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Normal Cardiovascular system
- Anatomy: closed loop, systemic circulation, pulmonary circulation
- Arterial system
- Capillary system
- Venous system
- Lymphatic system
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Lymphatics
- Collect fluids that leak out of the arteriole/capillary circuit under high hydrostatic pressure and return it to lymphatic channels
- -system of 1-way valves
- -Pass through lymph nodes
- -swelling: obstruction or infection
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Lymphedema
- Normal flow of lymph is blocked or altered.
- Lymph collects in the interstitium: inflammation
- Not much we can do about this; best treatment is through occupational therapists and PTs to work on to get fluid to return to vascular system
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Control of Heart Rate
- Intrinsic: SA, automaticity, rhythmicity
- Local mediators: baroreceptors (sense pressure) & chemoreceptors (chemcials)
- Nervous (autonomic): Sympathetic (turn up <3 rate) and parasympathetic (turn down <3 rate) nerves
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Inotropy
strength of heart contraction
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Dromatropy
conduction of heart
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Stenosis (valvular disease)
- Failure of valve to open completely
- Develops a pressure gradient across the valve
- -normally pressure is 0 mmHg
- -Stenosed valve 6-8 mmHg pressure gradient (blood must force through high resistance of the narrow opening)
- *Hypertrophy occurs as compensatory mechanism
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Regurgitation
- Insufficiency (opposite of stenosis)
- Failure of valve to close completely
- Allows blood to leak back/flow in reverse
- Increases heart's workload
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Mitral stenosis
- Mitral Valve Disease of LEFT HEART
- Atrial pressure > ventricular pressure
- Thickening of L atrium -> chamber enlarges -> hypertrophy -> ↑ pul. vasc. pressure -> chronic pul HTN -> R ventricle hypertrophy -> R heart failure
- Pulmonary congestion
- Diastolic murmur
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Mitral regurgitation
- Mitral valve disease (Left heart)
- Backflow from L ventricle into L atrium:
- -both dilate, hypertrophy
- -increased afterload increases the regurgitation
- -If not fixed, leads to L heart failure
- Systolic murmur (backflow during L ventricle contraction)
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Preload
The volume and associated pressure generated in the ventricle at the end of diastole (before contraction)
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Mitral valve prolapse (MVP)
- mitral valve balloons up into the L atrium
- valve is "floppy" and doesn't close tightly
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Aortic stenosis
- Due to age-related calcification
- Obstruction of aortic outflow from L ventricle (systole)
- L ventricle hypertrophies and ↑ afterload leads to L HF and pulmonary compliations
- Systolic murmur (when L ventricle contracts)
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Aortic regurgitation
- blood leaks back into L ventricle from aorta
- L ventricle volume overload --> hypertrophy, dilation, ↑ systolic BP
- Left HF from increased workload
- High-pitched blowing murmur during diastole
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Infective Endocarditis (IE)
- Infection and inflammation of the endocardium, especially the cardiac valves
- Bacteria most common cause (Streptococci, staphylococci)
- -bacterial adherence -> fibrin and thrombus formation (Bad!)
- Risk: history of rheumatic heart disease, congenital disease, prosthetic valves (bacteria like to sit on these), valvular heart disease, trauma (procedure)
- S/S: fever, new or changed heart murmur, petechial lesions, chest pain
- Physical findings specific to endocarditis:
- -janeway lesions (usually nonpainful and on hands)
- -Osler nodes (painful, block flow, can eat away tissue)
- Complications: HF, systemic spread of microemboli (everywhere.. can lodge in kidney and cause kidney failure)
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Acute pericarditis
- acute inflammation of the pericardium
- idiopathic (unknown) or viral most common
- membranes inflamed and roughened
- A pericardial effusion may develop (buildup of fluid.. up to 2 L!)
- S/S: fever, chest pain, SOB (pt usually sits forward to relieve SOB)
- Complications: effusion (small ones will usually reabsorb), constriction, tamponade (acute type of pericardial effusion
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Cardiac Tamponade
- buildup of blood or fluid in the pericardial sac, putting pressure on the heart which can prevent it from pumping effectively.
- systemic venous congestion
- Treatment: pericardiocentesis
- Emergency!!
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Shock
- Widespread impairment of cellular metabolism
- Many causes and manifestations
- Progresses to organ failure if not treated!!
- Syndrome.. when cells are not receiving or cannot use oxygen
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Compensatory mechanisms in SHOCK
- Homeostatic mechanisms maintain adequate tissue perfusion despite reduction in CO: RAAS, baroreceptors (signal to brain to turn up <3 rate)
- SNS activation: tries to maintain BP even though CO has fallen by temporarily increasing venous return to heart by:
- -E/NE: B1 stimulation to ↑ HR, vasoconstriction
- -gastric vessels constrict
- -urine output = 0 to conserve fluid --> renal damage (ARF)
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Cardiogenic shock
- Heart muscle is damaged and contractility is impaired, usually from MI, cardiomyopathy
- HypOtension, cool, clammy skin, altered mentation reduced urine output, metabolic acidosis, pulmonary edema
- GOAL: improve CO and myocardial O2 delivery (<3 transplant, VAD, Intra-aortic balloon pump [IABP])
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Hypovolemic shock
- Inadequate circulation of blood volume
- -dehydration
- -hemorrhage
- -3rd spacing: loss of volume in intracellular, vascular, and interstitial spaces
- Cool, clammy skin, tachycardia, delayed capillary refill, decreased urinary output, thirst, thready pulse
- GOAL: stop bleeding and replace fluid/blood
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Neurogenic
- AKA 'vasogenic' shock
- massive, widespread vasodilation of PNS overstimulation and SNS understimulation
- Caused by spinal cord or medulla trauma
- Causes a "relative hypovolemia"
- GOAL: return fluids and vasoconstriction
- Low HR and BP, blood pooling in extremities,
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Anaphylactic
- Widespread hypersensitivity reaction
- Leaky vessels and massive vasodilation from histamine release
- Treat with Epinephrines and histamine blockers (to stop dilation)
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Septic Shock
- Form of distributive shock
- Severe systemic inflammatory response to infection, characterized by release of immune mediators
- Common causes: Gram - and + bacteria, fungal infections, endotoxins
- Clotting cascade, complement system, and kinin system are activated
- Widespread inflammation leads to profound peripheral vasodilation w/ hypOtension, maldistribution of blood flow w/ cellular hypoxia, and increased permeability w/ edema formation
- Complications: ARDS, DIC
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Acute Respiratory Distress Syndrome (ARDS)
- Most commonly associated with septic shock
- Neutrophils release proteolytic enzymes, produce oxygen-free radicals, and secrete inflammatory chemicals that make pulmonary capillaries leak-Inflammation of the lung parenchyma leads to impaired gas exchange with systemic release of inflammatory mediators, causing inflammation, hypoxemia and frequently multiple organ failure.
- -Has a 90% death rate in untreated patients. With treatment, usually mechanical ventilation in an ICU, the death rate is 50%
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Disseminated Intravascular Coagulopathy (DIC)
- Immune activation of clotting cascade
- -leads to the formation of small blood clots inside the blood vessels throughout the body
- -small clots consume coagulation proteins and platelets
- -normal coagulation is disrupted and abnormal bleeding occurs from the skin, GI tract, respiratory tract and surgical wounds
- -The small clots also disrupt normal blood flow to organs (such as the kidneys), which may malfunction as a result
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Acute Renal Failure (ARF)
- Complication of all types of SHOCK
- Kidneys undergo long periods of hypoperfusion
- -vasoconstriction causes decreased glomerular blood flow
- -OR-
- -Acute tubular necrosis (ATN) associated decreased urinary excretion of waste products --> intrarenal failure
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Multiple Organ Dysfunction Syndrome (MODS)
- Most common causes: sepsis and septic shock
- Initiated by immune mechanisms that are overactive and destructive
- Cytokines affect endothelium, recruit neutrophils, and activate inflammation in
- vascular beds leading to tissue destruction and organ dysfunction
- *We can often recover for this, but once organs start to shut down, DOWNHILL -> mortality ↑
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Embryonic heart (Congenital HD, heart disease)
- Lungs are collapsed in human fetus
- 2 passageways in embryonic heart permit blood flow to bypass the lungs
- -Foramen ovale: Flow is RA -> LA (blood bypasses pulmonary circulation and no O2!)
- -Ductus Arteriosus: Connects pulmonary artery and aorta; Flow is Pulm art -> Aorta (can cause no symptoms or heart murmur, etc.)
- *Foramen and ductus usually close shortly after birth.
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Right to Left Shunt
- Allows unoxygenated blood from the R heart to enter the L heart and systemic circulation w/o passing through the lungs first
- -Leads to cyanosis and ↓ PaO2 (arterial partial pressure of O2 - tissue oxygenation)
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Left to Right Shunt
- Allows oxygenated blood from the L heart (aorta) to enter the R side
- -No cyanosis b/c recirculated through lungs
- -Over time leads to R ventricular hypertrophy due to increased pressure in R heart
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Acyanotic Defects
- Atrial-septal defect (ASD): Foramen ovale stays open to some degree
- Ventricular-septal defect (VSD): Most common; L>R pressure after birth leads to R heart failure.
- Coarctation of the Aorta: Narrowing/stricture impedes blood flow
- Patent Ductus Arteriosus (PDA): The pulmonary artery (deox. O2) remains connected to aorta (ox. O2)
- *All are Acyanotic b/c L>R, so oxygenated blood wins
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Cyanotic Defects: Tetralogy of Fallot (TOF)
- A congenital heart defect which involves four anatomical abnormalities of the heart:
- 1) Ventricular-septal defect (VSD)
- 2) Over-riding Aorta: aorta positioned above VSD opening
- 3) Pulmonary stenosis: obstructs R ventricular outflow
- 4) R ventricular hypertrophy
- *TOF is the most common cause of blue baby syndrome.
- Cyanosis occurs from overriding aorta that receives deoxygenated blood
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Cyanotic Defects: Transposition of the Great Arteries
- Aorta arises from the R ventricle and pulmonary artery arises from the L ventricle (opposite from normal)
- 2 separate but non-communicating circulations
- Fatal unless septal defects are also present
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Atherosclerosis
- Thickening and hardening of arterial wall
- Begins w/ injury to endothelial cells that line artery walls
- inflammation -> accumulation of lipid-laden macrophages -> formation of plaque
- Hyperlipidemia is the major cause/risk factor in development
- Consequences: angina pectoris, CHF
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Angina Pectoris
- Supply-demand problem: myocardial ischemia w/o cell death (cells are hungry for O2 but haven't died yet)
- Higher demand for O2 than supply
- Myocardium has little tolerance for hypoxia: cardiac cells go into anaerobic metabolism and are viable for only 20 mins under ischemic conditions
- S/S: substernal chest pain that can radiate to jaw or left arm, squeezing sensation, EKG changes, usually brought on by physical activity & subsides w/ rest.
- *Atypical symptoms!* -> Often hard to tell and catch b/c large portion of population will not express symptoms above!**
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Myocardial Ischemia
- Angina: O2 supply is not adequate to meet demands
- Stable: predictable and can take medicine ahead of time.
- Unstable: unpredictable from thrombus movement
- Prinzmetal's Angina (Variant): unpredictable, often at rest, vasospasm, night chest pain, > in women, coronary artery vasospasm (seems like <3 attack but not from blockage but from spasms.
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Myocardial Infarction (MI)
- prolonged ischemia causing irreversible damage to heart muscle
- Heart attack!! Cells die and form scar tissue
- Mostly caused by thrombotic occlusion
- 2 types:
- -Non ST elevation MI (N-STEMI)
- -ST elevation MI (STEMI)
- Clinical manifestations: prolonged chest pain, progresses, pallor, cyanosis, SOB, diaphoresis, nausea, radiating pain, BP changes, crackles in lungs, EKG changes
- Complications: changes in electrical currents, dysrhythmias, thromboemboli, sudden death, myocardial rupture, pericarditis, organ failure
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Acute Coronary Syndrome (ACS)
- Form of MI
- Time is MUSCLE! #1 rxn to chest pain is denial.
- *Educate patients to call ambulance!!*
- Irreversible cell injury after occlusion happens after 20 minutes
- Necrotic tissue: replaced by 6 weeks by tough fibrous scar tissue
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Heart Failure (HF)
- heart cannot meet metabolic and/or O2 demands - insufficient pump
- impaired systole or diastole or both
- Not a disease, a syndrome
- L or R heart failure
- Limitations to compensation:
- -Frank-Sterling: heart cannot pump the extra blood and heart stretches and enlarges
- -RAA activation: adds to blood volume and diastolic preload, making things worse! Also vasoconstriction, ↑ BP
- -Hypertrophy: increased stress, myocardial cells increase in size, not number, EF (ejection fraction) and CO ↓
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Types of Failure
- R-sided:
- -pulmonary stenosis or HTN
- -R ventricular MI
- -pulmonary embolism
- -cor pulmonale (failure of the R side of the heart brought on by long-term high blood pressure in the pulmonary arteries and right ventricle of the heart)
- *Pulmonary disorders; backward (congestion in systemic venous system - hepatomegaly, ascites, splenomegaly, anorexia, edema, jugular vein distensions); forward (Low output to L vent leading to low CO - fatigue, oliguria, ↑ HR, faint pulses, confusion, anxiety)
- L-side:
- -aortic stenosis
- -L vent MI
- -HTN
- -Mitral stenosis
- *Most associated with: backward effects (accumulation of blood in pulmonary circulation - dyspnea, orthopnea, cough, cyanosis, crackles) & forward (same as R-side)
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Cardiomyopathy (CM)
- Dilated/Congestive (DCM)
- -all 4 chambers dilated & weak,
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