Comprehensive Cardiovascular Nursing Study Guide: RAAS, Hypertension, Coronary Syndromes, and Heart Failure

Renin-Angiotensin-Aldosterone System (RAAS)

Step 1: The kidneys release renin.
Step 2: Converts Angiotensin 1 in the liver.
Step 3: Angiotensin 1 is converted to Angiotensin 2 in the lungs.
Step 4: Angiotensin 2 causes vasoconstriction and stimulates the secretion of aldosterone (alclusterone).
Step 5: Aldosterone causes $Na^+$ and $H_2O$ retention.
Step 6: Blood volume increases.
Step 7: Vascular resistance increases ( $\uparrow$ ).
Step 8: Hypertension develops.

Blood Pressure Categories and Diagnostic Workup

Blood Pressure Classification Criteria:
- Normal Blood Pressure: Systolic and diastolic values less than $120/80\,\text{mmHg}$ .
- Elevated Blood Pressure: Systolic pressure ranging from $120\text{--}129\,\text{mmHg}$ and diastolic pressure $< 80\,\text{mmHg}$ .
- Stage 1 Hypertension: Systolic pressure ranging from $130\text{--}139\,\text{mmHg}$ or diastolic pressure ranging from $80\text{--}89\,\text{mmHg}$ .
- Stage 2 Hypertension: Systolic pressure of $140\,\text{mmHg}$ or higher, or diastolic pressure of $90\,\text{mmHg}$ or higher.
Hypertension Diagnostic Evaluations:
- Routine Urinalysis (routine UA).
- Blood Urea Nitrogen (BUN).
- Serum Creatinine.
- Electrolyte assessment, specifically evaluating potassium levels ( $K^+$ levels).
- Blood glucose / blood sugar.
- Lipid profile.
- Electrocardiogram (ECG/EKG).
- Chest X-ray.

Cardiovascular Pharmacotherapy

Thiazide Diuretics:
- Mechanism of Action: Reduce preload.
- Hemodynamic Effects: Produce a decrease ( $\downarrow$ ) in total blood volume, renal blood flow, and cardiac output.
Loop Diuretics (Loup Diuretics):
- Mechanism of Action: Reduce preload through substantial volume depletion.
- Monitoring Parameters: Closely monitor blood pressure (BP) and potassium levels ( $K^+$ levels).
- Pharmacological Agents: Furosemide, bumetanide.
Beta-Blockers:
- Hemodynamic Effects: Produce a reduction ( $\downarrow$ ) in heart rate (HR) and blood pressure (BP).
- Nomenclature: Agents ending with the suffix "-lol" (LOL's).
- Clinical Consideration: Can mask signs of hypoglycemia.
Angiotensin-Converting Enzyme (ACE) Inhibitors:
- Mechanism of Action: Reduce afterload by inhibiting the conversion of Angiotensin 1 to Angiotensin 2.
- Nomenclature: Agents ending with the suffix "-pril" (pril's).
- Adverse Effects: Dry cough is the primary/main side effect.
Angiotensin Receptor Blockers (ARBs):
- Mechanism of Action: Reduce afterload by blocking the direct physiological effects of Angiotensin 2.
- Nomenclature: Agents ending with the suffix "-sartan" (Sartan's).
Nitrates:
- Mechanism of Action: Reduce preload by dilating blood vessels and lowering ( $\downarrow$ ) blood pressure.
- Pharmacological Agents: Nitroglycerin, isosorbide (iso Sorbicle).
- Specific Protocols and Nursing Considerations for Nitroglycerin:
- Storage: Keep in original container due to being light-sensitive.
- Dosing Protocol: Administer $3$ sublingual tablets spaced $5\,\text{mins}$ apart.
- Emergency Action: If chest pain is not relieved following administration, call EMS.
- Safety Precaution: Have the patient sit down during administration because the medication causes syncope.
- Side Effects: Flushing, hypotension, headache, and tachycardia.
Human B-Type Natriuretic Peptides:
- Mechanism of Action: Reduce afterload.

Cardiac Anatomy and Hemodynamic Circulation

Sequential Pathway of Blood Flow Through the Heart:
- 1. Superior vena cava.
- 2. Right atrium.
- 3. Tricuspid valve.
- 4. Right ventricle.
- 5. Pulmonary valve.
- 6. Pulmonary artery.
- 7. Lungs.
- 8. Pulmonary vein.
- 9. Left atrium.
- 1. Mitral valve.
- 1. Left ventricle.
- 1. Aortic valve (Cortic valve).
- 1. Aorta.
- 1. Out into systemic circulation/body.
Heart Valve Classifications:
- Atrioventricular (AV) Valves: Tricuspid valve, mitral valve.
- Semilunar Valves: Aortic valve (Cortic), pulmonic valve.

Auscultatory Heart Sounds

S1 ( $S_1$ ):
- Caused by the closure of the tricuspid and mitral valves.
- Best heard at the apical auscultation site.
S2 ( $S_2$ ):
- Caused by the closing of the pulmonic and aortic valves.
S3 ( $S_3$ ):
- An abnormal early diastolic sound occurring when the ventricle will not open properly.
S4 ( $S_4$ ):
- An abnormal late diastolic sound.

Angina Pectoris and Myocardial Infarction

Angina Presentations:
- Stable Angina: Pain that occurs intermittently over a prolonged period of time, exhibiting a consistent pattern of onset, duration, and intensity of symptoms; typically precipitated by prolonged exertion.
- Unstable Angina: Unpredictable chest pain caused by plaque that ruptures; occurs at rest; characterized by an increasing intensity and frequency of episodes.
- Prinsmental Angina (Prinzmetal / Vasospastic): Chest pain that occurs characteristically at night, associated with vasospasms and reversible changes on EKG.
Myocardial Infarction (MI) Classifications:
- ST-Elevated Myocardial Infarction (STEMI): Characterized by visible ST elevation on electrocardiography; causes significant transmural damage to the heart, killing all $3$ anatomical layers of the myocardium.
- Non-ST-Elevated Myocardial Infarction (NSTEMI): Presents with no ST elevation evidence on ECG; occurs from a partially occluded vessel; causes partial necrosis killing $1$ or $2$ layers of the myocardium.

Diagnostic Biomarkers and Laboratory Tests for Myocardial Infarction

Cardiac Enzymes:
- Myoglobin: Marker present in both cardiac and skeletal muscle tissue.
- Creatine Kinase-MB (CK-MB): Found primarily in the heart tissue; serves as an indicator of acute myocardial infarction.
- Troponin: The most cardiac-specific biomarker; found exclusively in heart tissue.
Adjunctive Laboratory Tests for MI:
- B-Type Natriuretic Peptide (BNP): Increases ( $\uparrow$ ) in the setting of myocardial infarction.
- Leukocytosis: Elevated white blood cell count visible within several hours of myocardial damage.
- C-Reactive Protein (CRP): Elevated inflammatory marker indicating the occurrence of multiple ischemic events.
- Erythrocyte Sedimentation Rate (ESR): Demonstrates an elevation ( $\uparrow$ ) within $3\,\text{days}$ post-infarction.

Heart Failure Pathophysiology, Clinical Manifestations, and Risk Factors

Left-Sided Heart Failure:
- Pathophysiological Flow: Fluid and pressure back up into the lungs.
- Clinical Signs and Symptoms: Dyspnea, orthopnea, cough, pulmonary crackles, pulmonary congestion, cyanosis, hemoptysis, and confusion.
- Etiological Risk Factors: Hypertension (HTN), coronary artery disease (CAD), history of angina, myocardial infarction (MI), cigarette smoking, and obesity.
Right-Sided Heart Failure:
- Pathophysiological Flow: Fluid and venous pressure back up into the systemic circulation/body.
- Clinical Signs and Symptoms: Peripheral edema, anorexia, unexpected weight gain, hepatomegaly, ascites, jugular venous distention (JVD), and generalized fatigue.
- Etiological Risk Factors: Preexisting left-sided heart failure (left sided HF), right ventricular myocardial infarction, chronic obstructive pulmonary disease (COPD), pulmonary hypertension (Pulmonary HTN), pulmonary embolism, coronary artery disease (CAD), heart valve disease, and cigarette smoking.

Diagnostic Evaluation for Heart Failure

Laboratory Biomarkers and Chemistries:
- Blood Urea Nitrogen (BUN).
- Comprehensive renal function panel.
- Urinalysis (U/A).
- Hemoglobin and Hematocrit (H&H).
- B-Type Natriuretic Peptide (BNP).
- Arterial Blood Gas (ABG).
- Liver Function Tests (LFT's).
- Cardiac Troponin.
Diagnostic Imaging and Invasive Testing:
- Chest X-ray.
- Echocardiogram (Echo).
- Electrocardiogram (EKG).
- Cardiac Catheterization (Cardiac cath).