropic.
less important in regulating cardiac function
Proprioceptor effect on the heart
Stimulated by muscular and joint movement.
Increases HR during exercise.
Preload and afterload effects on EF
Increase preload –> Increase Ejection Fraction
Increase afterload–> Decrease Ejection Fraction
Specific Testing for LV Function
- Angiographic Assessment – this is where you determining the actual motion of the ventricle
- Echocardiography – allows you to measure the ejection fraction in relation to the cardiac filling as well as to visualize the other structures which may be interfering with the cardiac output such as any fluid within the pericardial sac.
- CT Scan – Excellent visualization of the cardiac structures including reproducible measure of wall thickness as well as ESV and EDV
Gold standard: MRI
Allows visualization even in patients with abnormal geometry
Heart Failure defining criteria
Heart Failure basically is any condition which reduces myocardial efficiency. This inefficiency will eventually produce changes within the heart.
Heart Failure etiology examples
- Reduced contractility, or force of contraction, due to overloading of the ventricle.
- A reduced stroke volume, as a result of a failure of systole, diastole or both.
- Increased heart rate, stimulated by increased sympathetic activity in order to maintain cardiac output.
- Hypertrophy of the myocardium, caused by the terminally differentiated heart muscle fibers increasing in size in an attempt to improve contractility.
- Enlargement of the ventricles, contributing to the enlargement and spherical shape of the failing heart.
CHF Causes
Coronary artery disease
Heart attack
High blood pressure
Heart valves disorders
Inflammation
Kidney Disease
Abnormal Heart Rhythms
Severe Anemia
Hyperthyroidism
Hypothyroidism
Timing Classifications of HF
Systolic failure- dec. contractility
Diastolic failure- dec. filling
Etiologies of Systolic Heart Failure
- Coronary Artery Disease (65%)
- Idiopathic dilated cardiomyopathy
3 .Alcohol/toxin-induced cardiomyopathy - Infectious/inflammatory process
- Familial dilated cardiomyopathy
- Postpartum cardiomyopathy
- Stress induced cardiomyopathy
- Endocrine/nutritional causes
- Iron overload cardiomyopathy
- Tachycardia mediated cardiomyopathy
Characteristics of Systolic Heart Failure 1
More readily recognized.
- Described as failure of the pump function of the heart.
Characterized by a decreased ejection fraction (less than 45%). - The strength of ventricular contraction is attenuated and inadequate for creating an adequate stroke volume, resulting in inadequate cardiac output.
- Caused by dysfunction or destruction of cardiac myocytes or their molecular components.
- Most common mechanism of damage is ischemia causing infarction and scar formation which casues dead myocytes are replaced by scar tissue, then decreased function of myocardium causing wall motion abnormality.
Characteristics of Systolic Heart Failure 2
- Since the ventricle is inadequately emptied, ventricular end-diastolic pressure and volumes increase affecting the atrium.
- On the left side of the heart, the increased pressure is transmitted to the pulmonary vasculature creates extravasation of fluid into the lung parenchyma –> pulmonary edema.
- On the right side of the heart, the increased pressure is transmitted to the systemic venous circulation and systemic capillary beds which creates extravasation of fluid into the tissues of target organs and extremities –> dependent peripheral edema.
Ejection fraction drops below 40%.
Characteristics of Diastolic Heart Failure 1
- Described as failure of the ventricle to adequately relax and typically denotes a stiffer ventricular wall.
- Inadequate filling of the ventricle results in an inadequate stroke volume.
- Failure of ventricular relaxation also results in elevated end-diastolic pressures with pulmonary edema in left heart failure and peripheral edema in right heart failure.
- Caused by processes that affect cardiac remodeling which may be asymptomatic.
Characteristics of Diastolic Heart Failure 2
- Sensitive to increases in heart rate
Sudden bouts of tachycardia (caused simply by physiological responses to exertion, fever, or dehydration) can lead to flash edema. - Pathological tachyarhythmias (e.g., atrial fibrillation with rapid ventricular response) may result in flash pulmonary edema.
- Diastolic function worsens with age even in individuals without ischemic heart disease.
- Low stroke volume
Reduced cardiac output despite a normal ejection fraction. - Limited exercise tolerance as a result of elevated left ventricular diastolic and pulmonary venous pressure –> reduction in lung compliance –> increase in the work of breathing
Epidemiology of Diastolic Heart Failure
- About one third of all patients with congestive heart failure have diastolic heart failure.
- Prevalence is highest in patients older than 75 years old.
- Mortality rate is about 5-8 % annually as compared to 10-15% among patients with systolic heart failure.
- Mortality rate is directly related to age and the presence/absence of coronary disease.
Factors that Exacerbate Diastolic Heart Failure
- Uncontrolled hypertension
- Atrial Fibrillation (AF)
- Non-compliance with or inappropriate discontinuation of medications for heart failure
- Myocardial ischemia
- Anemia
- Renal insufficiency
- Use of nonsteroidal anti-inflammatory drugs (NSAIDS) or thiazolidinediones
- Dietary indiscretion with over-indulgence in salty foods.
Diagnosis of Diastolic Heart Failure
A clinical diagnosis based on the finding of typical symptoms and signs of heart failure in a patient who is shown to have normal left ventricular ejection fraction and no valvular abnormalities on echocardiogram according to the American College of Cardiology (ACC) and the American Heart Association (AHA).
Determinants of Venous Return
- Mean systemic filling pressure
- Right Atrial Pressure
Pressure change is slight. Thus, small increase in RA Pressure causes dramatic reduction in venous return. (mean systemic filling pressure).
Venous Return & Cardiac Output 2
- Cardiac output increases with atrial pressure.
Normal atrial pressure is about 10mm Hg.
