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321 Cards in this Set
- Front
- Back
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What is the importance of the cardiovascular system?
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1. Delivers oxygen and nutrients to organs and removes carbon dioxide and waste products
2. Transports hormones 3. Regulation of temperature 4. Transports drugs 5. Regulation of blood pressure |
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Three main components of the circulatory system
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1. Heart: pumps blood through system
2. Blood vessels: connecting tubes that transports the blood 3. Blood: tissue composed of water, solutes, cells, and formed elements |
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What is the arrangement of the circulatory system?
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1. Pulmonary circulation
2. Systemic circulation |
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What is pulmonary circulation?
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Blood is carried between the heart and lungs.
Receives blood from the [R] ventricle and delivers blood to the [L] atrium. Carries deoxygenated blood through lungs for gas exchange Low pressure, Low resistance |
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What is systemic circulation?
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Blood carried between the heart and organ systems.
Receives blood from [L] ventricle and delivers blood to the [R] atrium. Carries oxygenated blood to tissues of the organ systems High pressure, High resistance |
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Heart, pulmonary and systemic circulation, is arranged in ________.
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SERIES (blood flows through in sequence)
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Individual beds in the systemic circulation are arranged in _______.
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PARALLEL (total blood volume is divided among different vascular beds)
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Body can dynamically adjust blood flow through different _______ _________.
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VASCULAR BEDS (the body adjusts the blood volume as needed)
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Blood flow is distributed within the cirulatory system by:
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Arterial system & venous system
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What is the arterial system?
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Blood vessels that carry blood from the heart to capillaries - carries oxygenated blood
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What is the venous system?
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Blood vessels that carry blood back to the heart from capillaries - carries deoxygenated blood
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Not all arterial blood is oxygen rich which includes ________.
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PULMONARY ARTERIES
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Not all venous blood is oxygen poor which includes ________.
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PULMONARY VEINS
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Two components that affect blood flow.
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1. Pressure
2. Resistance |
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What is blood pressure (mmHg)?
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The force that causes blood flow through vessels
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What is pressure (P)?
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The force exerted by pumped blood on a vessel wall
Primarily created by the [L] ventricle |
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What is pressure gradient?
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P1 - P2
Blood flows from high pressure to low pressure Needed in order for the blood to propel forward |
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What is resistance (R)?
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Opposes blood flow
Friction on the blood vessel walls and controlled by BV diameter R = 1/r^4 (decrease in radius, increase in resistance, decrease in blood flow) |
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Blood flow (F) equals:
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F = (P1 - P2)/R
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Blood flow within organs is determined by:
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1. Arterial pressure (generated by pumping action heart against a systemic vascular resistance)
2. Changes in diameter of blood vessels (via contraction of relaxations) within organs |
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What is the pulmonary semilunar valve?
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Valve that makes sure the blood flows from the [R] ventricle to the pulmonary circulation.
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Waht is the right atrioventricular (AV) valve?
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Valve that makes sure the blood flows from the [R] atrium to the [R] ventricle
Also called the TRICUSPID valve |
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What is the left (AV) valve?
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Valve that makes sure the blood flows from the [L] atrium to the [L] ventricle
Also called the MITRAL valve |
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What is the aortic semilunar valve?
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Ensures that the blood flows from the [L] ventricle to the systemic circulation
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What is the purpose of the four (4) one-way valves?
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Ensure that blood flows in the proper direction (uni-directional)
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What are the pressure effects on the valves to open and close?
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There is a greater pressure behing the valve so the valve opens [THEN] the pressure is greater in front of the valve so the valve closes and does not open in the opposite direction
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What is the chordae tendineae?
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The anchor onto the myocardial wall of the heart to ensure that the valves stay in place
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What happens to the AV valves during ventricular filling?
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Atria pressure > ventricular pressure so the AV valves open to allow blood to flow from the atria into the ventricles
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What happens to the AV valves during ventricular emptying?
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Ventricular pressure > atrial pressure so the AV valves close which prevents the blood to flow backwards
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What is the heart wall composed of?
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Spirally arranged cardiac muscle fibers
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What are the three layers of the heart wall?
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1. Endocardium
2. Myocardium 3. Epicardium |
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What is the endocardium?
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Inner layer of the epithelium
Lines the entire circulatory system |
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What is the myocardium?
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Middle layer of the cardiac muscle
Full of myocytes - muscle fibers arranged in a spiral formation Bulk of the heart wall |
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What is the epicardium?
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External membrane covering the heart
Where the coronary vessels are located |
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Heart wall is surrounded by the _________ __________.
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PERICARDIAL SAC
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What is the cardiac muscle?
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Striated smooth muscle uniquely arranged
Fibers are interconnected to form branching fibers |
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What are intercalated discs?
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Adjacent cells joined end to end at specialized structures
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What are the two types of membrane junctions within the discs?
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1. Desmosomes (mechanical adherence)
2. Gap junctions (electrical spread) |
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The two types of membrane junctions form _________ _________ which are:
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FUNCTIONAL SYNCYTIA - a group of interconnected muscle cells that function electrically and mechanically as a unit
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What are desmosomes?
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"Glue"
Adherence molecules that keep the muscle fibers together |
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What are gap junctions?
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Electrical conducting pathway that spreads the action potential from once cardiac muscle to the next
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The heart beats in absence of any nervous connection because:
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There are specialized cells (pacemaker cells) with pacemaker activity (auto-rhythmicity)
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Contraction of the heart is based on:
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1. Electrical event within the heart itself, key to turn on the engine
2. Specialized conduction system in the heart |
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The conduction system within the heart allows for:
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1. Rapid, organized near-synchonous depolarization
2. Contraction of ventricles |
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Why is the conduction system essential?
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1. To allow sufficient rest time for filling of ventricles
2. Generate pressure efficiently during ventricular contraction and pumping of blood into arterial system |
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What are the pacemaker cells?
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Possess the ability to produce a spontaneous electrical stimulus initiating an impulse
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What are the types of pacemaker cells?
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SA node, AV node, Bundle of His, and Purkinje fibers
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What is the predominate pacemaker cell in the heart?
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SA NODE = pacemaker of the heart
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What are the latent pacemaker cells?
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AV node [THEN] Purkinje fibers
They take over and provide contractions in the heart if the SA node is damaged |
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Pathway of impulse conduction:
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SA node -> Bachmanns bundle -> Internodal pathways -> AV node -> Bundle of His -> Bundle branches -> Purkinje fibers
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Pacemaker cells have ________.
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CONDUCTIVITY
These cells generate action potentials on their own |
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What is the HIGHEST conduction velocity pacemaker cell?
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PURKINJE FIBERS - allows for efficient contraction and emptying of the ventricles
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What is the LOWEST conduction velocity pacemaker cell?
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AV NODE - allos time for complete atrial depolarization, contraction and emptying of atrial blood into ventricles prior to ventricular depolarization and contraction
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Factors that increase conduction velocity within the heart:
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Sympathetic stimulation, muscarinic receptor antagonist, beta agonist, catecholamines, hyperthyroidism
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Factors that decrease conduction velocity within the heart:
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Parasympathetic stimulation, muscarinic receptor agonist, beta-blockers, ischemia/hypoxia, CCB
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T/F: All action potentials have their own unique shape.
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TRUE
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The change in the action potential generated is dependent on:
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specific ions moving through unique ion channels
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What is involved in pacemaker action potentials?
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SA node, AV node, Bundle of His and Purkinje fibers
Do NOT have a resting membrane potential therefore ALWAYS trend toward depolarization |
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What is involved in non-pacemaker action potentials?
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Includes atria and ventricles
Have a true resting membrane potential (~ -90mV) which is maintained by potassium channels |
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T/F: The duration of cardiac action potentials (pacemaker and non-pacemaker) is shorter than the action potential of a neuron and skeletal muscle.
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FALSE - they are longer because it prevents the contraction of the heart to happen too quickly
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What are the phases of an action potential in the SA node?
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Phase 4 = Diastole
Phase 0 = Depolarization Phase 3 = Repolarization |
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What happens during Phase 4 of an action potential in the SA node?
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Pacemaker current is SLOW
Sodium channels open and sodium moves slowly INTO the cell |
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What happens during Phase 0 of an action potential in the SA node?
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Voltage-dependent calcium channels open
Calcium moves INTO the cell |
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What happens during Phase 3 of an action potential in the SA node?
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Voltage-gated potassium channels open
Potassium moves OUT of the cell |
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What causes the generation of an action potential to occur (depolarization)?
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CALCIUM
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What are the phases of an action potential in a purkinje fiber?
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Phase 4 = Diastole
Phase 0 = Depolarization Phase 1 = Early repolarization Phase 2 = Plateau Phase 3 = Repolarization |
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What happens in Phase 4 of an action potential in a purkinje fiber?
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Pacemaker potential
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What happens in Phase 0 of an action potential in a purkinje fiber?
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Voltage-dependent Sodium channels open FAST
Sodium moves rapidly INTO the cell |
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What happens in Phase 1 of an action potential in a purkinje fiber?
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Sodium channels close
Potassium channels open Potassium flows OUT of the cell |
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What happens in Phase 2 of an action potential in a purkinje fiber?
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Voltage-dependent Calcium channels open
Calcium ions move INTO the cell Potassium channels open Potassium flows OUT of the cell |
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What happens in Phase 3 of an action potential in a purkinje fiber?
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Calcium channels close
Potassium flows OUT rapidly |
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How does the cardiac cell get ready to generate another action potential?
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1. Ion pumps and exchangers return the ions that have moved in and out of the cardiac cell during an action potential
2. Maintains the concentration gradients for each of these ions 3. Returns membrane potential back to the baseline |
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Two reasons to have a Resting/Refractory Period:
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1. Protective mechanism for the heart itself by limiting the number of AP it can generate
2. Protects tatanic contraction of the heart (protection of one contraction after another) |
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What is the Absolute Refractory Period (ARP)?
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Unexcitable to stimulation
Between Phase 0-2 Can NOT stimulate another AP |
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What is the Effective Refractory Period (ERP)?
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Breif period beyond ARP where stimulation produces weak depolarization that does not propagate
AP would disipate and NOT go anywhere -EX- Flushing the toilet twice in a row, first time the toilet flushes, second time it only bubbles |
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What is the Relative Refractory Period (RRP)?
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Stimulation produces a weak AP that does propagate but more slowly than usual
Phase 3 - very weak contraction that would propagate very slowly |
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What is the EKG?
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Records the electrical activity of contraction of the heart muscle
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What is the P wave?
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Atrial depolarization and contraction
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What is the QRS wave?
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Ventricle depolarization and contraction
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What is the T wave?
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Ventricle repolarization and relaxation
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What is the PR interval?
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Time from atrial depolarization to spread of impulse through AV node
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What is the QT interval?
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Time from ventricular depolarization to repolarization
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What is the ST segment?
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End of ventricular depolarization and beginning of ventriclar repolarization
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What is cardiac arrhythmias?
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Are disorders of rate and rhythm of the heart, which can occur as the result of abnormal impulse generation or abnormal impulse conduction
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Arrhythmias can originate in:
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1. Specialized conduction system: SA node, AV node, Bundle of His, Purkinje fibers
2. Atrial muscle 3. Ventricular muscle |
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Arrhythmias that develop can cause the heart to:
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1. Beat too slowly
2. Beat too rapidly 3. Respond to AP's that travel down pathways outside the conduction system 4. Respond to impulses originating from non-SA node sites |
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T/F: Arrhythmias can happen anywhere in the heart.
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TRUE
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All arrhythmias result from alteration in:
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1. Impulse formation - fault in pacemaker cells in the heart
2. Impulse conduction - problems w/ nervous signal initiated in PM cells and fails to reach the non-PM tissue 3. Both impulse formation and conduction |
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What are the types of atrial arrhythmias?
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Sinus tachycardia, Paroxysmal tachycardia, Atrial Flutter, Atrial Fibrillation
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What are the types of supraventricular tachycardias?
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AV node reentry, Wolf-Parkinson White Syndrome, Paroxysmal and Acute Supraventricular tachycardias
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What are the types of ventricular tachycardias?
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Paroxysmal ventricular tachycardia, Monomorphic ventricular tachycardia, Polymorphic ventricular tachycardia
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What are the types of atrioventricular conduction
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First-degree AV block, second-degree AV block, third-degree AV block
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What are atrial arrhythmias?
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Disorders of atrial rhythm or conduction
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What are supraventricular tachycardias?
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Disorders of atrial rhythm/conduction OR AV node conduction where impulses from atria to ventricles are disrupted
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What is ventricular tachycardias?
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Disorders of ventricular rhythm or conduction
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What is atrioventricular conduction?
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Disorders of AV node conduction where impulses from atria to ventricle are blocked
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Sinus Tachycardia
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Abnormally fast heart beat
Length between the QRS complexes is much SHORTER |
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Mechanism of Atrial Fibrillation
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Continuous rapid firing of multiple etopic foci of atrial cells
"Hot spots" of depolarization occuring in the atria |
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Characteristics of Atrial Fibrillation
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Atria beats way too fast
NO P wave, replaced by erratic fibrilatory waves Rhythm has an irregular pattern Ventricular filling is sporadic resulting in weak contractions |
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Mechanism of AV Nodal Re-entry
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Continuous re-entry of impulse through AV junction region
Depolarizing stimulus to atria and ventricle each time it passes through |
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Characteristics of AV Nodal Re-entry
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Palpitations, light-headedness, feeling faint
Atria and AV node beat at a high frequency NO P waves and NARROW QRS wave (therefore short time between contraction & relaxation) |
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What is AV Nodal Re-entry?
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When 2 conducting pathways are present
Premature atrial depolarization arrives at the AV node, one pathway is still refractory (resting) but the other can conduct impulse normally Reentry into the atrium occurs when SLOWED impulse undergoes retrograde (backward) conduction into atrium Reentry may occur with coronary artery disease cardiomyopathy or MI |
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Mechanism of Wolff-Parkinson-White Syndrome
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Presence of abnormal acccessory pathway connecting atria with ventricle, by passing AV conduction
Short circuits the usual delay at AV node Bundle of Kent forms the second pathway |
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Characteristics of Wolff-Parkinson-White Syndrome
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Rate - normal heart rate unless AFib present
Rhythm - regular unless AFib present Short PR interval Has a DELTA WAVE Wide QRS complex Congenital problem |
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Mechanism of Monomorphic Ventricular Tachycardia
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Presence of etopic focus in either ventricle
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Characteristics of Monomorphic Ventricular Tachycardia
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Lethal heart beat
Essential regular rhythm Bizarre QRS complex (WIDE) |
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Mechanism of Polymorphic Ventricular Tachycardia
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Prolonged AP duration caused by early after-depolarization (EAD's)
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Characteristics of Polymorphic Ventricular Tachycardia
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PROLONGED QT WAVE
Increased ventricular heart rate Twisting contractions |
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Early after-depolarization occurs during ________ of AP via excess ________ flowing into the cardiac cell and too little __________ flowing out
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PHASE 3, CALCIUM, POTASSIUM
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What is heart block?
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Failure of the transfer of an impulse from the atria to the ventricle
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What is the difference between first-degree, second-degree and third-degree heart block?
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First-degree: not every impulse is blocked, lengthening of PR interval
Second-degree: Missing QRS waves and increase P wave Third-degree: Complete failure of impulse from atrium to ventricle and more P waves |
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Mechanism of Heart block
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Results from defects in cardiac conducting system, atria beat regulary, but ventricles occasionally fail to be stimulated
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Characteristics of Heart block
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Normal P wave, and QRS and T waves occur regularly, but at a much slower rate
Completely independent of P wave rhythm |
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What is hyperkalemia?
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Elevated ECF of potassium
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Elevated ECF of potassium, decreases the gradient and therefore:
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1. Reduces resting membrane potential - very excited cells
2. Difference in magnitude from normal resting membrane potential to AP is reduced 3. Prolongs AP duration - slowing ventricular contraction due to potassium not able to leave the cell |
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Result of hyperkalemia
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Heart stops beating
The heart contracts but does not relax so the heart stops contracting |
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The flow of ________ ions into the atria and ventricle are responsible for contraction.
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CALCIUM
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Calcium enters the myocyte during Phase ___ depolarization
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2
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What causes sarcomeres to contract?
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1. Calcium from the ECF will enter the cell and bind to actin and myocin directly on the sarcomere (20%)
2. Calcium from voltage gated channels in the sacroplasmic reticulum will bind to the actin and myocin on the sarcomere (80%) |
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What causes sarcomeres to relax?
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Sarcomeres relax by removing calcium:
1. Calcium/Sodium exchange pump 2. Calcium ATPase pump 3. **Serca pump on the sarcoplasmic reticulum that pumps the calcium into the SR and stores it for the next contraction |
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What is phospholamban?
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Protein that becomes phosphorylated which inturn increases the activity of the serca pump and enables it to pump calcium back in
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T/F: The more calcium released from the SR, the stronger the force of contraction is up to a certain point.
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TRUE
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Rise in ECF of calcium:
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1. Prolongs plateau of AP
2. Augments strengths of contraction 3. Heart contracts spastically, however, little time between contractions |
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What is a refractory period?
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Time after AP during which excitable tissue's membrane is unresponsive
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What is the cardiac cycle?
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The time period from the start of one ventricular contraction to the beginning of the next
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What is systole?
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Contraction and emptying
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What is diastole?
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Relaxation and filling
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What are the 4 phases of the cardia cycle?
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1. Ventricular filling
2. Isovolumic ventricular contraction 3. Ventricular ejection 4. Isovolumic ventricular relaxation |
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What is atrial systole?
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When atrial contraction forces a small amount of additional blood into the ventricles
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What is end-diastolic volume?
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The maximum amount of blood in the ventricles occurs at the end of ventricular relaxation
EDV = 135 mL |
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What is isovolumic ventricular contraction?
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The first phase of ventricular contraction which pushes AV valves closed but does not create enough pressure to open semilunar valves
NO blood moves anywhere even thought the ventricles are starting to contract |
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What happens at the ventricular ejection phase?
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The ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected
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What is end-systolic volume?
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The blood left in the ventricles after ejection
ESV = 65 mL |
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What is islovolumic ventricular relaxation?
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As the ventricles relax, the pressure in the ventricles drops, blood flows back into curps of semilunarvalves and snaps them closed
NO volume exchange takes place |
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What is stroke volume (SV)?
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The volume ejected by the ventricles
SV = EDV - ESV = 135 - 65 = 70 mL |
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What are the 3 important points of the cardiac cycle?
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1. Well timed for contraction and relaxation
2. Determines the heart's sounds 3. s1 indicates the beginning of systole in ventricles and s2 indicates the end of systole in ventricles |
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What does the s1 sound of the heart tell you?
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Closure of the valves of the heart between the atrium and ventricle
Indicates the beginning of systole in the ventricles "Lub" |
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What does the s2 sound of the heart tell you?
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Mitral valves open
Indicates the end of systole in the ventricles "Dub" |
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What are heart murmurs?
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Abnormal heart sounds usually associated with heart disease which results in turbulence rather than laminar flow
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What is the difference between functional murmurs and murmurs?
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Functional murmurs are usually NOT associate with disease, usually in young people
Murmurs ARE associated with disease |
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What are stenotic valves?
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Stiff, narrowed valve that doesn't open completely
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What are insufficient valves?
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Valves that do NOT close completely, usually scarring of valve edges so they do not fit together properly
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What can cause stenotic valves and insufficient valves?
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RHEUMATIC FEVER
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What is cardiac output (CO)?
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A measure of cardiac performance
CO = volume of blood pumped by each ventricle/min (L/min) NOT the total amount of blood pumped by the heart, ONLY the amount that the heart will pump out per minute |
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T/F: The volume of blood flowing through the pulmonary circulation and systemic circulation is not equivalent.
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FALSE, they are equal
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What makes up the cardiac output? CO = ??
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CO = Heart rate X Stroke volume
(beats/min) (L/beat) |
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The heart rate is controlled by:
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1. Parasympathetic activity
2. Sympathetic activity |
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Heart rate is determined primarily by _________ influence on _________.
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Autonomic nervous system, SA node
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Parasympathetic innervation via ________ __________ which stimulates:
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VAGUS NERVE which stimulates the atria, SA and AV nodes
NOT the ventricles |
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Sympathetic innervation via several nerves which stimulate:
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Atria, SA and AV nodes and **VENTRICLES**
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What is the impact of the parasympathetic activity on cardiac output?
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Parasympathetic activity: decreases SA node firing -> increase potassium permiability -> decrease heart rate -> decrease cardiac output
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What is the impact of the sympathetic activity on cardiac output?
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Sympathetic activity: increases SA node firing -> decrease potassium permiability -> increase heart rate -> increase cardiac output
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What is the overall effect of the parasympathetic stimulation?
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Decreases HR via influence on the SA node
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Stroke volume is controlled by 3 factors:
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1. Preload
2. Contractility 3. Afterload |
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What is preload?
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The blood entering from the atrium to the ventricle which causes a tension due to the increase volume of blood in the ventricle
Has a positive effect on the stroke volume |
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What is conctractility related to stroke volume?
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Has a positive effect, if you increase contractility then there is an increase in SV
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What is afterload?
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Resistance that is needed to overcome
The blood pressure that is encountered outside the semilunar valves (aorta and pulmonary trunk) The pressure the ventricle muscle must generate to overcome the higher pressure in the aorta to pump blood out of the heart Opposing force |
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What is the overall effect of the sympathetic stimulation?
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Speeds up HR in emergency or exercise situations
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What is the influence of norephinephrine on the SA node?
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Decreases potassium permeability by accelerating inactivation of potassium channels, resulting in LESS negative inside of cells (depolarized)
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What is the sympathetic influence at the AV node?
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Increased conduction velocity, presumed via enhancement of slow, inward calcium current
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What is the result of norepinephrine acting on the SA node?
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Increased rate of depolarization, reaching threshold more rapidly and more frequent AP
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What is the result of the sympathetic stimulation on the AV node?
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Reduced AV nodal delay via increased conduction velocity
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Sympathetic and parasympathetic effects on heart rate are:
A. Antagonistic B. Agonistic |
A. Antagonistic
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Which line of the ANS dominates when the heart is resting?
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Parasympathetic
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What controls stroke volume?
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1. Strength of cardiac contraction
2. End-diastolic volume (max. amount of blood in relaxed ventricle) 3. Venous return (intrinsic) 4. Sympathetic activity (extrinsic) |
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Both the venous return and sympathetic activity increases stroke volume by:
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Increasing the cardiac contractility of the heart
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The heart has inherent ability to vary stroke volume through ________ _________.
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INTRINSIC CONTROL
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T/F: Increasing cardiac muscle fiber length brings length closer to optimal.
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TRUE
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What is the main determinant of fiber length?
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The degree of diastolic filling
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What is the Frank-Starling Law?
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**As EDV increases, stroke volume increases**
The more you stretch the cardiac fibers = increase in stroke volume Increase in venous return is related to preload (extent of filling) |
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Advantages of the Frank-Starling Law:
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1. Equalizes output between left and right sides
2. When large CO is needed, venous return increases by sympathetic stimulation, resulting in an increase in EDV automatically increases stroke volume |
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As cardiac muscle fibers stretch due to (greater/decreased) ventricular filling, myofilaments are pulled (farther apart/closer together)
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GREATER, CLOSER TOGETHER
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What is heart failure?
|
Inability of the heart to maintain adequate CO to meet the constant metabolic demands of all tissues
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Two basic types of cardiac dysfunction that lead to CHF:
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1. Systolic dysfunction
2. Diastolic dysfunction |
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What is systolic dysfunction?
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A decreased ejection of blood from heart during systole
Decrease contractility & decreased ejection fraction |
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What is diastolic dysfunction?
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Impaired filling of ventricles during diastole
Poor ventricular filling, small ventricle size, ventricular hypertrophy, poor compliance, congestion of tissue |
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T/F: Cardiac output of RHS and LHS heart does not have to be equal.
|
FALSE, they must be equal
|
|
|
Right heart failure can result in:
|
Congestion of peripheral tissues, dependent edema & ascites, liver congestion, GI tract congestion, signs related to impaired liver function, anorexia, GI distress, weight loss
|
|
|
Left heart failure can result in:
|
Decreased CO, pulmonary congestion, activity intolerance & signs of decreased tissue perfusion, impaired gas exchange, cyanosis & signs of hypoxia, pulmonary edema, cough with frothy sputum, orthopnea, paroxysmal nocturnal dyspnea (difficulty breathing at night)
|
|
|
What are generalized CHF symptoms?
|
Fluid retention/edema, respiratory (dyspnea, orthopnea), fatigue & weakness, cachexia & malnutrition, cyanosis
|
|
|
Left-side Heart Failure:
|
1. Right ventricular output exceeds left ventricular output
2. Pressure backs up 3. Fluid accumulates in pulmonary tissue |
|
|
Right-side Heart Failure:
|
1. Left ventricular output exceeds right ventricular output
2. Pressure backs up 3. Fluid accumulates in the systemic tissue |
|
|
Prime defect resulting from heart failure:
|
Decrease in cardiac contractility -> decrease in stroke volume -> decrease in CO
|
|
|
What are the 2 major compensatory measures in heart failure?
|
1. Sympathetic activity to heart is increased -> increasing contractility
2. Kidneys retain salt and water to increase blood volume -> increase EDV |
|
|
Positive effects of the sympathetic activity:
|
Increases contractility -> increases SV -> increases CO
|
|
|
Negative effects of the sympathetic activity:
|
Increases heart rate due to stimulating the SA node -> tachycardia possible
Increase HR will also increase CO |
|
|
Positive effects of the kidneys on a failing heart:
|
Releases aldosterone which results in salt & water retention -> increases vascular volume -> increases preload (EDV) -> increases stroke volume -> increases CO
|
|
|
Negative effects of the kidneys on a failing heart:
|
Releases angiotensin which is vasoconstrictor -> increases resistance in BV -> increases pressure -> increases afterload -> decreases stroke volume -> decreases CO
Harder for the heart to pump the blood so the heart starts to hypertrophy |
|
|
Increased sympathetic stimulation shifts the Frank-Starling curve of a failing heart to the _______ therefore ________ contractility towards normal
|
LEFT, INCREASES
|
|
|
What is decompensated heart failure?
|
When the heart can no longer pump out normal stroke volume, despite compensatory measures
Ventricles become floppy due to the cardiac muscle fibers stretched to the point at which they operate in descending limb of length-tension curve |
|
|
What does to mean for backward and forward failure occurs during decompensated heart failure?
|
Backward failure - blood cannot enter and be pumped out by the heart, so it backs up in the venous system (congestive heart failure)
Forward failure - heart fails to pump adequate blood volumes forward to tissues due to smaller and smaller SV |
|
|
What is HBP?
|
High blood pressure is an increase in workload
Ventricles contract, forcing out blood which must exceed the pressure in the major arteries (afterload) -> an increase pressure in the arteries means the ventricles must contract more forcefully to exceed this BP |
|
|
What are the two main components of the cardiac muscle cells?
|
Mitochondria (energy) and myoglobin (storing limited amounts of oxygen)
|
|
|
Blood passing through the heart muscle cannot supply oxygen or other nutrients because:
|
1. Endocardium lining muscle prevents blood from passing into the myocardium
2. Heart muscle walls are too thick for diffusion of oxygen and nutrients |
|
|
What is coronary circulation?
|
The heart's own blood supply
|
|
|
The heart gets most of its blood supply via coronary circulation during (diastole/systole).
|
DIASTOLE
|
|
|
The blood flow to the heart id reduced during systole because:
|
1. Major branches of the coronary arteries are compressed by contracting myocardium
2. Entrance to coronary vessels are partially blocked by the open aortic valve |
|
|
Where do the left and right coronary arteries branch from?
|
Aorta just beyond the aortic valve
|
|
|
What is the neurotransmitter that keeps the coronary vessels open and dialated?
|
ADENOSINE - formed from ATP during cardiac metabolism
|
|
|
Increased blood delivery to cardiac cells via (vasoconstriction/vasodialation) of the coronary vessels?
|
VASODIALATION
|
|
|
Why is there little oxygen reserve in the heart?
|
The heart, unlike other tissues, is unable to remve extra oxygen from blood passing through the vessels to meet increased metabolic needs
|
|
|
The heart under resting conditions removes ____% of available oxygen.
|
65%
|
|
|
What is the chain of events when there is an increase in metabolic activity of cardiac muscle cells (i.e. more oxygen needed)?
|
Increase adenosine -> vasodialtaion of coronary vessels -> increased blood flow to the cardiac muscle cells -> increased oxygen available to meet the increased oxygen need
|
|
|
What is coronary heart disease?
|
Disease of the heart due to impaired coronary blood flow
|
|
|
Diseases of the coronary arteries can cause:
|
ANGINA, myocardial infarction, arrythmias, CHF, and sudden death
|
|
|
What are the two main classifications of CHD?
|
1. Chronic ischemic heart disease
2. Acute coronary syndrome |
|
|
How is chronic ischemic heart disease broken down/subdivided?
|
1. Stable angina
2. Varian angina 3. Silent myocardial ischemia |
|
|
What are the subdivisions of acute coronary syndrome?
|
Unstable angina (no ST-segment elevation), non ST-segment elevation AMI (both no ST or ST-segment elevation) and Q-wave AMI (ST segment elevation)
|
|
|
What is the most common cause of CHD?
|
ATHEROSCLEROSIS
|
|
|
What is atherosclerosis?
|
Formation of plaques within the arterial walls of the heart
|
|
|
What do the plaques contain?
|
1. Lipid-rich core (oxidized LDL)
2. Abnormal overgrowth of smooth muscle cells 3. Covered with collagen-rich connective tissue cap |
|
|
T/F: Atherosclerosis can occur anywhere in the epicardial arteries and their branches.
|
TRUE
|
|
|
What are some complications of coronary artery disease?
|
Myocardial ischemia, possibly leading to acute MI via:
1. Vascular spasm of arteries 2. Formation of atherosclerotic plaques 3. Thromboembolism |
|
|
What occurs when fixed/stable plaques are formed?
|
Grows very slowly to obstruct blood flow but NOT prone to rupture
Implicated in chronic ischemic heart disease (stabe, variant angina) |
|
|
What occurs when unstable plaques are formed?
|
RUPTURE which causes a cascade of events:
1. Plaque disruption and platelet aggregation 2. Thrombus formation Implicated in unstable angina and myocardial infarction |
|
|
What is chronic ischemic heart disease?
|
Disorder in the coronary blood flow due to stable atherosclerotic plaques
|
|
|
Chronic Ischemic Heart Disease Classification:
|
1. Stable (classic) angina
2. Variant (Prinzmetal's) angina 3. Silent myocardial ischemia |
|
|
What is stable angina?
|
Stable atherosclerotic plaques produce a fixed obstruction to blood flow with mycardial ischemia (lack of blood flow to the heart) occurring during periods of increased metabolic needs
|
|
|
What are the characterizations of stabe angina?
|
1. CHEST PAIN, discomfort or pressure
2. Provoked by exertion or emotional stress 3. Reduced oxygen supply 4. Relieved within minutes of rest or NTG |
|
|
What is variant (Prinzmetal's) angina?
|
Abnormal spastic constriction, transientl narrowing of the coronary vessels
NO OVERT PLAQUES Occurs at rest, or withminimal exercise and frequently occurs at night |
|
|
What is the possible cause of variant angina?
|
Platelet activating factor (PAF): found in the endothelium of BV that line the heart and diffuse to smooth muscle and cause the smooth muscle to go into spastic contractions
|
|
|
What is silent myocardial ischemia?
|
Ischemia occurs in the ABSENCE OF ANGINA PAIN due to having an abnormal pain threshold (VERY HIGH)
|
|
|
What are the three populations that are affected by silent myocardial ischemia?
|
1. Asymptomatic without evidence of CAD
2. Previous myocardial infarct with continued episodes of silent ischemia 3. Angina with episodes of silent ischemia inbetween time |
|
|
In a normal heart, oxygen supply ______ oxygen demand.
|
EQUALS
|
|
|
When angina occurs, oxygen supply ______ oxygen demand, which causes:
|
DOES NOT EQUAL, reduction in blood flow
|
|
|
Two factors that leads to a decrease in oxygent supply to the myocardium:
|
1. Vessel narrowing (stable angina)
2. Abnormal vascular tone (variant angina) |
|
|
What are the two vasoactive substances that the endothelial cells of the heart and coronary vessels release?
|
1. NO (nitric oxide)
2. Endothelins |
|
|
What does nitric oxide (NO) do upon release from endothelial cells and coronary vessels?
|
Dilates vessels by relaxing smooth muscle
Prevents coagulation (anti-coagulant) |
|
|
What does endothelins do upon release from endothelial cells and coronary vessels?
|
Cause vasoconstriction which will restrict blood flow
Promotes coagulation in blood Levels are elevated in atherosclerosis, acute MI, CHF, HTN which will increase thickness of BV and decrease blood flow |
|
|
Key factors that affect the myocardial oxygen supply:
|
1. Oxygen-carrying capacity
2. Coronary blood flow which can be altered by several factors |
|
|
Key factors that affect the myocardial oxygen demand:
|
1. Preload (blood volume, venous tone)
2. Afterload (peripheral resistance) 3. Heart rate 4. Contractility (heart force, ejection time) |
|
|
What happens to the heart during angina?
|
1. Oxygen supply decreases due to the coronary arteries cannot supply sufficient oxygen to the myocardium
2. Oxygen demand increases due to the affects of afterload, preload, heart rate and contractility |
|
|
What is the goal of angina therapy?
|
To restore imbalance between the oxygen supply and demand by:
1. Increasing oxygen supply by increasing blood flow to the ischemic myocardium 2. Decreasing oxygen demand 3. BOTH |
|
|
What does acute coronary syndomes (ACS) include?
|
1. Unstable angina
2. Non-ST-segment elevation (non-Q-wave) MI 3. ST-segment elevation (Q-wave) MI |
|
|
What are the determinants of ACS status?
|
1. Presenting characteristics and timing (e.g. pain)
2. EKG variables 3. Serum cardiac markers |
|
|
What are serum cardiac markers?
|
They are indicators of myocardial injury (AMI)
Include: 1. Myoglobin 2. Creatine kinase 3. Troponin |
|
|
What occurs with unstable angina/non-ST-segment elevation MI?
|
Clinical syndrome ischemia ranging between stable angina and MI
Pain is much greater than stable angina and could last longer than 20 minutes |
|
|
What are the causes of unstable angina/non-ST-segment elevation m.i.?
|
1. Atherosclerotic plaque disrutpion
2. Platelet aggregation w/ secondary hemostasis 3. Coronary vasoconstriction |
|
|
How would you diagnosis a patient with unstable angina/non-ST-segment elevation m.i.?
|
1. Pain severity and presenting symptoms
2. Hemodynamic stability (instability in the blood) 3. EKG and serum cardiac markers **Unstable angina - you will NOT see serum cardiac markers; Non-ST-segment elevation - you WILL see serum cardiac markers |
|
|
What is ST-segment elevation m.i.?
|
HEART ATTACK
Ischemic death of myocardial tissue associated with atherosclerotic disease of coronary arteries Abrupt onset or progression from unstable angina/non-ST-segment elevation m.i. **Complete occlusion of the coronary arteries** **Sudden onset of pain which is so severe that the patient feels like they are suffocating** |
|
|
The extent of damage from ACS depends upon:
|
1. Location and extent of occlusion
2. Amount of heart tissue supplied by the vessels 3. **Duration of occlusion** 4. Metabolic needs of affected tissue 5. Extent of collateral circulation |
|
|
The rupture of atherosclerotic plaques can be classified as:
|
1. Transmural - total thickness of the heart wall becomes ischemic
2. Subendocardial - 50% of the heart wall becomes ischemic |
|
|
What occurs in a severely ischemic patient?
|
1. Anaerobic metabolism (loss of myocardial function)
2. Irreversible cell death begins within 20 - 40 minutes 3. Necrosis starts in the subendocardial tissue (inner layer) and moves out |
|
|
What is some pharmacologic treatments for ACS?
|
Oxygen, NTG, ASA, morphine, beta-blocker, thrombolytic (to prevent further clotting)
|
|
|
What are some medical treatments for ACS?
|
1. PTCA (angioplasty)
2. CABG (coronary artery bypass graph) |
|
|
What is the function of arteries?
|
PRESSURE RESERVOIR
Rapid-transit conduit for blood flow to tissues Influence afterload - blood from [L] ventricle need to be ejected into the high pressure in the aorta which controls the BP |
|
|
What is the function of arterioles?
|
RESISTANCE VESSELS
Influence systemic vascular resistance which controls BP |
|
|
What is the function of veins?
|
BLOOD RESERVOIR
Conduit for return of blood to the heart Influence preload (influence BP) |
|
|
Arteries provides the driving force for blood when the heart is (relaxed/contracted)
|
RELAXED
|
|
|
What is a pressure gradient?
|
When blood moves from high pressure to low pressure (how blood moves forward
|
|
|
Arterial systolic pressure is ______, and diastolic pressure is ________.
|
HIGH, LOW
|
|
|
How do arteries act as a rapid conduit for blood flow?
|
Arteries have LARGE radii which means little resistance to flow of blood, therefore BLOOD FLOW INCREASES
|
|
|
The pressure gradient in the arteries is (low/high), and therefore teh flow in the arteries is (low/high).
|
HIGH, HIGH
|
|
|
Arterioles has a major influence on:
|
RESISTANCE
|
|
|
What is resistance?
|
Measure of the hindrance to blood flow through vessel which prevents the flow of blood through the system
Friction between fluid movement and stationary vascular walls |
|
|
Resistance is dependent upon 3 main factors:
|
1. Viscosity
2. Vessel length (not a big influence) 3. **Vessel radius** |
|
|
Effects of the viscosity of blood on resistance:
|
When there is an increase in thickness of a liquid, the viscosity increases
The more RBC in the blood, the more viscous the blood is |
|
|
Effects of the vessel length on resistance:
|
The greater the length of the vessel the higher the resistance to flow (at a constant radius)
|
|
|
Effects of the vessel radius on resistance:
|
**Major determinant of resistance to flow**
LESS resistance in a LARGER diameter = increased blood flow MORE resistance in a SMALLER diameter = decreased blood flow |
|
|
What causes changes in the resistance of an arteriole?
|
Contraction or relaxation of the smooth muscle cells in the vessel wall
|
|
|
What are the consequences of resistance?
|
Heart must work harder to push the blood through the vessels and contract more frequently
|
|
|
Mean arterial pressure (MAP) = _______ X _________
|
MAP = CO X TPR
|
|
|
How do your body control resistance?
|
1. Local (intrinsic) controls
2. Extrinsic controls |
|
|
Resistance to flow in arterioles is influenced by:
|
1. Local chemical influences (metabolic changes)
2. Local physical influences (application of heat or cold) |
|
|
Extrinsic control of resistance is influenced by:
|
Sympathetic nervous system which is important in BP regulation
|
|
|
Vasodilation (decrease in resistance) is caused by:
|
Decrease myogenic activity
Decrease oxygen Increase carbon dioxide & other metabolites Increase nitric oxide Decrease sympathetic stimulation Histamine release Heat |
|
|
Vasoconstriction (increase in resistance) is caused by:
|
Increase in myogenic activity
Increase oxygen Decrease carbon dioxide and other metabolites Increase endothelin Increase in sympathetic stimulation Vasopressin Angiotensin II Cold |
|
|
_________ binds to the _______ receptor on the muscular arteriole and causes the arterial to relax or __________ which __________ resistance and __________ TPR.
|
EPINEPHRINE, BETA, VASODILATION, DECREASES, DECREASES
|
|
|
_________ binds to the _______ receptor on the muscular arteriole and causes the arterial to constrict or __________ which __________ resistance and __________ TPR.
|
NOREPINEPHRINE, ALPHA, VASOCONSTRICTION, INCREASES, INCREASES
|
|
|
What is norepinephrine and where does it come from?
|
Neurotransmitter; SNS
|
|
|
What is epinephrine and where does it come from?
|
Hormone; adrenal medulla
|
|
|
What part of the brain is the integrating center for sympathetic motor pathways to the arterioles?
|
MEDULLA
|
|
|
Veins have ______ radii = _____ resistance to blood flow.
|
Large; low
|
|
|
Veins have an influence on ________ which is the volume of blood entering EACH atrium/minute from veins = ________ ________
|
Preload; venous return
|
|
|
Venous return is a component of _______ and therefore _______ _______ and therefore _______.
|
Preload; cardiac output; MAP
|
|
|
What are the long-term control measures on venous return?
|
Salt and water retention which will increase blood volume back to the heart!
|
|
|
What are the short-term control measures on venous return?
|
Sympathetic vasoconstrictor activity would squeeze more blood back to the heart and therefore increase the reservoir volume (preload)
|
|
|
What is blood pressure?
|
The pressure of blood as it moves through the arterial system
|
|
|
When does blood pressure reach its peak (systolic pressure)?
|
When the blood is ejected from the heart during systole
|
|
|
When does blood pressure reach its lowest level (diastolic pressure)?
|
When the heart is relaxing during diastole
|
|
|
What is the function of blood pressure?
|
To keep BLOOD FLOWING CONSTANTLY to vital organs (heart, brain, kidney, liver)
|
|
|
How is blood pressure regulated?
|
1. Short-term regulation - neural and humoral mechanisms (nervous & hormones)
2. Long-term regulation - kidneys and control of extracellular fluid volume |
|
|
What are the determinants of blood pressure?
|
1. Systolic blood pressure
2. Diastolic blood pressure 3. Pulse pressure 4. Mean arterial pressure |
|
|
What is systolic blood pressure?
|
Represents the ejection of blood into the aorta during ventricular systole/contraction
|
|
|
What causes the systolic blood pressure to rise or fall?
|
1. Stroke volume (amound of blood ejected into aorta with each beat)
2. Velocity of blood ejection from the heart 3. Aorta distensibility (ability for the aorta to stretch) |
|
|
What factors increase systolic blood pressure?
|
Large stroke volume
Rapid ejection Decreased distensibility/elasticity |
|
|
What is diastolic blood pressure?
|
Represents pressure in the arterial system during diastole/relaxing
|
|
|
What causes the diastoic blood pressure to rise or fall?
|
1. **Peripheral vascular resistance** - influenced by sympathetic stimulation
2. Aortic distensibilbiy - ability for the aorta to stretch (not a big factor) 3. Aortic valve competency - closure of valves is vital to hold pressure steady on the aorta |
|
|
What factors increase diastoic blood pressure?
|
Increased peripheral resistance
Increased sympathetic stimulation Decrease in distensibility/elasticity |
|
|
What is pulse pressure (PP)?
|
Reflects the pulsatile nature of the arterial blood
|
|
|
Pulse Pressure (PP) = ________ - _________
|
PP = SP - DP
|
|
|
What happens when the pulse pressure decreases?
|
Hypovolemic shock = decrease in stroke volume and systolic pressure
|
|
|
What is mean arterial pressure (MAP)?
|
Represents the average blood pressure in arterial system during ventricular contraction and relaxation (cardiac cycle)
|
|
|
Mean Arterial Pressure (MAP) has 2 equations, what are they?
|
MAP = DP + PP/3
MAP = CO X TPR |
|
|
T/F: The main force of blood flow into tissues is an indicator of tissue perfusion.
|
TRUE, also ICU and CCU measurements
|
|
|
Mechanisms of regulation of blood pressure:
|
1. Sympathetic nervous system
2. Baroreceptor reflexes 3. Vasopressin system 4. Renin-angiotensin-aldosterone system 5. Fluid retention or elimination by the kidneys |
|
|
Short-term regulation of blood pressure includes:
|
ANS responses (nerves) = baroreceptor reflex, chemoreceptor stimulation
Hormonal mechanisms = renin-angiotensin system, vasopressin |
|
|
Long-term regulation of blood pressure includes:
|
KIDNEY and regulation of ECF volume
|
|
|
What does renin do to the blood pressure?
|
Increases blood pressure
Renin is a vasoconstrictor which will increase TPR and therefore increase MAP |
|
|
What does angiotensin II do to the blood pressure?
|
Acts as a vasoconstrictor which will increase TPR
|
|
|
What does aldosterone do to the blood pressure?
|
**Long-term**
Regulates the salt and water balances in the kidneys |
|
|
What is baroreceptor reflexes?
|
Receptors tha sense the pressure in the artery system in the aorta so any change in an individuals BP, they will signal the brain to correct it
Sends neural signals to the CV control center in the medulla |
|
|
Two areas in the body that you can find baroreceptor reflexes:
|
1. Aortic arch
2. Carotid arteries |
|
|
What is the influence of afferent pathways for baroreceptors?
|
Baroreceptors continually generate AP through afferent pathways to CV centers in the medulla
|
|
|
What is the influence of efferent pathways for baroreceptors?
|
Efferent pathways is the ANS -> the CV centers alter ratio of sympathetic and parasympathetic activity to the heart and blood vessels to control the BP
|
|
|
What is normal blood pressure value?
|
<120/<80
|
|
|
What is considered prehypertension?
|
120-139/80-89
|
|
|
What is considered stage 1 hypertension?
|
140-159/90-99
|
|
|
What is considered stage 2 hypertension?
|
>160/>100
|
|
|
What is primary (essential) hypertension?
|
Typically asymptomatic (if any symptoms occur, it is related to long-term funcion on organs)
Target organ damage: heart, brain, peripheral vascular, kidney, retinal complications |
|
|
What is secondary hypertension?
|
Results from some other disorder or disease
|
|
|
What is hypertension in general?
|
All forms of HTN involve an increase in either cardiac output or peripheral resistance or both
|
|
|
T/F: Baroreceptors adapt to HTN, therefore maintaining it at a lower level.
|
FALSE, baroreceptors maintain it at a HIGHER level
|
|
|
What happens when you have uncontrolled HTN?
|
Increases the work demands on the heart, and blood vessels of arterial system resulting in:
Left ventricular hypertrophy/heart failure Atherosclerosis Kidney disease Stroke |
|
|
What is hypotension?
|
LOW BLOOD PRESSURE which occurs when there is too little blood to fill the vessels
|
|
|
What is orthostatic (postural) hypotension?
|
Transient condition, occurring when moving from horizonal to vertical position
Results from transient inadequate sympathetic activity |
|
|
What is circulatory shock?
|
Occurs when BP falls to such a low level that adequate blood flow to tissues not maintained
|
|
|
Define hypovolemic shock
|
Fall in blood volume
Could be due to vomiting, diarrhea, hemorrhage |
|
|
Define cardiogenic shock
|
Due to weakened heart
|
|
|
Define vasogenic shock
|
From widespread vasodialation due to a release of vasodilator substances
|
|
|
Define neurogenic shock
|
From widespread vasodialation, from loss of sympathetic vascular tone
|
