Coronary Artery Disease (CAD) Exam

Normal Regulation of Blood Pressure (BP)

• Systolic BP (SBP) should be less than 120mmHg.
• Diastolic BP (DBP) should be less than 80 mmHg.
• Blood pressure is the force exerted by the blood against the walls of the blood vessel.
• Maintaining BP requires adequate tissue perfusion during activity and rest.
• It also requires the integration of both systemic factors and local peripheral vascular effects.
• Arterial BP is calculated as Cardiac Output (CO) multiplied by Systemic Vascular Resistance (SVR): Arterial BP = Cardiac Output (CO) x Systemic Vascular Resistance (SVR)
• Mechanisms regulating BP can affect CO, SVR, or both.
• The complex process involves nervous, cardiovascular, renal, and endocrine functions.
• BP is regulated by short-term (seconds-hours) and long-term (days-weeks) mechanisms.

Factors Influencing Blood Pressure

• Cardiac factors: Heart rate, contractility, and conductivity.
• Sympathetic nervous system: a₁- and 2-Adrenergic receptors (vasoconstriction) and B2-Adrenergic receptors (vasodilation).
• Local Regulation: Vasodilators(Prostaglandins and Nitric oxide) and Vasoconstrictors(Endothelin).
• Renal fluid volume control: Renin-angiotensin-aldosterone system and Natriuretic peptides.
• Neurohormonal factors: Vasoconstrictors(Angiotensin and Norepinephrine).

Cardiac Output (CO)

• Cardiac Output is the amount of blood pumped by the ventricle in one minute.
• Reflects the mechanical ability of the heart.
• Cardiac Output (CO) = Stroke Volume (SV) x Heart Rate (HR)/min
• Factors that affect HR or SV.
• Preload is the volume of blood in ventricles at end diastole, before the next contraction.
• The volume of blood in ventricles at end diastole, before next contraction
• Contractility is the more fibers stretched (i.e., greater preload), greater force of contractility.
• Afterload is the peripheral resistance against which the left ventricle must pump.
• Atrial Kick occurs during the final phase of atrial systole, when the atria contract and eject a bolus of blood into the ventricles.
• Cardiac Reserve is the heart's ability to respond to demands by increasing cardiac output.

Systemic Vascular Resistance (SVR)

• Systemic Vascular Resistance (SVR): the force opposing the movement of blood within vessels.
• Determined principally by the radius of small arteries and arterioles.
• A small change in radius creates a major change in SVR.
• If SVR increases and CO remains constant or increases, arterial BP will increase.

Hypertension (HTN)

• Hypertension is the sustained elevation of systemic arterial blood pressure (BP)
• One of the most important modifiable risk factors of cardiovascular disease and mortality in Canada
• Increased BP increases the risk for myocardial infarction (MI), heart failure (HF), stroke, renal disease, and death
• WHO identifies HTN as a "silent killer”.
• Increased awareness and early detection crucial.
• Measure BP in all adult patients during their visits, to determine cardiovascular risk and monitor antihypertensive treatment.
• Systolic BP(SBP) greater than or equal to 140 mmHg is classified as Hypertension
• Diastolic BP(DBP) greater than or equal to 90 mmHg is classified as Hypertension.
• Stage 1 Hypertension: SBP: 140-159mmHg or DBP: 90-99 mmHg
• Stage 2 Hypertension: SBP:Greater than or equal to 160mmHg or DBP: greater than or equal to 100 mmHg
• Target for those with HTN and DM: SBP less than or equal to 130 mmHg.
• Target for those with HTN and DM: DBP less than or equal to 80 mmHg.

Primary (Essential) Hypertension

• Primary hypertension accounts for the majority of HTN cases.
• The exact cause is not identified due to the complex interaction of genes and the environment.
• Potential Factors are; increased SNS activity, increased sodium intake, overproduction of sodium retaining hormones and vasoconstrictors, increased body weight, DM, excess alcohol intake

Secondary Hypertension

• Affects 5-10% of adults with HTN and over 80% of children with HTN.
• A specific cause is identified and corrected.
• Clinical findings include unprovoked hypokalemia, abdominal bruit, variable pressures with a history of tachycardia, sweating, tremor, and a family history of renal disease.
• Potential causes include congenital conditions of the aorta, renal diseases, endocrine disorders, neurological disorders, sleep apnea, medications, and pregnancy.
• Treatment involves eliminating the underlying cause.

Primary Hypertension: Pathophysiology

• Genes: Familial heritability is a significant factor, likely arising from multiple genes.
• Excessive dietary intake of sodium is strongly linked to HTN; when sodium intake is restricted, BP often falls
• High plasma renin activity = increased conversion of angiotensinogen to angiotension 1 = direct arteriolar constriction promotes vascular hypertrophy and increases aldosterone secretion.
• Physiological responses to stress are normally protective, but ongoing results in prolonged increases in SNS activity will negatively effect.
• Insulin resistance is associated with endothelial dysfunction; hyperinsulinemia simulates SNS and RAAS activity. It also impairs nitric oxide-mediated vasodilation.
• Pressor effects of insulin include vascular hypertrophy and increased renal sodium reabsorption
• Vascular endothelial cells are the source of multiple vasoactive substances. Some people with HTN have reduced vasodilator responses to nitric oxide where ET is pronounced and prolonged vasoconstriction.
• Obesity is complex, and has an unclear relationship. Likely linked to hormone abnormalities.

Hypertension: Clinical Manifestations

• Frequently asymptomatic until severe and target-organ diseases occur.
• Symptoms of severe hypertension are related to effect on blood vessels in various organs/tissues or to increased workload of the heart.
• Fatigue
• Reduced activity tolerance
• Dizziness.
• Palpitations
• Angina
• Dyspnea
• Extremely high BP can cause headaches, nosebleeds, and dizziness.

Diagnostic Studies

• Diagnosis is not based on a single elevated reading; requires several elevated readings over several weeks.
• History and physical examination must be performed.
• Routine laboratory tests: -Urinalysis and urinary albumin excretion if patients also have diabetes. -Blood chemistry (potassium, sodium, creatinine, blood urea, nitrogen). -Fasting blood glucose. -Fasting total cholesterol and high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglycerides.
• Standard 12-lead electrocardiography should be performed.

Hypertension: Interprofessional Care

• Monitor BP at Home
• Ambulatory BP monitoring: Fully automated system, measures BP at preset intervals over 24-hour period. Do every 3-6 months once BP is stabilized.
• Nutritional therapy
• Restricted sodium intake (reduce to 2000mg per day).
• Restricted intake of cholesterol and saturated fats.
• Adequate intake of potassium, calcium, and magnesium.
• Weight management and regular, moderate physical activity.
• Tobacco cessation and moderation in alcohol consumption.
• Antihypertensive medications.
• Patient and caregiver teaching.

Hypertension: Antihypertensive Medication Therapy

• Medication therapy is recommended for all patients at low risk with stage 1 HTN (140-159/90-99mmHg)
• The general goal is BP less than 140/90mmHg
• Patients with chronic kidney disease or diabetes can be treated with a BP of less than 130/80mmHg
• Medications have two actions reduction of SVR and decrease the volume of circulating blood
• Full effects of antihypertensive medication may not be apparent for up to 6 weeks.
• If BP is not controlled, increase dosage off first-line medication, and/or substitute or add second medication from different class.
• Many patients require at least two medications plus lifestyle changes.
• Types of medications to treat HTN: -Diuretics, Adrenergic(sympathetic inhibitors), Direct vasodilators, Angiotensin inhibitors and Calcium channel blockers.

Primary Hypertension: Nursing Management

• Achieve and maintain individually determined target BP
• Understand, accept, and implement therapeutic plan
• Experience minimal to no unpleasant adverse effects of therapy
• Be confident about the ability to manage and cope with the condition
• Thorough assessment and health history is needed.
• Health promotion: -Primary prevention: public awareness, decrease risk factors, screening Initial assessment of BP for potential hypertension -Initial: Take 2-3 times, at least 2 minutes apart, and record average for visit -Ensure the size and placement of the BP cuff are correct -Measure both arms to detect differences between arms -Patient should be supine or sitting during the test and for at least 5 minutes of rest before the test

Hypertension: Patient and Family Teaching

• Sedentary lifestyle, diet, abdominal obesity, Diabetes Mellitus, smoking, dyslipidemia, stress, and adherence to treatment plans are all modifiable risks
• Prescription and over-the-counter prescriptions must be discussed with a doctor.
• Identify and minimize adverse effects, especially regarding potential sexual dysfunction, dry mouth, and the frequent voiding of diuretics.
• Lifestyle modifications include diet changes, limiting alcohol, regular physical activity, avoiding tobacco, and managing stress.
• Follow-up monitoring should be done every 3-6 months once stabilized.
• Hypertension cannot be cured but can be controlled and managed.
• When cooking, reading labels for hidden sources of sodium like baking soda-containing toothpaste.

Challenges with adhering to prescribed treatment plans for hypertension

• Long-term management of HTN is challenging.
• Many patients find it difficult to follow regimens because of inadequate patient teaching, unpleasant adverse effects of medications, a return of BP to normal range while on medication, lack of motivation or readiness to change, the high cost of medications, and a lack of trusting relationships with healthcare providers.
• Individual assessment is needed to determine why a patient is not willing/able to follow the treatment plan.
• Create plans individualized for the patients involving their input and are compatible with personality, habits, lifestyle, culture, and context.

Hypertension: Complications

• Most common disorders are Target-organ diseases.
• These mainly impact; the heart(hypertensive heart disease), the brain(cerebrovascular disease), Peripheral vasculature(peripheral arterial disease), kidneys (nephrosclerosis) and eyes(retinal damage).

Hypertensive Crisis

• This is shown as sudden, abrupt elevation in BP, over 120-130 mmHg.
• The *Rate of rise is more important than absolute value in determining the need for emergency treatment.
• Prompt recognition and management is essential.
• Most common in patients with a history of HTN who failed to adhere to a medication regimen or were un-medicated.
• The high BP is thought to trigger endothelial damage and the release of vasoconstrictor substances resulting in a vicious cycle of BP elevation
• Life-threatening damage to target organs (heart, brain, kidneys). Stroke, MI, encephalopathy, or illicit drug such as drug-induced seizures.
• Classified by the degree of organ damage and the rapidity with which BP must be lowered.
• Hypertensive emergencies include hypertensive encephalopathy, intracranial or subarachnoid hemorrhage Acute, acute left ventricular failure with pulmonary edema, myocardial infarct, renal failure and dissecting aorta aneurysms.

Hypertensive Crisis: Clinical Manifestations

• Sudden rise in BP headache, nausea, vomiting, seizures, confusion, stupor, coma, blurred vision, and transient blindness. Often shown with hypertensive encephalopathy.
• Range from minor impairment to complete renal shutdown. Commonly renal insufficiency.
• Rapid cardiac decompensation from unstable angina to infarction and pulmonary edema associated with chest pain and dyspnea.
• Aortic dissection occurs with excruciating chest and back pain, diaphoresis, and a loss of pulse in the extremity.
• Often a similar presentation to stroke, without focal or lateralizing.

Hypertensive Crisis: Nursing and Interprofessional Management

• BP alone is not a major factor in deciding treatment Association between elevated BP and signs of new/progressive end organ determines seriousness of hypertension crisis.
• Requires hospitalization, Parenteral administration of antihypertensive medications, oral agents may be administered in addition and critical care monitoting.
• The initial treatment goal is to decrease mean arterial pressure (MAP) 10-20% in first 1-2 hours. A gradual reduction is further reduced over the next 24 hours.
• Lowering bp to quickly or far, can decrease cerebral perfusion and percipitate stroke.
• A patient with severe elevation of BP but no target-organ damage may not require emergent therapy or hospitalization. Sitting for 20-30 minutes, quiet environment, institute/adjust ora medications and encourage verbalzining fears, eliminates excess noise.
• Once a hypertensive crisis is resolved it is important to determine the cause in order to avoid future.

Atherosclerosis

• A medical condition categorized as the major cause of coronary artery disease
• A progressive condition developed over many years
• Characterized by the deposits of lipids within the intuma of artery
• By the time of symptoms its advanced -Fatty Steaks
  • Fibrous Plaque -Complicated Lesion
• Risk Factors: -non-modifiable: age, sex, ethnicity -modifiable: elevated serum levels, hypertension, tobaccos, activity and obesity -Modifiable: diabetes mellitus, metabolic syndrome, homocysteine, substance us

Atherosclerosis: Etiology and Pathophysiology

• The endothelium is a inner lining of the wall. It is normally nonreactive to platelets, leukocytes, coagulation, fibrinolytic, and compliment factors.
• Can be injured by tobacco use, hyperlipidemia, HTN, toxins, diabetes, hyperholysteinemia, or infection
• Injury causes local inflammoation response ti occur
• High C-reactive protein or CRP is typically produced by the liver and a marker for non-specified inflammation. High CRP means they are increased.

Coronary Artery Disease (CAD)

• Also known as arteriosclerotic heart disease (ASHD),cardiovascular heart disease (CVHD);ischemic heart disease (IHD);coronary heart disease.
• A common heart condition, Involves atherosclerotic plaque formation in the vessel and leads to imparared oxygen and blood flow.
• Blood vessels in the disorder is Atherosclerosis. This is known as the greek word Ather (fatty mush and skleros (hard).
• Can be asymptomatic or stable angina. In most cases be the time the symptoms shows its advance.
• More sersious manifestations is ACS also known as acute coronary syndrome.

Coronary Artery Disease: Etiology

• Mechanisms: -shear stress response to injury hypothesis of atherogenesis - results in dysfuntion, causes impairment in synthesis and the realease of potent vasodilators -nitric oxide decreaeses and atherosclerosis plaque formation. -intimal layer exposed to the high pressure.
• artenolar changes may be account.

Coronary Artery Disease: Risk Factors

• -Modifiable: serum lipids, blood pressure, tobacco use, physical inactivity, obesity, elevated fasting blood and autoimmune disorders.
• Non modifiable: increasing age, men, ethnicity

Dyslipidemia Screening

• Men over 40 and women over 50 should undergo lipids every 3-5 years.
• Screen earlier high risk ethnic groups. Those in South east Asia.
• Screen earlier when previous pregnancy and induced. -The first test it a non fasting blood sample for lipid. -If trriglyceries are low you shoudl fasting the lipids after

CAD- Collaborative Management:

• Collaborative management invoves nutricional therapy. Decreasing fat intakes and increase complex cardio intakes.
• Diet would include DASH, medi, portfolios
• Goals with medication re to restrict lipoprotien production
• Must monitor for any signs or problems.

CAD: Promtoion

• Prevent or modify slower by progression
• Help indentidy at risk peoples
• risk screening - health, family, syptoms, pschosocial factors, employment and attitidues

CAD patient and family teaching

• Pt. should report BP over 140 and is very important
• Maintain ordered medication
• Eat heart healthy. Mediterrean.
• Do exercise and maintain heathy weight
• Stress reduction or sleep
• Manage condions and follow up with medication
• Diet and lifestyle modification.

Chronic Stable Angina:

• CAD is progressive -Some indviduals never shows syptomn s
• Angina: manifestations of reverisble mycaridal ischaemia. Mycaridal ischaemia can be increased daman or decreased.
• pain or tightness and the anigina will relieve that pain and uncomfrotable

Assesment of the angina

• Factors to look for quality of pain -preciptating event Radiations to the chest with the scale of severity.

###Chronic Stable Angina: Interprofessional Management and Nursing Interventions

• Meds are Nitrates which dilates Blood vessels
• Symtpoms are not changing. repeat does in 5 mins and do not use a mix of nitrates. Table 36.11 shows Angina or varient Angina

Acute Coronary syndrome

• A more sersious condition of coronary artery disease - unstable angina or ishemic
• ACS - goup of diseases that decrease BP. Diagnosie and related pathophyisiology.

Manifestation

• New onset with stable angina increase frequency
• Pt seek or support due to woman showing symtoms SOB, fatifue and anxiety.
• Primary use to check if ACS.

Cardiac markers

• Enzyymes after the MI. Can identify damage to extent to damage from myoglobin to find the right way to treatment.

###ACS

• Goal is to reduce pain. Most often found in ER.
• Early medication with ECG changes. Openn affected area if the cathter can do

Myocardial Infarction

• Sustatined isheca causing imnoblizing or revervible. Halts distsl ouccluison
• Infatction takes 5 to 6 hours to happen
• severe ches t pain and heaveiness.

ACS Manifestation.

• Chest pain is brand new and shows ACS.
• Patients for UA do and they will start treatment

Chronic and Ancute Syndrom.

Diagnostics studies.

• Detailed health histroy -Physical exam and chest rays
• Cardiac enzymes (CK-MB + Troponin. T wave

Chronic and Ancute: Management

• Maintain bed reast and comfort
• O2 suplementary
• Prompt pain care and vitals

Chronic Stabe, teaching

• Pt start to look at their needs for self goals
• Phyiscal actiity and counseling of self with the website,

Acs and death.

• Abrupt distruption in cardiac function. Most likely arrythmias
• Pt have lethal ventriucalr and require holter montior.

###Emeegency mangemtn

Etiolation = heart damage Assessment: pain, breathing and wheezing Interventison: VItals, o2 and obtaining labs

• Monitor LOC
• Prepare for CPR

Hyperthoophy

Increase the preload and doubles the obesitys It will decrease and lead to heart failure

Heart failure

Symptoims are fatigue tachy

Med mgt

Lodeing and reatment to help mobilize and balance it.

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