Patho Exam 2

What are the layers of the heart from external to internal?

Epicardium, myocardium, endocardium

pericardium

* fibrous covering of heart attached to great vessels, sternum, and diaphragm
* prevents acute dilation of heart chambers

pericardial cavity

* cavity around heart that contains serous fluid
* lubricates and minimizes friction during contraction and dilation

myocardium

* muscle of heart: ventricles and atria
* contraction of ventricles together and atria together (syncytium)
* contains many mitochondria
* actin and myosin filaments
* calcium need for contractions

PQRST complex

* electrical activity of the heart
* P: depolarization of SA node
* QRS: depolarization of ventricles
* T: repolarization of ventricles

Cardiac Output formula

stroke volume x heart rate

atrial pressure waves (3)

* A wave: atrial contraction
* C wave: ventricle contraction
* V wave: end of systole when AV valves close

Systole and diastole

* Systole: contraction
* Diastole: relaxed and filling

when does an atrial contraction occur?

last 1/3 of diastole

function of circulatory system

* transports nutrients and materials to tissues
* removes waste products

humoral control of vascular function (vasodilators)

* epinephrine
* histamine
* bradykinin (dilates arterioles, constricts venules)
* prostaglandins in E group

humoral control of vascular function (vasoconstrictors)

* norepinephrine
* angiotensin II
* serotonin
* bradykinin (dilates arterioles, constricts venules)
* prostaglandins in F group

what protein controls colloidal osmotic pressure?

albumin

which nerve helps regulate heart rate?

vagus CN X (increased activity= slower HR) = parasympathetic NS

vascular endothelium function

* transports nutrients and waste
* creates compounds that stimulate :
* vasoconstriction and vasodilation
* inflammation (cytokines)
* clot formation
* smooth muscle ?

vascular smooth muscle cells function

creates compounds that stimulate vasoconstriction/dilation and inflammation

arterial blood pressure (ABP) (formulas)

* systolic : ventricles contracts
* diastolic : ventricles relax
* pulse pressure= systolic - diastolic
* mean arterial pressure= (1/3)systolic +2/3diastolic
* cardiac output= heart rate x stroke volume
* blood pressure= cardiac output x total peripheral resistance

orthostatic hypotension

* drop of systolic bp >20mmHg
* drop of diastolic bp >10
* ex:
* laying down BP: 120/80 mmHg
* sitting up BP: 90/60 mmHg
* blood shifts to brain decreases
* blood pools in capillaries instead of circulating

what regulates systemic arterial BP?

* acute regulation: corrects temporary imbalances
* neural: autonomic NS (epi and norepi)
* humoral: RAAS (kidneys &lungs) = does take longer to work

Hypertension

* high BP; is a crisis, urgent, and an emergency
* primary causes: genetics, diet, alcohol
* secondary causes: renal hypertension, adrenocortical hormones, oral contraceptives
* calcification increases as you age= increase BP

how would the follow affect BP: vasodilation, decreased stretching of baroreceptors, hypoxemia, inhibiting ACE, beta-blockers, a2-agonists; calcium channel blockers, age?

* vasodilation: Decrease
* decreased stretching of baroreceptors: decrease
* hypoxemia (low O2 in blood): increase
* inhibiting ACE: decreases
* beta-blockers: decreases
* a2-agonists: Increase
* calcium channel blockers: Decrease
* age: increases as you age

what treatment is used for hypertension? (broad answers)

* treat underlying cause
* medications:
* lasix/furosemide (diuretic) (lower blood volume)
* ace inhibitors
* calcium channel blockers
* education

dyslipidemia (primary and secondary)

* Latin roots:
* dys: abnormal
* lipid
* -emia: blood
* imbalance of lipid components of blood
* primary: genetics, family hypercholesterolemia (LDL receptor is defective or deficient)
* secondary: dietary, obesity, type 2 diabetes

triglyceride function

energy metabolism

phospholipids function

* lipoproteins (membranes)
* blood clotting
* myelin sheath

do lipids have a higher or lower density compared to proteins?

lipids have a lower density than proteins

* more lipid= lower density

what is the function of chylomicrons?

transport dietary triglyceride to peripheral tissues and cholesterol to liver

LDL and HDL

* LDL (low density lipoproteins)
* more cholesterol, less lipid
* transports cholesterol
* can be oxidized and deposited into vascular bed (atherosclerosis)
* HDL (high density lipoproteins)
* more protein, less cholesterol
* transports cholesterol from cells to liver

hypercholesterolemia

* high cholesterol in blood
* high serum cholesterol levels: >240mg/dl
* effects: stroke, heart attack, atherosclerosis

atherosclerosis (risk factors)

* hardening of arteries (is full of plaque)
* cholesterol build up

atherosclerosis (effects)

* scavenger cells encounter fatty deposits in the artery lining and try to destroy the fats by oxidizing them or remove the fats by eating them
* oxidizing fats:
* injure endothelium
* clot formation (release of growth factors)
* smooth muscle grows over fatty core
* eating fats: become “foam cells” in the core of plaque
* lipids get into damaged vascular endothelium
* WBCs try to clear foam cells (inflammation)
* WBCs and endothelium release growth factors that promote plaque formation
* plaque forms and blocks arteries

lesions associated with Atherosclerosis

* fatty streaks
* fibrous plaque (embedded in tissue)
* complicated: contains hemorrahage, ulceration, scar tissue

complications and manifestations of atherosclerosis

* ischemic heart disease
* stroke
* peripheral vascular disease
* manifestations
* narrowing of vessel causing ischemia
* vessel obstruction due to plaque hemorrhage or rupture
* thrombosis and formation of emboli
* aneurysm formation (abnormal bulb)

arterial disease to extremities

* atherosclerotic occlusive disease: interruption of arterial blood flow to affected tissues and organs; emergency situation
* Raynaud disease: intense vasospasm of arteries and arterioles in fingers and maybe toes
* blood cut off (pale color) => low o2 (cyanosis)=> blood returns (pink) (is painful)

7 P’s of acute arterial embolism

1. pistol shot (acute onset)
2. pallor
3. polar (cold)
4. pulselessness
5. pain
6. paresthesia (pins and needles feeling)
7. paralysis
8. More blue colored

atherosclerotic occlusive disease (peripheral artery disease) manifestations and treatment

* blockage in large arteries (not coronary, aortic arch, or brain)
* risk factors similar to atherosclerosis
* clinical manifestations: gradual, cool extremities, weak pulses, color change
* pain upon walking; cramping
* diagnosis: ultrasound, MRI, arteriography, angiography
* treatment: injury prevention, meds, stent placement, surgery

aneurysm

* wall of blood vessel weakens and stretches
* risk of rupture and hemorrhage
* risk of clot formation
* bulb formation

aortic dissection (dissecting aneurysm)

* acute, life-threatening
* hemorrhage into the vessel wall with longitudinal tearing that forms a blood-filled channel
* rupture = death
* manifestations: abrupt onset of pain : tearing or ripping (chest/back)
* diagnosis: vascular imaging, CT, MRI, resection and replacement

disorders of venous circulation

* produce congestion of the affected tissues
* predispose to clot formation because of stagnation of flow and activation of the clotting system
* disorders:
* varicose veins
* thrombophlebitis

effects of venous insufficiencies

* edema
* redness
* brown pigment
* ulcers, ankle and lower leg

VTE

* venous thromboembolism
* Blood pools in calves of leg (stasis) = clot
* Virchow’s Triad: venous stasis, increased blood coagulability, vessel wall injury
* prevent is better than treatment
* Ultrasound
* blood clot in calves of leg= pooling (stasis)

Virchow’s triad for VTEs

* venous stasis
* increased blood coagulability
* vessel wall injury

risk factors of venous stasis

* bed rest
* immobility

high and low bp

* low blood pressure: not enough blood to tissues
* high blood pressure: damage to endothelial tissue, increased likelihood of atherosclerotic vascular disease and vascular rupture

organs and hypertension affect

* heart: hypertrophy; heart failure
* brain: dementia, stroke
* peripheral vascular: atherosclerosis
* kidney: nephrosclerosis
* eyes: retinal complications; blindness

pericardium (what is it and what does it do?)

* double-layered serous membrane
* prevents overfilling of heart
* isolates heart from other thoracic structures
* maintains its position in the thorax
* contributes to coupling the distensibility between the 2 ventricles during diastole= fill equally

pericardial disorders

* pericarditis: inflammation of pericardium; heart beats against pericardial sac
* cardiac tamponade: slow or rapid compression of heart due to accumulation of fluid, pus, or blood in pericardial sac
* pericardial effusion: accumulation of fluid in pericardial cavity

pericarditis

* inflammation of pericardium
* causes:
* ECG changes
* pain
* exudate
* serous: pericardial effusion (cardiac tamponade)
* fibrous: friction rub, adhesions
* restricts heart movement due to pericardial effusion and fibrous scar tissue (constrictive pericarditis)

cardiac tamponade

* blood or fluid compressing the pericardial sac= increasing pressure on heart = disrupts diastole= causes back flow of blood (muffle heart sounds)
* treatment: need aspiration, surgery, dopamine
* risk factors: effusion, trauma, coagulation tissues, MI (myocardial infarction), drug reaction
* Beck’s triad: JVD, muffled heart sounds, low BP
* medical emergency

consequences of pericardial effusion (left ventricle)

1. fluid in pericardial cavity
2. restricts heart expansion
3. L ventricle cannot accept enough blood
4. low cardiac output
5. decreased BP and shock

consequences of pericardial effusion (right ventricle)

1. fluid in pericardial cavity
2. restricts heart expansion
3. R ventricle cannot accept enough blood
4. increased jugular venous pressure ; jugular distention

coronary circulation

* coronary arteries: right and left main
* site on surface of heart
* vasodilation in response to need
* feed the epicardium first

CHD

* coronary heart disease
* atherosclerosis blocks coronary arteries
* effects:
* angina
* MI or heart attack
* cardiac arrhythmias
* conduction defects
* heart failure
* sudden death

tests to evaluate coronary blood flow and myocardial perfusion

* ECG: pattern of wave forms (electrical activity)
* Echocardiogram: M-mode, two-dimensional, Doppler, esophageal (muscle function)
* Exercise stress testing: motorized treadmill and bicycle ergometer (stresses the heart to see where there is less blood flow)

acute coronary syndrome & chronic ischemic heart disease

* ACS: ranges from unstable angina to MI
* chronic ischemic HD: chronic stable angina, silent myocardial ischemia, variant or vasospastic angina

determinants of ACS status

* presenting characteristics
* ECG variables: T-wave inversion, ST-segment depression or elevation, abnormal Q wave
* serum cardiac markers: proteins released from necrotic heart cells (myoglobin, creatine kinase, troponin)
* stable: exercising and chest pain
* unstable: at rest and chest pain

Manifestations of a STEMI

* STEMI: ST-segment elevation myocardial infarction
* abrupt onset
* crushing pain, radiates to left arm, neck, or jaw
* GI issues (vomiting, nausea)
* pallor, cool skin
* fatigue and weakness: blood stops being sent to the muscles
* tachycardia, anxiety, restlessness, impending doom feeling

factors determining the extent of an infarct

* infarct: dead heart tissue
* location and extent occlusion
* amount of heart tissue supplied by vessel
* duration of occlusion
* metabolic needs of affected tissue
* extent of collateral circulation
* heart rate, BP, cardia rhythm

complications of AMI

* acute myocardial infarction
* heart failure
* cardiogenic shock: nausea, fatigue, vomiting (acute phase of MI)

medical management of infarct

* meds: morphine, nitroglycerin (vasodilates), oxygen
* thrombolytic therapy: aspirin
* revascularization: coronary artery bypass graft (CABG: making new vascular flow from skin), percutaneous coronary intervention (PCI)
* cardiac rehab programs

chronic ischemic heart disease

* imbalance in blood supply and the hearts O2 demands
* less blood: atherosclerosis, vasospasm, thrombosis
* higher oxygen demand: stress, exercise, cold

angina classification

* silent myocardial ischemia: MI without pain


* note: diabetics don’t tend to have chest pain as a symptom of heart attack

unstable angina (characteristics: 3 features)

* occurs at rest, lasts longer than 20 minutes (not interrupted by nitroglycerin)
* severe and described as frank pain and of new onset
* pattern that is more severe, prolonged, or frequent than previously experienced

unstable angina (causes)

* atherosclerotic plaque disruption
* platelet aggregation
* secondary hemostasis

myocardial diseases

* primary cardiomyopathies: unknown origin


* secondary cardiomyopathies: results from another cardiovascular disease (most common)

hypertrophic cardiomyopathy

* defects in contractile proteins make cells too weak
* cells hypertrophy to do the same amount of work as normal cells
* need more oxygen and perform less efficiently= prone to heart failure and sudden death upon exertion

S/S of left ventricular dysfunction

* orthopnea (difficulty breathing while lying down)
* dyspnea: shortness of breath
* tachypnea: faster breathing rate
* crackles: fluid in lungs
* blood tinged sputum

valve defects (stenosis, regurgitation)

* stenosis: valve doesn’t open all the way
* blood cannot enter
* will hear murmur of blood shooting through narrow opening when the valve is open
* could occur b/c of calcification for older people
* more pressure
* regurgitation: valve doesn’t lose all the way
* leakage
* will hear a murmur of blood leaking back through when the valve should be closed

left-sided valve disorders

* mitral valve: stenosis, regurgitation, prolapse
* aortic valve: stenosis, regurgitation
* more pressure= more work= more damage

Stenotic and regurgitant heart murmurs

* stenotic: heard when valve should be open
* regurgitation: heard when valve should be closed

right and left sided heart failure

* diastolic: RV/LV does not accept enough blood from body
* systolic: RV/LV does not pump enough blood to body
* lungs don’t oxygenate enough blood
* body fills with blood (blood backs up in cycle)
* right sided: neck and feet aches
* left sided: lung issues

manifestations of heart failure

* impaired pumping
* decreased renal blood flow (low BP)
* sympathetic NS
* congestion
* low cardiac output

circulatory failure

* shock
* hypoperfusion of organs and tissues
* insufficient O2 supply and nutrients for cellular function
* compensatory mechanisms: sympathetic and renal systems

types of shock

* hypovolemic
* cardiogenic
* distributive: sepsis

hypovolemic shock

* acute loss of 15% or more of circulating blood volume
* hemorrhage
* excessive dehydration
* third spacing : fluid moves to area where it doesn’t circulate
* compensatory mechanisms
* treatment: blood and fluid

cardiogenic shock

* heart fails to pump blood adequately
* decreased output lowers BP

distributive or vasodilatory shock

* blood vessels dilate
* not enough blood to fill the circulatory system
* blood flow decreases
* less blood returned to heart
* less blood circulates through body

causes of distributive shock

* vasodilatory substances in blood:
* type I hypersensitivity (anaphylactic shock)
* inflammatory response to infection (sepsis)

Sepsis (SIRS)

* SYSTEMIC inflammatory response syndrome
* inflammatory mediators released into circulation
* systemic: fevers, increased respiration, vasodilation, warm flushed skin
* significant hypotension

complications of shock

* pulmonary injury: lungs don’t oxygenate well
* acute renal failure: no BP available
* gastrointestinal ulceration: no BP available
* disseminated intravascular coagulation: clotting and bleeding at the same time
* multiple organ dysfunction syndrome: not enough blood to organs

acute respiratory distress syndrome (ARDS) (shock complication)

* may be the cause or result of shock
* rapid onset of profound dyspnea that usually occurs 12-48 hours after initiating event
* exudate enter alveoli: blocks gas exchange, inhalation is difficult
* neutrophils enter alveoli: inflammatory mediators and proteolytic enzymes released

GI complications (shock complication)

* loss of appetite, nausea, vomiting
* constriction of blood vessels= redistribution of blood flow= decrease in mucosal perfusion= GI ulceration and bleeding

DIC (shock complication)

1. coagulation pathways activated
2. clots form in small blood vessels / platelets and clotting proteins used up
3. microinfarcts, ischemia / bleeding problems

multiple organ dysfunction syndrome (MODS) (shock complication)

* rapidly depletes the body’s ability to compensate and recover from a shock state
* affects multiple organ systems (lungs, liver, kidneys, brain, heart)
* risk factors: sepsis, hepatic dysfunction, hypotension, infarcted bowel

treatment measures to correct and reverse shock

* fluid resuscitation: fix blood pressure (currently very hypotensive)
* restore blood flow
* improve O2 delivery
* hemodynamic stability

how many angles are used to view the heart? (ECG)

12- lead angles

waveform deflections (depolarization and repolarization)

* depolarization: electrical impulse moves towards the positive electrode= upward deflection
* repolarization: electrical impulse moves away from positive electrode = downward deflection

PQRST complex

* P: atrial depolarization
* QRS: ventricular depolarization, atrial repolarization
* T: ventricular repolarization

3 I’s of myocardial infarctions

* zone of ischemia: inversion of T wave
* zone of injury: elevated S-T segment
* zone of infarction: (tissue death) Q or QS deflated

ventilation, perfusion, diffusion of gases (respiratory)

* ventilation: movement of gases into and out of lungs
* perfusion: movement of blood through lungs
* diffusion: movement of gases between lungs and blood

other functions of the lungs other than respiration

* inactivate vasoactive substances
* convert angiotensin I to angiotensin II
* reservoir for blood

common upper respiratory tract infections

* cold ( rhinovirus, parainfluenza, RSV, corona)
* rhinosinusitis
* influenza

common lower respiratory tract infections

* pneumonia
* tb
* fungal infections

what are the common portals of entrance for viruses?

* fingers
* nasal mucosa
* conjunctival surface of eyes
* cough
* sneeze

rhinosinusitis

* obstructs sinus drainage/passages
* acute: facial pain, headache, purulent nasal discharge (colored mucus), decreased sense of smell, fever
* viral (mainly) or bacterial
* lasts 5 days - 4 weeks
* subacute: 4-12 weeks

Influenza

* direct contact precaution or aerosol
* viral pneumonia: fever, tachypnea, tachycardia, cyanosis, hypotension
* respiratory viral infection followed by a bacterial infection

influenza vaccines

* TIIV (trivalent inactivated influenza vaccine) : IM injection
* LAIV (live, attenuated influenza vaccine) : nasal

pneumonia

* inflammation of the lung structures (alveoli more so than bronchioles): macrophage abundance
* causes:
* infectious: bacteria and viruses,
* non-infectious: gastric secretions aspirated into lungs
* typical:
* lobar (affects entire lobe of lung)
* bronchopneumonia: patchy distribution over more than one lobe

pneumonia classifications

* source of infection:
* community: within 48 hours of admission
* hospital: after 48 hours of admission
* immune status of host

tuberculosis

* can infect any part of the body; lungs frequently involved
* bacteria: Mycoplasma tuberculosis
* airborne precaution