HSC4555 Exam 2
Terms in this set (263)
The pathology of having too many RBCs
The pathology of having a decrease in the oxygen carrying capacity of RBCs
Red Blood Cells Circulate for how many days? And transports what to tissues? And Removes what from tissues?
(also buffers blood pH)
The oxygen carrying protein in the mature red blood cell
Consists of two pairs of polypeptide chains
Gives RBCs their characteristic color
What're the normal ranges for Hemoglobin (gm/dL) in men and women?
(Definition) Volume % of RBCs in the blood
What're the normal ranges for Hematocrit (%) in men and women?
What're the normal ranges for Red Cell Count (10/microL) in men and women?
An immature RBC without a nucleus
(Premature RBC; no hemoglobin in it)
What're the normal ranges for Reticulocyte Count (%) in men and women?
0.5-1.5 for both
Comprises 90% of a cell's dry weight
Each globulin contains heme molecule composed of __________ and __________________ molecule
Regulated by the concentration of hemoglobin in blood and made in the kidney
Why does the kidney secrete erythropoietin?
B/c of decreased hemoglobin
Pulmonary Gas Exchange is what type of respiration?
Systemic Gas Exchange is what type of respiration?
What are the pressures of Oxygenated Blood?
Po2 = 100 mmHg
PCO2 = 40 mm Hg
What are the pressures of Deoxygenated Blood?
Po2 = 40 mm Hg
PCO2 = 45 mm Hg
(Systemic Tissue Cells have the same pressure)
This reflects the pressure or tension that oxygen exerts when it is dissolved in blood
Partial Pressure of Oxygen
Oxygen combines with heme portion to form what?
Each hemoglobin molecule can bind ____ atoms of oxygen
Oxygen gets transported by the?
Most of Co2 is transported through the blood by as?
(Hemoglobins can transport it also)
Hemoglobin binds with CO2 to form?
This is the RBC help to form carbonic acid
This reflects the pressure or tension carbon dioxide it exerts when dissolved in blood
Partial Pressure of Carbon Dioxide
Carbon Dioxide is transported in the blood by?
Dissolved Gas, Bicarbonate Ion, and Bound to Hemoglobin
Low oxygen-carrying capacity leads to?
Normal total red cell mass with disturbances in regulation of plasma volume
Actual decrease in numbers of red blood cells
Excess of red blood cells.
Increased blood viscosity and volume.
Types of RBC Disorders?
Anemia and Polycythemia
What're the 3 Types of Anemia?
-Acute (trauma, like getting stabbed but once blood is replaced you're out of this phase)
- Chronic (Can't see you're loosing blood, You become Anemic as a result)
*Increased Destruction (Hemolytic)
RBCs are lysing like crazy
Causes of decreased production of RBCs
1. Bone Marrow not working to full capacity (No making enough RBC's)
2. Kidney Failure (Leading to decreased erythropoietins and decrease of RBC production)
3.Iron, B12, and/or Folate deficiency (causing decreased RBC production)
Deficiency of all three cellular components of the blood (red cells, white cells, and platelets)
What're the causes of Aplastic Anemia?
1. Viral Causes ( Hepatitis, Epstein-Barr Cytomegalovirus)
2. Autoimmune Causes (Lupus- Immune system attacks the bone marrow)
3. Drug Causes (Chloramphenicol)
Loss of hematopoietic cells causing pancytopenia
Infections (or easily bruising) along with anemia is telling you that you have?
Why would a person have Pallor (unnatural color) in the skin when they are anemic?
The blood will be going to all the major organs first (like the brain)
Pallor, Tiredness, Weakness (The oxygen isn't going to the blood properly), Dyspnea (difficult respiration), Palpitations, Heart Failure (The heart will work to hard-->Hypertrophy-->Heart Failure)
These features of all of what?
General Effects of Anemia?
1. Reduction in oxygen-carrying capacity (tissue-hypoxia)
2. Compensatory Mechanism to restore tissue oxygenation (increased heart rate, cardiac output, circulatory rate, and flow to vital organs)
Increase in 2,3-DPG (enzyme) in erythrocytes and decreased oxygen affinity of hemoglobin in tissues
When Hemoglobin above 8g/dl (not that low)
Elderly with cardiovascular, pulmonary disease may have symptoms
When Hemoglobin below 8g/dl (falls tramendously)
If RBC on a blood smear look really pale and small this is?
Iron Deficiency Anemia
Blood Smears Test?
Anemias based on the appearance
(Microcytic and Macrocytosis Anemias)
This occurs in iron deficiency (RBC to small)
What're the types of Microcytic Anemias
*Anemia of Chronic Disease
*Thalassemia (body making abnormal form of hemoglobin)
* Lead Poisoning
This occurs when RBCs are released from the bone marrow too early
What're the types of Macrocytosis Anemia?
B12 or Folate Deficiency (WBC nuclei are also affected resulting in hyper segmented PMNs)
On a CBC what do you look at 1st and 2nd too see if you have anemia?
1st: look at hemoglobin and hematocrit levels
2nd: (if those are low) look at MCV level (these tell size of cell so you know which type of anemia you're suffering from)
What're the types of Normocytic Anemias?
*Anemia of Chronic Renal Failure
Intracellular protein that stores iron. Amount of this reflects amount of iron stored.
Available binding sites for iron on transferrin
TIBC (Transferrin Iron Binding Site)
This takes iron from GI Tract, takes from digestion system and takes to RBC in order for you to make Hemoglobin
Microscopic visualization of blood
When you loose blood this count increases
For Normacytic Anemia what is the Reticulocyte Count for loosing RBCs and Not Making RBCs
Loosing RBCs: >4%
Not Making RBCs: <1%
The formation of blood cellular components
Reticulocytes >4% means?
RBC Destruction (lysis)
Reticulocytes <1% means?
Decreased production of RBCs from bone marrow
Enzyme that increases in the blood b/c its trying to clean the destroyed RBCs itself
Stem cell disorder characterized by REDUCTION of HEMATOPOIETIC TISSUE in the bone marrow, fatty marrow replacement and pancytopenia
Caused by toxic, radiant, or immunologic injury to the bone marrow stem cells
What differentiates Aplastic Anemia from other Anemias?
Decrease in platelets and WBCs
1. Identify and avoid further toxic exposure
2. Used HLA and ABO to find donors
3. Maintain essential levels of hemoglobin and platelets
4. Administer immunosuppressive therapy or stimulate hematopoiesis and bone marrow regeneration
These treatments are for?
*Failure of the renal endocrine function and impairs erythropoietin production
*Decreased RBC count
*Low hematocrit (HCT) and hemoglobin (HGB) level
Anemia of Chronic Renal Failure
Treatment of Anemia of Chronic Renal Failure
Dialysis and administration of erythropoietin
This binds to intrinsic factor and is absorbed by the body
This binds to receptor in terminal ileum and is excreted in stomach by parietal cells
Disruption in DNA Synthesis of Blast Cells in bone marrow produces?
Low RBC, WBC, and platelet counts with increased mean corpuscular volume is?
Treatment of Folate or B12 Deficiency
Replacing nutritional deficiencies
Decreased intrinsic factor
Defective uptake in terminal ileum
Results in what deficiency?
What tests for B12 Deficiency?
Examples of Megaloblastic Anemias?
Folate and B12 Deficiency
Due to inadequate intake (ex. vegetarian)
See in alcoholism and strict veg. diets
or increased demand (seen in pregnancy and malignancy)
Supplementation helps with this
Site of absorption for B12/intrinsic factor complex
Autoimmune disorder in which the body destroys parietal cells
Without _____________ you can't make intrinsic factor and you can't absorb vitamin B12
Looking at what would help you in deciding if you have microcytic anemia?
Total Iron Binding Capacity (TIBC)
MCV <80, Low Ferritin, Increased TIBC, Hypochromia
Most common nutritional deficiency
Insufficient iron for hemoglobin synthesis
Iron Deficiency Anemia
The only way we can lose Iron is by ________________ b/c Fe is recycled
Treatment for Iron Deficiency Anemia
Oral administration of ferrous sulfate or intravenous ferric gluconate
Crave and want to eat non-food things like ice and chalk
From Iron Deficiency
In Iron Deficiency Anemia
Pre Menopausal Women:
Post Menopausal Women:
Adult Men: GI Blood Loss
Pre Menopausal Women: Menorrhagia (abnormally heavy bleeding at menstruation)
Post Menopausal Women: GI Blood Loss
Low Serum Iron
Iron Deficiency Anemia
Low Serum Iron
Anemia of Chronic Disease
Cause RBCs to be released prematurely when still large
Hypersegmentation of PMN's
Affects dorsal column-medial lemniscus
What Vitamin Deficiency is this?
B12 or Folate Deficiency
Relative Polycythemia is due to?
(Due to lack of plasma it seems there is an increase in RBCs but there isn't)
Absolute Polcythemia is? and has what subtypes?
Actual Increase in RBCs
*Polycythemia Vera (primary) (LOW EPO)
*Polycythemia (secondary) (HIGH EPO)
A "myeloproliferative" disease where all cell lines are increased, not just RBCs (cells are proliferating like crazy)
Increased Red Cell Mass and Blood Viscosity, WBCs, and platelets
No Cure (You have to Reduce blood volume, viscosity, platelet count; decrease the symptoms itself)
You can survive at least a decade if it's managed well
Secondary Polycythemia is due to?
*EPO Tumors (Forcing bone marrow to make more RBCs)
*EPO "Doping" (Forcing your body to make more RBCs, increasing more oxygen to use to deliver to your tissues)
What two things causes diseases of blood vessels?
*Blockage (Preceded by narrowing)
*Rupture (Preceded by weakness)
What're the two types of vascular diseases that the professor discussed?
Atherosclerosis and Hypertension
The inside space of a tubular structure (Artery or Vein)
What're the Layers of Artery or Vein (Inner to Outer)
Lumen-->Intima-->Media-->Adventitia (outermost layer)
These cells cover the Intima layer
These muscle cells cover the Media Layer
Smooth Muscle Cells
Adventitia layer is made up of?
What layer gets damaged first in arteriosclerosis (generic term for anything which hardens)
What're the two examples of arteriosclerosis that the professor gives?
Atherosclerosis (99%) and Monckeberg Medial Calcific Sclerosis (Rare; 1%)
Sclerosis of the medial layer (more in depth than intima layer so it doesn't cause for disruption of the lumen) A lot less common.
Monckeberg Medial Calcific Sclerosis
Involves small arteries and arterioles, generally regarded as NOT strictly being part of atherosclerosis, but more related to hypertension and/or diabetes
Medial layer is calcified
Chronic inflammatory response of the arterial wall initiated by injury to the endothelium
If the fibrous cap during atherosclerosis ruptures this causes what to occur?
Thrombosis leading to total occlusion of that area
When do you actually get signs and symptoms of atherosclerosis?
When you're 90% occluded
What're the morphological concepts of artherosclerosis?
Macrophages infiltrate, Intimal thickening, lipid accumulation, fatty streaks (start to cause swelling), atheroma (thicker area of the wall itself from the fatty streaks), smooth muscle hyperplasia and migration (migrate out of media and into intima layer), Fibrosis, Calcification, Aneurysm, Thrombosis (worse thing that can happen if plaque ruptures.)
This helps prevent accumulation of plaques itself but once you hit menopause everyone is at the same risk of getting atherosclerosis
What sex is at a higher risk for atherosclerosis
What risk factors are for atherosclerosis
Age, Sex, Genetics, Lifestyle (US and Western Europe highest; Decreased since 1963 b/c of awareness and dietary restrictions)
What're the non-modifiable risk factors for atherosclerosis
Increasing Age, Male Gender, Family History, and Genetic Abnormalities
Can atherosclerosis be reversed?
No (you can't reverse it but you can slow it down)
Weight reduction, smoking cessation, drug therapy (like beta blockers), Ballon angioplasty, Laser angioplasty, and coronary bypass
These are treatments of?
How much pressure is outside
How much pressure is in the ventricle (has to outweigh afterload or won't have enough cardiac output)
What allows systemic movement of blood?
The pressure differences b/t the left and right sides of the heart that produce the gradient
What is produced by the force of left ventricular contraction overcoming the resistance of the aorta to open the aortic valve?
Arterial Blood Pressure
What is blood pressure regulation usually affected by?
Neural (brain, hypothalamus), humoral (how much sodium is in the blood), and renal (renin from the kidneys) factors
Fluctuates over 24 hrs. due to physiologic changes associated with circadian rhythm
The normal fluctuations in systemic blood pressure
1. Suprachiasmatic nuclei in the brain govern daily variations in bodily functions
2. Neural and hormonal regulation influences BP
3. Lifestyle influences can affect BP
Types of blood pressure regulations
Short-Term Regulation of Systemic Blood Pressure and Long-Term Regulation of Systemic Blood Pressure
Changes in ________ are mediated through activation of the sympathetic nervous system
This results in release of neurotransmitters epinephrine and norepinephrine
Short-Term Regulation of Systemic Blood Pressure
(Changes in the blood pressure that happens quickly throughout the day; like running to catch the shuttle and then sitting down and relaxing)
In Short-Term Regulation of Systemic Blood Pressure Vasomotor center indirectly activated via ________________
(Activates a1 receptors in smooth muscle of arterioles and activates B1 receptors of the heart)
In Long-Term Regulation of Systemic Blood Pressure increased serum sodium level = increased osmolality = increased _____________________
(Antidirectic Hormone = retains water)
*Increased ADH Secretion
*Increase in extracellular fluid volume
*Renin-angiotensin-aldosterone system (RAAS) important regulator of BP
Long-Term Regulation of Systemic Blood Pressure
Functions as a neurohormonal regulatory mechanism for body water and Na+
(increases water volume and increases Na+ reabsorption)
Renin-Angiotensin-Aldosterone System (RAAS)
Hypertension has a systolic pressure of ______________________________ and a diastolic pressure of __________________________
1. 140 mm Hg or greater
2. 90 mm Hg or greater
What stage of hypertension should you start doing interventions to stop it from going further and getting worse?
What is the normal Systolic and Diastolic Blood Pressures of Hypertension
SBP: <120 mm Hg
DBP: <80 mm Hg
What is the prehypertension systolic and diastolic blood pressures levels
SBP: 120-139 mm Hg
DBP: 80-89 mm Hg
What is the stage 1 hypertension systolic and diastolic blood pressure levels
SBP: 140-159 mm Hg
DBP: 90-99 mm Hg
What is the stage 2 hypertension systolic and diastolic blood pressure levels
SBP: > or = to 160 mm Hg
DBP: > or = to 100 mm Hg
Most common primary diagnosis in the US
Increases morbidity and mortality associated with heart disease, kidney disease, peripheral vascular disease, and stroke
Responsible for an annual worldwide death of 7 million
Can hypertension cause atherosclerosis?
Yes, b/c the high blood pressure is putting added force against artery wall
What're the two classifications of hypertension?
Primary (you just have it, it could be genetic or environmental) and Secondary (you aquire b/c you have some other type of organ failure as a result)
(If you can't find an actual reason why the person has secondary hypertension then they're diagnosed with primary hypertension)
Most common form
Rare prior to age 10
What're the subtypes of primary hypertension?
Isolated Systolic Hypertension
Isolated Diastolic Hypertension
Combined systolic and diastolic hypertension
What're the outcomes of primary hypertension?
A common disorder in which blood pressure remains abnormally high (a reading of 140/90 mm Hg or greater)
What is the first and most important prevent and treatment strategy for primary hypertension?
Drug therapy for hypertension addresses what?
Heart rate and stroke volume
What are some lifestyle modifications to prevent and treat primary hypertension in adults?
Weight Reduction, DASH Diet, Decreased sodium intake, exercise plan, and moderate intake of alcohol
Hypertension attributed to a specific identifiable pathology or condition
Most common form in children <10 years of age
Abnormally low blood pressure
A decrease in systolic blood pressure (great than or equal to 20 mm Hg or greater than or equal to 10 mm Hg w/in 3 min.) when moving to an upright position
Excessive increase in heart rate (by 20-30 beats/min.) may also be diagnostic
When symptoms begin, squatting/bending forward or crossing legs may reduce effects of?
How does blood flow through the right side of the heart?
1. Blood enters the heart through two large veins, the inferior and superior vena cava, emptying DEOXYGENATED (Venous) blood from the body into the Right Atrium of the heart
2. As the atrium contracts, blood flows from your right atrium through the open TRICUSPID VALVE into your Right Ventricle
3. When the Right Ventricle is full, the tricuspid valve shuts. This prevents blood from flowing backward into the atria while the ventricle contracts.
4. As the ventricle contracts, blood leaves the heart through the Pulmonary (Pulmonic) Valve, into the Pulmonary Artery and to the Lungs where it is oxygenated.
(This is happening at the same time with the left side)
How does blood flow through the left side of the heart?
1. The pulmonary vein empties oxygenated blood from the lungs into the Left Atrium of the heart
2. As the atrium contracts, blood flows from your left atrium through the open Mitral Valve into your Left Ventricle
3. When the ventricle is full, the mitral valve shuts. This prevents blood from flowing backward into the atrium while the ventricle contracts
4. As the ventricle contracts, blood leaves the heart through the Aortic Valve, into the aorta and to the body
How does blood flow through your lungs?
Once blood travels through the pulmonic valve, it enters your lungs. This is called the pulmonary circulation. From your pulmonic valve, blood travels to the pulmonary artery to tiny capillary vessels in the lungs.
Here, oxygen travels from the tiny air sacs in the lungs, through the walls of the capillaries, into the blood. At the same time, carbon dioxide, a waste product of metabolism, passes from the blood into the air sacs. Carbon dioxide leaves the body when you exhale. Once the blood is purified and oxygenated, it travels back to the left atrium through the pulmonary veins
Right-side heart chambers pump _____________ blood through the lungs
Left-sided heart chambers pump _____________ blood through the systemic circulation
This ECG wave complex corresponds to atrial depolarization
This ECG wave complex represents ventricular depolarization
This ECG wave complex reflects ventricular repolarization
Useful for detecting conduction and rhythm disturbances
Professors examples of coronary arteries
Left Coronary Artery
LAD (Anterior Interventricular Branch)
Right Coronary Artery
Posterior Interventricular Branch
Feeds blood to left (right) side of the heart
Left (right) coronary artery
Most commonly occluded of the coronary arteries. It provides the major blood supply to the interventricular septum. Blockage of this can lead to impairment or death (infraction) of the conduction system
LAD (Anterior Interventricular Branch)
The diff. types of muscles are?
Skeletal, Cardiac, and Smooth Muscle
Composed of unbranched, cylindrical muscle cells (myofibers) that're multinucleated, and arranged in parallel bundles
Composed of branched muscle cells that contain 1-2 nuclei per cell
Composed of elongated, nonstriated cells w/ a single centrally located nucleus
What're the two general types of cardiac myocytes (type of cell found in muscle tissue)
Working (mechanical pumping functions)
Electrical cells (transmit electrical impulses)
(Both produce and transmit action potentials)
What Proteins form contractile aparatus; they're arranged in contractile units called _________________
Actin and Myosin
Professors examples of alterations in cardiac function diseases
Coronary Heart Disease (CHD)
Endocardial & Valvular Diseases
Congenital Heart Diseases
Insufficient delivery of oxygenated blood to the myocardium due to atherosclerotic coronary arteries
Coronary Heart Disease
Atherosclerosis causes narrowing of the arterial lumen that can lead to cardiac ischemia through?
1. Thrombus Formation (These cause for rupture)
2. Coronary Vasospasm (The actual vessel itself begins to spasm and causes for contration)
3. Endothelial Cell Dysfunction
This is almost always the result of atherosclerosis (hardening of the arteries)
Coronary Artery Disease (CAD)
These transport cholesterol atheromatous plaque from peripheral tissue back to the liver clearing tissues
High-Density Lipoproteins (HDL)
Lipids are transported via?
Lipoproteins all contain?
Triglycerides, Phospholipids, Cholesterol, and Protein
1. The increase in the % of lipids in lipoprotein, _________ its density
2. The increase in the % of protein in lipoprotein, __________ its density
What're the types of lipoproteins
1. High density lipoprotein (HDL)
2. Intermediate Density lipoprotein (IDL)
3. Low density lipoprotein (LDL)
4. Very low density lipoprotein (VLDL)
These are produced by the intestine, packaged with dietary lipids. They transport dietary lipids to hepatic and peripheral cells.
An elevated concentration of lipids in the blood
Major plasma lipids include?
1. Total Cholesterol
Classifications of Risk in Adults Based on Low-Density Lipoprotein Cholesterol.
2. Optimal or above Optimal
Classifications of Risk in Adults Based on Low-Density Lipoprotein Cholesterol.
Classifications of Risk in Adults Based on Low-Density Lipoprotein Cholesterol.
2. Very High
Vulnerable Plaques Have:
Large lipid core
High Shear Stress
When vulnerable plaques may rupture or become eroded, which stimulates clot formation on the plaque. This leads to?
Local, temporary deprivation of the coronary blood supply
Occurs when oxygen supply is insufficient to meet metabolic demands
Critical factors in meeting cellular demands for oxygen include?
Rate of coronary perfusion
Syndromes with slow progression due to chronic obstruction from stable atherosclerotic plaques.
Chronic Coronary Syndrome
Syndrome associated with acute changes in plaque morphology and thrombosis
Plaque rupture with acute thrombus development
Acute Coronary Syndrome (ACS)
Types of Chronic Coronary Syndromes
-Stable angina pectoris (no plaque associated thrombus; Occlusion usually remains about 75% and only have symptoms when you increase demand (like walking up the stairs))
Types of Acute Coronary Syndromes
-Unstable angina (occlusion is partial)
-Myocardial infarction (complete occlusion)
(ECG and biomarkers used for diagnosis)
Chest pain associated with intermittent myocardial ischemia
May result in inefficient cardiac pumping w/ resultant pulmonary congestion and shortness of breath
*Reduced perfusion, but NO infarction
Angina with exertion
Short Duration of pain
Treat by rest or medication
Chest pain may spread to arm, back, and other areas
(Chronic Coronary Syndrome)
Insufficient blood flow to the heart muscle from narrowing of coronary artery may cause ______________
Angina (chest pain)
Angina w/o exertion
Have no idea when it's going to happen (unpredictable)
Long duration of pain
Nor relieved by rest nor medicaiton
Pain may be a signal that a myocardial infraction will occur soon
(Acute Coronary Syndrome)
Pain typically occurs at rest, during the night or early morning hours
Pain and discomfort may be severe
Pain is relieved by medication
Variant (Prinzmental's) Angina
Cholesterol lowering drugs
Aspirin/Other platelet inhibitors)
Decrease Heart's Demand for Oxygen (Beta-blockers and calcium channel blockers)
Increase vasodilation - both arteries & veins (calcium channel blockers and nitrates)
Angioplasty, stenting, bypass surgery
These are treatments of?
Sudden and extended obstruction of the myocardial blood supply
Can be present w/ severe chest pain
Can be minor or asymptomatic (Silent)
Sympathetic nervous system activation leads to increased myocardial workload by increasing?
Heart Rate, Contractility, and Blood Pressure
Treatment of Myocardial Infarction
Reperfuse the Heart
Anticoagulants (Aspirin, Herparin)
(Also the same treatments as for angina)
What're the Cardiac Analytes?
1. Cardiac Troponin T and I (cTnT, cTnl)
Troponin complex consists of what three proteins:
The combination of what regulate muscle contraction?
1. Troponin C (binds to Ca+2, found in heart and skeletal muscle)
2. Troponin T (binds to tropomyosin, cTnT is cardiac specific)
3. Troponin I (inhibit binding of myosin to actin, cTnl is cardiac specific)
Troponin complex. Ca+2, and Tropomyosin
Used as indicators of acute myocardial infraction, similar in sensitivity to CK-MB
Remains elevated 3-7 days after acute myocardial infraction
Cardiac Troponin (cTnl & cTnT)
(cTnl is not elevated in patients with extreme muscle injury)
Found in both cardiac and skeletal muscle
Increase in this is detected 1-2 hrs after onset of symptoms, that make it sensitive for myocardial infraction diagnosis
Testing for this helps to say the MI just occured
Change in myoglobin concentration is seen in:
2. Renal Failure Injury
4. Skeletal Muscle Disease
This cytosolic enzyme is involved in the transfer of energy in muscle metabolism
Creatine Kinase (CK)
It is a dimer composed of two subunits: B (brain form) and M (muscle form) --> Resulting in what three CK Isoenzymes:
1. CK-BB (CK-1): (Of brain origin, found in blood if blood-brain barrier has been breached)
2. CK-MM (CK-3): (accounts for most of the CK activity in skeletal muscle
3. CK-MB (CK-2): (Has the most specificity for cardiac muscle, even though it accounts for only 3-20% of total CK activity in the heart; peak is at 12-24 hrs)
Why would CK-MB might lead to false positive results of an acute myocardial infraction?
Because it is also found in the skeletal muscle
What helps increase survival of Sudden Cardiac Death?
Use of external defibrillators and CPR
Heart failure develops insidiously due to progressive ischemic myocardial damage
Typically have history of angina or myocardial infraction
More common in older adults
Chronic Ischemic Cardiomyopathy
Cause altered hemodynamics of the heart and increase myocardial workload
Endocardial and Valvular Diseases
Endocardial and Valvular structures may be damaged by?
1. Inflammation and Scarring
3. Congenital Malformations
Failure of the valve to open completely results in extra pressure work for the heart
(Endocardial and Valvular Diseases)
Inability of a valve to close completely results in extra volume work for the heart
(Endocardial and Valvular Diseases)
Degeneration of the Mitral Valve
Associated with connective tissue disorders (marfan syndrome & scoliosis)
More in female
Easily seen and heard on echocardiogram
Mitral Valve Prolapse (MVP)
What is the Click sound on an echocardiogram
The actual prolapsing of the valve in mitral valve prolapse
What is the murmur sound heard on an echocardiogram
The ventricle blood trying to flow back through to the atrium
Holosystolic murmur if regurgiation present
Occasional chest pain, dyspnea
3% infective endocarditis, mitral insufficiency, arrythmias, and sudden death
These are all clinical features of?
Mitral Valve Prolapse (MVP)`
What're the types of artificial valves?
1. Mechanical (most common, made of graphite like carbon. on chronic anticoagulants)
2. Xenografts (porcine; animal derivatives; typically from a pig)
(60% have complications w/in 10 years)
Caused by hypersensitivity II reaction
Diffuse, inflammatory disease caused by delayed immune response to infection by the group A beta-hemolytic streptococci
Febrile illness (inflammation of the joints, skin, nervous system, and heart)
If rheumatic fever is left untreated it causes ____________________
Rheumatic Heart Disease
What helps diagnose acute rheumatic fever?
Two major criteria, or one major and two minor criteria needed for diagnosis when there is also evidence of a previous strep infection, support the diagnosis of rheumatic fever
(C: Carditis, A: Migratory Ployarthritis, N: Nodules, C: Sydenham Chorea, ER: Erythema Marginatum)
Acute inflammatory disease that follows infection w/ group A B-hemolytic streptococci
Occurs mainly in children
Rheumatic Heart Disease
Invasion and colonization of endocardial structures by microorganisms with resulting inflammation
Infective Endocarditis (Diseases of the Endocardium)
Pathogenesis of Endocarditis
-Blood-borne microorganism adherence
-Proliferation of the microorganism
What is Inflammation of the endocardium?
(Agents: Bacteria, viruses, fungi, rickettsiae, and parasites
Inflammatory conditions (SLE))
What are the 2 common bacterial causes of infective endocarditis?
Streptococcus (usually) and Staphylococcus (sometimes)
Inflammatory disorder of the heart muscle characterized by necrosis and degeneration of myocytes
disorders of the heart muscle, may be genetic or acquired and is noninflammatory
Causes include microbial agents, immune-mediated diseases, and physical agents
Viral etiology most common: Virus, Inflammatory Disease, and Toxins
Characterized by left ventricular dysfunction and general dilation of all four chambers
Classified by cause of functional impairment:
Dilated, Hypertrophic, or Restrictive
An enlarged, weakened left ventricle struggles to pump enough blood to meet the body's needs
Typically heart enlarges 2 to 3x bigger than its actual size
Hard Time Contracting
Walls become very thick and the cells have hypertrophyed over time. Left ventricle can't fully relax b/t heartbeats, resulting in less blood flow
Hard Time Relaxing
Thickened, Hyperkinetic Ventricular Muscle Mass
Walls their self are restricted and unable to move
What're the two main causes of Dilated Cardiomyopathy?
In hypertrophic cardiomyopathy if the septum thickens as well this leads to?
Decrease in chamber volume, Decrease in SV, and decrease in diastolic filling describes?
Rarerest form of cardiomyopathy
Normal chamber size and wall thickness
What're the disorders of the pericardium?
-Pericardial Effusion (Tamponade)
Something common that you'll see in tamponade. Causes jugular vein to distend from the excess blood.
Jugular Vein Dissention (JVP)
Treatment for Tamponade
Relieving the pericardial pressure by aspirating the offending fluid
Acute or chronic inflammation of the pericardium
Acute is normally viral
Pleuritic chest pain affected by position
Treat underlying cause
Abnormality of the heart that is present from birth
Congenital Heart Diseses
Abnormal path of blood through the heart or great vessels
a bluish discoloration of the skin resulting from poor circulation or inadequate oxygenation of the blood
(Hole in the heart) (Blue Baby)
Right to Left Shunt = _________
Left to Right Shunt = _________
2. No Cyanosis
interference with blood flow leading to increased workload of affected chamber
Abnormal opening b/t the atria
Atrial Septal Defect
Abnormal communication b/t the ventricles
Most common type of congenital heart lesion
Ventricular Septal Defect (VSD)
General term used to describe several types of cardiac dysfunction that result in inadequate perfusion of tissues
Inability of the heart to maintain sufficient cardiac output to meet metabolic demands of tissues and organs
1. Failure of myocardium to contract?
2. Failure of myocardium to relax?
1. Systolic Failure
2. Diastolic Failure
BP in the left ventricle after filling and before ventricles contract
From the Venous System
BP in the systemic system that heart must work against
Created by the arteries
What are the compensatory Mechanisms and Remodeling of restoring cardiac output toward normal (in heart failure)
1. Sympathetic Nervous System Activation
2. Increase Preload
3. Myocardial Hypertrophy and Remodeling
Primarily a result of baroreceptor reflex stimulation, which detects fall in pressure
CNS increases activity in the sympathetic nerves to the heart resulting in venoconstriction
Juxtaglomerular cells release renin, activating the RAAS cascade, resulting in increased sodium and water retention
Sympathetic Nervous System Activation
Initially a consequence of reduced EF with resultant increase in residual ESV
Decreased CO to the kidney reduced glomerular filtration = fluid conservation
RAAS cascade activated = elevated blood volume
Results from a chronic elevation of myocardial wall tension
High systolic pressure in the ventricle needed to overcome a high afterload leading to hypertrophy
Neurohormonal factors have hypertrophic effect on the heart
Angiotensin II involved in remodeling
Myocardial Hypertrophy and Remodeling
Results in accumulation of blood within the pulmonary circulation, pulmonary congestion, and edema
Backward Effects associated with Left-Sided Heart Failure
Results in insufficient CO with diminished delivery of oxygen and nutrients to peripheral tissues and organs
Forward Effects associated with Left-Sided Heart Failure
Backward effects due to congestion in the systemic venous system
Forward effects cause low output to left ventricle leading to low CO
Right-Sided Heart Failure
Most often result of primary left-sided HF progressing to right-sided HF
Pulmonary congestion due to left-sided HF
Systemic venous congestion due to right-sided HF
Biventricular Heart Failure
What helps you diagnose Heart Failure?
FACES (fatigue, activity limitation, congestion, edema, shortness of breath)
Assessments including x-ray and echocardiography
B-type natriuretic peptide level
Severity of symptoms used to identify class/stage of HF
What're the Treatments of heart failure?
1. Increased forward flow (cardiac output must be increased)
2. Decrease backup of flow (heart's workload must be decreased)
Disturbance of the heart rhythm
Range from occasional "missed" or rapid beats to severe disturbances that affect the pumping ability of the heart
Electrical activity of the heart is uncoordinated
What're the three major types of cardiac dysrhythmias/arrhythmias
Abnormal rates of sinus rhythm
Abnormal sites (ectopic) of impulse initiation (Random cells start leading except for SA Node controlling)
Disturbances in conduction pathways
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