Patho Test 3 (Cardiovascular) PDF

Preview

Summary

Test study guide...

Description

Cardiovascular A&P o Understand factors affecting cardiac output  Differentiate:  Preload:  Amount of ventricular stretch  Determined by venous return  Amount of volume in ventricles at the end of diastole  Afterload  Resistance against which heart must pump to circulate blood  Increases cardiac workload  Contractility  Heart rate: increased heart rate  increased CO o Heart wall Layers:  Pericardium: double walled sack encasing heart made up of connective/fibrous tissue and serous fluid  Myocardium: middle layer of heart wall composed of muscle  Endocardium: inner lining of heart o Blood pressure regulation via  RAAS  Baroreceptors o Calculate and understand importance of mean arterial pressure  Average pressure in circulation, based on length of cardiac cycle  Calculation: MAP = SBP+2(DBP)/3 Disease of Arteries and Veins o Primary (Essential) Hypertension: “Essential idiopathic” 92-95% of cases 

Risk factors: 

family hx (genetic predisposition)



advancing age



African American



Men> Women (before age 55)



Women> Men (after age 55)



Smoking



Obesity, diabetes, sedentary lifestyle





Diet = heavy alcohol (increase Na and decreases K+, calcium, and magnesium)

Causes/pathophysiology 

1. SNS Hyperactivity: 



2. Overactive RAAS: 



Should excrete Na with increased arterial pressure, but hypertensive people do not

4. Insulin resistance – obesity hormones 



Increased volume and vasoconstriction = increased BP

3. Defect in natriuresis 



increased HR, systemic vasoconstriction = increased BP

Causes structural changes in vessels and endothelial dysfunction  SNS/RAAS activation = vasoconstriction

5. Inflammation and Endothelial Dysfunction 

Endothelial injury  chronic inflammation  vascular remodeling  vasoconstriction  narrowing and smooth muscle contraction

Note importance and functioning of RAAS 

Symptoms: (early) no signs or symptoms 

Headaches



Dizziness



Blurred vision



Tinnitus



Anxiety









Chest pain



Shortness of breath



Nausea

Values for: 

Normal: Systolic 60  Triglyceride 240 is high Understanding that complications/progression of atherosclerosis leads to other cardiac disorders such as CAD, MI, etc. o Atherosclerosis is primary risk factor for CAD, myocardial ischemia, and acute coronary syndromes Peripheral artery disease – intermittent claudication o Atherosclerosis of the arteries that perfuse the limbs o Intermittent claudication: pain with ambulation 











Coronary Artery Disease: a continuum of diseases from atherosclerosis to myocardial ischemia to myocardial infarction  Risk Factors – modifiable vs nonmodifiable o Modifiable:  Dislipidemia  HTN  Smoking (leads to vasoconstriction)  Obesity  Sedentary lifestyle  Atherogenic diet o Nonmodifiable:  Advanced age  Male gender  Women after menopause  Family hx  Angina – cause and associated symptoms o Angina Pectoris is chest pain or discomfort secondary to myocardial ischemia – heaviness, pressure, or pain may radiate to back, shoulder, arm, neck, jaw, epigastric region o Patho: build-up of lactic acid, stretch that causes irritation to myocardial nerve fibers o Physical assessment findings:  May have normal physical  Hear assessment: tachycardia, gallops/murmurs, carotid artery bruits, ECG changes (T wave inversion, ST segment depression)  Head/Neck: xanthelasmas, arcus senilis o Diagnostic tests:  Stress test  Coronary arteriography  Noninvasive: CT, MRI, ultrasound  Single photon emission computerized tomography o Types: Stable, prinzmetal, silent, unstable  Stable  Recurrent predictable chest pain  Cannot vasodilate with increased myocardial demand  Transient 3-5 mins  Usually relieved by nitroglycerin or rest  Prinzmetal/variant  Caused by coronary vasospasm, decreased vagal cavity, decreased NO, hyperactive SNS  Unpredictable  Almost always occurs during rest, at night during REM sleep  Silent: mental stress induced ischemia

Asymptomatic, may be a problem with LV afferent sympathetic nerve innervation  DM is most common cause  Unstable: form of acute coronary syndrome  Occurs randomly or unpredictably and is unrelated to any obvious trigger  Considered a medical emergency- escalates rapidly, signs that plaques are complicated and MI is pending  Reversible myocardial ischemia that results from a sudden obstruction of a coronary vessel by thrombus over atherosclerotic plaque o Characteristics of stable vs unstable angina (see above) 



Myocardial Infarction: prolonged ischemia that results in damage to the heart muscle – irreversible after 20 minutes o Risk factors- causes  Typically from a ruptured plaque, clot formation, blood flow being dramatically obstructed  Decreased blood supply – increased demand  Unstable angina o Pathophysiology  Concepts of ischemia and time to irreversible loss of cell function  Begins 8 to 10 seconds after decreased blood flow  Aerobic to anaerobic metabolism  Glycogen decreases  Hydrogen ions, lactic acid increases (acidosis)  Loss of intracellular ions (K, Mg, Ca)  Release of catecholamines  Inflammatory cascade at injury  Angiotensin II released  Vasoconstriction/fluid retention  Growth factor for cardiac smooth muscle/fibroblast/myocyte = remodeling o Clinical manifestations  Biomarkers: Troponin I, CK-MB (increase in these biomarkers  ST segment elevation  Gender differences in symptom profiles  Chest pain, HTN, diaphoresis, N/V, paleness, cyanotic o STEMI vs. Non-STEMI o STEMI  ST segment elevation MI  Greater damage, change in ECG screen at this point (ST elevation)  Complete obstruction has probably occurred  Biomarkers are elevated

Transmural- infarction through the wall  Highest risk for heart failure and complication o Non-STEMI  Non ST segment elevation MI  Acute ischemia present based on symptoms and cardiac marker  No ST elevation on ECG, cardiac biomarkers are elevated, so acute changes are present  Complete obstruction has probably not occurred at this point o Concept of myocardial remodeling and how this impacts recovery treatment  Myocardial remodeling: myocyte hypertrophy, loss of contractile function (angiotensin II)  Begins within 24 hours, recovery 10-14 days after MI, scar tissue complete after 6 weeks  ACEI, Beta-Blockers, and aldosterone antagonists are able to inhibit or reverse remodeling ECG changes with: Ischemia, Injury, Infarction o Ischemia: T wave inversion, ST wave segment depression o Injury: ST segment elevation, increased biomarkers Troponin I and CK-MB o Infarction: deep Q waves after 24 hours Prophylaxis of CAD: therapy focus of lowering LDL LDL vs HDL cholesterol o Know appropriate ranges for each and for total cholesterol (see atherosclerosis) o Methods of control, including pharmacological 



 

Heart Wall Disorders  Define: o Acute Pericarditis: acute inflammation of pericardial membranes, fibrotic process - roughening  Symptoms: precipitating fever, sudden onset, severe retrosternal chest pain that worsens with breathing and laying down  Signs: fever, tachycardia, cardiac friction rub at apex and left sternal border, ECG changes o Pericardial Effusion: fluid in pericardial sac can occur with pericarditis  Exudate (inflammatory): acute pericarditis, autoimmune disorders, infection  Transudate (serous): heart failure, overhydration, hypoproteinemia  Classic Symptoms: dyspnea on exertion, dull chest pain  Signs: muffled heart sounds, X-ray water bottle o

Complications of heart wall disorders:  

Tamponade: pressure exerted by pericardial fluid that equals or exceeds diastolic pressure in the heart Symptoms: same as rheumatic heart failure



Interferes with atrial filling, increases venous pressure/congestion, decrease ventricular filling (decreased SV, decreased CO)

o

Relationship between Acute Rheumatic Fever and Rheumatic Heart

o

Acute Rheumatic Fever 

Delayed exaggerated, systemic inflammatory disease



Results from autoimmune response to group A beta-hemolytic strep (GABHS) pharyngitis (strep-throat)



Symptoms: 



Acute: fever, lymphadenopathy, polyarthritis- red swollen joints/large joint, chorea, rash on neck

Prevention: 

Antibiotics within 9 days of GABHS



Completion of antibiotics for GABHS

o

Disease and prevention strategies  Cause GABHS  Acute phase symptoms and progression  If ARF left untreated- carditis- scar heart valves resulting in rheumatic heart disease  RHD: S/S of Endocarditis/Myocarditis (Ashcoff bodies) Pericarditis  Endocarditis  Vegetation on valve  Scar tissue forms  > may take decades  Mitral and aortic stenosis  Mitral valve affected 50-60% of time  Myocarditis  Ashcoff bodies- fibrin deposits surrounded by necrosis  Pericarditis  Serofibrinous effusion

o

Infective Endocarditis 

Process of infection: 1. Endocardial damage; 2...3... 

Endocardial Damage:





Adherence of bloodborne microorganisms 





o

From systemic infection adhere via adhesions to damaged endocardium

Formation of endocardial vegetations 



Valve disease, turbulent blood flow = exposes endothelial basement membrane/collagen inflammation and thrombus formation

Bacteria infiltrate the thrombus and become embedded in the fibrin clots making them resistant to natural immune defenses

Risk factors and rationale for prophylactic antibiotic treatment 

Can occur whenever a valve is damaged



Infection from bacterium during invasive procedures (urinary, GI, dental)

S/S specific to embolization of vegetations 

Petechiae



Splinter hemorrhages



Osler nodes (painful)



Janeway lesions (not painful)

Differentiate cause and complications associated with:  Stenosis: valve narrowing, constriction, hard to open  Chamber before valve has increased work to move blood through narrow opening  Aortic Stenosis  Causes:  Rheumatic fever (most common)  Congenital malformation  Valve calcification – from damaged surface, inflammation, HTN in elderly   

results ■ narrowing of the orifice decreasedSV Systolic murmur

     

LVhypertrophy

Mitral Stenosis o causes rheumatic fever bacterial endocarditis congenital-least common ○ results

    

narrowing of orifice atrial hypertrophy increased pulmonary pressures PE, dyspnea, cough ■ decreased CO

 

Regurgitation: incompetent valve, does not close fully Increased workload of atria/ventricle, L heart valves most commonly affected

Heart Failure  Define: heart is unable to generate adequate cardiac output, causing inadequate tissue perfusion/increased diastolic filling pressures  Major risk factors: o o o 

Left Heart Failure (Systolic – HFrEF) o

Concepts of contractility, preload, afterload 

With causes/risk factors



As goals for treatment

o

Symptoms

o

Cycle of progression

Difference in symptoms of HFrEF and HFpEF Right Heart Failure o Causes and symptoms o Difference in symptoms of right vs. left heart failure o



Ejection Fraction – know values indicative of failure HFrEF and HFpEF

o

Typical medication regimen for patients with Heart Failure . What drug(s) you could expect to see used

Shock  

 

Define – General Types and their differentiating mechanisms o Hypovolemic: caused by insufficient fluid volume o Cardiogenic: heart failure o Neurogenic: caused by a neural alteration o Anaphylactic: caused by an immune response o Septic: caused by an infection Clinical Manifestation – general Multiple organ dysfunction:

Cardiac Pharmacology For All Drugs, Know:  Mechanism of Action – Classification  Effects – why it is used  Common and/or life threatening side effects  Specific teaching  Specific monitoring (labs, ADRs) Classes: 

Diuretics o

Loop 

Action:



Most effective diuretic



Blocks significant amount of NaCl reabsorption



Uses:





Conditions requiring significant fluid loss



Acute pulmonary edema with CHF



Edema of liver disease

Adverse effects 

Dehydration





Hypotension



Electrolyte imbalance



Ototoxicity

Drug: 

o

o

Thiazide 

Best at reducing BP, improving HTN



Major side effect – K+ loss resulting in hypokalemia resulting in fatal cardiac arrhythmias

K-sparing 

Lab values to be monitored -Potassium



Action:







Blocks actions of aldosterone in distal tubule and collecting duct



Causes excretion of Na and retention of K

Uses: 

HTN



Edema

Side effects: 



Lasix

Hyperkalemia

Lipid Lowering Agents o

Differentiate between statins and bile acid resin drugs

o

Statins

o



Atorvastatin – top selling drug in US



Adverse reactions: 

Well tolerated with much fewer side effects



Mild GI upset, constipation, cramps, nausea, dizziness, blurred vision, fatigue, insomnia



Hepatic injury: jaundice



Myopathy: muscle ache, injury, inflammation



Rhabdomyolysis- rare but serious can lead to AKI/renal failure

Bile Acid Sequestrants 

Drug: cholestyramine



Sequestrant 

Drugs bind with bile acids and increase their excretion



Are inert, insoluble to water



Pass through GI tract unabsorbed – very safe 







Main effect is reduction of cholesterol = increase in LDL receptors in the liver 

Lowers cholesterol



Can lower LDL 15 to 30%



Very small increase in HDL

Bile acids contain large amounts of cholesterol

Adrenergic Antagonists o

Effect: cholesterol is excreted in feces

Beta 1 – blockade

o

Beta 2 blockade

o

Alpha 1 Blockade 

Prazosin (Minipress)



Ace Inhibitors



ARBs o







Bradykinin

Calcium channel blockers (all are essentially vasodilators) o

Dihydropyridines are vascularly selective (Vasodilators)

o

Non-dihydropyridnes are non-selective – therefore, they affect both cardiac smooth muscle to slow the heart rate and vascular smooth muscle to cause vasodilation

Vasodilators – Nitrates o

Nitroglycerin: venous dilator decreases preload

o

Administration

Anticoagulants o Heparin  Administration  Required lab value monitoring  Have a thorough understanding of therapeutic range  Do NOT need to know exact values, but know which values need to be monitored  Antidote o Coumadin

 



Patient teaching Antidote

Thrombolytics (fibrinolytics) o Know major/life-threatening side effects



Adrenergic Agonists   



Mechanism of action Clinical uses Precautions (side effects & adverse reactions)

Digoxin   

What class of drug: Cardiac Glycoside, increases cardiac contractility Clinical manifestations of toxicity Dangers of toxicity: o Bradycardia o Arrhythmias o Vision changes o N/V anorexia o Hypokalemia...