PATH 370 WEEK 3 Chapters 16, 18, 19, and 20 Flashcards

Flashcards covering blood pressure mechanics, hypertension classifications, coronary heart disease, heart failure types, and various forms of shock.

Blood Pressure Equation

Calculated as Cardiac output $(\text{CO}) \times \text{Resistance (R)}$.

Systolic Blood Pressure

The onset of Korotkoff sounds, typically $120$; stroke volume (SV) is the primary factor influencing this value.

Stroke Volume

The amount of blood pumped per beat.

Diastolic Blood Pressure

The disappearance of Korotkoff sounds, typically $80$; systemic vascular resistance (SVR) is the major determinant.

End Diastolic Volume (EDV)

The amount of volume left in the ventricle after diastole; it is proportionate to stroke volume and equivalent to venous return or preload.

Pulse Pressure (PP)

The difference between systolic and diastolic pressure, typically a range of $40-80$: $\text{Systolic} - \text{Diastolic}$.

Mean Arterial Pressure (MAP)

The average pressure in the circulatory system throughout the cardiac cycle; calculated as $\text{Diastolic} + \frac{1}{3}\text{PP}$.

Preload

The amount of blood present in the ventricles before systole.

Systemic Vascular Resistance (SVR)

Also known as afterload; the pressure against which the heart must pump blood.

Cardiac Output (CO)

The amount of blood pumped per minute, typically $5-6 \text{ liters}$; calculated as $SV \times HR$.

Fluid Volume Increase/Decrease…

so does to preload, contractility, BP, and cardiac output.

If peripheral vasodilation increases…

peripheral vascular resistance, afterload, and BP will DECREASE.

Peripheral vasocontriction increases…

so does peripheral vascular resistance, afterload, and BP.

Short-term Regulation

Body’s immediate response→ Baroreceptors will detect the drop in BP and send signals to the medulla oblongata and hypothalamus to activate the SNS. SNS acts on A1 and B1 receptors.

α-receptors

Adrenergic receptors stimulated by the SNS that cause vasoconstriction, leading to increased resistance ($R$) and BP while decreasing blood flow.

β-receptors

Adrenergic receptors stimulated by the SNS that increase heart rate ($HR$), contractility, and stroke volume ($SV$).

RAAS System Pathway

$\text{Angiotensinogen} \rightarrow \text{ANG 1} \rightarrow \text{ACE} \rightarrow \text{ANG 2}$. ANG 2 causes vasoconstriction, aldosterone release, and sodium/water retention.

Primary Hypertension

Essential or idiopathic hypertension making up 95% of all cases; known as the Silent Killer because damage to organs occurs before diagnosis.

Secondary Hypertension

Hypertension resulting from a specific cause (e.g., renal disease), making up 5% of cases; the most common form in children.

Normal Blood Pressure

Categorized by a reading of $120/80$.

Prehypertension

Categorized by a range of $120-139 / 80-89$.

Stage 1 Hypertension

Categorized by a range of $140-159 / 90-99$.

Stage 2 Hypertension

Categorized by a reading of $160+ / 100+$.

Isolated Systolic Hypertension

Defined by a systolic reading of $140+$.

Isolated Diastolic Hypertension

Defined by a diastolic reading of $90+$.

End Organ Damage of Hypertension

Includes renal failure (nephrosclerosis), stroke (high BP can cause thin brain blood vessels to pop), heart disease (plaque buildup), atherosclerosis acceleration, and retina microcirculation bleeding.

Modifiable Risk Factors

Includes dietary factors, sedentary lifestyle, obesity, elevated blood glucose, elevated cholesterol, alcohol, and smoking; lifestyle modifications are the most important intervention.

Treatment for Hypertension:

lifestyle modifications (weight loss, exercise, diet change, decreased sodium intake); Drug Therapy (reduces stroke volume, reduces systemic vascular resistance, decreases heart rate).

ACE Inhibitors

Medications that reduce systemic vascular resistance and stroke volume (less vasocontriction in the aorta); they help protect kidneys, especially in diabetic patients, by preventing the conversion of ANG 1 to ANG 2.

Hypertensive Emergencies

sudden increase in either or both systolic or diastolic blood pressure, WITH evidence of end-organ damage. INJECTION/MEDICATION FOR BOTH REGARDLESS OF END-ORGAN DAMAGE

Hypertensive Urgencies

sudden increase in either or both systolic or diastolic blood pressure without evidence of end-organ damage. INJECTION/MEDICATION FOR BOTH REGARDLESS OF END-ORGAN DAMAGE

Orthostatic Hypotension

An extreme response to shifting from supine to upright; characterized by a decrease in systolic BP and an increase in HR by $20-30 \text{ beats/min}$. This happens because it takes longer for blood to travel upwards to brain once u stand up.

S/S of Orthostatic Hypotension:

dizziness, blurred vision, confusion, and possible syncope (temporary loss of consciousness). Associated with cardiovascular disease and is a risk factor for stroke, cognitive impairment, and death.

Importance of Sodium in Hypertension:

When there is more sodium in the blood, the kidneys retain more water to combat that, but increased fluid will increase blood volume, causing high blood pressure. Long-term excessive sodium can cause the blood vessels to stiffen and constrict; treatment for hypertensionr-> reduce sodium intake.

Coronary Heart Disease (CHD)

Also known as Ischemic Heart Disease or Coronary Artery Disease (CAD); insufficient oxygen delivery due to atherosclerotic coronary arteries.

Etiology of CHD:

atherosclerosis -> endothelial cell dysfunction -> thrombus formation

Factors in meeting cellular demands for oxygen:

Rate of coronary perfusion and myocardial workload; O2 Supply — Workload (O2 Demand)

Long-term (Sequelae) of CHD:

Angina pectoria (3 types), MI, dysrhythmias, heart failure, and sudden cardiac death.

Stable Plaque

Plaque containing more collagen and fibrin with a stable cap; unlikely to rupture.

Vulnerable Plaque

Plaque with a large lipid core and a thin cap; has a high possibility of rupture.

Stable (Classic) Angina + path of Angina

(Chronic Occlusion) Predictable angina pain due to similar stimuli each time– relieved by rest and nitroglycerin.

When your body wants more oxygen, it'll tell your heart to start pumping more blood (more workload bc increase O2 demand), but O2 supply does not change because of plaque, and heart becomes overworked and sends chest pain.

Angina Pectoris

Chest pain associated with intermittent myocardial ischemia, described as burning, crushing, squeezing, or referred pain.

Unstable (Crescendo) Angina

Unpredictable anginal pain that is not relieved by rest or nitroglycerin; requires admission to telemetry as it may lead to MI (total occlusion).

Prinzmetal (Variant) Angina

Unpredictable chest pain unrelated to physical or emotional exertion; caused by vasospasms in smooth muscles of arteries.

ECG

measures the heart's electrical activity in waves. There should be a P, QRS, and T wave with spaces in between.

ST Elevation:

Shown on an ECG, blood test (bio markers) to confirm STEMI diagnosis–treat with acute thromboytic therapy

NO ST Elevation

Blood test; Negative biomarkers mean unstable angina; positive biomarkers mean NSTEMI diagnosis– treat with antiplatelet drugs

Acute Coronary Syndrome (ACS)

Condition where myocardial infarction causes decreased cardiac output, triggering a detrimental SNS response that increases HR and workload; treated with immediate Beta blockers.

SNS Response to MI

detrimental to myocardial tissue in ACS because SNS is making the heart increase HR, BP, and contractibilty but part of the heart muscle is dead. Treatment is immediate Beta blockers to stop SNS response.

MONA Therapy

The clinical mnemonic for treating MI: Morphine (pain), Oxygen (ischemia), Nitroglycerin (vasodilation), and Anticoagulants (platelet thinning).

Coronary Artery Bypass Grafting (CABG):

surgical procedure used to restore blood flow in cases of severe CAD; bypass occlusion; it looks like a bridge detour going around the occlusion

LDL Role in CAD

Low-density lipoproteins enter the intima and oxidize; macrophages ingest them to become foam cells, forming atherosclerotic plaque. Increased foam cells = atherosclerotic plaque, which can narrow the artery, reducing blood flow -> CAD.

Heart Failure (HF)

The inability of the heart to maintain sufficient cardiac output to meet the metabolic demands of tissues.

Left-sided Heart Failure

congestion of blood flow in the pulmonary venous circulation; results in blood clot or edema; causes fluid to build up (pulmonary edema), shortness of breath

Forward LHF effect:

Systemic hypoxia/ischemia & SNS activation; Fatigue, oliguria, anxiety

Left-sided Heart Failure (LHF) Backward Effects

Results in pulmonary edema, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, respiratory crackles (rales), and S3 sound.

Right-sided Heart Failure:

congestion of blood in the systemic (cor pulmonale)

Forward RHF

low oxygen/hypoxia/ ischemia

Right-sided Heart Failure (RHF) Backward Effects

Causes congestion in the systemic system (peripheral edema), jugular vein distention (JVD), hepatomegaly, and splenomegaly.

Bi-ventricular Heart Failure:

combine LHF + RHF

Baroreceptor Response:

senses change, signals brain to activate SNS to increase heart rate and contractility

RAAS Activation/Decreased GFR:

kidneys increase fluid retention to increase preload

Increase ventricular wall tension:

causes myocyte growth leading to hypertrophy of the heart muscle

Diuretics:

reduce preload; makes the kidneys retain less sodium and water = peeing; helps decrease total blood volume which decreases preload

Beta-blockers

inhibit SNS effects/reduce afterload

Digitalis

A heart failure drug used to improve cardiac output and contractility.

Paroxysmal Nocturnal Dyspnea

Difficulty breathing while sleeping; the patient cannot sleep without multiple pillows under their head.

Shock

An imbalance between cellular oxygen supply and requirements due to extremely low cardiac output (hypoperfusion- no oxygen to tissue).

Etiology of Shock

valvular, myocarditis, trauma, inflammation/infection, ischemia

Cardiogenic Shock Define + Management

Shock caused by inadequate cardiac output due to decreased contractility ($MI$ or severe $HF$). PCI, Inotopes (Dobutamine, dopamine), vasodilators (NGT), IABP, Impella, ECMO, VAD

Cardiogenic Shock Pathogenesis:

decreased contractility, which causes decreased stroke volume and cardiac output, which decreases BP, causing decreased perfusion pressure, hypoperfusion, and ischemia.

Hypovolemic/Hemorrhagic Shock Define + Management

Shock resulting from loss of blood volume due to hemorrhage, severe diarrhea, or vomiting; Control bleeding, IV Isotonic crystalloids (Normal Saline/Lactated Ringer’s), blood transfusion if hemorrhage.

Classification of Hemorrhagic Shock

Class I (initial stage), Class II (Compensated Stage), Class III (Progressive stage), Class IV (Refractory Stage).

Class I Hemorrhagic Shock

An initial stage of hemorrhagic shock characterized by a blood loss of up to 15% (approximately 750 mL) of total blood volume, with minimal tachycardia and normal/increased pulse pressure.

Class II Hemorrhagic Shock

Compensated Stage; blood loss between 15% and 30% (750-1500 mL), resulting in tachycardia, tachypnea, decreased pulse pressure, cool/clammy skin, delayed capillary refill, and possible anxiety.

Class III Hemorrhagic Shock

The progressive stage of hemorrhagic shock, characterized by blood loss between 30% and 40% (1500-2000 mL), leading to tachycardia, hypotension (decreased systolic), altered mental status, oliguria, and marked changes in skin perfusion.

Class IV Hemorrhagic Shock

The refractory stage of hemorrhagic shock, defined by blood loss greater than 40% (more than 2000 mL), resulting in profound hypotension, tachycardia, altered mental status, anuria, loss of consciousness, narrowed pulse pressure, and very poor skin perfusion.

Hypovolumic Shock Pathogenesis:

decreased blood volume will decrease preload and cardiac output, which will decrease BP and perfusion pressure, leading to hypoperfusion and ischemia

Distributive Shock:

greatly expanded vascular space; not distributing blood enough (inappropriate vasodilation)

Distributive Shock Pathogenesis:

the vasodilation causes a decrease in central blood volume, which decreases preload, cardiac output, and BP, leading to perfusion pressure, hypoperfusion, and ischemia.

Different Types of Distributive Shock:

Anaphylactic, Neurogenic, and Septic

Anaphylactic Shock Define + Management

A type of distributive shock involving Type 1 Hypersensitivity where histamine causes systemic vasodilation and bronchoconstriction. Mast cells -> histamine -> hypotension; treated with epinephrine (first-line), airway support, oxygen, IV fluids, bronchodilators, antihistamines, and corticosteroids.

Neurogenic Shock Define + Management

A type of distributive shock involving the loss of sympathetic activation of smooth muscle, leading to vasodilation, decreased HR, and decreased contractility. IV Fluids, vasopressors, compression stockings, and gradual position changes.

Septic Shock Define + Management

Severe systemic inflammatory response to infection, where endotoxins cause increased permeability and damage to the endothelium. Infection (histamine/endotoxin) can travel into the bloodstream, causing vasodilation and increased permeability. They can damage the endothelium, causing protein to be outside the cell, pulling water outside the blood vessel into the tissue. CO will be high at first, then go low. Broad-spectrum antibiotics ASAP, IV fluids, vasopressors, inotropes if needed

Obstructive Shock Define + Management

Shock resulting from a circulatory blockage such as a large pulmonary embolus, tension pneumothorax, or cardiac tamponade. PE→ thrombolytics/embolectomy; cardiac tamponade →pericardiocentesis; tension pneumothorax→ needle decompression/chest tube.

Shock Clinical Manifestations

Includes hypotension ($SBP < 90$), decreased urine output, cool/clammy skin, and release of aldosterone and cortisol.

Acute Respiratory Distress Syndrome (ARDS)

A complication of shock involving development of refractory hypoxemia and pulmonary edema.

Disseminated Intravascular Coagulation (DIC)

A shock complication involving widespread clot formation followed by depletion of platelets and clotting factors, leading to bleeding.

Acute Renal Failure:

Kidneys undergo long periods of hypoperfusion → Acute tubular necrosis (ATN)

Multiple Organ Dysfunction Syndrome (MODS)

A state where immune mechanisms initiate destructive failure of multiple organs after shock.