Week 4 - Cardiovascular System

• Anatomy: closed loop, systemic circulation, pulmonary circulation
• Arterial system
• Capillary system
• Venous system
• Lymphatic system

• 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

• 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

• 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

strength of heart contraction

heart rate

conduction of heart

• 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

• Insufficiency (opposite of stenosis) 
• Failure of valve to close completely
• Allows blood to leak back/flow in reverse
• Increases heart's workload

• 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

• 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)

The volume and associated pressure generated in the ventricle at the end of diastole (before contraction)

• mitral valve balloons up into the L atrium
• valve is "floppy" and doesn't close tightly

• 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)

• 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

• 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)

• 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

• 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!!

• 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

• 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)

• 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])

• 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

• 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,

• Widespread hypersensitivity reaction 
• Leaky vessels and massive vasodilation from histamine release
• Treat with Epinephrines and histamine blockers (to stop dilation)

• 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

• 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%

• 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

• 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

• 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 ↑

• 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.

• 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)

• 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

• 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

• 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

• 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

• 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

• 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!**

• 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.

• 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

• 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

• 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 ↓

• 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)

• Dilated/Congestive (DCM)
• -all 4 chambers dilated & weak,