cardiac disorders

how does the heart change with age?

1. lipofuscin accumulation

   • protein that makes cell ineffective → cell death

2. interstitial fibrosis

   • free radical damage

3. collagen crosslinking

   • heart becomes less elastic → Decreases stretch = contract interruption

4. amyloid accumulation

   • stresses cells → dysfunction

how does the heart valve change with age

• mild fibrosis

• calcification

• focal thickening

• makes it harder to open/close

what are general cardiovascular changes with aging

1. decrease in cardiac reserve

2. increase in workload of the heart

   • blood vessel changes → increase TPR → increase afterload → increase workload )

3. conduction abnormalities

   • ex. arrhythmias

4. decrease in maximal achievable HR

how do the blood vessels change with age

1. loss of elasticity

2. collagen fixation

3. fibrosis

4. smooth muscle proliferation and calcification

• increases ability to get HTN

  • easier for constriction

auscultation

• diagnostic test

  • listens to heart for turbulent blood flow (Laminar blood flow cannot be heard)

  • valvular abnormalities → murmurs

what condition does an auscultation detect?

• turbulent blood flow

  • stenosis of superficial vessels

  • heart murmurs / valvular abnormalites

chest rays

• diagnostic test

  • determine shape + size of heart

  • show silhouettes/size of heart

what conditions do chest x-rays detect?

1. cardiomegaly

   • enlarged heart

2. left/right ventricular hypertrophy

   • increased muscle thickness (Cardiomyocytes can not divide)

3. pulmonary congestion

   • opacities = fluid build up from heart failure

4. calcifications in the heart

what conditions does an electrocardiogram (ECG) detect?

1. cardiac arrhythmias

2. myocardial infarctions

3. inflammation of the heart/pericardium

holter monitor

• at home device version of electrocardiogram

what are the 2 types of echocardiogram

1. transthoracic echocardiogram (TTE)

   • across the chest

2. transesophageal echocardiogram (TEE)

   • through esophagus

echocardiogram

• give info about size of heart, chambers, and movement of heart valves

  • can see the opening/closing of valves

definition of stress tests

• assesses general cardiovascular function

  • how does the heart respond to stress or increase demand

  • uses echocardiogram to see

  • may or may not inject radioisotope (ex. thallium)

what are the 2 types of stress tests?

1. exercise

   • bicycle, stairs, or treadmill

2. non-exercise

   • uses drugs like adenosine + persantine to simulate what happens in the heart during exercise

what conditions does a stress test detect?

• selective coronary dilation

  • no dilation = blockage/active atherosclerosis

cardiac catherization

• tread a catheter into the heart + Inject dye → visualize coronary arteries, heart valves, and heart muscle

• measure pressures within the heart

what heart pressures does a cardiac catherization measure

1. central venous pressure

   • pressure in vena cava + Amount of blood returning to the heart

2. pulmonary capillary wedge pressure

   • pressure in pulmonary artery → Elevated in pulmonary edema

angiography

• assess coronary artery blood flow

  • use radio-opaque dye + imaging technique (CT/MRI)

• usually in combination with cardiac catherization

what conditions do angiography detect?

• occlusions in all types of blood vessels

  • includes cerebral vessels

doppler studies

• use sound waves to evaluate how blood flows through a vessel

what conditions do doppler studies detect?

• occlusions in blood vessels (Ex. DVT)

• venous insufficiency

what substances do blood tests look for?

• serum triglyceride + cholesterol levels

• electrolytes

• arterial blood gases (O2 saturation, acid-base balance)

• high sensitivity c-reactive protein (hs-CRP)

high sensitivity c-reactive protein (hs-CRP) marks what?

• general marker of inflammation and infection

• high CRP = increased risk for cardiovascular disease

 Describe the general dietary and lifestyle changes that can help prevent many cardiovascular disorders, or at least delay the progression of certain existing cardiovascular conditions.

1. low fat diet

   • decrease saturated fat intake (animal fat)

   • decrease trans fats (hydrogenated fat)

2. low sodium intake

   • bc salt increases osmolality → Increases ADH → increases blood volume → increases BP

3. increased omega 3 fatty acid intake

   • omega 3s are anti-inflammatory

4. regular exercise

5. cessation of smoking

6. control diabetes

what causes advanced glycation and products (AGEs)

• from sustained hyperglycemia

• nonenzymatic process

advanced glycation and products (AGEs) process

1. AGEs bind to AGER and RAGE (receptors)

2. releases MAPK, NF-kB, JAK/STAT

advanced glycation and products (AGEs) can cause…

1. nephropathy

2. retinopathy

3. neuropathy

4. atherosclerosis

5. cardiomyopathy

increase of lipoproteins has a strong association with …

• accelerated/premature development of cardiovascular disease (specifically atherosclerosis )

what is the rate limiting step in cholesterol synthesis?

• HMG-CoA Reductase

  • HMG-CoA → mevalonate

what are the 5 types of lipoproteins

1. chylomicrons

   • absorb fats in small intestine

2. VLDL

3. IDL

4. LDL

   • bad cholesterol when oxidized

5. HDL

   • good cholesterol → removes cholesterol in blood vessel walls

list the 2 pathways involved in lipid synthesis and storage

1. exogenous pathway

   • diet → Intestine → liver

2. endogenous pathway

   • liver → synthesizes/uses lipids to make bile

exogenous pathway for lipid synthesis and storage

1. dietary fat and cholesterol digested by small intestine→

2. produce chylomicrons absorbed by lymph →

3. travel in blood →

4. lipoprotein lipase →

5. break down some of the triacyl glycerides → glycerol and fatty acids

   • glycerol → goes back to liver

   • fatty acids → beta oxidation → energy OR stored by adipocytes

6. chylomicron remnants (removed a lot of triacylglyerols) → liver

7. liver uses them to make cholesterol or bile

endogenous pathway for lipid synthesis

1. liver makes VLDL →

2. travels in blood →

3. lipoprotein lipase acts on VLDL →

4. break down some of the triacyl glycerides → glycerol and fatty acids

   • glycerol → goes back to liver

   • fatty acids → beta oxidation → energy OR stored by adipocytes

5. IDL (remnants) → lipoprotein lipase →

6. LDL →

7. peripheral tissues can take up LDL to be used

8. OR IDL → lipoprotein lipase→ HDL

HDL

• heterogenous small particles

• cholesterol esters + various proteins

• retrieves cholesterol from periphery + return to liver

• antiatherogenic

HDL process

• reverse cholesterol transport

  • enters endothelial cells

  • picks up esters

  • circulation

  • liver

  • break down cholesterol esters

coronary heart disease includes …

1. angina pectoris

2. myocardial infarction

angina pectoris

• temporary ischemic episode → causes chest pain

  • because of narrowing of blood vessels

  • oxygen demand > o2 supply

• cardiac muscles switch to anaerobic respiration → lactic acid → pain

• SYMPTOM

myocardial infarction

• COMPLETE OCCLUSION

• damage of myocardium due to coronary vessel occlusion, inflammation, and plaque instability → cell death (Myocardium) because of ischemia

• myocardial cells get replaced by scar tissue (hypokinetic)

• more PERMANENT

in theory, angina pectoris can be corrected by either…

1. decrease O2 demand

   • avoid activity (decrease activity = decrease demand)

2. increase O2 supply

   • ssels use nitroglycerin → dilate blood vessels

increased O2 demand in the normal heart are counteracted by …

• increased coronary blood flow

atheroma

• plaques within blood vessels containing lipids, cells, fibrin, and/or thrombi on their surface

list the 3 types of angina

1. stable angina/atherosclerotic/classic

2. vasospastic angina /variant angina / Prinzmetal’s angina

3. unstable angina/crescendo/ACS

atherosclerotic angina

• also known as stable angina

• most common

• lipid deposition in walls / plaques → partial occlusions of coronary arteries → Ischemia

  • increased demand for O2 → chest pain

• stable for many years or may deteriorate into unstable angina

what can help with stable angina

• pain relieved by a few minutes of rest

  • nitroglycerin can also help → decrease demand + relieve pain

vasospastic angina

• due to reversible spasm of coronaries usually at site of a plaque

  • sudden spasms/constrictions of coronary arteries

  • can happen at any time

• may occur during sleep

• can deteriorate into unstable angina

unstable angina

• increased frequency + severity

  • repeated episodes of diminished blood flow from plaques

• immediate precursor of an MI

• medical emergency

what type of angina is the immediate precursor of an MI

• unstable angina / crescendo /ACS

what is arteriosclerosis

• any change in normal structure of arteries

  • loss of elasticity

  • thickening of the artery walls

  • narrowing of the lumen

  • happens in age + diabetes

what is atherosclerosis

• deposition of fat into endothelial layer of the arteries → plaques

fibrous cap

• keeps the plaque from rupturing

• but buildup of free radicals + necrotic cells → rupture of fibrous cap

what substance is a good predictor for atherosclerosis ?

• c-reactive protein

atherosclerotic plaque development

1. LDL binds to receptors on surface of cell wall →

2. cell-receptor mediated endocytosis to bring LDL into subendothelial layer →

3. ROS oxidize LDL →

4. oxidized LDL binds to LOX-1 receptors on macrophages →

5. phagocytosis →

6. foam cell formation →

7. release pro-inflammatory cytokines →

8. release GF, PDGF, bFGF →

9. bFGF → stimulates fibrous cap, proteolyiss + Apoptosis + migrate to form lipid-rich necrotic core

what happens when the fibrous cap starts to weaken?

• shedding of endothelial cells → blood in contact with subendothelial layer (Collagen) → forms thrombus

what type of drugs can help decrease LDL / oxidized LDL

• statins

with a pt with heart attack experience, to prevent thrombus formation, you should give them what type of drug?

• antiplatelets

partial occlusion in the brain causes ____, while a complete occlusion in the brain causes ____

1. transient ischemic attack (TIA)

2. cerebral vascular accident (CVA) / stroke

atherosclerosis in the aorta can cause …

an aneurysm (weakened walls)

atherosclerosis in the legs can cause …

• peripheral vascular disease → ischemia, gangrene → possible amputation (severe)

what are 2 types of surgeries that can help treat CAD

1. angioplasty

2. coronary artery bypass graft (CABG)

angioplasty

• surgery for CAD treatment

• use catheter in femoral artery → clogged coronary artery → inflate balloon at occlusion site → smooshes plaque

  • can damage endothelial cells → still lead to occlusions

• with/without stent

  • stent = metal mesh inserted to keep vessel open (can still restenosis over time)

  • can be covered with drug to help more

coronary artery bypass graft (CABG)

• open heart surgery for CAD treatment

  • only used for failed stents or extensive blood vessel occlusions

• take blood vessel from arm → connect to artery → make new conduit to bypass blockage

general drug classes for CAD treatment

1. antihyperlipidemic

   • lower cholesterol

2. anti-platelets

   • arterial clots

3. anticoagulants

   • venous clots

4. antihypertensives

   • decrease BP → decrease workload on the heart

5. antihyperglycemics

the most common cause of myocardial infarction is …

• atherosclerosis

• less frequent:

  • embolus

  • sickle cell crisis

some signs/symptoms of myocardial infarction include

• pain

  • chest pain

  • left arm pain, shoulder, jaw, back, etc (referred pain)

• shortness of breath

• diaphoresis

• weakness + fatigue

• nausea, indigestion

• anxiety, fear

• pallor

what are the diagnostic tests for MI

1. ECG changes

   • STEMI

   • nSTEMI

2. measure serum cardiac markers

   • CPK-MB

   • troponin T + I

   • (both released w/ cell death)

STEMI vs nSTEMI on an ECG

• STEMI

  • complete + prolonged coronary blood occlusion

  • ST elevation

• nSTEMI

  • severe narrowing → thrombus

  • ST depression

• both = indicators for MI

possible complications of MIs

• death

• cardiac arrhythmias

• cardiogenic shock

• congestive heart failure

• rupture of necrotic heart tissue

• mural thrombus

what are the general treatment strategies for MI

1. reperfusion (restore blood flow)

   • thrombolytics

   • angioplasty

   • CABG

2. other (depending on individual presentation)

   • antiarrhythmics

   • defibrillation

   • pacemaker

what are cardiac arrhythmias?

• any change in the normal rate or rhythm of the heart (electrical activity is not correct)

  • decreases the heart’s ability to pump blood

what are the 2 types of arrhythmias

1. supraventricular arrythmias

   • sinus node abnormalities

   • atrial conduction abnormalities

   • AV node abnormalities (heart block)

2. ventricular conduction abnormalities

what are the different types of supraventricular arrhythmias

1. sinus node abnormalities

2. atrial conduction abnormalities

3. AV node abnormalities (heart block)

why is AV node abnormalities called a heart block

• AV node is unable to transfer electrical activity → ventricle

which is worse? supraventricular arrhythmias ? or ventricular conduction abnormalities?

• ventricular conduction abnormalities

what is reentry

• region of myocardium = damaged

• electrical pathway = slowed

  • 1 AP = multiple contractions (atria is not in the absolute refractory period) → can be restimulated

• can be global or local

sinus node abnormalities

• SA = pacemaker → Problems will affect HR

• bradycardia or tachycardia

bradycardia

• regular rhythm but slow

• <60 BPM (except for athletes)

tachycardia

• regular rhythm but fast

• 100-160 BPM

sick sinus syndrome

• sinus node abnormality

• alternating bradycardia and tachycardia

T/F: you can treat sick sinus syndrome with drugs

false

• alternating bradycardia and tachycardia (Don’t know which drug to use)

• pacemaker is required

  • FOR LIFE

  • may be replaced for battery reasons

pacemaker

• in chest cavity

  • 1 electrode to atrial wall + ventricular wall

  • sends electrical signals at intervals that mimic SA node

AV conduction abnormalities

• premature atria contractions or beats

  • ectopic beats = region of heart = AP when it SHOULDNT be

• may feel palpitations

• may result from re-entry

atrial flutter

• av conduction abnormality

• fast rhythm, regular rhythm

• ventricles respond to every 2nd /3rd impulse

• usually caused by re-entry

atrial flutter symptoms

• heart palpitations

• shortness of breath

• chest tightness

• fatigue dizziness

atrial fibrillation

• AV conduction abnormality

• multiple ectopic foci → atria quiver

• fast rhythm, irregular rhythmn

• CO compromised as the ventricles dont have enough time to fill

atrial fibrillation symptoms

• heart palpitations

• shortness of breath

• chest tightness

• fatigue

• dizziness

which is worse? atrial flutter or fibrillation?

• atrial fibrillation

aflutter and afib can both cause ….

• thrombi in atria → Cardiac embolic stroke

complications of aflutter and afib

• blood clot formation due to sluggish blood flow/pooling

• high risk of embolic strokes

• require long-term / life long sometimes anticoagulation

heart block

• conduction from the atria to the ventricles is delayed/stopped

• partial block + third degree/total heart block

first degree vs second degree partial heart blocks

• first degree

  • prolongation of PR interval → increase time between atrial and ventricular contractions

• second degree

  • LONGER delay → leads to missed ventricular contraction

what is a third degree/ total heart block

• ZERO transmission from AV → Bundle of His /ventricles

• ventricles take over as pacemakers of the heart

  • 30-45 BPM

• severely compromised CO → syncope/fainting

• can lead to cardiac arrest

• patient needs a pacemaker

wold-parkinson-white syndrome

• congenital accessory conduction pathway

  • second pathway for electrical pathway → tachycardia

treatment for wolf-parkinson-white syndrome

• ablation

  • use laser to cap area causing problem

bundle branch block

• ventricular contraction abnormality

  • problems with electrical conduction in one of the bundle branches

  • bundle of his blocked

• may have no effect on CO

  • depends on location, Purkinje fibers may allow electrical activity to bypass blockage

• wide QRS wave

ventricular tachycardia

• rapid contractions of the ventricles

  • compromised CO due to insufficient time for ventricular filling

  • may require implantable ICD (defibrillator)

implantable ICD (defibrillator)

• implanted in chest

• wries

  • 1 = sensor to detect heart rhythm/rate

  • other = deliver jolt of electricity create normal rhythm

ventricular fibrillation

• ventricular contraction abnormalities

• uncoordinated quivering of the ventricles

  • NO CARDIAC OUTPUT

  • multiple areas have AP → quivering

• myocardial damage due to hypoxia

• requires defibrillation

which cardiac arrhythmias can lead to cardiac arrest.

• ventricular tachycardia

• ventricular fibrillation

premature ventricular contractions

• ventricular contraction abnormalities

  • additional beats from ventricular ectopic focus

  • can be benign or progress → Ventricular fibrillation + cardiac arrest

cardiac arrest

• all activity in the heart stops

  • ECG = FLAT LINE

  • NO CARDIAC OUTPUT → hypoxia =fast

• pt requires resuscitation (CPR)