Cardiovascular Study Guide

8/6/2019 Cardiovascular Study Guide

http://slidepdf.com/reader/full/cardiovascular-study-guide 1/19

Cardiovascular – 36 questions3 questions- atherosclerosis, arteriosclerosis, effect of LDLs & triglycerides, effect on BP (Melinda) McCance p. 1157-60; slides 2-8 Cardiovascular Fx. lecture.Arteriosclerosis - chronic; thickening & hardening of vessel wall d/t smooth muscle & collagen migration to tunicaintima (innermost layer of endothelium; endo = inside).Atherosclerosis - Form of arteriosclerosis; progressive, inflammatory disease proces; thickening & hardening d/taccumulation of lipid-filled macrophages (foam cells) deposited in tunica intima of endothelium → fatty streaks(accumulated foam cells) → fibrous plaquesVLDLs (triglycerides) & LDLs (cholesterol) role in atherosclerosis:

• Abnormal concentrations of serum lipoproteins associated with ↑ risk for atherosclerosis, especially LDLs

• Serum LDL controlled by liver; ↑ serum LDL levels w/ high fat diets and genetic factors

• Small dense LDLs = most atherogenic because they oxidize in endothelium

• Oxidized LDL→ endothelial injury, inflammation, immune response (key steps in atherosclerosis)

BP

• HTN = 2 to 3-fold risk for atherosclerotic CVD

• ↑ BP due to forming plaques→ further endothelial injury & myocardial hypertrophy→↑ BP demands &overactivity of SNS & RAAS

Atherosclerosis schematic: 1. Endothelial injury The usual suspects: release of

• Inflammation proinflammatory cytokines: TNF, INF,

• Impaired ability to make IL-1, & heat shock proteins

a.) antithromboticb.) vasodilating cytokines

Oxidation

• Oxidized LDL penetrates the wall of tunica intima in endothelium

• Macros engulf oxidized LDL at tunica intima = foam cells (just as pac-manswallows the ghost)

• Accumulated foam cells = fatty streaks (these don’t obstruct, smooth muscle +collagen build up on top - see bullet below)

• Fatty streaks produce more 02 radicals→inflammation + immuneresponse→further damage to vessel wall

• Smooth muscle + collagen proliferation over fatty streak = fibrous plaque (this isatherosclerosis)

3. Macrophages (aka: pac-man)• They go after (think: pac-man) and adhere to injured endothelium (thru adhesion molecules, like VCAM-1);

• Macros release enzymes & toxic 02 radicals→oxidative stress and oxidized LDL→smooth muscleproliferation and inflammation + immune response

• GF released: angiotensin II, Fibroblast GF, platelet-driven GF→smooth muscle proliferation

1 question aneurysm: dissecting vs fusiform vs saccular (Melinda) -please feel free to add; not a whole lot here



McCance p. 1146; slides 22 & 23 for Cardiovascular Fx.Fusiform

• Circumferential and saccular

• True aneurysms: involve all 3 layers of arterial wall (from outside in: adventitia, tunica media, & tunicaintima) vs. False aneurysm: there is previous damage to a vessel and the clot is formed outside of thevessel wall (same outline as a saccular aneurysm)

• Caused by weakened vessel wall

Dissecting

• Saccular

• Break in vessel wall, usually a result of trauma (most critical); as a result of damage in the vessel wall, bloodenters into the damaged area --> bleeding in between layers of the vessel wall; as more blood isaccumulated, more blood is being pushed through, leading to more tension in the balloon area

1 question angina (Victoria) (power point pg 9-10, book 1165-1167)

• Angina Pectoris : chest pain (angina) occurs when there is deficient oxygen for the heart muscle. Often

presents as: substernal chest discomfort, may radiate to lower neck/jaw, left arm/shoulder, commonlymistaken for indigestion.

○ Supply and demand issue

○ Angina Pectoris: 3 Types

Classic- exertional

Variant- spasms of coronary arteries

Unstable- due to plaque disruption (leads to MI and myocardial ischemia)

○ S/S : (stops when exertion stops)

Typically recurrent, intermittent, brief episodes of tightness in the chest

Pain can radiate (not as severe as MI)

Diaphoresis and nausea often present• Angina: 3 Kinds (these are reversible)

○ Stable angina : pain when heart’s oxygen demand increases (transient, lasts 3-5 minutes, can

happen with stress, exercise d/t vessel narrowing, hardening wall = vessel can’t dilate in responseto increased myocardial demand.. Recurrent and predictable.)

○ Variant angina or Prinzmetal: pain when coronary arteries spasm (unpredictable, transient, chest

pain, almost always happens at rest/at night)

○ Silent myocardial ischemia : myocardial ischemia without pain; no specific symptoms (can present

as fatigue, dyspnea or feeling of unease).

•

1 question cardiomyopathy: dilated vs hypertrophic (Lindsay) (Slides p. 12) (McCance p. 1178-1180)• 3 types of Cardiomyopathies , ALL caused by infection:

• Dilated (congestive) - ventricular dilation and grossly impaired systolic function --> dilated heart failure. Mostcommonly d/t ischemic heart disease or valvular heart disease. Diminished myocardial contractility -->diminished systolic function. All 4 chambers of heart are enlarged and weakened resulting incongestive heart failure and need for heart transplant. ⅔ of cases are idiopathic. Most commonsymptoms are dyspnea and fatigue, initial elevated bp, but hypotension indicates progressive decrease incontractility. Tx includes salt restriction and meds.



• Hypertrophic - defects in contractile proteins make cells weak and unable to contract/relax in coordinatedfashion --> cells hypertrophy (oblique and perpendicular orientation) to do same amount of work as normalcells --> cells need more oxygen and so perform less efficiently (vicious cycle) --> makes person prone toheart failure and may suffer sudden death during exertion. Always happens during exertion. Think of the b-ball player who drops dead. Often genetic (autosomal dominant inheritance). .

• Restrictive - heart chambers unable to fill w/ blood completely b/c of stiffness of heart and inability of heartmuscle to relax during diastole. Most common manifestation is right-sided heart failure w/ systemic venous

congestion.

3 questions hypertension/hypotension (Tracy C.)Definition of HTN according to American Heart Association(http://www.heart.org/HEARTORG/Conditions/HighBloodPressure/AboutHighBloodPressure/Understanding-Blood-Pressure-Readings_UCM_301764_Article.jsp):

Blood Pressure Category Systolic (upper #) mm Hg Diastolic (lower #)mm Hg

Normal < 120 AND < 80

Prehypertension 120-139 OR 80-89

Hypertension (Stage 1) 140-159 OR 90-99

Hypertension (Stage 2) 160 or higher OR 100 or higher

Hypertensive Crisis (Emergency Careneeded)

> 180 OR > 110

“Etiologic” Risk Factors (BBJ uses “etiologic” in the slides, but these are more like risk factors p.2 of cardiolecture):

• Family history

• Advancing age

• Race

• Increased salt intake

• Obesity

• Hyperinsulinemia

• High alcohol consumption

• DECREASED K, Ca, and Mg intake (slide is wrong in lecture)

• Use of oral contraceptives

TWO TYPES (p.2-3 of cardio lecture):1) Primary HTN:

• Essential or idiopathic HTN (unknown cause)

• d/t: genetic and environmental factors (e.g. exercise, high fat diet, etc.)

○ Leads to increased peripheral resistance and/or increased blood volume → sustained HTN (look at

p.3 of cardio lecture for more detailed diagram)

• Affects 90-95% of individuals with HTN

2) Secondary HTN:

• Caused by systemic disease process that raises peripheral vascular resistance or cardiac output



Isolated Systolic HTN*: Elevated systolic pressure caused by increases in CO or total peripheral vascular resistanceor BOTH.Complicated HTN*: chronic hypertensive damage to walls of systemic blood vessels → hypertrophy and hyperplasiaof smooth muscle cells w/ fibrosis of tunica intima and media aka “vascular remodeling” → reduced blood flow andperfusion to organs

• Target organs: kidney, brain, heart, extremities, and eyes

Malignant HTN*: rapidly progressive HTN. Diastolic pressure usually > 140 mm Hg

• Can increase capillary permeability → edema (e.g. cerebral edema, papilledema)

*p.3 of cardio lecture - BBJ only said there were two types of HTN: primary and secondary, so I’m thinking these 3can fall under one of those types depending on the cause. Feel free to elaborate on this.Orthostatic (postural) Hypotension (p.3 of cardio lecture): Decrease in both systolic and diastolic BP uponstanding. Lack of normal BP compensation in response to gravitational changes on circulation

• Acute Orthostatic Hypotension (temporary type)

○ Caused by sluggish regulatory mechanisms

• Chronic Orthostatic Hypotension

○ 2 forms: 1) Primary or idiopathic 2) Secondary to a disease (e.g. DM, metabolic disorders, or CNS

or PNS diseases)

•

8 questions & Case Study (for MI)-MI: relationship of CAD & MI and relationship of MI & HF, chronic ischemic heart disease, lab values, ECGchanges,-types of MI Slides pg11, McCance pg 1171 ( SW )Transmural: most common type, full thickness. If thrombus lodges permanently in the vessel, infarction will extendthrough the myocardium all the way from endocardium to epicardium (transmural), resulting in severe cardiacdysfunction. Clinically, individuals with transmural are at highest risk for serious complications, need interventionimmediately. Individuals usually have marked elevations in the ST segments on ECG, categorized as STEMI.Subendocardial: inner half of heart wall. If the thrombus breaks up before complete distal

tissue necrosis has occurred, infarction only involves myocardium directly beneath the endocardium. Usuallypresents with ST depression and T wave inversion without Q waves, clinically termed non-STEMI.-effects of angiotensin II, (SW) McCance 1126-1127. Powerful vasoconstrictor, considered a growth promoter incardiovascular tissues. The resulting vascular hypertrophy is a significant factor in pathogenesis of hypertension.Chronically elevated Ang II in heart (like that seen in hypertension) contribute to myocardial hypertrophy and heartfailure. Renin-angiotension-aldosterone system (RAAS): After hemorrhage or extracellular volume deficits(dehydration), there is a decrease in blood pressure or sodium delivery to kidneys, this stimulate secretion of renin,which forms Ang I, which is converted to Ang II which restores blood pressure.-SNS stimulation effects on heart (SW) Slides pg 15 (not much there), McCance 1150-1151. In healthy person,SNS helps maintain adequate blood pressure and tissue perfusion by promoting cardiac contractility and heart rate(maintains adequate cardiac output) and by inducing arteriolar vasoconstriction. In individuals with hypertension,overactivity (due to inc. production of catecholamines) of the SNS can result which causes increased heart rate andsystemic vasoconstriction, results in raised blood pressure àcontributes to pathogenesis of HTN. SNS contributes toinsulin resistance, which is associated with endothelial dysfunction and decreased production of vasodilators. SNShas procoagulant properties which make vascular spasm and thrombosis more likely.

3 questions-peripheral vascular disease: venous disease, arterial disease, Buerger disease/Raynaud’sdisease (Moya)

Peripheral ArterialDiseases

ThromboangiitisObliterans (Buerger Disease) --from slides &McCance pg. 1149

General:• Occurs mainly in young men who smoke

• 95% cases: associated with smoking

• 5% cases: related to frostbite, trauma, or the use of



sympathomimetic drugs

• Inflammatory disease of peripheral arteries resulting in theformation of nonatherosclerotic lesions (non-plaques)

• inflammation, thrombus formation, and vasospasm obliteratesthe small and medium-sized arteries

• typical areas: digital, tibial and plantar arteries of the feet andthe digital, palmar, and ulnar arteries of the hands

S/S:• pain, tenderness and hair loss in the affected area

ClinicalManifestations:

• sluggish blood flow and include rubor (redness of the skin) dueto dilated capillaries under skin, and cyanosis, which is causedby blood that remains in capillaries after its oxygen hasdiffused into the interstitium

• Chronic ischemia: skin thin & shinny; nails thicken &malformed

• Advance disease: ischemia can cause gangrene

• disease associated with cerebrovascular disease andrheumatic symptoms

Raynaud Phenomenon--slides & McCance pg1149-1150

General:• characterized by attacks of vasospasms in the small arteries

and arterioles of the fingers and, less commonly, the toes

• secondary to systemic diseases (ie: scleroderma,chemotherapy, cocaine use, hypothyroidism, pulmonaryhypertension, smoking, and environmental factors (cold andprolonged exposure to vibrating machinery)

Clinicalmanifestations:

• changes in skin color & sensation caused by ischemia

• vasospams: varying frequency and severity and causes pallor,numbness & the sensation of cold in the digits

• attacks: bilateral, begins distal at tips of digits and progressproximally

• sluggish blood flow, rubor w/ throbbing and paresthesisas

• can cause ulceration & gangrene (extremely rare)

Tx:• remove stimulus & treat the primary disease process

• associated with malignancy, surgal removal of the tumor mayresolve the ischemia

• no malignancy: calcium channel blockers or other vasodilators





S/S:• chronic pooling of blood in veins of lower extremeties

• hyperpigmentation of the skin of feet & ankles

• edema can extend to knees

Clinicalmanifestation: • circulation becomes sluggish

○ metabolic demands of cells for O2, nutrients, & waste are

barely met

• any trauma or pressure can lower O2 supply

○ causes cell death & necrosis (venous stasis ulcers)

Deep VenousThrombosis (DVT)--slides & McCancepgs 1143-1143

General:• formation of a thrombus in a deep vein

Causes: Triad of Virchow:

1. venous stasis (ie: immobility, obesity, prolonged leg dependency,

age, CHF

2. venous endothelial damage (ie: trauma, medications)

3. hypercoaguable states (inherited disorders, malignancy,

pregnancy, oral contraceptives, hormon replacement, etc.)

-------

• hospitalized individuals: significant risk

• orthopedic trauma or surgery, spinal cord injury, and OB/GYNconditions associated w/ up to 100% likelihood of DVT

-------

• genetic abnormalities, esp with hypercoagulability

Clinicalmanifestations

• accumulation of clotting factors & platelets leads to thrombusformation in vein, often near venous value

○ inflammation around thrombus

○ further platelet aggregation & propagates or grows

proximally

• can create venous flow obstruction

○

increase pressure behind the clot causing edema of theextremity

• DVT can dissolve without treatment but untreated can cause:

○ thromboembolization of a part of the clot from the leg to

the lung (pulmonary embolism)

○ post-thrombotic syndrome (PTS): frequent DVT

complication -- chronic, persistent pain, swilling, andulceration of the affected limb



Prevention:• due to being asymptomatic and difficult to detect clinically,

prevention in at-risk individuals is CRUCIAL

• people should be mobilized ASAP after illness, injury or surgery

• prophylactic tx with anticoagulation meds

• anticoagulation contraindicated: inferior vena caval filter

8 questions & 1 case study -heart failure: right side vs left side failure, edema, clinical manifestations(Marcus)LEFT HF (aka, congestive heart failure): Think SYSTOLIC or DIASTOLIC HF (or both)

• SYSTOLIC LHF (inability of ht to generate adequate CO to perfuse tissue)

○ (Remember: CO=HR x SV; and SV depends on contractility, preload, afterload - Starling forces)

○ Contractility (Pathology: in general, disrupted MYOCYTE activity)

MI is most common cause of ↓ contractility (other causes: myocarditis, cardiomyopathies)

SECONDARY causes of ↓ contractility (as seen in myocardial ischemia, ↑ myocardial

workload) predispose to inflamm., immune, & neurohormonal changes that mediateVENTRICULAR remodeling.

• Ventricular remodeling: where myocardial hypertrophy and dilation causemyocyte contractile dysfxn

• ↓ contractility → ↓ SV, causing ↑ LVEDV → ↑ dilation → ↑ pre-load

○ Preload (essentially LVEDV, filling volume)

Remember: ↓ contractility results in ↑ LVEDV; up to a certain point, ↑ LVEDV can actuallyimprove CO, but after a certain point, myocardium is too stretched out, dysfxn of sarcomeres, and ultimately ↓ contractility (think of a simple rubber band, and whatoverstretching can do)

↑ LVEDV often caused by: IV fl.administration, renal failure, MV dz

○ Afterload

Most often a result of ↑ PVR (as seen in HTN)

W/ ↑ PVR, LV has more emptying workload, resulting in myocardial hyperTROPHY

• Hypertrophy is mediated by angiotensin 2 and catecholamines, to increase O2and energy supply for thickened myocardium

• Myocardium depends on efficient ATP production and c-kinase system

• Energy-starved state contrib’s to ventricular remodeling, hence fxn

• Remodeling also results in COLLAGEN deposition b/w myocytes, which disruptmuscle integrity

○ Vicious cycle

↓ CO and activation of RAAS leads to ↓ renal perfusion → ↑ PVR and plasma vol. → ↑

preload + afterload Central baroreceptors cause vasoconstr, hypothal.release of ADH → ↑ pre-/after-load

○ Catecholamine release

Sympathetics compensate by ↑ PVR + HR

Cytotoxic to myocytes (apop, remodeling, dysrhythmias... good stuff!)

○ RAAS

↑ preload + afterload



Cytotoxic as well

Ang2: contrib.to remodeling, sarcomere death, loss of collagen matrix, fibrosis

Aldosterone: myocardial fibrosis, autonomic dysfxn, dysrhythmia

○ Arginine Vasopressin (ADH)

Peripheral vasoconstriction, renal fluid retention, exacerbat’n of hyponatremia + edema

○ ANP + BNP

Protective effect in ↓ preload, but not adequate in HF

○ Inflammatory mediators

Endothelin (bad), TNF-a, IL-6 (both of which contrib.to remodeling)

○ Myocyte calcium transport: decrease contractility

○ Insulin resistance: causes abnormal myocyte FA metabolism and ATP gener’n, leading to ↓

contractility, remodeling

• Chronic LHF

• DIASTOLIC LHF

○ In isolate: Pulmonary Congestion (despite noraml CO, SV)

○ Causes 50% of all LHF cases, and is more common in WOMEN

○ Causes

HTN-induced myocardial hypertrophy, myoc.ischemia w/ resultant remodeling

Hypertrophy and ischemia: impair myocyte pumping of CALCIUM from cytosol, resulting inIMPAIRED RELAXATION

Aortic valve dz, MV dz, pericardial dz

Diabetes

○ ↓ Compliance

Alterations seen in collagen, resulting in altered myoc.structure

Abnormality found in titin: intracellular protein component

○ Abnormal lusitropy (relaxation)

Abnormal relaxation caused by CA transport from myocyte, related to sarco.retic CAATPase

Result: poor acceptance of filling blood without resistance and ↑ wall tension

LVEDP (LVEDV) causes backing up of fluid into pulm.circ, resulting in pulm.edema

CL.PRESENTATION of SYSTOLIC vs. DIASTOLIC HF

• Systolic

○ Result from pulm.vasc congestion and inadequate systemic circ.perfusion

○ Dyspnea, orthopnea, frothy sputum, fatigue, ↓ urine output, CARDIOMEGALY

○ S3 gallop

• Diastolic

○ Dyspnea on exertion w/ fatigue

○ If severe, pulm.edema; S4 gallop

○ LV hypertrophy

○ Pulmonary congestion w/o cardiomegaly



○ NORMAL ejection fractions, but poor ventricular filling

RIGHT HF

• RV cannot provide adequate bl.flow to pulm.circ at normal central venous pressure (CVP)

• Most often SECONDARY to LHF w/ ↑ LV filling pressure, reflected into pulm.circ

• When pressure in pulm.circ rises, resistance to RV emptying increases

• RV generally cannot accommodate increased workload, leading to dilation and RV failure

• Result

○ ↑ pressure in systemic venous circ.

○ Triad: JVD, peripheral edema, hepatosplenomegaly

• Cor pulmonale (ch.33)

○ When RHF occurs in absence of LHF

○ Results from diffuse hypoxic pulm.dz (COPD, CF, ARDS)

4 questions-Valvular heart disease: stenosis vs regurgitation or incompetence, rheumatic heart disease (Dylan)

Valve Defects

• These can occur in any of the 4 heart valves

• However, more common in Mitral and Aortic Semilunar valves of LeftHeart

• Stenosis

○ Orifice is constricted and narrowed, impeding forward flow

○ This makes chamber proximal to the stenosis work harder to eject

blood → hypertrophy of myocardium in chamber proximal to stenosedvalve

• Aortic Stenosis (stenosis of Aortic Semilunar valve)

○ Most common valvular abnormality

○ Impedes blood flow from LV to Aorta

○ 3 major causes are 1) congenital bicuspid valve, 2) degeneration with

aging, 3) inflammatory damage caused by rheumatic heart disease

○ Linked with hyperlipidemia → Chronic inflammation → calcification of

valve leaflets

○ Causes hypertrophy of Left Ventricle → Increased oxygen demand →

Angina → MI

○ Clinical manifestations: Angina, syncope, heart failure, weak pulses,

decreased systolic BP

• Mitral Stenosis

○ Impedes blood flow from LA to LV



○ Most common cause is Acute Rheumatic Fever

○ 2-3 times more common in women

○ Leads to hypertrophy and dilation of LA →Atrial Fibrillation → thrombus

formation

○ Can cause blood to back up into lungs causing Pulmonary Edema and

Right heart failure

• Regurgitation

○ AKA insufficiency or incompetence

○ Valvular leaflets fail to close completely → blood leaks back into

chamber proximal to valve

○ This increases the volume of blood the heart must pump → chamber

dilation

○ Increased workload of the chamber → hypertrophy

Aortic regurgitation (regurgitation of the Aortic semilunar valve)

• Causes: Congenital defect, rheumatic heart disease,bacterial endocarditis, syphillis, HTN, trauma,atherosclerosis, connective tissue disorders, idiopathic

• Leads to LV dilation and hypertrophy → Heart failure

• Clinical Manifestations: Widened pulse pressure,dysrythmias

Mitral regurgitation

• Causes include mitral valve prolapse, Rheumatic heartdisease

•

Leads to dilation and hypertrophy of LA → pulmonaryedema → Right heart failure

Tricuspid regurgitation

• Usually secondary to pulmonary HTN

• Leads to volume overload in RV → increased systemicveinous BP

• Rheumatic Heart Disease

○ Scarring and Deformity of Cardiac structures

○ Caused by Rheumatic fever, a diffuse inflammatory disease caused by

a delayed immune response to infection by Group A beta-hemolyticstreptococci

○ Usually occurs in children aged 5-15

○ Immune response causes inflammatory lesions to occur in connective

tissue of the heart

○ Clinical Manifestations



Stenosis/regurgitation of valves

Pericarditis and pericardial effusions

Heart murmur

Enlarged heart

4 questions & (1 case study) -shock: septic, cardiogenic, circulatory shock (Yesol)

• Shock: Condition of acute and progressive circulatory dysfunction that results in inadequate delivery of oxygen and nutrients to tissues.

• Types:

○ cardiogenic: caused by heart failure

○ hypovolemic: insufficient intravscular fluid volume

○ obstructive: mechanical obstruction of blood flow through the central circulation

○ distributive (vasodilatory): widespread dilation of small vessels -- ↓ effective blood volume. “relative

hypovolemia”

septic: severe infection, endotoxins ⇒ massive release of inflammatory mediators

neurogenic (vasogenic): parasympathetic overstimulation or sympathetic understimulationd/t SCI, anesthesia, etc.

anaphylactic: type I hypersensitivity

• Septic shock: (will finish up tonight)

• Cardiogenic shock: heart failure of any cause (acute MI, valve failure, etc) -- impaired myocardial functioncompromises cardiac output

○ unresponsive to treatment

○ widespread impairment of cellular metabolism

○ Compensatory mechanism:

Activation of renin-angiotensin, neuro-hormonal, sympathetic NS ⇒ fluid retention,systemic vasoconstriction, tachycardia

Catecholamine (epinephrine, NE, etc) release ⇒ vasoconstrction, ↑ contractility, ↑ HR

These responses normalize BP and increase cardiac performance, but increasedmyocardial demands for O2 and nutrients further strain the already failing heart.

It will be helpful to understand how an MI leads to left side heart failure and then leads to right side heart failure.(Note: I took a crack at this, please add accordingly if there are gaps (Marcus))

Apart from the relatively rare occurrence of cor pulmonale (pure RV dysfxn), myocyte necrosis as seen in MIis directly related to ↓ in CO, which is a key component of LHF (remember systolic HF, which is inability of heart togenerate adequate CO to perfuse tissue), and less so RHF. Ischemic myocytes (MI) underlie systolic and diastolic

dysfxn, which are sub-types of LHF.If the LHF is sufficiently severe, pulm.congestion and edema occur, resulting in RHF (direction of pathology

is reverse; think UPSTREAM damage).Also, look at FUNCTIONAL changes seen in MI (McCance 1173):1. ↓ contractility; 2. altered LV compliance; 3. ↓ SV; 4. ↓ EF; 5. ↑ LVEDP (LVEDV); 6. SA or AV node malfxn*** All these functional changes are characteristic of LHF pathophys; RHF is secondary to LHF...... usually.

Pulmonary - 29 questions4 general; types of respiratory patterns (Kussmaul’s vs Cheyne-stokes), effect of PNS stimulation on bronchioles,causes of chest wall restriction (NEH-DUH)



• Kussmaul respirations, or Hyperpnea: Slightly increased Respiratory Rate, effortless tidal volumes and noexpiratory pause.

• Cheyne-stokes respiration: Alternating periods of deep and shallow breathing with apnea (15-60sec)followed by increased respiration. Decreased Blood Flow to brain or respiratory center in brain stem.

Effect of PNS stimulation on bronchioles::

Restrictive diseases restrict lung or chest wall expansion. There are different types:Atelectasis: The collapse of previously expanded lung tissue which results in no alveolar gas exchange. Atelectasisis caused by airway obstruction and absorption of air from the involved lung area and by compression of lung tissue.

○ Compression by external pressure.

○ Absorption: Removal of air from obstructed or hypoventilated alveoli or from inhalation of

concentrated oxygen.

• Lung tissue is collapsed. This can be caused by physical blockage or surgery. Clinical manifestationsincreased secretions and decreased breath sounds.

○ Atelactasis can result from a tumor, fluid, or air in the pleural space OR

○ Abdominal distention, bronchi obstruction

Pneumothorax: the presence of air or gas in the pleural cavity caused by rupture of the pleura. This destroys thenegative pressure in the pleural space disrupting the recoil forces of the lung and chest wall. Air enters the pleuralcavity, takes up space, restricting lung expansion. The affected lung can go through partial or complete collapse. Thetypes are classified by cause

• Spontaneous: an air-filled blister on the lung ruptures (bullae)

• Traumatic: air enters through injuries

○ Tension: air enters pleural cavity through wound on inhalation, cannot leave on exhalation. Clinical

manifestations: Hypoxemia, dyspnea, hypotension, shock, bradychardia. When chest tube isplaced, hear rush of air on insertion. Pleural pain, tachypnea, and mild dyspnea are experienced inTension pneumothorax.

○ Open: air enters pleural cavity through wound on inhalation, leaves on exhalation. Air pressure in

the pleural space equals the barometric pressure because air that is drawn in during inspiration is

forced back out during expiration.

○ Pleural Effusion: Occurs when there is a collection of fluid in the pleural cavity, can collapse the

lung partially or totally. This type is not a disease.

• Types of pneumothorax:

• Primary- occurs spontaneously

• Secondary- secondary to complications of pulmonary disease.

• Tension- secondary to trauma, requires emergent care (you will see this in people who have been impaled).

1 influenza (Lindsay) (Slides p.2)

•

In U.S., 36,000 die/year of flu-related illness (used to be the #1 killer)• Transmitted by aerosol or direct contact --> RESP system affected first

• 3 types: A, B, C: We see Type A every year and epidemic form every 3-4 years; Type B epidemic every 4-6years; Type C is endemic

• Leads to URI (rhinotracheitis) - like common cold w/ profound maliase

• Leads to Viral Pneumonia (lobar or bronchial)- fever, tachypnea, tachycardia, cyanosis, hypotenstion -->2dary bacterial infection



3 pulmonary edema, paroxysmal nocturnal dyspnea, hypoxia (Julia Kwon)pulmonary edema (p. 1279) (Figure 33-7 on p. 1279 illustrates pathogenesis of pulmonary edema) (Julia Kwon)

DEFINITION: excess water in the lungo Capillary fluid moves into alveoli and respiratory airways

o When fluid flow out of capillaries > lymphatic system’s removal of fluid (fluid builds up)

o Can occur when circulatory system is overloaded with fluids

Causes: MOST COMMON: Heart diseaseo Left ventricular failure/dysfunction

o ARDS

o Inhalation of toxic gases (i.e. ammonia)

o Obstruction of lymphatic system

Pathophysiology : Depends on causeo SEVERE pulmonary edema: capillary fluid moves into alveoli

o Fluid accumulates in alveoli and respiratory airways

o This causes lung stiffnesso So, lung expansion is more difficult

o Thus, gas exchange is impaired

Clinical Manifestations:o Air hunger, dyspnea

o Productive cough, often frothy, maybe blood tinged

o Hypoxemia, in severe increase partial pressure of CO2

o Tachycardia

o Skin: Moist and cool

o Nail beds/Lips: Cyanotic

o Confusion and stupor

paroxysmal nocturnal dyspnea (p. 1267)o An alteration of pulmonary functiono Dyspnea – subjective sensation of being unable to get enough air

o Air hungry, breathlessness

o A positional dyspnea in which individuals with heart failure or lung disease wake up at night gasping

for air ando must sit up or stand to relieve dyspnea

hypoxia (p. 1269) – Blood inadequately oxygenated. Reduced oxygenation of tissues, maybe caused byalterations of other systemso mistaken for hypoxemia

o can result from other abnormalities

o low cardiac output

o cyanide poisoning

o can’t get patient’s to breathe

o hypoxia can be caused by hypoxemia

2 TB (Victoria) power point pg. 5-6, book pg. 1293 - 1294• World’s foremost cause of death from a single infectious agent

• Drug-resistant forms (require multiple therapies, very long duration: 6-12 mo. treatment)

• Myobacterium tuberculosis hominis (acid fast bacillus that affects lungs and may invade other systems)

○ Airborne (droplets)--transmit person to person

○ Protective waxy capsule (stays alive/protected)

○ Can stay alive in “suspended animation” for years (latent)



• More than half of new cases occur in foreign-born individuals

• Individuals with AIDS are highly susceptible

• Clinical Manifestations :

○ Fatigue

○ Weight loss

○ Lethargy and anxiety

○ Change in appetite

○ Low grade fever

○ Night sweats

• Diagnosis

○ PPD (skin test, usually double test)

○ CXR (chest x-ray to confirm)

○ Sputum culture

• Initial TB Infection/Pathophysiology

○ Macrophages begin a cell-mediated immune response

○ Takes 3-6 weeks to develop positive TB test (need time to develop enough antibodies for + test)

○ Results : granulomatous lesion or Ghon focus containing (triggered by immune response, walls off

inactive TB bacteria)

Macrophages

T cells

Inactive TB bacteria

Central portion becomes caseous (cheese-like) and necrotic

○ Ghon Complex

Nodules in lung tissue and lymph nodes

Caseous necrosis inside nodules

Calcium may deposit in the fatty area of necrosis

Visible on x-ray (why we confirm with CXR)

• Primary TB (First exposure, if healthy --> wall off)

○ Usually isolated in Ghon foci --> bacteria are inactive AND not contagious OR

○ If immune response is inadequate, bacteria multiply in lungs (immune suppressed can’t wall off TB)

--> progressive primary TB

• Secondary TB (Already exposed--see frequently with health care workers)

○ Reinfection from inhaled droplet nuclei OR

○ Reactivation of previously healed primary lesion

○ Immediate cell-mediated response walls off infection in airways

○ Bacteria damages tissues in the airways, creating cavities

○ Signs of chronic pneumonia: gradual destruction of lung tissue

○ “Consumption”: eventually fatal if untreated

2 lung cancer (NERDA)The types of lung cancer:

• Squamous cell: slow growth, late mets, cough, sputum.



• Adenocarcinoma: Moderate growth, early mets, pleural effusion

• Large cell: Rapid growth, early wide mets, pain, pleural effusion, cough, sputum

• Small cell: Very rapid growth, very early to mediastinum, airway obstruction.

Bronchiogenic carcinoma: arises from epithelial cell lining.

Small-cell lung cancer: have metastasized by the time of diagnosis. The prognosis is very poor in this type of cancer because it is not amenable to surgery.

• Strong association with smoking.

• Without treatment, half of those diagnosed die within 12-15 weeks.

Non-small-cell lung cancer

• Large cell carcinoma- poor prognosis, tend to spread to distant sites early in their course.

• Squamos cell: associated with smoking. This type is more amenable to early detection.

• Adenocarcinoma: most common type in North America. This type is more common in women andnonsmokers.

Manifestations of Lung Cancer • Changes in organ function (damage, inflammation, and failure)

• Local effects of tumors (compression of nerves or veins, GI obstruction)

• Ectopic hormones secreted by tumor cells (paraneoplastic disorders). Such disorders includehypercalcemia, Cushing syndrome, SIADH, neuromuscular syndrome

• Nonspecific signs of tissue breakdown (protein wasting, bone breakdown)

Taken from McCance study guide: (Moya)

Type/Frequency GrowthRate

Metastasis Menifestations/Tx

Adenocarcinoma; 35%-

40%

Moderate Early Pleural effusion; surgical tx/adjunctive

chemotherapy

Squamous cell; 30% Slow Late Cough, sputum production, airway obstruction;surgical tx/adjunctive chemotherapy

Large cellundifferentiatedcarcinoma; 10%-15%

Rapid Early andwidespread

pain, pleural effusion, cough, sputum production,hemoptysis, airway obstruction results inpneumonitis or pleural effusion; treated surgically

small cell (oat cell)carcinoma

very rapid very early tomediastinum or distally in lung

airway obstruction, excessive ACTH secretionwith its signs and symptoms; chemotherapy andradiation

3 asthma (Julia Kwon)

(Pg. 1283-1286; slides 58-65 on Respiratory Pathology Powerpoint)Asthma is an obstructive pulmonary disease ASTHMA: lung disease characterized:o Airway obstruction,

o Airway inflammation,

o Airway hyperresponsiveness,

o Episodes of bronchospasm

· Pathophys : GENETICS. Abnormality in IL4 gene -à Increased IgE synthesiso Bronchial hyperresponsiveness=

Exaggerated bronchospastic response,



Increased functions of inflammatory response,Degranulation of Eosinophils

o Smooth muscle contraction

o Microvascular leakage

· Clinical Manifestations:o Asymptomatic during full remission

o ACUTE ATTACK: anxiety, cyanosis, chest constriction, inspiratory and expiratory wheezing, dyspnea,

nonproductive coughing, prolonged expiration, acidosis, tachycardia, tachypnea, with severe attacks on theaccessory muscles of respiration· TYPE I HYPERSENSITIVITYo ACUTE RESPONSE/Immediate or Early Phase Response

Allergen àMast cells’ release inflammatory mediatorsChemical mediators à increased mucous production

opening of mucosal intercellular junctions10-20 minutes

o LATE PHASE RESPONSE

Airway inflammationEpithelial injury with decreased mucociliary function and accumulation of

mucous.Release of inflammatory mediators

· Recruitment of Neutrophils, eosinophils, and basophils.Increased vascular permeability and edema

Increased airway responsiveness and4-8 hours4 pleural effusion (types of exudates) & pneumothorax (understand the different types) (AK47)Note: pneumothorax is considered a restrictive disorder, which is why I listed the types of pneumothoraxunder that section. But for less confusion, I am pasting it under this section as well.Restrictive diseases restrict lung or chest wall expansion. There are different types:Atelectasis: The collapse of previously expanded lung tissue which results in no alveolar gas exchange. Atelectasisis caused by airway obstruction and absorption of air from the involved lung area and by compression of lung tissue.

○ Compression by external pressure.

○ Absorption: Removal of air from obstructed or hypoventilated alveoli or from inhalation of

concentrated oxygen.

• Lung tissue is collapsed. This can be caused by physical blockage or surgery. Clinical manifestationsincreased secretions and decreased breath sounds.

○ Atelactasis can result from a tumor, fluid, or air in the pleural space OR

○ Abdominal distention, bronchi obstruction

Pneumothorax: the presence of air or gas in the pleural cavity caused by rupture of the pleura. This destroys thenegative pressure in the pleural space disrupting the recoil forces of the lung and chest wall. Air enters the pleuralcavity, takes up space, restricting lung expansion. The affected lung can go through partial or complete collapse. Thetypes are classified by cause

• Spontaneous: an air-filled blister on the lung ruptures (bullae)

• Traumatic: air enters through injuries

○ Tension: air enters pleural cavity through wound on inhalation, cannot leave on exhalation. Clinical

manifestations: Hypoxemia, dyspnea, hypotension, shock, bradychardia. When chest tube isplaced, hear rush of air on insertion. Pleural pain, tachypnea, and mild dyspnea are experienced in

Tension pneumothorax.

○ Open: air enters pleural cavity through wound on inhalation, leaves on exhalation. Air pressure in

the pleural space equals the barometric pressure because air that is drawn in during inspiration isforced back out during expiration.

○ Pleural Effusion: Occurs when there is a collection of fluid in the pleural cavity, can collapse the

lung partially or totally. This type is not a disease.

• Types of pneumothorax:

• Primary- occurs spontaneously



• Secondary- secondary to complications of pulmonary disease, mechanical ventilation, or chest trauma.

• Tension- secondary to trauma, requires emergent care (you will see this in people who have been impaled).

Pleural Effusion

• Presence of fluid in pleural space, causes compression atelectasis (from pressure) and mediastenaldisplacement.

• Clinical manifestations-dyspnea (most common symptom), compression atelectasis, impaired ventilations,mediastenal shift, pleural friction rub.

The 5 types of Pleural Effusion - great chart on table 33-2, pg 1274

• Transudates- water diffuses out of capillaries- CV, HTN, hypoproteinemia

• Exudates- Protein rich fluid- infection, inflammation, malignancy

• Empyema- Pus--infection

• Hemothorax or hemmorhagic pleural effusion- blood present- this means trauma to blood vessels.

• Chylothorax- milky fluid with lymph and fat dumped by lymph vessels.

5 ARDS: pathophysiology and clinical manifestations (Marcus)

• Fulminant resp failure char.by:

○ Acute lung inflammation

○ Diffuse alveolocapillary injury

• Results often from injury to lung by numerous unrelated causes

• Predisposing factors:

○ MOST COMMON: Sepsis, multiple trauma (transfusions esp); Other: burns, pneumo,

aspiration, pancreatitis, drug OD, smoke, DIC

• Pathophys

○ Cause massive pulm.inflamm injuring alveolocapillary membrane, producing severe pulm.edema

○ Alveolocapillary damage can be direct (aspiration) or indirect (chem. mediators released in

response to systemic disorders, eg, sepsis)

○ Initial injury

Complement activ’n: lung capillary damage

Platelet aggreg’n

Intravascular thrombus formation

Inflamm’y cascade by macrophages (MO’s): TNF, IL-1, alpha-, beta-chemokines

○ Neutrophils

Attracted/activated by substances released by platelets

Release inflamm.mediators: proteolytic enzymes, oxygen free radicals, PAF

Result in: damage to alveolocapillary membrane and ↑ capillary permeability

○ ↑ Capillary permeability

***Hallmark feature of ARDS***

Allows fluid, protein, blood cells to leak from cap.bed into pulm.interstitium & alveoli

Result in: pulm.edema & hemorrhage, resulting in ↓ lung compliance

○ Vasoconstriction

Caused by mediators released by PMN’s (and in part by MO’s)



Causes secondary pulm.HTN

Uneven distribution of vasoconstriction underlies V/Q mismatch in some areas of lung

○ Surfactant

Produced by type 2 alveolor cells, Inactivated by inflamm’n

↓ lung compliance

Result in: ↑ work of breathing, ↓ minute ventilation, hypercapnia

○ After 24 hours...

W/in 24-48 hrs: hyaline membrane formation

W/in 7 days: fibrosis obliterates alveoli, resp.bronchioles, interstitium

• Leading to ↓ functional residual capacity (FRC), V/Q mismatch, R-to-L shunt

○ ARDS can lead to MODS: MODS often is cause of death, not necess the initial ARDS

• Clinical Presentation

○ Primary symptom: Progressive dyspnea

○ 24-48 hrs: CxR reveals interstitial and alveolar infiltrate; HYPOXEMIA and resp ALK

○ As pulm.edema worsens

Hypoxemia becomes refractory to O2 therapy

Hypoventilation develops (↑ PaCO2)

○ Worsening hypoxemia and hypercapnia → Resp.failure

○ ↓ O2 delivery: met.ACIDOSIS, organ dysfxn

○ ↓ CO, hypotension: death

○ ***7 steps***:

• Dyspnea + Hypoxemia →

• Hypervent + Resp.ALK →

• ↓ Tissue perfusion + Organ dysfxn + Met.ACID →

• ↓ TV + Hypoventilation →

• Resp.ACID + Hypoxemia →

• ↓ CO + Hypotension →

• DEATH

5 & 1 case study: COPD, emphysema, chronic bronchitis: be able to differentiate pathophysiology and clinical

manifestations (Carla) I’ll be posting this tonight***

It will be very helpful to be able to differentiate between emphysema and chronic bronchitis (Sakhiba)

Documents

Cardiovascular Study Guide