Cardiovascular System Notes

Yellow: arrhythmias + hypertension Red: heart failure + intro to CV Purple: arteriosclerosis Blue: valvular diseases Green: vascular diseases

What characterizes Normal Sinus Rhythm (NSR) in terms of heart rate, rhythm, and intervals?

• 60-100 bpm

• Normal rate, rhythm & intervals

How is Sinus Tachycardia defined?

• 100-160 bpm

• No other ECG abnormalities

• Regular distance between RR

• All p waves present

What are some common causes of sinus tach?

• Exercise

• Anxiety

• Caffeine & nicotine

• Fever & shock

• CHF & HTN

• Pain

Define Sinus Bradycardia, and under what circumstances is it typically not concerning?

• < 60 bpm

• No other ECG abnormalities

• Not typically concerning if you can pinpoint a cause & also asymptomatic

What are some causes of sinus brady?

• SA node dysfunction

• Athletes

• Vasovagal response

• Hypothermia

• Inferior MI

• Meds (digoxin, BBs)

What is the general heart rate range for Supraventricular Tachycardias (SVTs), and where do these beats originate?

• 160-250 bpm

• Beats originate from above the ventricles

• Most SVTs have a p wave

What are some treatments for SVT?

• vasovagal maneuvers

• rate-lowerings meds

• cardioversion

• ablations

What are the types of SVTs?

• Paroxysmal

• Wolff-parkinson-white

• AV nodal reentrant

• Atrial tachycardia

• Atrial fibrillation

• Atrial flutter

What is Atrial Flutter, and how does it affect atrial and ventricular rates?

• Atrial rate: 250-400 bpm

• Ventricular rate: 70-150 bpm

• P waves have saw tooth pattern

• Can lead to a-fib or alternate between the 2

What are some causes of atrial flutter?

• Ischemic ♥ disease/MI

• Meds (digoxin)

• Valvular disease

• Stress & hyperthyroidism

• Pulmonary embolism

Describe atrial fibrillation

• Atrial rate: 350-600 bpm

• Ventricular rate: variable but can be “rate controlled”

• If < 100 = controlled a-fib

• If > 100 = uncontrolled a-fib

• Wavy & fibrillating p waves

What are some causes of a-fib?

• Ischemic ♥ disease/MI

• CHF

• Valvular disease

• Meds (digoxin)

What defines a 1st-degree heart block?

• PR interval > 0.20s & p waves can get buried in preceding T wave

• Not typically serious but can progress to more dangerous ♥ blocks

What are the causes of 1st degree heart block?

• Increasing age

• Hyperthyroidism

• Electrolyte abnormalities

• Damage to ♥ tissue

• Extreme athletes

• Genetics

Explain the characteristics of 2nd-degree heart block Type I (Mobitz I or Wenckebach).

• Irregular rhythm

• PR interval gets longer & longer, eventually QRS complex is dropped

• QRS gets bigger & bigger, then is gone

What are some causes of 2nd degree heart block?

• Ischemia

• Myocarditis

• Medications

Explain the characteristics of 2nd-degree heart block Type II (Mobitz II).

• Irregular rhythm

• Intermittent losses of the QRS complex

• Single, double, triple dropping of QRS

What distinguishes 2nd-degree heart block Type II (Mobitz II) from Type I?

• In type I QRS eventually gets dropped

• In type II QRS is intermittently lost

Describe 3rd-degree heart block (complete heart block).

• Atria & ventricles are completely dissociated from each other

• Independent p wave & QRS complex activity

• Regular PP & RR intervals

What are some causes of 3rd degree heart block?

• Ischemia

• Meds

• Nodal ablation

• Electrolyte imbalance

• Post op

• Lyme disease

What are Premature Ventricular Contractions (PVCs), and why is the number of consecutive PVCs important?

• Ventricular muscle is stimulated w/o signal from the atria

• This causes the ventricular contraction

• Contraction shows up on ECG as a wide & bizarre ectopic beat

• The # of PVCs in a row

  • Considered a “run of vtach”

  • 2 = couples, 3 = triplets

What can PVCs lead to?

vtach, which may then lead to vfib, etc.

What are the causes of PVCs?

• Stress

• Caffeine

• Meds

• Underlying disease

Define Ventricular Tachycardia (VT) in terms of heart rate, presence of P waves, and QRS characteristics.

• > 100 bpm

• P waves are absent

• QRS complexes are wide & abnormal

• All beats are ventricular in nature

What are some causes of vtach?

• MI/ischemia

• Myocarditis/endocarditis

• Cardiac scarring (Sx)

• Conduction disorder

Explain what Torsades de Pointes is.

• Specific form of polymorphic vtach

• Twisting or helical tracings

• Defibrillate

What are some causes of torsades de pointes?

• Myocardial ischemia/MI (most common)

• Long QT syndrome (genetics)

• Electrolyte imbalances

• Meds

What is the purpose of cardioversion?

delivers low-energy shocks to the ♥ to restore an arrhythmia

What types of rhythms can be cardioverted?

• A-fib

• Atrial flutter

• SVTs

• Vtach

• Vfib

Describe the difference between synchronized and unsynchronized cardioversion.

• Synchronized: Shocks are delivered in a very precise point & time + synchronizes with pt’s rhythm

• Unsynchronized: Delivers a not-so precise & not synchronized shock + must be correct amount of electricity & given at the right time

What must be present in order to defibrilate?

a true rhythm

What are 2 nonshockable rhythms?

asystole & pulseless electrical activity (PEA)

What do you do for nonshockable rhythms?

ACLS, CPR, or admin epinephrine

What does PEA look like?

can look like a normal rhythm, would never know the pt has no pulse

How does an Automated External Defibrillator (AED) work, and what are the basic steps for its use?

• Step 1: turn on AED

• Step 2: place pads on pt in correct locations

  • Shave any hair & pat site with towel if sweaty

• Step 3: follow AED instructions

Explain the functions of an Implantable Cardioverter Defibrillator (ICD) and the settings it can have.

it can cardiovert (administers precise low-energy shocks) & defibrilate (shocks a dangerous [or potentially] rhythm)

• has settings to control at what HR to start cardioverting (shock zones)

What is the role of an Implantable Pacemaker, and how does it function when a patient's heart rate falls below certain parameters?

it paces the ♥ following provided parameters & starts functioning when the HR goes below parameters

What is an ablation procedure and how does it treat arrhythmias?

• Problem areas of electrical misfiring are shocked/ablated until the tissue no longer creates impulses

• Can be used to help treat majority of SVT-based conditions

What is heart failure, and what does it involve in terms of the heart's ability to function?

The inability of the ♥ to pump sufficient blood to meet needs of the tissues (CO is not high enough)

Explain what ejection fraction (EF) measures.

fraction of blood ejected out of the left ventricle during systole vs. how much is left in the ventricle after systole; the higher the more efficient

What is the normal ejection fraction range?

50-70%

What is the formula for ejection fraction?

stroke volume / end diastolic volume

What is the formula for stroke volume?

end diastolic - end systolic

Define heart failure with preserved ejection fraction (HFpEF)

the ♥ muscle contracts normally, but the ventricles don’t relax as they should during ventricular filling; aka diastolic HF

Define heart failure with reduced ejection fraction (HFrEF)

the ♥ muscle doesn’t contract effectively, therefore less oxygenated blood is pumped out to the body; aka systolic HF

What are some of the common causes or etiologies of heart failure?

• Ischemic ♥ disease

• MI

• Myocarditis

• Peripartum cardiomyopathy

• Stress cardiomyopathy

• Genetic ♥ disease

• Infiltrative ♥ disease

• Chemotherapy/cardiotoxic meds

• HTN

List the risk factors associated with heart failure, both non-modifiable and modifiable.

• CAD

• Diabetes

• HTN

• Obesity

• Valvular ♥ disease

• Race (African Amer: 70% ⬆)

• Hx of MI

• Sleep apnea

• Smoking

• Alcohol

• Increasing age

• Familial Hx (immediate)

• Gender (men: lower survival)

Describe the pathophysiology of heart failure with preserved ejection fraction (HFpEF) as explained in the text.

it can be 1 of 2 issues, or can be both:

• Stiff ventricles leads to less stretch, thus an inability to accommodate adequate volumes of blood

• Ventricle hypertrophy & reduced chamber size lead to reduced space/volume for blood

What does less blood volume in the left ventricle lead to?

less CO, even in the presence of strong ventricular contractions

How is the EF in HFpEF (diastolic)?

normal despite reduced CO

Which gallop is specific to HFpEF (diastolic)?

S4

What is the pathophysiology of heart failure with reduced ejection fraction (HFrEF)?

The ♥ cannot contract with enough force to meet the systemic needs

Progression to systolic HF:

• Ventricular remodeling → dilation → dysfunction → Reduced EF

Which gallop is specific to HFrEF (systolic)?

S3

What are some compensatory mechanisms of heart failure?

RAAS system activation & sympathetic nervous system

How do compensatory mechanisms, such as the RAAS system and sympathetic nervous system, come into play in heart failure, and what are their effects on the heart?

• These mechanisms ⬆ BP & blood volume, therefore ⬆ ♥ strain

• ♥ will eventually “gas out” which is why pts with chronic HF are given an estimated time to life

How does the RAAS system activate during HF?

juxtaglomerular cells/apparatus (inside of Bowman’s Capsule within the kidneys) sense low sodium chloride concentration & low BP, releasing renin

Renin is converted into angiotensin II, causing sympathetic response, increased sodium retention, stimulates aldosterone secretion, stimulates ADH secretion

• Sympathetic response — vasoconstriction, ⬆ HR

• Aldosterone — leads to sodium reabsorption (water retention)

• ADH — causes ⬆ water reabsorption in collecting ducts in kidneys

How does the sympathetic nervous system activate during HF?

baroreceptors in aortic arch receive less stimulation with reduction in BP, so increasing sympathetic activity & decreasing parasympathetic activity leads to ⬆ HR, contractility & vasoconstriction

What are some of the common manifestations and symptoms of heart failure?

• Dyspnea

• Fatigue

• Edema

• Coughing or wheezing

• Tachycardia

• Ascites

• S3 (vent gallop)

• Nausea, lack of appetite

• Confusion

• Weight gain

• Anorexia

• Nocturia

• Angina

• JVD

What are some symptoms of left sided HF?

• Orthopnea & dyspnea

• Low O2 sat

• Crackles & wheezing

• Blood-tinged sputum

• Cough

• Tachycardia

• Decreased EF

What are some symptoms of right sided HF?

• Weakness/fatigue

• Ascites

• Splenomegaly & hepatomegaly

• Dependent edema

• JVD

• Weight gain

• Anorexia & nausea

What are some ways to manage HF?

Best outcome involves fixing underlying pathologies (i.e. diseased ♥ valves, coronary artery bypass surgery or PCI for CAD)

• O2 admin — to ⬇ oxygen demand & supply

• Diuretics — loop, thiazides, potassium sparing

• CCBs (HFpEF/diastolic) — blocks calcium from entering ♥, causing it to squeeze harder during systole; also blocks calcium in arteries causing vasodilation & ⬇ BP (reduced workload on ♥) not for systolic HF

• ACE inhibitors & ARBs — induce vasodilation & ⬇ BP

• Digoxin — ⬆ contraction, regulates rhythm

• Implantable cardioverter-defibrillator (ICD)

• Ventricular assistive devices (VADs)

• ♥ transplant

What is HF care centered around?

improving functional status (quality of life), extending survival & relieving client symptoms (quality of life)

What are the 2 classifications of acute heart failure?

• Acute decompensation heart failure (ADHF)

• De novo acute heart failure

Define acute decompensation heart failure (ADHF)

considered to be acute on chronic, a rapid ⬇ in CO in existing HF pts

Define de novo acute heart failure

occurs in those with 0 Hx of ♥ disease

What distinguishes acute heart failure from chronic heart failure?

acute HF has a sudden, rapid onset

What are some of the potential causes or etiologies of acute heart failure?

• Advanced kidney disease

• Alcoholism

• Pulmonary embolism

• Diabetes

• HTN & HT crisis

• Hyperthyroidism

• Sleep apnea

• Stroke (ischemic & hemorrhagic)

• Viral ♥ infections

• Exacerbations of existing ♥ disease (CAD, valvular disease)

• Dysrhythmias

Mention some of the diagnostic tests or procedures that can help diagnose acute heart failure.

• BNP

• Electrocardiogram (ECG)

• Chest x ray

• Echocardiogram

• Catheterization

What does BNP determine?

fluid volume status (stretch)

What does ECG determine as far as acute HF?

if cause of acute HF is anything electrophysiology-related

What does chest x-ray determine as far as HF?

cardiomegaly & pulmonary edema

What does echocardiogram determine?

EF & potential cause (valvular, muscular, etc.)

What does catheterization determine as far as HF?

if cause is from coronary artery origins

Define cardiogenic shock

lack of perfusion to the body caused by the heart

What are the medications and interventions for cardiogenic shock?

• Vasopressors — dopamine, epinephrine, norepinephrine

• Inotropic — dobutamine, dopamine, milrinone (PDE3 inhibitor)

  • Inotropic = ⬆ or ⬇ muscle contractions, in this case we would need to ⬆ in order to increase CO

• Fluid resuscitation — NS, LR, albumin (be careful because you can easily overload the ♥)

What is the function of an ECMO (Extracorporeal Membrane Oxygenation) machine?

• Pumps blood throughout the body (helpful in HF)

• Oxygenates the blood (helpful in acute pulmonary conditions)

What is arteriosclerosis, and what are the types?

hardening of the arteries

• atherosclerosis

• arteriolosclerosis

• monckeberg

Define atherosclerosis

arteries develop plaque deposits, which lead to hardening & narrowing

Define arteriolosclerosis

same as atherosclerosis but it affects the smaller arteries

Define monckeberg

calcium build up in the middle layer of artery wall

What is the word for deposited plaque?

atheromas

Describe what effects atherosclerosis has on arterial walls

arterial wall hardness + ⬇ lumen size = CV complications (⬇ blood flow)

Pathophysiology of atherosclerosis: First step

fatty streaks of lipids deposit into arterial wall

Pathophysiology of atherosclerosis: What occurs after the fatty streaks are deposited into the arterial wall?

immune inflammatory response in the form of WBCs

Pathophysiology of atherosclerosis: Fatty streaks → WBC immune inflammatory response → _____?

WBCs ingest the lipids through phagocytosis & turn themselves into foam cells

Pathophysiology of atherosclerosis: Fatty streaks → WBC immune inflammatory response → WBCs ingest lipids & turn into foam cells → _____?

diseased foam cells release toxic substances contributing to endothelial damage

Pathophysiology of atherosclerosis: Fatty streaks → WBC immune inflammatory response → WBCs ingest lipids & turn into foam cells → diseased foam cells release toxic substances contributing to endothelial damage → _____?

platelets respond to endothelial damage by forming fibrous caps

Pathophysiology of atherosclerosis: Fatty streaks → WBC immune inflammatory response → WBCs ingest lipids & turn into foam cells → diseased foam cells release toxic substances contributing to endothelial damage → platelets respond by forming fibrous caps → ____?

fibrous caps take up volume within endothelium to ⬇ arterial wall lumen space

Pathophysiology of atherosclerosis: Fatty streaks → WBC immune inflammatory response → WBCs ingest lipids & turn into foam cells → diseased foam cells release toxic substances contributing to endothelial damage → platelets respond by forming fibrous caps → fibrous caps decrease lumen space → _____?

fibrous caps & atheroma break off & cause an embolus

Complete pathophysiology of atherosclerosis

Fatty streaks → WBC immune inflammatory response → WBCs ingest lipids & turn into foam cells → diseased foam cells release toxic substances contributing to endothelial damage → platelets respond by forming fibrous caps → fibrous caps decrease lumen space → fibrous caps & atheroma break off & cause an embolus

What are the risk factors for atherosclerosis, both non-modifiable and modifiable?

• Non modifiable

  • Increasing age

  • Gender (men)

  • Fam Hx/genetics

  • Race (African Amer, Mexican Amer, Native/Asian Amer)

• Modifiable

  • Comorbidities (HTN, dyslipidemia, diabetes mellitus)

  • Smoking & tobacco use

  • Diet (⬆ in fat, salt)

  • Lack of exercise

  • Obesity

  • Stress

  • Metabolic syndrome (HTN, cholesterol, lipids, obesity, diabetes)

What complications can arise with atherosclerosis in the heart?

ACS (unstable angina, NSTEMI, STEMI), stable angina

What complications can arise with atherosclerosis in the extremities?

PAD, arterial wounds

What complications can arise with atherosclerosis in the neck (carotids)?

vision loss, carotid sinus syndrome (CSS)

What complications can arise with atherosclerosis in the brain?

transient ischemic attacks (TIAs), cerebral infections (stroke), vascular dementia

What complications can arise with atherosclerosis in the kidneys?

kidney hypoperfusion, CKD

What complications can arise with atherosclerosis in the intestines?

mesenteric artery ischemia (only 30%-50% survival rate)

What complications can arise with atherosclerosis in the reproductive organs?

erectile dysfunction (ED)

Define metabolic syndrome

a group of conditions that together raise your risk of CAD, diabetes, stroke, etc.

What is the criteria for metabolic syndrome?

• elevated waist circumference

• elevated triglycerides

• reduced HDL-C

• elevated BP

• elevated fasting glucose