final study guide

HEART

● Hypertension

○ Essential vs secondary hypertension

○ Hypertensive crisis is BP over 180/120. Emergency, treat with

anti-hypertensives

○ Increased vasoconstriction of arteries leads to increased cardiac workload

● Causes of hypertension:

○ Adrenergic nervous system

○ Baroreceptors

○ RAAS

● Anti-hypertensives:

○ Beta blockers (-alol)

■ Decrease HR and BP and myocardial oxygen demand

■ Used in HTN, MI, HF

■ Check HR and BP before giving. Hold for HR under 60 or SBP under

90-100mmHg

■ Non-selective vs selective

● Avoid non-selective in COPD/emphysema/asthma as they can

cause bronchoconstriction/bronchospasm

■ Caution in diabetes as they can mask tachycardia which can be a

symptom of hypoglycemia

■ Side effects: bradycardia, hypotension, depression, erectile dysfunction,

fatigue

○ Calcium channel blockers (-pines)

■ Decrease HR, contractility, vasodilators

■ Used in HTN, angina, dysrhythmias

■ Side effects: bradycardia, hypotension, constipation

○ ACE inhibitors (-prils)

■ Block RAAS to decrease BP and decrease heart afterload

■ Side effects: dry cough, hyperkalemia, angioedema (life threatening)

○ ARB (-sartans)

■ Similar to ACE inhibitors but can be used if they cause cough or

angioedema

● Chest pain

○ Stable vs unstable angina

■ Stable- chest pain with activity that stops with rest

■ Unstable- chest pain at rest or chest pain not relieved by rest. No

troponin elevation. Treatment similar to MI.

■ If there is troponin elevation, indicates damage to heart muscle

● Nitroglycerin

○ Vasodilator

○ Decreases preload

○ Decreases myocardial oxygen demand

○ Improves blood flow to the heart and relieves angina

○ Check BP before giving, hold if SBP under 90-100 mmHg

○ Side effects: headache, hypotension, dizziness, flushing

○ Can be given SL (acute chest pain), Transdermal patch

(prevention), IV (emergency). Not swallowed whole.

■ Heart failure- inability of heart to pump effectively to oxygenate body

● Digoxin

○ Increases contractility of heart muscle (positive inotrope)

○ Decreases heart rate

○ Improves cardiac output in heart failure and controls rate in

A fib

○ Before giving digoxin:

■ Check apical pulse for one minutes

● Hold if under 60 BPM

■ Monitor potassium- if low, greater chance of digoxin

toxicity (dig competes with K at the cellular level)

○ Digoxin toxicity symptoms

■ N/V

■ Decreased appetite

■ Fatigue

■ Bradycardia

■ Vision changes (yellow/green halos)

■ Dysrhythmias- can be fatal

■ Loop diuretics like Lasix can increase risk of toxicity

because they lower serum potassium

○ Monitor digoxin levels (0.5-2.0 ng/mL), K, mag, Ca

○ Antidote- digoxin immune Fab (Digibind)

○ Patient teaching: take pulse before taking dig, do not

double dose, report N/V or vision changes, irregular pulse.

Maintain consistent potassium intake.

● Loop diuretics (ex Lasix)

○ Heart unable to keep up with demand so fluid can back up

into lungs (pulmonary edema). Loop diuretics like lasix

can help kidneys clear excess fluid to decrease/eliminate

pulmonary edema.
SHOCK

Fundamental Hemodynamic Calculations

● Pulse Pressure (PP): SBP-DBP=PP (systolic blood pressure minus diastolic blood

pressure equals pulse pressure)

○ A narrowing pulse pressure (e.g., 90/70) is often an early sign of shock.

● Mean Arterial Pressure (MAP): The average pressure in a patient's arteries during one

cardiac cycle. It is considered a better indicator of perfusion to vital organs than systolic

BP. A MAP of 65 mmHg is typically the goal.

MAP = SBP+ (2 x DBP) / 3

■ Systolic blood pressure plus two times diastolic blood pressure divided by

three

● Stages of Shock

● Shock is a continuum, but can be classified as early, progressive and refractory

● In the Early Stage, body compensates

○ HR elevated

○ Baroreceptors sense decreased BP and cause vasoconstriction

○ SNS stimulated to increase cardiac output, increase vascular resistance to

increase BP

○ RAAS triggered

● In the Progressive Stage, compensatory mechanisms (like the RAAS and SNS) begin

to fail.

○ Hallmarks: MAP falls below 60 mmHg, mental status deteriorates

(lethargy/confusion), and multi-system organ dysfunction (MODS) begins.

○ Lungs: Often the first to fail; increased capillary permeability leads to interstitial

pulmonary edema, crackles, and tachypnea.

○ Kidneys: Acute Kidney Injury (AKI) develops as urine output drops below 30

mL/hr.

○ Increased HR, decreased BP, increased RR as body attempts to compensate

● In the Refractory Stage, compensation has failed

● Classification of Shock Types

● Hypovolemic Shock (Hemorrhagic)

○ Caused by a loss of intravascular fluid volume. Hemorrhagic shock is a subset

specifically involving blood or other fluid loss (trauma, GI bleed, excessive

nausea/vomiting/GI losses).

○ Pathophysiology: decreased preload, decreased stroke volume, decreased

cardiac output.

○ Key Finding: increased heart rate, decreased blood pressure, flat neck veins,

cool/clammy skin.

○ Treatment: stop the bleeding/fluid loss, replace with isotonic fluid or blood

products

● Cardiogenic Shock

○ The heart’s inability to pump blood effectively, most commonly following a

massive MI.

○ Pathophysiology: increased Preload (fluid backs up because the pump fails)

leads to decreased cardiac output and can lead to Interstitial Pulmonary Edema.

○ Clinical Presentation: Tachycardia, hypotension, and pulmonary congestion

(crackles).

○ Treatment: Medications: Inotropes (Dobutamine, Milrinone): Increase the heart's

ability to pump. Vasopressors (Norepinephrine, Dopamine): Increase blood

pressure to sustain organ perfusion. Antiplatelets/Anticoagulants (Aspirin,

Clopidogrel): Prevent further clotting.

● Distributive Shock (Septic & Anaphylactic)

○ The volume is there, but it is in the wrong place due to massive vasodilation.

○ Septic Shock: A subset of sepsis with profound circulatory and cellular

metabolism abnormalities.

■ Two Primary Pathophysiological Changes:

1. Profound Vasodilation: Massive drop in Systemic Vascular Resistance

(SVR).

2. Increased Capillary Permeability: Fluid leaks out of the vessels

(third-spacing).

Symptoms: increased HR, decreased BP, increased T

Treatment: fluid replacement, broad spectrum antibiotics, draw

cultures/labs/other tests to find source of infection

○ Anaphylactic Shock: An acute, life-threatening hypersensitivity (allergic)

reaction.

■ The Mechanism: An Antigen-Antibody Reaction triggers the release of

histamine, causing massive vasodilation and bronchospasm.

■ Symptoms: uritcaria, itching, difficulty breathing, angioedema

○ Obstructive Shock (PE, cardiac tamponade, tension pneumothorax)

■ Blocked flow of blood causes intravascular volume depletion

■ Impaired ventricle filling leads to decreased cardiac output

Pharmacological Management (Vasoactive Meds)

Vasoactive medications are used when fluid resuscitation is insufficient to maintain a MAP > 65

mmHg.

Medication

Norepinephrine

Dopamine

Primary Action

Strong alpha-1 agonist

(Vasoconstriction). Positive

inotrope

beta-1 (Inotropic) and alpha-1

(pressor) effects.

Clinical Use Case

First-line treatment for Septic Shock.

Increases SVR and BP.

Often used in bradycardia or when a

boost in contractility is needed with BP

support. Know effect of dopamine at

low, medium and high doses.

Dobutamine

Selective beta-1 agonist

(Inotrope).

Other meds to know in relation to shock:

●

●

Epinephrine

First-line for cardiogenic shock.

Increases heart contractility without

significantly increasing SVR.

Isotonic fluids (0.9%NS, LR) (best for maintaining BP)

●

●

Albumin (keeps fluid in vessels)

Lasix (for pulmonary edema)